1/Structure and func ons of respiratory system, signi cance for organism :

The respiratory system is responsible for the exchange of gases between an organism and its environment.

Struture : Nose and Nasal Cavity/ pharynx / larynx / trachea / Bronchi / Lungs / Alveoli

The respiratory system begins with the nose is the primary entrance for air. The nasal cavity lters, warms, and
humidi es the incoming air .The air then passes through the pharynx The trachea is a tube connects the larynx to the
bronchi. The trachea branches into two bronchi, one entering each lung. They are composed of bronchioles, alveolar
ducts, and alveoli.

Func on : Pulmonary Ven la on: The respiratory system facilitates the process of breathing, which involves the
movement of air into and out of the lungs. During inhala on, the diaphragm and intercostal muscles contract, expanding
the thoracic cavity and causing air to be drawn into the lungs. During exhala on, these muscles relax, and air is expelled
Func ons 1. Supplies the body with oxygen and disposes of carbon dioxide 2. Filters inspired air 3. Produces sound 4.
Clears the body from excess water and heat 5. Control blood pH

signi cance for organism *Oxygen Supply : Oxygen is necessary for cellular respiration, which generates
energy for the organism's metabolic activities. *Removal of Carbon Dioxide: The respiratory system helps
eliminate carbon dioxide,*pH Regulation: by controlling the excretion of carbon dioxide, which is an
important component of the body's acid-base balance. Immune Defense: The respiratory system filters,
humidifies, and warms the air, protecting the body from harmful particles, pathogens, and irritants

2/Main stages in the process of respira on. External respira on

The main stages in the process of respiration include:

Breathing (Ventilation):involves the inhalation of oxygen-rich air and the exhalation of

carbon dioxide. It includes the movement of air in and out of the lungs through the
respiratory system.

External Respiration:occurs in the lungs and involves the exchange of gases between the
alveoli and the surrounding capillaries. Oxygen from the inhaled air diffuses across the
thin alveolar walls into the bloodstream, while carbon dioxide moves from the
bloodstream into the alveoli to be exhaled.

Transport of Gases: Oxygen binds to hemoglobin in red blood cells, forming

oxyhemoglobin, and is transported throughout the body via the circulatory system.
Carbon dioxide produced by cells is carried by the bloodstream, mostly in the form of
bicarbonate ions, to the lungs for exhalation.

Internal Respiration:occurs in the body's tissues and involves the exchange of gases
between the systemic capillaries and the cells. Oxygen diffuses from the capillaries into
the cells, where it is utilized in cellular respiration to produce energy (in the form of
ATP) and carbon dioxide as a waste product.

Cellular Respiration:is the process that occurs within the cells to generate energy from
glucose and oxygen. It involves a series of chemical reactions in the mitochondria,
converting glucose and oxygen into carbon dioxide, water, and ATP (adenosine
triphosphate),

*External respiration is the exchange of gases between the external environment and
the lungs. It involves the following stages:

Ventilation: which includes inhalation and exhalation. During inhalation, the diaphragm
and intercostal muscles contract, expanding the thoracic cavity and causing air to enter
the lungs. During exhalation, the diaphragm and intercostal muscles relax, reducing the
volume of the lungs, and air is expelled.
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Pulmonary Gas Exchange: Once air enters the lungs, it reaches the alveoli. The alveolar
walls facilitating the exchange of gases. Oxygen from the inhaled air diffuses across the
alveolar walls into the surrounding capillaries, where it binds to hemoglobin in red blood
cells. At the same time, carbon dioxide, a waste product produced by cells, moves from
the capillaries into the alveoli to be exhaled.

Transportation of Gases: Oxygen molecules attach to hemoglobin in red blood cells,

forming oxyhemoglobin, which is then transported through the bloodstream to the
body's tissues and organs. Carbon dioxide, on the other hand, is mostly transported in
the blood as bicarbonate ions (HCO3-) but can also bind to hemoglobin or dissolve
directly in plasma.

Diffusion: The exchange of gases between the alveoli and the blood occurs via diffusion,
which is the passive movement of molecules from an area of high concentration to an
area of low concentration. Oxygen moves from the alveoli, where its concentration is
higher, to the capillaries, where it is lower. Carbon dioxide, which has a higher
concentration in the capillaries, moves in the opposite direction, from the blood into the
alveoli.

3/Respiratory cycle. Biomechanism of inspira on and expira on

The respiratory cycle refers to the complete sequence of events involved in one breath,
including both inspiration (inhalation) and expiration (exhalation). *Inspiration
(Inhalation):

Diaphragm Contraction: Inspiration begins with the contraction of the diaphragm, a

dome-shaped muscle located at the base of the chest cavity. When the diaphragm
contracts, it moves downward, flattening and increasing the volume of the thoracic
cavity.

Intercostal Muscle Contraction: In addition to the diaphragm, the external intercostal

muscles between the ribs also contract during inspiration. This contraction lifts the
ribcage upward and outward, further expanding the thoracic cavity.

Expansion of the Lungs: As the thoracic cavity expands, the volume of the lungs
increases, causing the pressure inside the lungs to decrease. This drop in pressure
creates a pressure gradient, and air flows from an area of higher pressure (the
atmosphere) to an area of lower pressure (the lungs).

Air Entry: The expansion of the thoracic cavity and the decrease in lung pressure allow
air to enter the respiratory tract. The air passes through the nose or mouth, travels down
the trachea, and enters the bronchial tree, ultimately reaching the alveoli in the lungs.

*Expiration (Exhalation): Diaphragm Relaxation: Expiration begins when the diaphragm

and intercostal muscles relax. The diaphragm moves back to its dome-shaped position,
and the intercostal muscles relax, causing the ribcage to move downward and inward.

Decrease in Thoracic Cavity Volume: The relaxation of the diaphragm and intercostal
muscles reduces the volume of the thoracic cavity. This decrease in volume increases the
pressure within the lungs.

Air Expulsion: As the pressure in the lungs becomes higher than the atmospheric
pressure, air is forced out of the lungs. The air flows from the lungs through the
respiratory tract and exits through the nose or mouth.
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 4/The pressure in the pleural cavity, its changes with breathing.

The pressure in the pleural cavity undergoes changes during the breathing cycle. The
pleural cavity is the space between the two layers of the pleura that covers the lungs
and lines the chest cavity. the pressure in the pleural cavity changes with breathing:

*During Inhalation: At rest, the intrapleural pressure is slightly negative, When the
diaphragm and external intercostal muscles contract during inhalation, the thoracic
cavity expands, causing an increase in the volume of the pleural cavity. As the volume of
the pleural cavity increases, the pressure within it decreases further, reaching a more
negative value.The negative intrapleural pressure helps maintain the lung's adherence to
the chest wall and keeps the lungs inflated by opposing the elastic recoil of the lung
tissue.

*During Exhalation: During normal, passive exhalation, the diaphragm and intercostal
muscles relax. As the thoracic cavity decreases in volume, the pleural cavity volume also
decreases. The reduction in pleural cavity volume leads to a slight increase in the
intrapleural pressure, but it remains negative compared to atmospheric pressure. The
elastic recoil of the lung tissue helps expel air from the lungs.

5/ Pneumothorax, its types. Pneumothorax is a condition characterized by the presence of air

in the pleural cavity, There are several types of pneumothorax:

*Spontaneous Pneumothorax: Primary Spontaneous Pneumothorax: This type occurs in

individuals without any underlying lung disease. It often happens spontaneously,
without any apparent cause

Secondary Spontaneous Pneumothorax: This type occurs in individuals with pre-existing

lung diseases

*Traumatic Pneumothorax: Closed Traumatic Pneumothorax: It occurs due to an injury

or trauma to the chest, such as a fall or a direct blow to the chest. The trauma can cause
a lung injury or damage to the chest wall, leading to air leakage into the pleural cavity.

Open Traumatic Pneumothorax: This type occurs when there is an open chest wound,
such as a penetrating injury from a gunshot or a stabbing. The wound acts as a direct
pathway for air to enter the pleural cavity.

*Tension Pneumothorax: Tension pneumothorax is the most severe form of

pneumothorax. It occurs when air enters the pleural cavity during inhalation but cannot
escape during exhalation

6/ Elas c proper es of lungs and chest. The lungs and chest possess elastic properties that are
essential for the process of breathing. the key elastic properties of the lungs and chest:
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Lung Elasticity: The lung tissue has the ability to stretch and recoil. The elastic fibers
within the lung tissue provide the necessary support and resilience. When the lungs
expand during inhalation, the elastic fibers are stretched, storing potential energy. This
energy is then released during exhalation when the elastic fibers recoil, causing the
lungs to return to their original shape and expel air.

Surface Tension: The alveoli, tiny air sacs within the lungs, are lined with a thin layer of
fluid. This fluid creates surface tension, which is the force that resists the expansion of
the alveoli. Surface tension is necessary to prevent the collapse of the alveoli during
exhalation.

Chest Wall Elasticity: The chest wall, including the ribcage and intercostal muscles,
During inhalation, the contraction of the diaphragm and intercostal muscles causes the
chest wall to expand outward. The elastic recoil of the chest wall during exhalation helps
to reduce the volume of the thoracic cavity,

Pleural Linkage:which lines the lungs and chest wall, plays a crucial role in linking the
elastic properties of the lungs and chest. The pleural membranes are in close contact
with each other.This linkage ensures that the expansion and recoil of the lungs are
transmitted to the chest wall, maintaining coordinated movement during breathing.

7/ The surface tension of alveoli, its origin.

The surface tension of alveoli, is primarily due to the presence of a thin layer of fluid
lining the alveolar walls. This fluid layer consists of a mixture of water and a substance
called pulmonary surfactant. * The origin of the surface tension in alveoli can be
attributed to the well-organized forces between water molecules. Water molecules have
strong attractive forces between them, known as hydrogen bonds. These hydrogen
bonds create surface tension

In the absence of surfactant, the surface tension of the alveoli would be very high,
making it difficult for the alveoli to expand during inhalation. This would result in the
collapse of the alveoli and impair gas exchange in the lungs. However, the presence of
pulmonary surfactant significantly reduces surface tension and prevents alveolar
collapse.

Pulmonary surfactant is a complex mixture of lipids and proteins produced by specialized

cells called type II alveolar cells in the lungs. It is released into the alveolar fluid, where
it spreads across the surface of the alveoli. The surfactant molecules have a hydrophobic
region and a hydrophilic region.

8/ Surfactants, their value Surfactants, including pulmonary surfactant in the lungs, have
significant value and play roles in various aspects of our daily lives and biological
systems. Here are some key values of surfactants:

*Pulmonary surfactant is essential for proper lung function. It reduces the surface
tension in the alveoli, preventing their collapse during exhalation and promoting the
expansion of the lungs during inhalation

*Surfactants are widely used in cleaning products, such as detergents and soaps.
Surfactants act by emulsifying or dispersing oils and other hydrophobic substances,
allowing them to mix with water and be easily washed away.

*Surfactants are commonly found in personal care products, including shampoos, body
washes, and toothpaste. They help to create lather, distribute the product evenly, and
remove dirt, oils, and impurities from the skin, hair, and teeth.
 *Surfactants play a role in the food industry as emulsifiers and stabilizers. They are used
to create and stabilize emulsions in products such as salad dressings, sauces, and
mayonnaise. Surfactants also enhance the texture, appearance, and shelf life of various
food products.

-surfactants have immense value and versatility across various industries and biological
systems. They facilitate important processes, such as lung function, cleaning, personal
care, food production, pharmaceuticals, and industrial applications, making them
integral to many aspects of our daily lives.

9/ Sta c indicators of external respira on. Static indicators of external respiration refer to the
parameters that are measured to assess the efficiency and adequacy of gas exchange in
the lungs. These indicators provide information about the respiratory function at a given
moment and are measured when the individual is at rest. -----static indicators of
external respiration:

*Partial Pressure of Oxygen represents the partial pressure of oxygen dissolved in

arterial blood. It is an indicator of the oxygen level in the blood and reflects how well the
lungs are oxygenating the blood. Normal values for PaO2 range from 75-100 mmHg.

*Partial Pressure of Carbon Dioxide represents the partial pressure of carbon dioxide
dissolved in arterial blood. It indicates the efficiency of carbon dioxide removal by the
lungs. Normal values for PaCO2 range from 35-45 mmHg.

*Oxygen Saturation is a measure of the percentage of hemoglobin in arterial blood that

is bound to oxygen. It represents the oxygen-carrying capacity of the blood and
indicates how well oxygen is being transported to the tissues. Normal values for SaO2
are typically above 95%.

*Arterial Blood Gas Analysis involves measuring the levels of oxygen, carbon dioxide,
pH, and bicarbonate in arterial blood. It provides a comprehensive assessment of acid-
base balance and respiratory function. ABG results are used to evaluate oxygenation,
ventilation, and acid-base status.

*Alveolar-Arterial Oxygen Gradient measures the difference between the partial

pressure of oxygen in the alveoli (PAO2) and the arterial blood (PaO2). It reflects the
efficiency of oxygen diffusion from the alveoli to the blood and helps assess the presence
of any ventilation-perfusion (V/Q) mismatch or lung pathology.

*Respiratory Quotient is the ratio of carbon dioxide production to oxygen consumption.

It provides information about the substrate being metabolized for energy. RQ values can
vary depending on the type of fuel being utilized (e.g., carbohydrates, fats) and can
indicate the metabolic state of the individual.

---help assess the efficiency of gas exchange, oxygenation, and acid-base balance in the
body. They are commonly measured through blood tests, such as arterial blood gas
analysis, and provide valuable information for diagnosing and managing respiratory
disorders.

10/ General characteris cs of the research methods of respira on:

- spirometry, - spirography, - pneumotachometry

Spirometry, spirography, and pneumotachometry are common research methods used to

assess various aspects of respiration. their general characteristics:

*Spirometry is a widely used method to measure lung volumes and airflow. It involves
the use of a spirometer, which is a device that measures the volume of air inspired and
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 expired by a person. Spirometry provides quantitative data on lung function parameters,
including tidal volume, inspiratory reserve volume, expiratory reserve volume, forced
vital capacity , forced expiratory volume in one second, and more. Spirometry is a non-
invasive procedure and is commonly performed in clinical settings to assess lung
function, diagnose respiratory conditions (such as chronic obstructive pulmonary
disease, asthma, or restrictive lung diseases), monitor disease progression, and evaluate
the effectiveness of interventions.

*Spirography, is a graphical representation of lung function obtained during spirometry.

It illustrates the flow rate of air during inspiration and expiration plotted against lung
volume. Spirography provides a visual representation of the airflow patterns and can
help identify abnormalities, such as airflow limitation, obstruction, or restriction.

*Pneumotachometry involves the use of a pneumotachograph or flowmeter to measure

airflow rates during respiration. It utilizes a device that incorporates a flow sensor (such
as a pneumotachograph) placed in line with the airflow. The flow sensor measures the
volume of air passing through it per unit of time, providing real-time airflow data.
Pneumotachometry allows for the assessment of inspiratory and expiratory flow rates

spirometry, spirography, and pneumotachometry are valuable research methods for

studying respiration.

11/ Gas exchange in the lungs.

Gas exchange in the lungs refers to the process by which oxygen is taken in from the
atmosphere and carbon dioxide is removed from the body. This vital process occurs in
the alveoli . how gas exchange occurs in the lungs:

*Breathing is begins with inhalation, where air is drawn into the lungs through the nose
or mouth. The air travels down the trachea and enters the bronchial tubes, which branch
out into tubes called bronchioles. The bronchioles continue to divide into numerous
smaller passageways, eventually leading to alveoli. The walls of the alveoli are
extremely thin and surrounded by a dense network of blood vessels called capillaries. *
Oxygen-rich air in the alveoli comes into contact with the capillaries' walls, which have a
higher concentration of carbon dioxide. Through the process of diffusion, oxygen
molecules move from the alveoli into the capillaries, while carbon dioxide moves in the
opposite direction—diffusing from the capillaries into the alveoli. * Oxygen binds to
hemoglobin in red blood cells, forming oxyhemoglobin. The oxygenated blood then
leaves the lungs and is transported throughout the body via the circulatory system. *
Carbon dioxide, produced as a waste product of cellular respiration, diffuses from the
body's cells into the capillaries. It binds with hemoglobin to form carbaminohemoglobin,
and some of it dissolves directly in the plasma. The deoxygenated blood carrying carbon
dioxide returns to the lungs through the pulmonary arteries.* During exhalation, the
diaphragm and intercostal muscles relax, causing the chest cavity to decrease in size.
This leads to an increase in pressure within the lungs, pushing the air rich in carbon
dioxide out of the alveoli, through the bronchioles, and eventually out of the body
through the nose or mouth.

12/ The composi on of the air exhaled, inhaled, alveolar air.

The composition of the air exhaled, inhaled, and alveolar air differs due to the processes
of gas exchange and the addition of metabolic waste products. *breakdown of the
composition of each type of air:

Inhaled Air:* The inhaled air contains approximately 21% oxygen, which is essential for
cellular respiration and energy production in the body. *Nitrogen (N2) makes up around
78% of the inhaled air and is mostly inert, serving as a diluent gas.*Inhaled air also
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 contains small amounts of other gases like argon, carbon dioxide, neon, helium,
methane, and hydrogen, though these are present in very low concentrations.

Exhaled Air:*The exhaled air still contains some oxygen, although its concentration is
lower compared to inhaled air. It is typically around 16-17% oxygen. * The exhaled air
has a higher concentration of carbon dioxide compared to inhaled air. It usually contains
about 4-5% carbon dioxide, as it is a waste product of cellular respiration. *Exhaled air
is also enriched with water vapor due to the moisture present in the respiratory system.
*Exhaled air may contain traces of other gases present in inhaled air, depending on the
environment and individual factors.

Alveolar Air: *The concentration of oxygen in alveolar air is lower than inhaled air but
higher than exhaled air. It is typically around 13-15% oxygen. *The concentration of
carbon dioxide in alveolar air is higher than inhaled air. It ranges from about 4-6%
carbon dioxide. *Alveolar air is saturated with water vapor, as it comes into contact with
moist surfaces in the respiratory system. *Alveolar air may contain traces of other gases
found in inhaled air, including nitrogen and small amounts of other gases like argon and
neon.

13/ The rela ve constancy of the composi on of alveolar air.

The composition of alveolar air is relatively constant due to several factors that help
maintain a stable balance of gases. This relative constancy is important to ensure
efficient gas exchange in the lungs. Here are the key factors contributing to the stability
of alveolar air composition:

*Ventilation-Perfusion Matching: The process of ventilation refers to the movement of

air in and out of the lungs, while perfusion refers to the blood flow through the
pulmonary capillaries. The lungs regulate ventilation and perfusion to maintain a
balance. This matching of ventilation and perfusion helps maintain the composition of
alveolar air.

*Breathing Control: The respiratory control centers in the brainstem, particularly the
medulla oblongata, monitor and regulate the rate and depth of breathing to maintain the
appropriate levels of oxygen and carbon dioxide in the alveoli. Feedback mechanisms
involving chemoreceptors detect changes in the blood's oxygen and carbon dioxide
levels and adjust breathing accordingly to maintain homeostasis.

*Gas Exchange Efficiency: The thin walls of the alveoli and the surrounding capillaries
facilitate efficient gas exchange. The large surface area and short diffusion distance
between the alveoli and capillaries promote rapid diffusion of oxygen from the alveoli
into the blood and carbon dioxide from the blood into the alveoli. This efficiency helps
maintain the relative constancy of alveolar air composition.

*Buffering Capacity: The blood's buffering capacity plays a role in maintaining the
constancy of alveolar air composition. Carbonic acid-bicarbonate buffering system helps
regulate the pH of the blood, preventing significant changes caused by the production of
carbon dioxide during cellular respiration. This buffering capacity helps stabilize the
concentration of carbon dioxide in the alveolar air.

*Physiological Adaptations: The body has physiological adaptations that optimize gas
exchange in the lungs. For example, the presence of surfactant in the alveoli reduces
surface tension, preventing alveolar collapse and improving gas exchange. Additionally,
the alveolar-capillary membrane's selective permeability allows for efficient diffusion of
gases while minimizing the transfer of other substances.

14/ The par al pressure of gases in the alveolar air (PCO2, PO2).
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The partial pressure of gases in the alveolar air refers to the pressure exerted by each
gas within the alveoli. The partial pressures of carbon dioxide and oxygen in alveolar air
are crucial for efficient gas exchange. The typical values for partial pressures of gases in
alveolar air at sea level, breathing ambient air,:

*Partial Pressure of Carbon Dioxide in alveolar air is around 40(millimeters of mercury)

or 5.3(kilopascals). This represents the equilibrium between carbon dioxide production
through cellular metabolism and its removal through respiration.

*Partial Pressure of Oxygen in alveolar air is approximately 100 mmHg (13.3 kPa) at sea
level. This oxygen partial pressure is sufficient to facilitate diffusion of oxygen from the
alveoli into the pulmonary capillaries, allowing for oxygenation of the blood.

-the partial pressures of gases can vary depending on factors such as altitude, inspired
air composition, and individual physiological conditions.

15/ Tension of gases dissolved in the blood

The tension of gases dissolved in the blood refers to the partial pressures of gases
dissolved in the plasma component of the blood. The two main gases of interest are
oxygen and carbon dioxide . The tensions of these gases are important for gas exchange
between the alveoli in the lungs and the tissues throughout the body.

*Oxygen Tension: Oxygen is carried in the blood primarily bound to hemoglobin in red
blood cells, but a small amount is also dissolved directly in the plasma. The oxygen
tension indicates the partial pressure of oxygen dissolved in the blood. In arterial blood
leaving the lungs, the PO2 is typically around 100(millimeters of mercury) or 13.3 kPa.
As blood circulates through the body and oxygen is delivered to tissues, the PO2
decreases.

*Carbon Dioxide Tension : refers to the partial pressure of dissolved carbon dioxide in
the blood. In arterial blood leaving the tissues, the PCO2 is typically around 40 mmHg or
5.3 kPa. As blood returns to the lungs, the PCO2 increases as carbon dioxide is
eliminated during exhalation.

-are influenced by various factors such as metabolic rate, ventilation, and overall health
conditions.

16/ The mechanism of gas exchange in the lungs.

The mechanism of gas exchange in the lungs involves several processes that allow for
the exchange of oxygen and carbon dioxide between the alveoli in the lungs and the
surrounding pulmonary capillaries. *step-by-step the gas exchange mechanism:

*Pulmonary Ventilation: The process begins with breathing. During inhalation, the
diaphragm and intercostal muscles contract, expanding the chest cavity and creating a
pressure gradient. This causes air to flow into the lungs, filling the alveoli with fresh
atmospheric air.

*Diffusion of Gases: Oxygen in the inhaled air diffuses across the walls of the alveoli and
into the surrounding pulmonary capillaries. This diffusion occurs due to the difference in
partial pressure of oxygen between the alveoli (high PO2) and the capillaries (lower
PO2). Simultaneously, carbon dioxide, produced as a waste product by the body's cells,
diffuses in the opposite direction—moving from the capillaries into the alveoli—due to
the difference in partial pressure of carbon dioxide (high PCO2 in capillaries, lower PCO2
in alveoli).
 *Oxygen Transport: Once in the pulmonary capillaries, oxygen molecules bind to
hemoglobin within red blood cells, forming oxyhemoglobin. The oxygenated blood then
leaves the lungs and is transported through the systemic circulation, delivering oxygen
to tissues and cells throughout the body.

*Carbon Dioxide Elimination: In the systemic capillaries, carbon dioxide produced by

cellular metabolism diffuses from the tissues into the blood. Some of it combines with
water in the red blood cells to form carbonic acid (H2CO3), which quickly dissociates into
bicarbonate ions (HCO3-) and hydrogen ions (H+). Bicarbonate ions are transported
back into the plasma, while hydrogen ions bind to hemoglobin or are buffered by other
substances. As blood returns to the lungs, the carbon dioxide-rich blood enters the
pulmonary capillaries.

*During exhalation, the diaphragm and intercostal muscles relax, causing the chest
cavity to decrease in size. This leads to an increase in pressure within the lungs, forcing
air rich in carbon dioxide out of the alveoli, through the bronchial tree, and eventually
out of the body through the nose or mouth. This process removes the carbon dioxide
waste from the body.

17/ Di usion capacity of the lungs.

The diffusion capacity of the lungs, refers to the ability of the lungs to facilitate the
diffusion of gases, particularly oxygen and carbon dioxide, across the alveolar-capillary
membrane. It quantifies the efficiency of gas exchange in the lungs. The diffusion
capacity is typically measured by a pulmonary function test called the single-breath
carbon monoxide diffusing capacity (DLCO) Several factors can influence the diffusion
capacity of the lungs, including:

*The diffusion capacity is dependent on the surface area available for gas exchange.
Conditions that reduce the effective surface area, such as lung damage, scarring, or
reduced alveolar surface, can decrease the diffusion capacity.

*thickness of the alveolar-capillary membrane plays a crucial role in gas exchange. Any
thickening or damage to the membrane can impair diffusion and reduce the diffusion
capacity.

*The diffusion capacity is influenced by the concentration of hemoglobin in the blood.

Hemoglobin carries oxygen, and its presence affects the uptake and release of gases
during diffusion.

*Pulmonary Blood Flow: Adequate blood flow through the pulmonary capillaries is
necessary for efficient gas exchange. Any factors that affect pulmonary blood flow, such
as pulmonary hypertension or pulmonary embolism, can impact the diffusion capacity.

*The lung volume, specifically the volume of air in the alveoli, can affect the diffusion
capacity. Changes in lung volume, such as restrictive lung diseases or conditions that
affect lung compliance, can alter the diffusion capacity.

18/ The rela onship between pulmonary circula on and ven la on of the lungs.

Pulmonary circulation and ventilation of the lungs are closely interconnected processes
that work together to facilitate efficient gas exchange. Here's an overview of their
relationship:

*Pulmonary circulation refers to the circulation of blood between the heart and the
lungs. It involves the flow of blood from the right side of the heart (right ventricle) to
the lungs and back to the left side of the heart (left atrium).
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*Ventilation involves the movement of air in and out of the lungs. It is the process by
which fresh oxygen is brought into the lungs, and carbon dioxide, a waste product, is
expelled from the lungs.

The relationship between pulmonary circulation and ventilation can be understood

through the following points:

*The primary function of pulmonary circulation is to oxygenate deoxygenated blood and

remove carbon dioxide. During inhalation, oxygen-rich air enters the lungs, and oxygen
diffuses from the alveoli into the pulmonary capillaries. At the same time, carbon dioxide
diffuses from the capillaries into the alveoli, ready to be exhaled during exhalation.

*The alveoli are the sites where gas exchange takes place. Ventilation ensures that fresh
air rich in oxygen is constantly brought into contact with the alveoli, allowing for
efficient diffusion of oxygen into the pulmonary capillaries and carbon dioxide out of the
capillaries into the alveoli. This gas exchange is facilitated by the proximity of the alveoli
to the surrounding pulmonary capillaries, creating a large surface area for diffusion.

*Pulmonary Blood Flow: Ventilation is closely linked to pulmonary blood flow. As air
enters the lungs during inhalation, it reaches the alveoli, creating an oxygen-rich
environment. Simultaneously, deoxygenated blood from the right side of the heart is
pumped into the pulmonary arteries, which branch into a network of capillaries
surrounding the alveoli. The oxygen-depleted blood releases carbon dioxide into the
alveoli and takes up oxygen through diffusion. Oxygenated blood then returns to the left
side of the heart via the pulmonary veins.

*The regulation of ventilation and pulmonary blood flow is coordinated to ensure

efficient gas exchange. Ventilation is controlled by the respiratory centers in the brain,
which adjust the rate and depth of breathing based on the body's oxygen and carbon
dioxide levels. Pulmonary blood flow is regulated by factors such as the diameter of
pulmonary blood vessels,

19/ Anatomical and physiological "dead spaces"

Anatomical and physiological "dead spaces" refer to areas within the respiratory system
where gas exchange does not occur efficiently. These spaces are not involved in the
exchange of oxygen and carbon dioxide between the alveoli and the pulmonary
capillaries.

*Anatomical dead space refers to the portion of the respiratory system where no gas
exchange occurs. It includes the conducting airways, such as the trachea, bronchi, and
bronchioles, where air passes during inhalation and exhalation but does not participate
in gas exchange with the alveoli. The anatomical dead space is primarily involved in the
conduction of air and the conditioning of inhaled air

*Physiological dead space refers to the total volume of the respiratory system that does
not participate in gas exchange. It includes both the anatomical dead space and any non-
functioning or poorly-perfused alveoli. Physiological dead space can occur when certain
areas of the lungs receive inadequate blood flow, such as in pulmonary embolism or lung
diseases that affect the alveoli's ability to exchange gases effectively.

Measurement of physiological dead space is important for assessing lung function and
detecting abnormalities in gas exchange. The most common method to estimate
physiological dead space is the Bohr equation, which compares the carbon dioxide
concentration in exhaled air (end-tidal CO2) to the carbon dioxide concentration in
arterial blood.
 20/ Transport of gases (O2 and CO2) in a blood.

The transport of gases in the blood involves different mechanisms and forms of
attachment to ensure efficient delivery of oxygen to tissues and removal of carbon
dioxide from the body. how O2 and CO2 are transported in the blood:

Oxygen (O2) Transport: A small portion of oxygen dissolves directly in the plasma of the
blood. This dissolved oxygen accounts for only a small fraction of the total oxygen
transported (about 1-2%). The majority of oxygen is bound to hemoglobin, a protein
found in red blood cells. Each hemoglobin molecule can bind up to four oxygen
molecules. Oxygen binds to the iron component of hemoglobin, forming oxyhemoglobin.
This form of oxygen transport is highly efficient and allows for the bulk of oxygen to be
carried in the blood (approximately 98-99%).

Carbon Dioxide (CO2) Transport: Similar to oxygen, a small portion of carbon dioxide
dissolves directly in the plasma. Dissolved carbon dioxide accounts for about 5-10% of
the total carbon dioxide transported in the blood. Some carbon dioxide binds to
hemoglobin, forming carbaminohemoglobin. This form of carbon dioxide transport
accounts for approximately 20-30% of total carbon dioxide transport. The majority of
carbon dioxide is converted into bicarbonate ions in the red blood cells. Carbon dioxide
combines with water in the presence of an enzyme called carbonic anhydrase to form
carbonic acid (H2CO3), which then rapidly dissociates into bicarbonate ions (HCO3-) and
hydrogen ions (H+). Bicarbonate ions are transported out of the red blood cells into the
plasma, while hydrogen ions bind to hemoglobin or are buffered by other substances.
This form of transport is the most significant, accounting for approximately 60-70% of
total carbon dioxide transport.

21/ Oxyhemoglobin dissocia on curve.

The oxyhemoglobin dissociation curve is a graphical representation of the relationship

between the partial pressure of oxygen and the saturation of hemoglobin with oxygen. It
illustrates how readily hemoglobin binds to or releases oxygen molecules in response to
changes in oxygen partial pressure.

The shape of the oxyhemoglobin dissociation curve is "S-shaped," which reflects the
cooperative binding of oxygen by hemoglobin. characteristics:

*Plateau Region: At high PO2 levels, such as in the lungs, hemoglobin has a high affinity
for oxygen. This means that even a small change in PO2 results in a substantial increase
in the saturation of hemoglobin with oxygen

*Steep Region: As PO2 decreases, such as in the peripheral tissues where oxygen is
released from hemoglobin to support cellular respiration, the curve transitions to a steep
portion. In this range, a small decrease in PO2 leads to a significant decline in
hemoglobin's saturation with oxygen.

*Bohr Effect: The position of the oxyhemoglobin dissociation curve can shift based on
factors that influence oxygen binding to hemoglobin. One such factor is the pH of the
blood. A decrease in pH shifts the curve to the right, indicating a decreased affinity of
hemoglobin for oxygen.

22/ Factors that in uence the forma on and dissocia on of oxyhemoglobin.

*The presence of carbon dioxide and bicarbonate ions influences the formation and
dissociation of oxyhemoglobin. As carbon dioxide levels increase in the blood, carbonic
acid is formed, which then dissociates into bicarbonate ions and hydrogen ions. The
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 release of hydrogen ions reduces the affinity of hemoglobin for oxygen, promoting the
dissociation of oxyhemoglobin and facilitating oxygen release.

*Higher temperatures tend to decrease the affinity of hemoglobin for oxygen, promoting
oxygen release to the tissues. Lower temperatures, on the other hand, increase the
affinity of hemoglobin for oxygen, facilitating oxygen binding. This temperature effect
can be observed, for example, during exercise when the increased heat in muscles
promotes oxygen release from oxyhemoglobin to meet the metabolic demands.

*2,3-Bisphosphoglycerate (BPG) is a molecule produced in red blood cells as a byproduct

of glycolysis. It binds to hemoglobin and reduces its affinity for oxygen, promoting the
dissociation of oxyhemoglobin. BPG levels increase under conditions such as high
altitude or chronic hypoxia, allowing for more efficient oxygen unloading in tissues.

23/ Oxygen capacity of the lungs. The oxygen capacity of the lungs refers to the maximum
amount of oxygen that can be held or carried by the respiratory system at a given time.
It is determined by the volume of oxygen that can be bound to hemoglobin in the blood
and the amount of oxygen dissolved in the plasma. The oxygen capacity of the lungs
plays a crucial role in ensuring adequate oxygen delivery to the body's tissues and
organs. It allows for the transportation of oxygen from the lungs, where it is taken up
during inhalation, to the peripheral tissues, where it is released for cellular respiration

*Oxygen Bound to Hemoglobin: The majority of oxygen in the blood is carried by

hemoglobin, a protein found in red blood cells. Each hemoglobin molecule can bind up to
four oxygen molecules. The oxygen binding capacity of hemoglobin is influenced by
factors such as the concentration of hemoglobin in the blood and its affinity for oxygen.
On average, the oxygen-carrying capacity of hemoglobin is about 1.34 mL of oxygen per
gram of hemoglobin.

*Dissolved Oxygen: A small fraction of oxygen can dissolve directly in the plasma of the
blood. The solubility of oxygen in plasma is relatively low compared to the amount that
can be carried by hemoglobin. The dissolved oxygen contributes only a small portion to
the total oxygen capacity of the lungs.

To calculate the total oxygen capacity of the lungs, both the oxygen bound to
hemoglobin and the dissolved oxygen are considered: Total Oxygen Capacity = Oxygen
Bound to Hemoglobin + Dissolved Oxygen

24/ The forma on and dissocia on of bicarbonate and сarbohemoglobin The formation and dissociation of
bicarbonate and carbohemoglobin occur as part of the transport and regulation of carbon
dioxide in the blood. Here's an overview of the processes involved:

Formation of Bicarbonate : Carbon dioxide produced in tissues diffuses into red blood
cells (RBCs) due to its partial pressure gradient. Once inside the RBCs, it can be
transported in multiple ways. In the presence of an enzyme called carbonic anhydrase,
carbon dioxide combines with water (H2O) within the RBCs to form carbonic acid
(H2CO3). This reaction occurs rapidly and is reversible. Carbonic acid then dissociates
into hydrogen ions (H+) and bicarbonate ions (HCO3-). Bicarbonate ions are transported
out of the RBCs into the plasma in exchange for chloride ions (Cl-) through a transporter
called the bicarbonate-chloride exchanger. Inside the RBCs, hydrogen ions bind to
hemoglobin, acting as a buffer to prevent excessive changes in pH.

Dissociation of Bicarbonate : As bicarbonate ions are transported out of the RBCs,

chloride ions move into the RBCs to maintain electrical neutrality, a process known as
the chloride shift. In the pulmonary capillaries, where the partial pressure of carbon
dioxide is low and the partial pressure of oxygen is high, the reaction can reverse
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 Bicarbonate ions re-enter the RBCs in exchange for chloride ions, and under the
influence of carbonic anhydrase, carbonic acid is reformed. Carbonic acid then breaks
down into carbon dioxide and water. Carbon dioxide diffuses out of the RBCs and into the
alveoli of the lungs to be exhaled.

Carbohemoglobin refers to the complex formed when carbon dioxide binds directly to
hemoglobin. However, the affinity of hemoglobin for carbon dioxide is relatively low
compared to its affinity for oxygen. As a result, only a small fraction of carbon dioxide
(~5-10%) binds directly to hemoglobin to form carbohemoglobin. The majority of carbon
dioxide is transported as bicarbonate ions, as described above.

25/ The signi cance of carbonic anhydrase. Carbonic anhydrase is an enzyme that plays a role in
various physiological processes, particularly in the regulation of acid-base balance and
carbon dioxide transport in the body. significant roles of carbonic anhydrase:

Carbon Dioxide Transport: Carbonic anhydrase facilitates the interconversion between

carbon dioxide and carbonic acid. In the presence of carbonic anhydrase, CO2 rapidly
combines with water to form carbonic acid. This reaction allows for efficient conversion
of CO2 into a soluble form (H2CO3) that can be transported in the blood.

Bicarbonate Ion Formation: The carbonic acid formed by carbonic anhydrase further
dissociates into bicarbonate ions (HCO3-) and hydrogen ions (H+). Bicarbonate ions are
crucial for the transport of carbon dioxide from tissues to the lungs. Carbonic anhydrase
catalyzes the formation of bicarbonate ions, which are then transported out of red blood
cells (RBCs) into the plasma.

Acid-Base Balance: Carbonic anhydrase plays a vital role in maintaining the acid-base
balance of the body. By facilitating the interconversion between CO2 and carbonic acid, it
helps regulate the concentration of hydrogen ions in the blood. This process is especially
important in buffering and maintaining the pH within a narrow range in various tissues
and fluids, including the blood.

Salivary and Gastric Secretion: Carbonic anhydrase is also present in the salivary glands
and gastric mucosa, where it aids in the production of bicarbonate ions. In saliva,
carbonic anhydrase converts CO2 into carbonic acid, which then dissociates to release
bicarbonate ions, contributing to the buffering capacity and pH regulation of saliva. In
the gastric mucosa, carbonic anhydrase participates in the production of bicarbonate
ions, which play a role in gastric acid secretion and the protection of the gastric lining.

26/ Gas exchange between blood and ssues. Gas exchange between the blood and tissues,
specifically the exchange of oxygen (O2) and carbon dioxide (CO2), is a vital process for
cellular respiration and the removal of metabolic waste. Here's an overview of how gas
exchange occurs:

*Oxygen Delivery to Tissues: Oxygenated blood from the lungs is pumped by the heart to
the systemic circulation, which carries oxygen-rich blood to the body's tissues. Oxygen
diffuses from the capillaries into the interstitial fluid surrounding the cells and then into
the cells themselves. This diffusion occurs due to the partial pressure gradient, as the
partial pressure of oxygen is higher in the capillaries than in the cells.

*Oxygen Utilization by Cells: Inside the cells, oxygen is used in the process of cellular
respiration to produce energy in the form of ATP. Oxygen is consumed in the
mitochondria, where it participates in the electron transport chain, enabling oxidative
phosphorylation and ATP synthesis.

*Carbon Dioxide Removal from Tissues: As cells metabolize oxygen, carbon dioxide is
produced as a waste product. Carbon dioxide diffuses out of the cells into the interstitial
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fluid and then into the capillaries, driven by the partial pressure gradient. The partial
pressure of carbon dioxide is higher in the cells than in the capillaries. Some of the
carbon dioxide binds to hemoglobin in red blood cells, forming carbaminohemoglobin,
but the majority is transported as bicarbonate ions (HCO3-) in the plasma.

*Carbon Dioxide Transport: In the red blood cells, carbon dioxide combines with water
under the influence of carbonic anhydrase to form carbonic acid (H2CO3), which then
dissociates into bicarbonate ions (HCO3-) and hydrogen ions (H+). Bicarbonate ions are
exchanged for chloride ions (Cl-) via the bicarbonate-chloride exchanger, allowing
bicarbonate to leave the red blood cells and enter the plasma. Carbon dioxide can also be
directly dissolved in plasma or bound to hemoglobin as carbaminohemoglobin.

*Return of Deoxygenated Blood: Deoxygenated blood, rich in carbon dioxide, returns to

the heart through the systemic veins and is eventually pumped to the lungs for
oxygenation. The carbon dioxide-rich blood is transported from the tissues to the lungs
via the systemic circulation to facilitate gas exchange.

27/ CNS structures that provide respiratory periodic ac vity The respiratory periodic activity, which
controls the rhythm and pattern of breathing, is primarily regulated by several structures
in the central nervous system (CNS). These structures work together to coordinate the
inhalation and exhalation phases of breathing. The main CNS structures involved in
respiratory periodic activity are:

Medullary Respiratory Centers:

*Dorsal Respiratory Group (DRG) Located in the dorsal portion of the medulla oblongata,
the DRG is responsible for initiating the inspiratory phase of breathing. It contains
inspiratory neurons that send signals to the muscles involved in inhalation, such as the
diaphragm and external intercostal muscles.

*Ventral Respiratory Group (VRG) Situated in the ventral portion of the medulla
oblongata, the VRG is involved in both inspiratory and expiratory activities. It contains
inspiratory neurons similar to the DRG, as well as expiratory neurons that activate the
muscles responsible for forced expiration, such as the internal intercostal and abdominal
muscles.

Pontine Respiratory Centers:

*Pneumotaxic Center (Pontine Respiratory Group) Located in the pons, the pneumotaxic
center helps regulate the timing and depth of each breath. It sends inhibitory signals to
the medullary inspiratory centers, limiting the duration of inhalation and facilitating
smooth transitions between inhalation and exhalation.

*Apneustic Center (Pontine Respiratory Group): Also situated in the pons, the apneustic
center stimulates the medullary inspiratory centers, promoting prolonged inhalation.
However, its exact role in normal breathing is still not fully understood.

These CNS structures work in a coordinated manner to generate the rhythmic pattern of
breathing. The medullary respiratory centers, particularly the DRG and VRG, provide the
primary drive for inspiration and expiration. The pontine respiratory centers, including
the pneumotaxic and apneustic centers, modulate the activity of the medullary centers,
fine-tuning the breathing rhythm and controlling the duration and depth of each breath.

28/ The dorsal respiratory group of neurons, its role in the genera on of the basic rhythm of breathing and the regula on
of breathing
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*The dorsal respiratory group of neurons, located in the dorsal portion of the medulla
oblongata in the brainstem, plays a role in the generation of the basic rhythm of
breathing and the regulation of breathing.DRG's functions:

*Generation of Basic Rhythm: The DRG contains inspiratory neurons that are responsible
for initiating the inspiratory phase of breathing, which is the active process of inhalation.
These inspiratory neurons in the DRG fire action potentials in a rhythmic pattern,
generating a burst of signals that activate the muscles involved in inhalation, such as the
diaphragm and external intercostal muscles. The rhythmic firing of the inspiratory
neurons in the DRG sets the basic rhythm or pattern of breathing.

*Integration of Sensory Inputs: The DRG receives inputs from various sensory receptors
involved in respiratory control, such as peripheral chemoreceptors that detect changes in
blood oxygen and carbon dioxide levels, as well as stretch receptors in the lungs and
airways. These sensory inputs provide feedback information about the internal and
external conditions related to breathing, allowing the DRG to adjust the breathing
pattern and respond to changing demands.

*Modulation of Breathing: The DRG integrates sensory inputs with descending inputs
from other respiratory centers, such as the pontine respiratory centers, to modulate the
breathing pattern and adjust the timing and depth of each breath. Feedback from
chemoreceptors and other sensory receptors allows the DRG to respond to changes in
blood gas levels and pH, helping to maintain homeostasis. Additionally, the DRG receives
inputs from higher brain centers, including those involved in voluntary control of
breathing, which allows for conscious control over breathing patterns when necessary.

Coordination with Ventral Respiratory Group (VRG): The DRG works in coordination with
the ventral respiratory group (VRG), another group of neurons in the medulla oblongata,
which is responsible for the expiratory phase of breathing. The DRG provides the primary
drive for inspiration, while the VRG is involved in both inspiratory and expiratory
activities, coordinating the muscles for forced expiration. The interaction between the
DRG and VRG ensures smooth transitions between inhalation and exhalation and
controls the overall breathing rhythm.

29/ Ventral respiratory group of neurons, its role. The ventral respiratory group (VRG) is a cluster of
neurons located in the ventral portion of the medulla oblongata in the brainstem. It plays
a role in the regulation of breathing, specifically in controlling the expiratory phase of
respiration. the VRG's functions:

*Inspiratory and Expiratory Neurons: The VRG contains both inspiratory and expiratory
neurons. These neurons are responsible for coordinating the muscles involved in both
inhalation and exhalation.

*Expiratory Activity: The expiratory neurons in the VRG are particularly important for
controlling the active process of exhalation, especially during forced expiration. They
stimulate the contraction of expiratory muscles, such as the internal intercostal and
abdominal muscles. During normal, quiet breathing, the expiratory neurons in the VRG
are relatively inactive, and expiration is primarily passive.

*Coordination with Dorsal Respiratory Group (DRG): The VRG works in coordination with
the dorsal respiratory group (DRG), another group of neurons in the medulla oblongata.
While the DRG is primarily involved in initiating the inspiratory phase of breathing, the
VRG contributes to both inspiration and expiration. It helps coordinate the transition
between inhalation and exhalation, ensuring smooth and coordinated respiratory cycles.

*Modulation of Breathing: The VRG receives inputs from various sources, including the
dorsal respiratory group (DRG), peripheral chemoreceptors, and other sensory receptors
involved in respiratory control. These inputs provide feedback information about the
internal and external conditions related to breathing. The VRG integrates this
information to modulate the breathing pattern and adjust the timing and depth of each
breath. For example, when there is a need for increased ventilation, such as during
physical exertion or in response to increased carbon dioxide levels, the VRG plays a role
in activating the expiratory muscles for more forceful expiration.

Interaction with Higher Brain Centers: The VRG also receives inputs from higher brain
centers, including those involved in voluntary control of breathing. This allows for
conscious control over breathing patterns when necessary, such as during activities like
speaking, singing, or breath-holding.

**the ventral respiratory group (VRG) of neurons is responsible for coordinating the
expiratory phase of breathing. It works in coordination with the dorsal respiratory group
(DRG) to ensure smooth transitions between inhalation and exhalation and helps
modulate the breathing pattern in response to changing demands and feedback from
sensory receptors. The VRG's role is essential in maintaining proper ventilation and
regulating the overall respiratory rhythm.

30/ Role of pneumotaxic center in the inhibi on of inspira on, regula on of volume and respiratory rate.

The pneumotaxic center is a structure located in the pons of the brainstem. It plays a
crucial role in the regulation of breathing by influencing the duration and rate of
inspiration. the pneumotaxic center's functions:

Inhibition of Inspiration: One of the primary functions of the pneumotaxic center is to

inhibit the inspiratory phase of breathing, thereby preventing excessive lung inflation.
The pneumotaxic center sends inhibitory signals to the inspiratory neurons located in the
dorsal respiratory group (DRG) of the medulla oblongata. These inhibitory signals help
regulate the duration and intensity of inspiration, preventing over-inflation of the lungs
and promoting efficient gas exchange.

Regulation of Volume: The pneumotaxic center is involved in controlling the volume of

each breath, primarily by modulating the duration of inspiration. By adjusting the
duration of the inspiratory phase, the pneumotaxic center can fine-tune the amount of
air taken in during each breath. Increased activity of the pneumotaxic center results in
shorter inspiratory bursts and quicker transitions to expiration, leading to smaller tidal
volumes (the volume of air inhaled or exhaled in one breath). Conversely, decreased
activity of the pneumotaxic center allows for longer inspiratory bursts and larger tidal
volumes.

Regulation of Respiratory Rate: The pneumotaxic center also plays a role in regulating
the respiratory rate, which refers to the number of breaths taken per minute. Higher
activity of the pneumotaxic center increases the rate of respiration by shortening the
inspiratory phase and promoting a faster transition to expiration. Lower activity of the
pneumotaxic center decreases the respiratory rate by allowing for longer inspiratory
bursts and slower transitions to expiration.

Coordination with Other Respiratory Centers: The pneumotaxic center works in

coordination with other respiratory centers, including the dorsal respiratory group (DRG)
and ventral respiratory group (VRG), to regulate the overall breathing pattern. The
pneumotaxic center interacts with the medullary respiratory centers, adjusting their
activity and influencing the timing and depth of each breath. It modulates the activity of
the inspiratory neurons in the DRG, providing fine-tuning of the inspiratory phase and
coordination between inhalation and exhalation
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 31/Apneus c center, its role in the regula on of breathing. The apneustic center is a structure located in
the pons of the brainstem, specifically in the lower portion of the pons. Its exact role in
the regulation of breathing.However, research has provided some insights into its
potential role:

Breathing Pattern: The apneustic center is believed to be involved in the regulation of

the breathing pattern, particularly in relation to the inspiratory phase. Stimulation of the
apneustic center in animal studies has been shown to prolong the inspiratory phase and
delay the transition to expiration, resulting in a prolonged inspiratory gasp. It is thought
to influence the activity of the inspiratory neurons in the medullary respiratory centers,
potentially affecting the duration and intensity of inspiration.

Interaction with Other Respiratory Centers: The apneustic center interacts with other
respiratory centers, particularly the pneumotaxic center and dorsal respiratory group
(DRG), to modulate the overall respiratory rhythm and pattern. It is believed to provide
a tonic stimulatory influence on the medullary inspiratory centers, contributing to their
activity.

Control of Breathing Rate and Depth: While the primary function of the apneustic center
is not fully understood, studies suggest that it may play a role in regulating the
breathing rate and depth. Activation of the apneustic center has been associated with
slower and deeper breaths, suggesting its involvement in setting the respiratory
parameters.

32/E ect of gas composi on and pH of arterial blood on the frequency and depth of breathing. The composition of
arterial blood, including the levels of gases such as oxygen (O2), carbon dioxide (CO2),
and the pH value, plays a crucial role in the regulation of breathing. Here's how changes
in gas composition and pH can affect the frequency and depth of breathing:

Oxygen (O2) Levels: Low arterial oxygen levels, known as hypoxemia, can stimulate an
increase in the frequency and depth of breathing. Peripheral chemoreceptors, located in
the carotid bodies and aortic bodies, detect low levels of arterial oxygen and send
signals to the respiratory centers in the brainstem. The respiratory centers respond by
increasing the drive to breathe, leading to a higher respiratory rate (frequency) and
deeper breaths (depth) in an attempt to increase oxygen uptake and improve
oxygenation.

Carbon Dioxide (CO2) Levels: High arterial carbon dioxide levels, known as hypercapnia,
can stimulate an increase in the frequency and depth of breathing. Central
chemoreceptors, located in the medulla oblongata, are sensitive to changes in arterial
carbon dioxide levels, indirectly sensed through the pH of the cerebrospinal fluid. An
increase in arterial carbon dioxide levels or a decrease in pH (resulting from increased
carbon dioxide levels) stimulates the central chemoreceptors, which in turn increase the
respiratory drive. The increased respiratory drive leads to a higher respiratory rate and
deeper breaths to eliminate excess carbon dioxide and restore normal pH levels.

pH Levels: Changes in arterial blood pH can directly influence the regulation of

breathing. Acidosis, which occurs when arterial blood pH decreases below the normal
range, can stimulate an increase in the respiratory rate and depth to blow off excess
carbon dioxide and increase pH. Conversely, alkalosis, which occurs when arterial blood
pH increases above the normal range, can lead to a decrease in the respiratory rate and
depth to retain carbon dioxide and lower pH. The changes in respiratory rate and depth
aim to restore the acid-base balance and maintain physiological pH levels.

33/Central and peripheral chemoreceptors, and their importance in ensuring gas homeostasis. Central and
peripheral chemoreceptors are specialized sensory receptors that play a crucial role in
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maintaining gas homeostasis, particularly in regulating the levels of oxygen (O2) and
carbon dioxide (CO2) in the body. their importance:

Central Chemoreceptors:

*Location: Central chemoreceptors are primarily located in the medulla oblongata, which
is part of the brainstem.

*Response to CO2 and pH: Central chemoreceptors are highly sensitive to changes in the
levels of carbon dioxide (CO2) in the cerebrospinal fluid (CSF), indirectly reflected by
changes in the pH of the CSF.

*pH Regulation: As arterial CO2 levels increase, CO2 crosses the blood-brain barrier and
combines with water in the CSF, resulting in an increase in hydrogen ions (H+), which
decreases pH. Central chemoreceptors respond to the increased H+ concentration,
triggering an increase in respiratory drive to eliminate excess CO2 and restore normal
pH levels.

*Influence on Breathing: Activation of central chemoreceptors leads to an increase in the

respiratory rate and depth, stimulating ventilation and facilitating the removal of CO2
from the body. This response helps maintain the acid-base balance in the blood and
ensures proper gas exchange.

Peripheral Chemoreceptors:

*Location: Peripheral chemoreceptors are located in specialized structures known as

carotid bodies (in the carotid arteries) and aortic bodies (in the aortic arch).

*Response to O2, CO2, and pH: Peripheral chemoreceptors respond to changes in arterial
oxygen (O2) levels, carbon dioxide (CO2) levels, and pH.

*O2 Sensitivity: Peripheral chemoreceptors are most sensitive to arterial oxygen levels.
When arterial O2 levels decrease (hypoxemia), peripheral chemoreceptors are
stimulated and send signals to the respiratory centers in the brainstem to increase
ventilation and enhance oxygen uptake.

*CO2 and pH Regulation: Peripheral chemoreceptors also contribute to the regulation of

CO2 and pH. However, their response to CO2 is less pronounced compared to central
chemoreceptors. They mainly provide feedback related to changes in pH when arterial
CO2 levels are significantly elevated.

*Influence on Breathing: Activation of peripheral chemoreceptors leads to an increase in

the respiratory rate and depth, similar to central chemoreceptors. However, their
primary role is to regulate oxygen levels, ensuring adequate oxygenation of tissues.

Importance in Gas Homeostasis: Central and peripheral chemoreceptors are essential

for maintaining gas homeostasis by continuously monitoring the levels of O2, CO2, and
pH in the blood. They play a critical role in regulating ventilation (respiratory rate and
depth) to match the body's metabolic demands, ensuring proper oxygenation and
elimination of CO2.

Chemoreceptors respond to deviations from normal gas and pH levels, triggering

appropriate adjustments in breathing patterns to restore homeostasis.

Their sensitivity to changes in arterial O2, CO2, and pH allows for rapid adjustments in
respiratory drive, contributing to the overall balance of gas exchange, acid-base
regulation, and oxygen delivery to tissues.
It's important to note that other factors, such as lung receptors, mechanoreceptors, and
higher brain centers, also contribute to respiratory control. However, central and
peripheral chemoreceptors are particularly vital in sensing and responding to chemical
changes in the blood, enabling the respiratory system to maintain gas homeostasis and
support overall physiological functioning.

34/ Changes in ven la on during hypercapnia, hypoxia.

*During hypercapnia (elevated levels of carbon dioxide, or CO2) and hypoxia (low levels
of oxygen, or O2), the body undergoes specific changes in ventilation (respiratory rate
and depth) as part of the respiratory response to maintain gas homeostasis. Here's how
ventilation is affected during hypercapnia and hypoxia:

Hypercapnia:

*Increased Ventilation: Hypercapnia triggers an increase in ventilation to remove excess

CO2 from the body.

Stimulation of Chemoreceptors: Central chemoreceptors in the medulla oblongata and

peripheral chemoreceptors in the carotid bodies and aortic bodies sense the elevated
CO2 levels or the associated decrease in pH.

Increased Respiratory Drive: The stimulation of chemoreceptors leads to an increased

respiratory drive, resulting in an elevated respiratory rate and deeper breaths.

Enhanced Removal of CO2: The increased ventilation facilitates a more rapid elimination
of CO2 through exhalation, helping to restore normal CO2 levels and maintain acid-base
balance.

Hypoxia:

Increased Ventilation: Hypoxia triggers an increase in ventilation to improve oxygen

uptake and delivery to tissues.

Stimulation of Chemoreceptors: Peripheral chemoreceptors in the carotid bodies and

aortic bodies sense the reduced arterial oxygen levels.

Increased Respiratory Drive: The stimulation of peripheral chemoreceptors leads to an

increased respiratory drive, resulting in an elevated respiratory rate and deeper breaths.

Improved Oxygenation: The increased ventilation enhances oxygen intake, increasing

the oxygen supply to tissues and counteracting the hypoxic condition.

35/ Pulmonary stretch receptors, and their importance in the regula on of breathing Pulmonary stretch
receptors are specialized sensory receptors located in the smooth muscle of the airways,
particularly in the walls of the bronchi and bronchioles of the lungs. These receptors play
a crucial role in the regulation of breathing and the overall control of respiratory
functions. The primary function of pulmonary stretch receptors is to detect the
stretching or distension of the lung tissue. When the lungs expand during inhalation,
these receptors are activated by the increased tension in the airway walls. Conversely,
during exhalation, when the lungs recoil and the airways contract, the receptors are less
active.

The activation of pulmonary stretch receptors sends sensory signals through afferent
nerve fibers to the brainstem, specifically to the medulla oblongata, which is the
respiratory control center. These sensory signals provide important feedback to the brain
regarding the status of lung inflation and help regulate the duration and intensity of
breathing cycles.
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The regulation of breathing involves a negative feedback mechanism. When the
pulmonary stretch receptors detect excessive lung inflation, they send inhibitory signals
to the medulla oblongata, leading to the termination of the current inhalation. This
mechanism prevents overinflation of the lungs, which could potentially damage the
delicate lung tissue. On the other hand, if the receptors detect insufficient lung inflation,
they promote inhalation by reducing their inhibitory signals to the medulla oblongata.

The importance of pulmonary stretch receptors in the regulation of breathing is evident

in various physiological responses. For example, if the receptors are artificially
stimulated, such as through a mechanical stretch of the lungs, it can lead to a decrease
in respiratory rate and tidal volume. Conversely, the inhibition or impairment of these
receptors can disrupt the normal regulation of breathing, potentially resulting in
respiratory disorders.

36/ The Hering-Breuer re ex (in a on re ex). The Hering-Breuer reflex, is a respiratory feedback
mechanism that helps regulate the depth and frequency of breathing. It is named after
the physiologists Josef Breuer and Eduard Hering, who independently described this
reflex in the late 19th century.

*The Hering-Breuer reflex is primarily associated with the regulation of inspiration or

inhalation. It is activated by the stretching or distension of the lung tissue, particularly
the pulmonary stretch receptors located in the airway walls. These receptors are
sensitive to the increased lung volume that occurs during inhalation. When the
pulmonary stretch receptors detect lung inflation, they send sensory signals through
afferent nerve fibers to the brainstem, specifically the medulla oblongata. These signals
are processed by the respiratory centers in the medulla, leading to the initiation of the
Hering-Breuer reflex.

*The reflex response depends on the phase of the respiratory cycle. During the
inspiratory phase, the Hering-Breuer reflex inhibits further inspiration, helping prevent
overinflation of the lungs. The inhibitory signals from the pulmonary stretch receptors
inhibit the activity of the inspiratory neurons in the medulla, resulting in the termination
of inspiration and the initiation of expiration.

The Hering-Breuer reflex also contributes to the regulation of respiratory rate and tidal
volume. If the lung inflation is excessive, the reflex response leads to a decrease in the
duration and intensity of the current inspiration, thereby reducing tidal volume. It also
contributes to the adjustment of respiratory rate by modulating the duration of the
inspiratory and expiratory phases.

While the Hering-Breuer reflex primarily acts to prevent overinflation, it is important to

note that it does not play a major role in the normal regulation of breathing during quiet
respiration in healthy individuals. However, it becomes more prominent during situations
that require increased ventilatory effort, such as exercise or respiratory distress.

37/ The role of other receptors in the regula on of respira on: irritant, j-receptors, proprioceptors

In addition to pulmonary stretch receptors, there are several other types of receptors
involved in the regulation of respiration: irritant receptors, (Juxtacapillary Receptors),
and proprioceptors. Each of these receptors has a specific role in the respiratory control
system.

Irritant receptors are located in the airway epithelium and are sensitive to noxious
stimuli such as irritants, smoke, chemical fumes, and excessive mucus. When these
receptors are stimulated, they initiate a protective reflex known as the "cough reflex" or
"irritant reflex." The reflex response involves rapid and forceful expiration, which helps
expel the irritants from the airways and protect the respiratory system.
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 Juxtacapillary Receptors are found in the alveolar walls, particularly in the pulmonary
capillaries close to the alveoli. These receptors are sensitive to various stimuli, including
lung congestion, pulmonary edema, and certain chemicals. Stimulation of J-receptors
leads to the activation of the "J-receptor reflex" or "pulmonary C-fiber reflex." This
reflex response is characterized by rapid, shallow breathing, bronchoconstriction, and
the feeling of dyspnea The J-receptor reflex plays a role in the regulation of pulmonary
blood flow, the redistribution of blood within the lungs, and the modulation of ventilation
during exercise or pathological conditions.

*Proprioceptors are sensory receptors located in muscles, tendons, and joints

throughout the body, including the respiratory muscles. They provide feedback regarding
the position, movement, and tension of the muscles and joints. Proprioceptors involved
in respiration include muscle spindles, Golgi tendon organs, and joint receptors. These
receptors contribute to the regulation of breathing by providing feedback to the
respiratory centers in the brainstem. They help adjust the intensity and timing of
respiratory muscle contractions to match the body's metabolic demands, postural
changes, and physical activity levels.

38/ Protec ve respiratory re exes.There are several protective respiratory reflexes that play a
role in maintaining the health and integrity of the respiratory system. These reflexes
help protect the lungs and airways from potential These protective respiratory reflexes
are mediated by the integration of sensory inputs from various receptors, such as irritant
receptors, stretch receptors, and other specialized receptors present in the respiratory
system. The reflex responses are coordinated by the respiratory centers in the
brainstem, which generate appropriate motor outputs to the respiratory muscles and
airway smooth muscles to carry out the necessary protective actions. Here are some
important protective respiratory reflexes:

Cough Reflex: The cough reflex is a protective mechanism that helps clear the airways of
irritants, foreign particles, excessive mucus, or other substances that may be present. It
is initiated by the stimulation of irritant receptors in the airway epithelium. The reflex
involves a deep inhalation followed by a forceful expulsion of air through the mouth,
expelling the irritants or mucus from the respiratory tract.

Sneezing Reflex: The sneezing reflex is another protective mechanism that helps clear
the nasal passages and upper respiratory tract. It is typically triggered by the irritation
of the nasal mucosa due to allergens, irritants, or infectious agents. The reflex involves a
rapid and forceful expulsion of air through the nose, helping to remove the irritants and
maintain clear airways.

Swallowing Reflex: The swallowing reflex helps protect the lower respiratory tract by
preventing the entry of food or liquids into the airways. When food or liquids reach the
back of the throat, sensory receptors trigger the swallowing reflex, which initiates the
closure of the airway (epiglottis) and the relaxation of the muscles involved in
swallowing. This ensures that the ingested material is directed toward the esophagus
and not the trachea, reducing the risk of aspiration.

Vagal Reflexes: The vagal reflexes are a group of protective reflexes mediated by the
vagus nerve (cranial nerve X). These reflexes help regulate the diameter of the airways
and maintain optimal airflow. For example, the vagal reflexes play a role in
bronchoconstriction and bronchodilation in response to various stimuli. They can cause
bronchoconstriction in response to irritants or allergens to prevent further exposure, and
bronchodilation in response to increased metabolic demands or exercise to facilitate
increased airflow.
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 39/ Regula on of airway space sizes. The regulation of airway space sizes is crucial for maintaining
optimal airflow and gas exchange in the respiratory system The regulation of airway
space sizes is a complex and dynamic process involving the interplay of various factors
and mechanisms. The autonomic nervous system, inflammatory mediators, mechanical
factors, neural reflexes, and local factors all contribute to the control of airway caliber,
ensuring optimal airflow and gas exchange in the respiratory system

*The autonomic nervous system, specifically the parasympathetic and sympathetic

divisions, plays a significant role in regulating airway space sizes. Parasympathetic
stimulation, mediated by the vagus nerve, leads to bronchoconstriction, narrowing the
airways. This effect is primarily mediated by the release of acetylcholine and activation
of muscarinic receptors on airway smooth muscle cells. On the other hand, sympathetic
stimulation leads to bronchodilation, relaxing the smooth muscles and widening the
airways. Sympathetic activation releases norepinephrine, which binds to beta-adrenergic
receptors on airway smooth muscle cells.

*Inflammatory mediators released during respiratory inflammation, such as histamine,

leukotrienes, and prostaglandins, can influence airway space sizes. These mediators can
cause bronchoconstriction, leading to narrowing of the airways, increased resistance to
airflow, and reduced airway space. This response is often seen in conditions like asthma
and allergic reactions.

*Mechanical factors, including lung volume and intrapleural pressure, can influence
airway caliber. For example, during inspiration, as lung volume increases, the airways
tend to dilate, resulting in increased airway space. Conversely, during expiration, the
reduced lung volume can lead to airway constriction. Additionally, changes in
intrapleural pressure can affect the diameter of the airways. Positive pressure within the
airways tends to compress and narrow the airways, while negative pressure promotes
airway dilation.

*Various neural reflexes can regulate airway space sizes in response to specific stimuli.
For example, the Hering-Breuer reflex, mediated by pulmonary stretch receptors, helps
prevent overinflation of the lungs by inhibiting further inspiration and promoting
expiration. Other reflexes, such as the cough reflex and the J-receptor reflex, can also
influence airway caliber.

*Local Factors: Local factors within the airways, such as smooth muscle tone, mucus
production, and the presence of irritants or allergens, can directly affect airway space
sizes. Smooth muscle contraction leads to bronchoconstriction and reduced airway
diameter, while relaxation results in bronchodilation and increased airway space.
Excessive mucus production or the presence of irritants can contribute to airway
narrowing and obstruction.

40/ Voluntary regula on of breathing Voluntary regulation of breathing refers to the conscious
control an individual can exert over their respiratory pattern and rate. Normally,
breathing is an automatic and involuntary process governed by the respiratory centers in
the brainstem.

*One of the most direct ways to exert voluntary control over breathing is through breath
holding. This involves prolonging the duration of the respiratory cycle by intentionally
holding one's breath. Breath holding can be performed after a deep inhalation or
exhalation, and the duration can vary based on individual capacity and purpose.

*Voluntary regulation of breathing also includes consciously altering the breathing

pattern, such as deep breathing, shallow breathing, or altering the duration of inhalation
and exhalation. Techniques like diaphragmatic breathing, where the focus is on
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expanding and contracting the diaphragm during inhalation and exhalation, can be
employed to enhance relaxation and reduce stress.

*Meditation and Mindful Breathing: Many mindfulness and meditation practices

emphasize conscious attention to the breath as a means to cultivate present-moment
awareness and relaxation. By directing conscious attention to the inhalation and
exhalation, individuals can regulate their breathing pattern and foster a sense of calm
and mental focus. Mindful breathing techniques often involve slow, deep breaths and
sustained attention to the breath's sensations.

*Breathing Exercises: Various breathing exercises, such as pranayama in yoga or

specific breathing techniques taught in practices like the Wim Hof Method, offer methods
to voluntarily manipulate respiration. These exercises typically involve specific patterns
of inhalation, exhalation, breath retention, and rapid breathing sequences. The purpose
is to promote specific physiological and mental effects, such as increased energy,
relaxation, or focus.

*Speech and Singing: Voluntary regulation of breathing is essential for speech and
singing. These activities require conscious control over the timing, intensity, and
coordination of breath with vocalization. By modulating the rate and depth of breathing,
individuals can adjust their speech or singing volume, pitch, and phrasing.

41/ Breathing during physical work, with increased and reduced barometric pressure

*Breathing during Physical Work: During physical work or exercise, the body's oxygen
demand increases to meet the elevated metabolic requirements. This prompts
adjustments in breathing to supply adequate oxygen and remove carbon dioxide
efficiently.

*Respiratory Rate: During physical work, the respiratory rate typically increases to
accommodate the higher oxygen demand. This allows for a greater intake of air into the
lungs and facilitates oxygen exchange.

*Tidal Volume: Tidal volume, which is the amount of air inspired or expired with each
breath, also increases during physical work. The combination of an elevated respiratory
rate and larger tidal volume helps optimize the overall ventilation of the lungs.

*Increased Ventilation: The combination of higher respiratory rate and tidal volume
results in increased minute ventilation (the volume of air moved in and out of the lungs
per minute). This heightened ventilation helps maintain appropriate oxygen levels and
aids in the removal of carbon dioxide, ensuring efficient gas exchange during physical
exertion.

*Activation of Respiratory Muscles: During physical work, the respiratory muscles,

particularly the diaphragm and intercostal muscles, experience increased activity to
support the increased workload. These muscles work to expand and contract the chest
cavity, facilitating air movement into and out of the lungs.

*Breathing in Increased Barometric Pressure: In situations where barometric pressure is

increased, such as in hyperbaric environments or at high altitudes, breathing patterns
may be altered due to the differences in air density.

*Decreased Respiratory Rate: In environments with increased barometric pressure, the

respiratory rate may decrease as the denser air contains more oxygen molecules per
breath. This means the body can extract sufficient oxygen with fewer breaths.
 *Decreased Tidal Volume: The higher density of air can lead to a decrease in tidal
volume. However, the overall minute ventilation may still be sufficient due to the higher
oxygen content in each breath.

*Reduced Effort: Breathing in increased barometric pressure environments requires less

effort because the denser air provides greater lung expansion, facilitating oxygen
uptake. This can be observed in hyperbaric chambers or in pressurized aircraft cabins.

*Breathing in Reduced Barometric Pressure: In conditions of reduced barometric

pressure, such as at high altitudes, the lower oxygen availability can impact breathing
patterns.

*Increased Respiratory Rate: At higher altitudes or in low-pressure environments, the

reduced partial pressure of oxygen stimulates an increase in respiratory rate. This
compensatory response helps maintain adequate oxygen intake.

*Increased Tidal Volume: In reduced barometric pressure conditions, the tidal volume
tends to increase to compensate for the lower oxygen concentration. The larger breaths
allow for greater air intake to support oxygenation.

*Enhanced Ventilation: The combined increase in respiratory rate and tidal volume
promotes a higher minute ventilation, enabling a sufficient oxygen supply and carbon
dioxide removal in low-oxygen environments.

42/ Regula on of the rst breath of a newborn baby

The first breath of a newborn baby is event that marks the transition from obtaining
oxygen through the placenta to independent respiration. Several factors and reflexes
contribute to the regulation of the first breath:

Chemical Factors: Before birth, the fetus is in a low-oxygen environment. During labor
and delivery, as the baby passes through the birth canal, the compression of the chest
and the release of pressure during delivery help expel amniotic fluid from the airways.
This process helps clear the airways and creates a stimulus for the respiratory centers in
the brainstem to initiate breathing.

Mechanical Factors: The mechanical forces exerted during delivery, such as the
stretching of the lungs and chest, play a role in initiating the first breath. As the baby
passes through the birth canal, the chest is compressed, and the thoracic cavity is
squeezed. This compression helps expel lung fluid and promotes the expansion of the
lungs. Once the baby is delivered, the release of pressure allows the lungs to expand
fully, facilitating the first breath.

Chemical Changes at Birth: The abrupt changes in the baby's environment at birth,
including a decrease in blood oxygen levels and an increase in carbon dioxide levels,
trigger chemoreceptors in the carotid arteries and aortic arch. The stimulation of these
chemoreceptors sends signals to the respiratory centers in the brainstem, stimulating
the baby to take the first breath.

Thermal Changes: The transition from the warm intrauterine environment to the cooler
external environment at birth can stimulate the baby's respiratory drive. The sudden
exposure to cooler air and contact with the skin can trigger reflexes that initiate
breathing.

1/ The basic principles of hemodynamics, rela onship of the main hemodynamic parameters. Hemodynamics
refers to the study of the forces and movements involved in the circulation of blood
through the cardiovascular system. The main hemodynamic parameters include blood
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pressure, blood flow, and vascular resistance. The basic principles of hemodynamics are
governed by the laws of physics, including the laws of fluid dynamics. Blood flow in the
circulatory system is driven by the pressure gradient created by the pumping action of
the heart, and the resistance to flow offered by the blood vessels. The relationship
between the main hemodynamic parameters can be described by the following equation
/Blood pressure (BP) = Cardiac output (CO) x Vascular resistance (VR)

*Cardiac output is the volume of blood pumped by the heart per unit time/ Vascular
resistance is the resistance to blood flow offered by the blood vessels

Another important concept in hemodynamics is the relationship between flow velocity

and cross-sectional area of the blood vessels. As the cross-sectional area of a blood
vessel increases, the flow velocity decreases, and vice versa. This relationship is
described by the equation:

Blood flow (Q) = Velocity (v) x Cross-sectional area (A)

Therefore, an increase in the cross-sectional area of a blood vessel will lead to a

decrease in flow velocity, while a decrease in cross-sectional area will lead to an
increase in flow velocity.

2/ Linear and volumetric blood ow rate, the dura on of total blood ow circula on

*Linear blood flow rate refers to the rate at which blood flows through a particular blood
vessel, and is typically expressed in units of distance per time This is also known as the
velocity of blood flow.

Volumetric blood flow rate refers to the volume of blood that flows through a particular
blood vessel per unit time, and is typically expressed in units of volume per time (e.g.,
mL/min or L/min). This is also known as the cardiac output.

The relationship between linear and volumetric blood flow rates can be described by the
equation:

Volumetric flow rate = Linear flow rate x Cross-sectional area

The cross-sectional area of a blood vessel is a measure of the total area of the lumen
(the open space inside the blood vessel). As the cross-sectional area of a blood vessel
increases, the linear flow rate decreases, but the volumetric flow rate increases.

The duration of total blood flow circulation is the time it takes for all the blood in the
body to circulate through the cardiovascular system. This is known as the circulation
time, and it can be calculated by dividing the total blood volume by the cardiac output.

The average total blood volume in an adult is approximately 5 liters, and the average
cardiac output is approximately 5 liters per minute at rest. Therefore, the circulation
time at rest is approximately 1 minute. However, the circulation time can vary depending
on factors such as cardiac output, blood volume, and the resistance offered by the blood
vessels.

3/ The total peripheral vascular resistance (TPVR), its value.

Total peripheral vascular resistance refers to the overall resistance to blood flow offered
by the systemic circulation all the blood vessels in the body except for those in the lungs.
TPVR is primarily determined by the diameter of the arterioles (smaller arteries) and the
amount of smooth muscle tone in their walls. When the smooth muscle in the walls of
the arterioles contracts (vasoconstriction), the diameter of the arterioles decreases,
increasing the resistance to blood flow and increasing TPVR. When the smooth muscle in
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 the walls of the arterioles relaxes (vasodilation), the diameter of the arterioles
increases, decreasing the resistance to blood flow and decreasing TPVR. The value of
TPVR varies among individuals and can also change under different physiological or
pathological conditions. The normal range for TPVR is approximately 900-1400 dynes-
sec/cm5, where dynes is a unit of force and sec/cm5 is a unit of viscosity. Abnormal
increases in TPVR can occur in conditions such as hypertension, vasoconstriction due to
sympathetic nervous system activation, or obstruction in the blood vessels. Abnormal
decreases in TPVR can occur in conditions such as shock, vasodilation due to
parasympathetic nervous system activation, or certain medications.

4/ Func onal characteris cs of vessels. Blood vessels have different functional characteristics
depending on their size and location within the cardiovascular system. The main types of
blood vessels are arteries, arterioles, capillaries, venules, and veins, each with their own
unique features:

*Arteries are large, muscular vessels that carry oxygenated blood away from the heart
to the rest of the body. They have thick walls with a layer of smooth muscle that can
constrict or dilate to regulate blood flow and maintain blood pressure.

*Arterioles are smaller branches of arteries that regulate blood flow to the capillaries.
They have less muscle than arteries but are still capable of regulating blood flow through
vasoconstriction and vasodilation.

*Capillaries are tiny, thin-walled vessels that connect arterioles to venules. They are the
site of exchange between the blood and surrounding tissues, allowing for the exchange
of oxygen, nutrients, and waste products between the blood and the cells of the body.

*Venules are small vessels that collect blood from the capillaries and drain it into the
veins. They have thin walls and low pressure, and their primary function is to transport
blood back to the heart.

*Veins are thin-walled vessels that transport deoxygenated blood from the body back to
the heart. They have valves to prevent backflow and rely on muscle contractions to move
blood against gravity.

5/ Volume of blood and blood pressure. Blood pressure and the volume of blood in the circulatory
system are closely related. Blood pressure is the force exerted by the blood against the
walls of the blood vessels, while the volume of blood refers to the amount of blood in the
circulatory system at any given time. An increase in blood volume can lead to an
increase in blood pressure, as there is more blood in the system exerting pressure on the
vessel walls. Similarly, a decrease in blood volume can lead to a decrease in blood
pressure. The kidneys play a crucial role in regulating blood volume and blood pressure.
They do so by regulating the amount of fluid and electrolytes in the body through
processes such as filtration, reabsorption, and secretion.

Other factors that can influence blood volume and blood pressure include physical
activity, stress, medications, and certain medical conditions such as hypertension, heart
failure, and kidney disease.

6/ Blood pressure (BP), its types, waves, methods of registra on by Riva-Rochi and by Korotko .

Blood pressure (BP) is the pressure exerted by the blood on the walls of the arteries as it
flows through the circulatory system. There are two types of blood pressure
measurements:

Systolic blood pressure (SBP): This is the pressure exerted by the blood on the arterial
walls when the heart contracts and pumps blood out into the circulation.
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 Diastolic blood pressure (DBP): This is the pressure exerted by the blood on the arterial
walls when the heart is at rest between contractions.

*Blood pressure waves refer to the oscillations in pressure that occur during each
cardiac cycle. The two main waves are:

Systolic wave: This is the peak of the pressure wave that occurs during systole.

Diastolic wave: This is the lowest point of the pressure wave that occurs during diastole.

*There are two main methods of measuring blood pressure: the Riva-Rocci method and
the Korotkoff method.

Riva-Rocci method: This method involves using a sphygmomanometer, which is a cuff

that is wrapped around the upper arm and inflated to a pressure higher than the
patient's systolic blood pressure. The pressure in the cuff is gradually released while
listening for the Korotkoff sounds with a stethoscope placed over the brachial artery. The
first sound heard is the systolic pressure, while the disappearance of sounds is the
diastolic pressure.

Korotkoff method: This method also uses a sphygmomanometer, but instead of using a
stethoscope to listen for sounds, it uses a microphone and speaker to amplify the
sounds. The cuff is inflated to a pressure higher than the patient's systolic pressure, and
then the pressure is gradually released while listening for Korotkoff sounds. The first
sound heard is the systolic pressure, while the disappearance of sounds is the diastolic
pressure.

7/ Pulse-related uctua ons in blood pressure Pulse-related fluctuations in blood pressure refer to
the changes in blood pressure that occur with each heartbeat or pulse. These
fluctuations are normal and reflect the cyclic nature of the cardiovascular system.
During each heartbeat, the pressure in the arteries increases as blood is ejected from the
heart, resulting in the systolic blood pressure. As the heart relaxes between beats, the
pressure in the arteries decreases, resulting in the diastolic blood pressure. This cycle of
pressure fluctuations is known as the pulse pressure. The amplitude of the pulse
pressure can be affected by a number of factors, including age, gender, physical activity
level, and medical conditions such as hypertension and atherosclerosis. For example, as
people age, their arteries become stiffer and less able to expand and contract, leading to
a decrease in pulse pressure.

Pulse-related fluctuations in blood pressure can be measured using a variety of

techniques, including arterial tonometry, which involves measuring the pressure
waveforms in the arteries, and pulse wave analysis, which involves analyzing the shape
and timing of the pulse wave.

8/ Sphygmography, pulse. Parameters of pulse Sphygmography is a technique that measures the

pulse waveforms, which are the pressure fluctuations in the arteries that occur with
each heartbeat. This technique can provide important information about cardiovascular
health and is used to assess the properties of the arterial wall and the characteristics of
the pulse. The parameters of the pulse that can be measured using sphygmography
include:

*Amplitude: This refers to the height of the pulse wave and is influenced by factors such
as age, gender, physical activity level, and medical conditions such as hypertension and
atherosclerosis.
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 *Upstroke time: This refers to the time it takes for the pulse wave to reach its peak and
is influenced by factors such as arterial stiffness and peripheral resistance.

*Pulse duration: This refers to the length of time between the upstroke and downstroke
of the pulse wave and is influenced by factors such as arterial compliance and blood
viscosity.

*Pulse contour: This refers to the shape of the pulse wave and can provide information
about the properties of the arterial wall and the presence of cardiovascular disease.

*Pulse pressure: This refers to the difference between the systolic and diastolic blood
pressures and is influenced by factors such as cardiac output, peripheral resistance, and
arterial compliance.

8/ Capaci ve vessels, transmural pressure in the veins, blood ow indexes Capacitive vessels, also known as
capacitance vessels, refer to the veins and venules in the cardiovascular system. These
vessels are characterized by their ability to store blood and regulate blood flow to
maintain proper venous return and cardiac output. /Transmural pressure in the veins
refers to the pressure gradient across the wall of the vein. This pressure gradient is
influenced by factors such as blood volume, cardiac output, venous tone, and the ability
of the veins to distend and contract in response to changes in blood flow. / Blood flow
indexes in the veins can be measured using a variety of techniques, including venous
occlusion plethysmography, which involves measuring changes in limb volume as a
result of changes in venous blood flow. Other techniques include Doppler ultrasound and
venous pressure measurements. Some of the blood flow indexes that can be measured
in the veins include:

Venous capacitance: This refers to the ability of the veins to store blood and regulate
venous return. It is influenced by factors such as blood volume, venous tone, and the
distensibility of the veins.

Venous compliance: This refers to the ability of the veins to distend and contract in
response to changes in blood flow. It is influenced by factors such as venous tone, blood
pressure, and the properties of the venous wall.

Venous pressure: This refers to the pressure in the veins and is influenced by factors
such as blood volume, cardiac output, venous tone, and the ability of the veins to store
blood.

9/ Mechanisms of blood ow to the heart. Blood flow to the heart is essential for the delivery of
oxygen and nutrients to the cardiac muscle. The mechanisms that regulate blood flow
to the heart include:

*Coronary artery autoregulation: The coronary arteries have the ability to regulate their
own blood flow in response to changes in oxygen demand. This is achieved through the
release of vasoactive substances, such as adenosine and nitric oxide, which cause
vasodilation and increase blood flow to the heart.

*Myogenic regulation: The cardiac muscle cells themselves have the ability to sense
changes in blood pressure and regulate blood flow through the release of vasoactive
substances. This is achieved through a process known as myogenic regulation, which
involves the contraction and relaxation of the vascular smooth muscle cells in response
to changes in transmural pressure.

*Neurogenic regulation: The nervous system also plays a role in regulating blood flow to
the heart. The sympathetic nervous system, for example, can cause vasoconstriction of
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the coronary arteries in response to stress or exercise, increasing blood flow to the
heart.

*Endothelial regulation: The endothelium that lines the blood vessels also plays a role in
regulating blood flow to the heart. Endothelial cells produce nitric oxide, which causes
vasodilation and increases blood flow to the heart.

10/Microcirculatory bed, capillaries, blood ow in microcirculatory bed The microcirculatory bed refers to
the smallest blood vessels in the body, including arterioles, capillaries, and venules.
These vessels are responsible for delivering oxygen and nutrients to the tissues and
removing waste products.

*Capillaries are the smallest blood vessels in the body and are the site of exchange of
nutrients, oxygen, and metabolic waste products between the blood and tissues.
Capillaries are characterized by their thin walls, which allow for efficient exchange of
substances across the vessel wall.

*Blood flow in the microcirculatory bed is regulated through a variety of mechanisms,

including local metabolic control, autonomic control, and myogenic control. Local
metabolic control refers to the ability of the tissues to regulate blood flow based on their
metabolic needs. For example, during periods of increased metabolic activity, such as
exercise, tissues release vasoactive substances that cause vasodilation and increase
blood flow to meet their increased demand for oxygen and nutrients.

*Autonomic control refers to the role of the sympathetic and parasympathetic nervous
systems in regulating blood flow in the microcirculatory bed. The sympathetic nervous
system can cause vasoconstriction of the microcirculatory bed in response to stress or
exercise, while the parasympathetic nervous system can cause vasodilation.

*Myogenic control refers to the ability of the vascular smooth muscle cells in the
microcirculatory bed to sense changes in blood pressure and regulate blood flow through
the contraction and relaxation of the vessel walls.

11/Exchange processes in the microcirculatory bed Exchange processes in the microcirculatory bed
occur primarily at the level of the capillaries, where nutrients, oxygen, and metabolic
waste products are exchanged between the blood and the surrounding tissues. These
exchange processes are facilitated by several mechanisms:

*Diffusion: Nutrients and oxygen diffuse from the capillary lumen into the surrounding
tissue, while metabolic waste products diffuse from the tissue into the capillary lumen.
This is driven by concentration gradients, with substances moving from areas of high
concentration to areas of low concentration.

*Convection: Blood flow through the capillaries creates a convective force that helps to
move substances across the capillary wall. This is particularly important for larger
molecules, such as proteins, that may be too large to passively diffuse across the
capillary wall.

*Transcytosis: Some substances, such as insulin and certain nutrients, can be

transported across the capillary wall by specialized transport mechanisms known as
transcytosis.

*Filtration and reabsorption: Fluid and small solutes are filtered out of the capillary
lumen and into the interstitial space, where they can be taken up by surrounding cells or
returned to the circulation through the lymphatic system. This process is balanced by
reabsorption of fluid and solutes back into the capillary lumen, which helps to maintain
fluid balance in the tissues.
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12/The movement of blood in the capillaries, its peculiari es. The movement of blood in the capillaries is
characterized by a slow and intermittent flow, with blood cells passing through the
capillary bed in single file. This slow flow allows for efficient exchange of oxygen,
nutrients, and waste products between the blood and the surrounding tissues. /
Capillaries are characterized by their thin walls and narrow diameter, which allows for
efficient diffusion of substances across the vessel wall. Blood flow through the capillaries
is regulated by the precapillary sphincters, which are rings of smooth muscle that control
blood flow into and out of the capillary bed. These sphincters are sensitive to local
metabolic demands and can open or close in response to changes in tissue oxygenation
and metabolic activity. In addition to the slow and intermittent flow, blood flow in the
capillaries is also characterized by a high degree of heterogeneity. This is due to
differences in the diameter and density of the capillaries, as well as differences in the
distribution of the precapillary sphincters. This heterogeneity allows for efficient
distribution of oxygen and nutrients to the tissues, with high-flow areas delivering more
oxygen and nutrients to tissues with higher metabolic demands.

13/ Mechanisms of exchange of uids and other substances between blood and ssues. The exchange of fluids
and other substances between the blood and tissues occurs primarily through two
mechanisms: diffusion and bulk flow. These mechanisms play roles in maintaining
homeostasis and facilitating the delivery of oxygen, nutrients, hormones, and other
essential substances to cells while removing waste products. these mechanisms

*Diffusion is the passive movement of molecules or ions from an area of higher

concentration to an area of lower concentration. It occurs across the thin-walled
capillaries, which are the smallest blood vessels, forming an extensive network
throughout the body tissues. The capillary walls are composed of a single layer of
endothelial cells that allow for the exchange of substances between the blood and
tissues.

*Oxygen and Nutrient Exchange: Oxygen and nutrients, such as glucose and amino
acids, are transported in the bloodstream and diffuse out of the capillaries into the
surrounding tissues. This diffusion is driven by the concentration gradient between the
blood and tissues, with higher levels of oxygen and nutrients in the blood and lower
levels in the tissues. Simultaneously, waste products, such as carbon dioxide and
metabolic byproducts, diffuse from the tissues into the capillaries to be transported
away.

*Lipid-soluble substances, such as hormones and certain drugs, can diffuse directly
through the endothelial cell membranes of capillaries to enter or exit the bloodstream.
This process is facilitated by the lipid bilayer of the cell membranes, which allows the
substances to dissolve and pass through.

*Bulk flow refers to the movement of fluids, such as blood plasma, between the blood
capillaries and the interstitial spaces of tissues. It is driven by pressure gradients and
occurs through two processes: filtration and reabsorption.

*Filtration is the movement of fluid from the capillaries into the interstitial spaces. It is
primarily driven by hydrostatic pressure, which is the pressure exerted by the fluid
within the capillaries. This pressure pushes fluid and small solutes out of the capillaries
and into the surrounding tissues. Filtration helps deliver nutrients, oxygen, and other
substances to the tissues.

*Reabsorption is the movement of fluid from the interstitial spaces back into the
capillaries. It is influenced by osmotic pressure, which is the pressure exerted by
solutes, particularly plasma proteins, within the capillaries. Osmotic pressure draws fluid
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 back into the capillaries, preventing excessive fluid loss and maintaining the fluid
balance between the blood and tissues.

The balance between filtration and reabsorption is essential for maintaining fluid
homeostasis and preventing the accumulation of excess fluid in the tissues (edema).

These mechanisms of diffusion and bulk flow work together to ensure the exchange of
fluids, gases, nutrients, waste products, and other substances between the blood and
tissues. They rely on various factors, including concentration gradients, pressure
differentials, and the permeability of capillary walls, to facilitate efficient exchange and
support the metabolic needs of cells throughout the body.

14/ The lympha c system, the regula on of lympha c circula on, func ons of lymph. The lymphatic system is a
network of vessels, nodes, and organs that work together to transport lymph, a clear
fluid, throughout the body. It plays a crucial role in maintaining fluid balance, immune
function, and the absorption of fats from the digestive system. Here's an overview of the
lymphatic system, the regulation of lymphatic circulation, and the functions of lymph:

*Lymphatic vessels are thin-walled tubes that collect lymph from the tissues and
transport it back towards the bloodstream. They have one-way valves that prevent the
backflow of lymph and help maintain the unidirectional flow.

*Lymph nodes are small, bean-shaped structures scattered along the lymphatic vessels.
They filter lymph, removing foreign substances, such as bacteria, viruses, and abnormal
cells, and activating immune responses. Lymph nodes also produce lymphocytes, a type
of white blood cell involved in immune defense.

*Lymphatic Organs: The lymphatic system includes various organs, such as the spleen,
thymus, and tonsils, which are involved in immune responses. The spleen filters the
blood and removes old or damaged red blood cells, while also producing lymphocytes
and antibodies. The thymus plays a role in the development and maturation of T-
lymphocytes. The tonsils are collections of lymphatic tissue located in the throat that
help defend against inhaled or ingested pathogens.

*Lymphatic circulation is regulated by various factors, including muscle contractions,

respiratory movements, and the pulsations of nearby blood vessels. Smooth muscle cells
in the walls of lymphatic vessels contract to propel lymph forward, while valves ensure
the one-way flow. The pressure changes during muscle contractions and breathing assist
in the movement of lymph through the vessels.

Functions of Lymph: *Fluid Balance: One of the primary functions of the lymphatic
system is to maintain fluid balance in the body. Excess fluid, proteins, and solutes that
are not reabsorbed by the blood capillaries are taken up by the lymphatic vessels and
returned to the bloodstream, preventing the accumulation of interstitial fluid and the
development of edema.

*Immune Function: Lymph plays a role in immune defense. Lymphatic vessels collect
pathogens, foreign particles, and abnormal cells from the tissues and transport them to
the lymph nodes. Within the lymph nodes, immune cells such as lymphocytes and
macrophages eliminate these threats and initiate immune responses.

*Absorption of Fats: The lymphatic system also plays a role in the absorption of dietary
fats. Lacteals, specialized lymphatic vessels in the small intestine, absorb fats and fat-
soluble vitamins from the digestive system. The absorbed fats form a milky fluid called
chyle, which is transported through the lymphatic vessels to the bloodstream.
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 *Transport of Cells and Molecules: Lymph transports various cells and molecules,
including immune cells, hormones, and waste products, throughout the body. It serves
as a conduit for these substances, allowing them to reach their target tissues and
organs.

15/ The concept of vascular tone: basal and adjustable tone. E ect of blood volume on vascular tone. Vascular tone
refers to the degree of constriction or relaxation of blood vessels, which determines the
resistance to blood flow in the circulatory system. Basal vascular tone refers to the
inherent level of constriction or relaxation that is maintained in blood vessels, whereas
adjustable vascular tone refers to the ability of blood vessels to respond to various
stimuli by either constricting or dilating.

*The basal vascular tone is maintained by the balance between the vasoconstrictor and
vasodilator mechanisms that act on the smooth muscle cells in the vessel walls.
Vasoconstrictors, such as norepinephrine and endothelin, increase vascular tone by
causing smooth muscle contraction, while vasodilators, such as nitric oxide and
prostacyclin, decrease vascular tone by relaxing smooth muscle cells.

*Adjustable vascular tone is influenced by a variety of factors, including neural,

hormonal, and metabolic factors. For example, sympathetic nerve activity can cause
vasoconstriction, while parasympathetic activity can cause vasodilation. Hormones such
as adrenaline, angiotensin II, and vasopressin can also influence vascular tone.

Blood volume also plays a role in the regulation of vascular tone. When blood volume
increases, there is an increase in the amount of blood flowing through the blood vessels,
which stretches the vessel walls and stimulates the release of the hormone atrial
natriuretic peptide (ANP) from the heart. ANP acts as a vasodilator, causing relaxation of
the smooth muscle cells in the vessel walls and decreasing vascular tone. On the other
hand, a decrease in blood volume can stimulate the release of hormones such as renin
and aldosterone, which can cause vasoconstriction and increase vascular tone.

16/ Modula ng func on of the vascular wall The vascular wall, which is composed of endothelial
cells, smooth muscle cells, and extracellular matrix, plays an important role in regulating
blood flow and maintaining cardiovascular homeostasis. the ways in which the vascular
wall modulates its function:

*The endothelial cells that line the inner surface of blood vessels have many functions,
including the regulation of vascular tone, the prevention of platelet aggregation and
thrombosis, and the promotion of angiogenesis. Endothelial cells can also produce and
release various vasoactive substances such as nitric oxide, prostacyclin, and endothelin,
which can modulate vascular tone.

*The smooth muscle cells in the vascular wall can contract and relax to regulate blood
flow and vascular resistance. The degree of smooth muscle contraction is controlled by
various vasoactive substances, such as norepinephrine, angiotensin II, and endothelin,
which can cause vasoconstriction, and nitric oxide and prostacyclin, which can cause
vasodilation.

*The extracellular matrix provides structural support to the blood vessels and can also
modulate their function. For example, the ECM can regulate smooth muscle cell
proliferation and migration, as well as endothelial cell adhesion and migration.

*Inflammation can also modulate the function of the vascular wall. Chronic inflammation
can cause damage to the endothelial cells, leading to endothelial dysfunction, which is
characterized by a decrease in the production of nitric oxide and an increase in
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 vasoconstrictor substances such as endothelin. This can contribute to the development
of atherosclerosis and other cardiovascular diseases.

17/ Local mechanisms of regula on of vascular tone: 1.metabolic regula on; 2.reac ve hyperemia; 3.myogenic
autoregula on and endogenous vasomotor phenomena Local mechanisms of regulation of vascular
tone are critical for maintaining blood flow to different organs and tissues under various
physiological conditions. Here are three examples of local mechanisms of vascular tone
regulation:

*Metabolic regulation refers to the ability of tissues to produce and release metabolites
that can cause vasodilation and increase blood flow. During exercise, for example,
skeletal muscles produce metabolites such as adenosine, nitric oxide, and potassium
ions, which can dilate blood vessels and increase blood flow to meet the increased
metabolic demands of the muscle.

*Reactive hyperemia refers to the transient increase in blood flow that occurs in
response to a brief period of ischemia (lack of blood flow). This mechanism is mediated
by the release of vasodilator substances such as adenosine and nitric oxide, which dilate
blood vessels and increase blood flow to the ischemic tissue.

*Myogenic autoregulation and endogenous vasomotor phenomena: Myogenic

autoregulation refers to the ability of blood vessels to maintain constant blood flow
despite changes in perfusion pressure. When perfusion pressure increases, the smooth
muscle cells in the vessel walls contract to prevent excessive blood flow, while when
perfusion pressure decreases, they relax to maintain blood flow. Endogenous vasomotor
phenomena, such as the release of endothelial-derived relaxing factors, also contribute
to the regulation of vascular tone and blood flow.

18/ Nervous and humoral regula on of vascular tone The nervous and humoral systems both play
important roles in the regulation of vascular tone.

Nervous regulation:can regulate vascular tone through sympathetic and parasympathetic

inputs. Sympathetic nerve fibers release norepinephrine, which binds to alpha-
adrenergic receptors on smooth muscle cells in blood vessel walls and causes
vasoconstriction. In contrast, parasympathetic nerve fibers release acetylcholine, which
binds to muscarinic receptors on endothelial cells and causes the release of nitric oxide,
leading to vasodilation.

Humoral regulation: regulates vascular tone through the release of vasoactive

substances, such as hormones and peptides. For example, angiotensin II, a hormone
released by the renin-angiotensin-aldosterone system, can cause vasoconstriction by
binding to receptors on smooth muscle cells. Similarly, vasopressin, a peptide hormone
released by the posterior pituitary gland, can also cause vasoconstriction. In contrast,
hormones such as atrial natriuretic peptide and bradykinin can cause vasodilation.

19/ Mechanisms of short-term ac on, which regulate blood pressure: 4.barorecetpor re exes; 5.chemoreceptor re exes;
6.re exes, dependent on central nervous system ischemi Short-term regulation of blood pressure
involves several reflex mechanisms that act quickly to maintain blood pressure within a
narrow range. three examples of such mechanisms:

*Baroreceptor reflexes: Baroreceptors are stretch receptors located in the walls of blood
vessels and the heart that detect changes in blood pressure. When blood pressure
increases, the baroreceptors send signals to the brainstem, which in turn decreases
sympathetic nervous system activity and increases parasympathetic nervous system
activity. This leads to a decrease in heart rate and cardiac output, as well as
vasodilation, which collectively decrease blood pressure. Similarly, when blood pressure
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decreases, the baroreceptors send signals to the brainstem to increase sympathetic
nervous system activity and decrease parasympathetic nervous system activity, leading
to an increase in heart rate and cardiac output, as well as vasoconstriction, which
collectively increase blood pressure.

*Chemoreceptor reflexes: Chemoreceptors are located in the carotid arteries and aortic
arch and detect changes in oxygen, carbon dioxide, and pH levels in the blood. When
oxygen levels decrease or carbon dioxide and pH levels increase, the chemoreceptors
send signals to the brainstem to increase sympathetic nervous system activity and
decrease parasympathetic nervous system activity, leading to an increase in heart rate
and cardiac output, as well as vasoconstriction, which collectively increase blood
pressure.

Reflexes dependent on central nervous system ischemia: These reflexes involve the
release of vasodilator substances, such as adenosine, from the brain in response to a
decrease in cerebral blood flow. Adenosine causes vasodilation and a decrease in blood
pressure by decreasing sympathetic nervous system activity and increasing
parasympathetic nervous system activity.

*the mechanisms of short-term regulation of blood pressure involve various reflexes

that act quickly to maintain blood pressure within a narrow range. Baroreceptor and
chemoreceptor reflexes work together to regulate blood pressure in response to changes
in blood pressure and oxygen, carbon dioxide, and pH levels, respectively. Reflexes
dependent on central nervous system ischemia also play a role in regulating blood
pressure by causing vasodilation and a decrease in sympathetic nervous system activity.

20/ Mechanisms of intermediate-term ac on: 7.changes of transcapillary exchange; 8.decrease of the vascular wall
tension; 9.the renin-angiotensin system. Intermediate-term regulation of blood pressure involves
several mechanisms that act over hours to days to maintain blood pressure within a
narrow range. Here are three examples of such mechanisms:

*Changes of transcapillary exchange: The movement of fluids and solutes between the
blood and the tissues is regulated by the balance between hydrostatic pressure and
osmotic pressure. When blood pressure increases, there is an increase in hydrostatic
pressure, which leads to an increase in transcapillary filtration and a decrease in fluid
reabsorption, resulting in an increase in interstitial fluid volume. This increased
interstitial fluid volume can lead to an increase in lymph flow and a decrease in blood
volume, which can ultimately result in a decrease in blood pressure.

*Decrease of the vascular wall tension: The tension of the vascular wall is regulated by
the tone of the smooth muscle cells in the blood vessel walls. This tone is determined by
the balance between vasoconstrictors and vasodilators. For example, vasodilators such
as nitric oxide and prostacyclin can decrease the tension of the vascular wall and lead to
vasodilation and a decrease in blood pressure.

*The renin-angiotensin system: The renin-angiotensin system is a hormonal system that

regulates blood pressure by controlling the volume of extracellular fluid and the tone of
the blood vessels. The system is activated when blood pressure decreases, causing the
release of renin from the kidneys. Renin converts angiotensinogen, which is produced by
the liver, into angiotensin I. Angiotensin-converting enzyme (ACE) then converts
angiotensin I to angiotensin II, a potent vasoconstrictor that increases blood pressure
by stimulating the release of aldosterone and promoting sodium and water retention.

*the mechanisms of intermediate-term regulation of blood pressure involve changes in

transcapillary exchange, vascular wall tension, and the activation of the renin-
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pressure within a narrow range.

21/ Mechanisms of long-term ac on, which regulate blood pressure: 10. renal regula on of uid volume; 11. ac on of
vasopressin; 12. ac on of aldosterone Long-term regulation of blood pressure involves several
mechanisms that act over days to weeks to maintain blood pressure within a narrow
range. three examples of such mechanisms:

*Renal regulation of fluid volume: The kidneys play a crucial role in regulating blood
pressure by controlling the volume of extracellular fluid. The kidneys filter blood to
remove waste products and excess fluids, which are then excreted as urine. The kidneys
also regulate the reabsorption of sodium and water, which are important determinants
of blood volume. When blood pressure increases, the kidneys excrete more sodium and
water, leading to a decrease in blood volume and ultimately a decrease in blood
pressure.

*Action of vasopressin: Vasopressin, also known as antidiuretic hormone (ADH), is a

hormone produced by the hypothalamus and released by the posterior pituitary gland.
Vasopressin acts on the kidneys to increase water reabsorption, which leads to an
increase in blood volume and ultimately an increase in blood pressure.

*Action of aldosterone: Aldosterone is a hormone produced by the adrenal glands that

regulates the reabsorption of sodium and water in the kidneys. Aldosterone acts on the
distal tubules of the kidneys to increase the reabsorption of sodium and water, which
leads to an increase in blood volume and ultimately an increase in blood pressure.

*the mechanisms of long-term regulation of blood pressure involve renal regulation of

fluid volume, the action of vasopressin, and the action of aldosterone. These mechanisms
act over days to weeks to maintain blood pressure within a narrow range.

22/ Circula on under changes of the volume of blood in the body. The volume of blood in the body is
tightly regulated to maintain proper circulation and adequate delivery of oxygen and
nutrients to the tissues. Changes in blood volume can occur due to various factors such
as bleeding, dehydration, or fluid overload. how the circulatory system responds to
changes in blood volume:

*When there is a decrease in blood volume, such as in cases of bleeding or dehydration,

the body responds by activating several mechanisms to maintain blood pressure and
tissue perfusion. The sympathetic nervous system is activated, leading to increased
heart rate and constriction of blood vessels to maintain blood pressure. The renin-
angiotensin-aldosterone system is also activated, leading to increased retention of salt
and water in the kidneys, which helps to increase blood volume.

*When there is an increase in blood volume, such as in cases of fluid overload, the body
responds by reducing the amount of fluid in the body to maintain proper circulation. This
is achieved by increased excretion of water and sodium by the kidneys, as well as
increased vasodilation to lower blood pressure.

Overall, the circulatory system responds to changes in blood volume by activating

several mechanisms to maintain proper circulation and tissue perfusion. The sympathetic
nervous system and the renin-angiotensin-aldosterone system are activated to increase
blood pressure and fluid retention in cases of decreased blood volume, while increased
excretion of water and sodium and vasodilation help to lower blood pressure and
decrease fluid overload in cases of increased blood volume.

23/ Regula on of blood ow during changes of body posi on. Regulation of blood flow during changes of
body position is crucial to maintain adequate perfusion of all tissues in the body,
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particularly the brain. When the body changes position from lying down to standing up,
there is a rapid redistribution of blood volume from the upper body to the lower body,
which can lead to a decrease in blood pressure and decreased perfusion of vital organs.
how the body regulates blood flow during changes in body position:

*The baroreceptor reflex is a rapid reflex response that helps to regulate blood pressure.
When blood pressure decreases due to changes in body position, stretch receptors called
baroreceptors in the walls of the carotid arteries and aortic arch are activated. This
triggers a reflex response that increases heart rate and constricts blood vessels to
increase blood pressure and maintain adequate perfusion to the brain and other organs.

*Gravity-dependent autoregulation is a mechanism that helps to maintain blood flow to

the brain during changes in body position. When standing up, there is a decrease in
blood flow to the brain due to the gravitational force pulling blood towards the lower
body. To counteract this, the arterioles in the brain dilate in response to decreased blood
flow, which helps to maintain adequate perfusion.

The renin-angiotensin-aldosterone system is activated when blood pressure decreases

due to changes in body position. This system increases the reabsorption of salt and
water in the kidneys, which helps to increase blood volume and maintain blood pressure.

24/ Mechanisms of regula on of local blood ow and microcircula on Local blood flow and microcirculation
are regulated by several mechanisms to ensure an adequate supply of oxygen, nutrients,
and removal of waste products in specific tissues. The regulation of local blood flow
involves both intrinsic (local) and extrinsic (systemic) factors. Here are some
mechanisms of regulation:

*Autoregulation is an intrinsic mechanism that allows tissues to maintain a relatively

constant blood flow despite changes in perfusion pressure. It ensures that blood flow
matches the metabolic demands of the tissue. Autoregulation is mediated by local
factors such as:

*Metabolic Factors: Increased metabolic activity in tissues leads to the release of

vasodilator substances such as adenosine, carbon dioxide, and lactic acid. These
substances cause local arterioles to dilate, increasing blood flow to meet the metabolic
needs of the tissue.

*Myogenic Response: Changes in arterial pressure cause a myogenic response in the

smooth muscle of arterioles. When arterial pressure increases, arterioles constrict to
regulate blood flow. Conversely, when arterial pressure decreases, arterioles dilate to
maintain blood flow.

*Neural Regulation: Neural mechanisms provide extrinsic control of local blood flow
through sympathetic nervous system activity. The sympathetic nerves release
norepinephrine, which binds to alpha-adrenergic receptors on smooth muscle cells of
arterioles, causing vasoconstriction. This reduces blood flow to non-essential tissues
during periods of stress or increased systemic demand.

*Endothelial Factors: The endothelium lining the blood vessels plays a critical role in
regulating local blood flow. Endothelial cells release various substances that modulate
vascular tone, including:

*Nitric Oxide (NO): Endothelial cells release NO, a potent vasodilator. NO diffuses to the
underlying smooth muscle cells and causes relaxation, leading to vasodilation and
increased blood flow.
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*Prostacyclin and Endothelin: Endothelial cells also release prostacyclin, a vasodilator,
and endothelin, a vasoconstrictor. These substances help regulate vascular tone and
blood flow in response to specific physiological conditions.

*Local Inflammatory Response: During inflammation, local blood flow increases to

deliver immune cells and nutrients to the site of injury or infection. Inflammatory
mediators such as histamine and prostaglandins cause vasodilation and increased
capillary permeability, allowing increased blood flow and the recruitment of immune
cells to the area.

*Active Hyperemia and Reactive Hyperemia: Active hyperemia refers to the increase in
blood flow to a tissue in response to increased metabolic activity, while reactive
hyperemia occurs after a period of reduced blood flow Both responses involve the
release of vasodilator substances to restore blood flow to normal levels.

25/ Features of coronary blood ow and its regula on. Coronary blood flow refers to the blood supply
to the heart muscle (myocardium) itself. The coronary circulation ensures that the heart
receives sufficient oxygen and nutrients to meet its high metabolic demands. key
features of coronary blood flow and its regulation:

*The coronary arteries are the main blood vessels that supply the heart muscle. The left
coronary artery branches into the left anterior descending artery (LAD) and the left
circumflex artery, while the right coronary artery (RCA) supplies the right atrium and
most of the right ventricle. These arteries give rise to smaller branches and arterioles
that penetrate the myocardium.

*Diastolic Filling: The majority of coronary blood flow occurs during diastole (the
relaxation phase of the cardiac cycle) when the heart muscle is not contracting. During
diastole, the coronary arteries fill with blood, primarily through the aortic valve and the
openings of the coronary arteries located just above the aortic valve.

*Myogenic Autoregulation: The coronary circulation has the ability to autoregulate its
blood flow to meet the metabolic demands of the heart. When the heart muscle's
metabolic needs increase (e.g., during exercise or increased cardiac workload), local
factors cause vasodilation of the coronary arterioles, increasing blood flow to the
myocardium. Conversely, if metabolic demands decrease, the arterioles constrict to
maintain adequate blood flow.

*Metabolic Factors: play a crucial role in regulating coronary blood flow. Increased
metabolic activity in the myocardium, such as increased oxygen consumption or
accumulation of metabolic byproducts like adenosine, causes local vasodilation of
coronary arterioles. Adenosine acts as a potent vasodilator, helping to increase blood
flow to areas of increased demand.

*Neural Regulation: The sympathetic nervous system can influence coronary blood flow
through the release of norepinephrine. Stimulation of sympathetic nerves can cause
vasoconstriction of coronary arterioles, reducing blood flow. However, during periods of
increased cardiac demand (e.g., exercise), sympathetic stimulation can also lead to
vasodilation of coronary vessels, increasing blood flow to meet the heightened metabolic
requirements.

*Endothelial Factors: Endothelial cells lining the coronary arteries release substances
that regulate vascular tone and blood flow. Nitric oxide (NO) is a potent vasodilator
released by the endothelium, promoting coronary artery dilation and increased blood
flow. Endothelin, a vasoconstrictor, can also be released, contributing to
vasoconstriction under certain conditions.
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 *Collateral Circulation: The coronary circulation has the potential for collateral
circulation, where alternative routes of blood supply develop in response to chronic
obstruction or stenosis in a coronary artery. Collateral vessels help provide a backup
blood supply to regions of the heart in case of reduced blood flow through the main
coronary arteries.

26/ Circula on of the brain and its regula on. The circulation of the brain, known as cerebral
circulation, is responsible for delivering oxygen, glucose, and other essential nutrients to
the brain cells while removing metabolic waste products. The regulation of cerebral
circulation is vital to ensure a constant blood supply and maintain proper brain function.
Here are some key aspects of cerebral circulation and its regulation:

*Cerebral Arteries: The major arteries that supply blood to the brain are the internal
carotid arteries and the vertebral arteries. The internal carotid arteries supply the
anterior portion of the brain, while the vertebral arteries merge to form the basilar
artery, which supplies the posterior portion of the brain. These arteries branch into
smaller vessels, forming an extensive network throughout the brain.

*Blood-Brain Barrier: The blood-brain barrier is a specialized system of tight junctions

between the endothelial cells that line the brain's blood vessels. It restricts the passage
of certain substances, including large molecules and toxins, from the bloodstream into
the brain. The BBB helps maintain a stable and controlled environment for brain cells by
regulating the exchange of substances between the blood and brain tissue.

Autoregulation: The cerebral circulation has a remarkable autoregulatory mechanism

that helps maintain a relatively constant blood flow to the brain despite changes in
systemic blood pressure. Autoregulation allows for consistent perfusion of the brain,
ensuring an adequate oxygen supply. When blood pressure increases, cerebral arterioles
constrict to regulate blood flow, while they dilate in response to decreased blood
pressure. This autoregulatory mechanism helps protect the brain from potential damage
due to fluctuations in blood pressure.

Metabolic factors play a crucial role in regulating cerebral blood flow. When brain cells
become metabolically active, they produce metabolic byproducts such as adenosine,
carbon dioxide, and lactic acid. These substances cause local vasodilation of cerebral
blood vessels, increasing blood flow to meet the increased metabolic demands. This
mechanism ensures that regions of the brain with higher activity receive adequate
oxygen and nutrients.

Neural control through the autonomic nervous system can influence cerebral blood flow.
The sympathetic nervous system activation can cause vasoconstriction of cerebral blood
vessels, reducing blood flow. Conversely, parasympathetic stimulation can lead to
vasodilation and increased blood flow to the brain.

Cerebral Perfusion Pressure is the pressure gradient across the cerebral circulation that
ensures adequate blood flow to the brain. It is calculated as the difference between
mean arterial pressure (MAP) and intracranial pressure (ICP). Maintaining an
appropriate CPP is crucial for preventing ischemia or inadequate perfusion of brain
tissue.

Active Hyperemia and Reactivity: Similar to other tissues, cerebral blood flow can
increase in response to increased metabolic activity (active hyperemia). Additionally,
cerebral circulation exhibits reactivity, which refers to the ability to adjust blood flow in
response to various stimuli, such as changes in blood gas concentrations or neural
activation.
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27/ Physiological features of pulmonary blood ow. Physiological features of pulmonary blood flow
refer to the unique characteristics of the circulatory system that supplies blood to the
lungs. Here are some key features:

Pulmonary Artery: Deoxygenated blood from the right ventricle of the heart is pumped
into the pulmonary artery, which branches into the left and right pulmonary arteries.
These arteries carry deoxygenated blood to the lungs for oxygenation.

Pulmonary Capillaries: The pulmonary arteries further divide into smaller arterioles and
eventually into pulmonary capillaries. The pulmonary capillaries surround the alveoli, the
tiny air sacs in the lungs where gas exchange occurs. The thin walls of the capillaries
allow for efficient diffusion of gases (oxygen and carbon dioxide) between the capillary
blood and alveolar air.

Pulmonary Veins: Oxygenated blood from the pulmonary capillaries is collected by the
pulmonary veins. There are four pulmonary veins in total—two from each lung. These
veins transport oxygenated blood back to the left atrium of the heart, where it is then
pumped into the systemic circulation.

Low Resistance: Compared to the systemic circulation, the pulmonary circulation has
significantly lower resistance. This is due to the short distance between the pulmonary
artery and pulmonary capillaries and the relatively larger diameter of the pulmonary
vessels. The low resistance allows for efficient blood flow and facilitates the exchange of
gases in the lungs.

Pulmonary Vasculature: The pulmonary vasculature has a unique structure that allows it
to accommodate changes in blood volume. The walls of the pulmonary arterioles and
capillaries are thin and contain less smooth muscle compared to systemic vessels. This
design enables them to dilate and constrict more easily, facilitating adjustments in blood
flow to match the oxygen demands of the lungs.

Hypoxic Vasoconstriction: In response to low oxygen levels, the pulmonary arterioles

undergo vasoconstriction, directing blood flow away from poorly ventilated areas of the
lungs. This mechanism, known as hypoxic vasoconstriction, helps optimize gas exchange
by redirecting blood to regions with better ventilation.

Recruitment and Distension: The pulmonary capillaries have the ability to recruit and
distend to accommodate changes in blood flow. During exercise or increased metabolic
demand, capillaries in the alveolar walls open up to increase the surface area available
for gas exchange. Conversely, during periods of decreased blood flow, some capillaries
may collapse or constrict to maintain efficient blood flow in well-ventilated areas of the
lungs.

28/ Physiological features of blood circula on of the abdomen. The blood circulation of the abdomen
includes the major blood vessels and organs within the abdominal cavity. Here are some
key physiological features of the abdominal circulation:

The abdominal aorta :is a large artery that originates from the thoracic aorta and
descends through the abdominal cavity. It supplies oxygenated blood to the abdominal
organs, including the liver, spleen, stomach, intestines, and kidneys.

Branches of the Abdominal Aorta: The abdominal aorta gives rise to several major
branches that supply specific organs and regions within the abdomen. These branches
include the celiac artery, superior mesenteric artery, inferior mesenteric artery, and
renal arteries. These arteries provide oxygenated blood to the respective organs and
regions.
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 Portal Circulation: The abdominal circulation involves the unique portal venous system.
The portal vein collects nutrient-rich, deoxygenated blood from the gastrointestinal
tract, spleen, and pancreas. It carries this blood to the liver, where nutrients are
metabolized and detoxified before being released into the systemic circulation. This
portal circulation ensures efficient nutrient absorption and detoxification within the
liver.

The superior mesenteric artery and inferior mesenteric artery supply blood to the
intestines and colon, respectively. These arteries branch into smaller vessels that form
an extensive network within the intestinal walls, providing oxygen and nutrients for
digestion and absorption processes.

Hepatic Circulation: The blood flow within the liver is unique and complex. Oxygenated
blood is supplied to the liver via the hepatic artery, a branch of the celiac artery.
Deoxygenated blood from the intestines and other abdominal organs enters the liver
through the portal vein. The hepatic artery and portal vein merge within the liver
sinusoids, where nutrient-rich blood is processed by liver cells (hepatocytes).

Venous Drainage: Deoxygenated blood from the abdominal organs is collected by the
hepatic veins and eventually drains into the inferior vena cava, which carries the blood
back to the heart. Additionally, the renal veins collect deoxygenated blood from the
kidneys and drain into the inferior vena cava.

Autonomic Nervous System: The autonomic nervous system plays a significant role in
regulating abdominal circulation. Sympathetic nerve fibers innervate the abdominal
blood vessels, regulating their diameter and blood flow. Sympathetic stimulation can
cause vasoconstriction, reducing blood flow to non-essential organs during periods of
stress or exercise. Parasympathetic fibers also contribute to the regulation of blood flow
by modulating the vascular tone.

29/ Blood as a ssue and a system. The main func ons of blood. Blood can be considered both a tissue
and a system in the human body. As a tissue, blood is a specialized connective tissue
that is composed of various types of cells and an extracellular matrix called plasma. As a
system, the circulatory system is responsible for transporting blood throughout the
body. The main functions of blood are as follows:

Transportation: Blood carries oxygen from the lungs to the body's tissues and removes
carbon dioxide from the tissues to be exhaled from the lungs. It also transports
nutrients, hormones, waste products, and heat throughout the body.

Regulation: Blood helps to maintain the body's pH balance, temperature, and fluid
balance by carrying and distributing hormones, enzymes, and electrolytes.

Protection: Blood contains white blood cells (leukocytes) that help to fight infection and
disease by attacking foreign invaders such as viruses, bacteria, and cancer cells. It also
contains clotting factors that help to stop bleeding and prevent blood loss after an injury.

*blood plays a vital role in the functioning of the body by transporting essential
substances, regulating internal environment, and protecting against diseases and
injuries.

30/ Physic-and-chemical proper es of blood. Blood has a number of physical and chemical
properties that are essential for its normal functioning in the body. Some of these
properties include:

*Blood is a highly viscous liquid, meaning that it is thick and has a high resistance to
flow. This is due to the presence of various proteins and other molecules in the plasma.
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 *The pH of blood is tightly regulated and maintained within a narrow range of 7.35-7.45.
This is important for the proper functioning of enzymes and other molecules in the body.

*Osmolarity: Blood has an osmolarity of around 300 mOsm/L, which helps to maintain
the balance of water and electrolytes in the body.

*Temperature: The temperature of blood is typically around 37°C, which is the optimal
temperature for enzymatic reactions and other metabolic processes in the body.

*Clotting: Blood contains clotting factors that are activated in response to injury to help
stop bleeding and prevent blood loss.

*Blood is able to transport oxygen and carbon dioxide due to the presence of hemoglobin
in red blood cells.

*Antibody production: Blood contains white blood cells that are capable of producing
antibodies in response to foreign invaders such as viruses and bacteria.

31/ Acid-base status of blood, the role of bu er systems in its regula on. The acid-base balance of the blood
is critical for maintaining normal physiological functions. The pH of blood is tightly
regulated within a narrow range of 7.35-7.45. Any changes in blood pH can affect the
function of enzymes, alter cellular function, and ultimately lead to organ failure.

The regulation of blood pH is maintained by buffer systems. Buffer systems are

composed of weak acids and their corresponding conjugate bases. The buffer systems in
the blood include the bicarbonate buffer system, the phosphate buffer system, and the
protein buffer system. These buffer systems work together to maintain the pH of the
blood within the normal range.

The bicarbonate buffer system is the primary buffer system in the blood. Carbon dioxide
produced by metabolic processes reacts with water to form carbonic acid ,which is a
weak acid. Carbonic acid then dissociates into bicarbonate and a hydrogen ion .This
reaction is reversible, so if there is an excess of hydrogen ions, bicarbonate ions can
combine with hydrogen ions to form carbonic acid, which can then be converted back to
carbon dioxide and water. This helps to prevent any significant changes in pH.

The phosphate buffer system works in a similar way to the bicarbonate buffer system,
except that the buffer components are phosphate ions rather than bicarbonate ions. The
protein buffer system involves amino acids and proteins that can act as buffers,
accepting or donating hydrogen ions as needed to maintain the pH.

Overall, buffer systems play a crucial role in regulating the acid-base balance of the
blood. They help to maintain the pH of the blood within the normal range, ensuring that
the body's enzymes and cells function properly. Any imbalances in the buffer systems
can lead to acid-base disturbances, which can have serious consequences on the body's
overall functioning.

32/ The composi on of blood, and blood volume. Hematocrit value. Blood is a fluid connective tissue that
consists of cellular components and a liquid portion called plasma. The composition of
blood includes:

*Plasma: makes up about 55% of total blood volume. It is a straw-colored fluid that
contains water, proteins, electrolytes, hormones, gases, nutrients, and waste products.
Plasma serves as a medium for transporting cells, nutrients, and waste products
throughout the body.
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 *Red Blood Cells (Erythrocytes): make up the majority of cellular components in blood.
They constitute about 45% of total blood volume. Red blood cells contain the protein
hemoglobin, which binds and carries oxygen from the lungs to the body tissues. They
also play a role in carbon dioxide transport.

*White Blood Cells (Leukocytes): are involved in the body's immune response to
infection and play a role in defending against foreign substances. They are present in
much smaller numbers compared to red blood cells. There are different types of white
blood cells, including neutrophils, lymphocytes, monocytes, eosinophils, and basophils.

*Platelets (Thrombocytes) are small cell fragments involved in blood clotting and
hemostasis. They help in forming blood clots to prevent excessive bleeding from injured
blood vessels.

*The total blood volume in the body varies depending on factors such as age, sex, body
size, and overall health. On average, blood volume is about 7% to 8% of body weight.

*Hematocrit value refers to the percentage of red blood cells in the total blood volume.
It is a measure of the packed cell volume (PCV) and indicates the proportion of cellular
components in blood. Hematocrit values can vary based on age, sex, and overall health.
In healthy adult males, the normal hematocrit range is typically around 40% to 52%,
while in healthy adult females, it is around 36% to 48%.

Hematocrit values are used to assess the oxygen-carrying capacity of blood and
diagnose conditions such as anemia (low hematocrit) or polycythemia (high hematocrit).
Changes in hematocrit can also occur due to dehydration, certain diseases, or medical
treatments.

33/ The composi on of plasma and physiological signi cance of its components. Plasma is the liquid portion
of blood that constitutes about 55% of total blood volume. It is a complex mixture of
water, proteins, electrolytes, hormones, gases, nutrients, waste products, and other
substances. the major components of plasma and their physiological significance:

*Water: is the main component of plasma, accounting for approximately 90-92% of its
volume. It serves as a solvent, providing a medium for the transportation of substances
throughout the body. Water helps maintain blood pressure, regulates body temperature,
and facilitates chemical reactions in the body.

*Proteins: Plasma contains various proteins, including albumin, globulins, and

fibrinogen.

Albumin: Albumin is the most abundant protein in plasma and plays a vital role in
maintaining osmotic pressure. It helps regulate the distribution of water between the
blood and tissues, thereby maintaining fluid balance.

Globulins: Globulins are involved in various functions, including transport of lipids,

vitamins, and hormones, as well as immune response by functioning as antibodies.

Fibrinogen: Fibrinogen is essential for blood clotting. It plays a key role in the formation
of fibrin, a protein that forms a mesh-like structure to create blood clots and stop
bleeding.

*Electrolytes: Plasma contains electrolytes such as sodium, potassium, calcium, chloride,

bicarbonate, and phosphate. These electrolytes play crucial roles in maintaining the
balance of fluids, regulating pH levels, conducting nerve impulses, and supporting
muscle function.
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 *Hormones: Various hormones, such as insulin, cortisol, thyroid hormones, and
reproductive hormones, are transported in the plasma. They play essential roles in
regulating metabolism, growth, development, reproduction, and other

physiological processes.

*Gases: Oxygen (O2) and carbon dioxide (CO2) are transported in the plasma. Oxygen
binds to hemoglobin in red blood cells for transport to tissues, while carbon dioxide, a
waste product of cellular metabolism, is carried from tissues back to the lungs for
elimination.

Nutrients: Plasma carries nutrients derived from the digestive system, such as glucose,
amino acids, fatty acids, vitamins, and minerals. These nutrients are transported to the
body's cells to support energy production, growth, and repair.

Waste Products: Metabolic waste products, such as urea, creatinine, and bilirubin, are
carried in the plasma. They are transported to the kidneys and liver for excretion or
further processing.

The components of plasma work together to maintain homeostasis, transport essential

substances, regulate fluid balance, support immune function, facilitate blood clotting,
and ensure proper functioning of various physiological processes in the body. Changes in
the composition of plasma can indicate certain diseases or imbalances, making plasma
analysis an important diagnostic tool in healthcare.

34/ Osmo c resistance of red blood cells, factors that a ect it : Osmotic resistance of red blood cells
refers to the ability of red blood cells to resist lysis (bursting) when exposed to
hypotonic (low salt concentration) solutions. This is an important characteristic of RBCs
because it determines their ability to function properly in the body. Factors that affect
osmotic resistance of RBCs include:

*Membrane composition: The lipid and protein composition of the RBC membrane can
affect its ability to resist lysis. For example, changes in the ratio of cholesterol to
phospholipids can alter the fluidity of the membrane, which in turn affects its stability.

*Surface area-to-volume ratio: RBCs have a high surface area-to-volume ratio, which
allows for efficient gas exchange. However, this also means that they are more
susceptible to lysis in hypotonic solutions.

*Electrolyte concentrations: The concentrations of various electrolytes, such as sodium,

potassium, and chloride, can affect the osmotic resistance of RBCs. For example, a
decrease in extracellular sodium concentration can cause water to move into the RBCs,
leading to lysis.

*pH: Changes in pH can affect the charge on the RBC membrane and alter its ability to
resist lysis.

*Hemoglobin concentration: Hemoglobin is the protein responsible for carrying oxygen

in RBCs. Changes in hemoglobin concentration can affect the osmotic resistance of RBCs,
as it can alter the overall volume of the cell.

*Presence of other substances: Various substances, such as urea and glucose, can affect
the osmotic resistance of RBCs. For example, the presence of high levels of glucose in
diabetes can cause RBCs to become more susceptible to lysis.

35/ The sedimenta on of erythrocytes, factors that a ect it. The erythrocyte sedimenta on rate Erythrocyte
sedimentation rate (ESR) is a laboratory test that measures the rate at which red blood
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cells (erythrocytes) settle in a vertical tube over a period of time. The sedimentation rate
of erythrocytes can be affected by a number of factors, including:

*Inflammatory conditions: ESR is often used as a marker of inflammation, as it tends to

increase in conditions such as rheumatoid arthritis, lupus, and infections. Inflammation
can cause changes in the shape and size of erythrocytes, making them more likely to
settle faster.

*Age and gender: ESR tends to be higher in women than in men, and it also tends to
increase with age.

*Anemia: A low red blood cell count or hemoglobin level can cause erythrocytes to settle
faster, resulting in an elevated ESR.

*Pregnancy: ESR tends to increase during pregnancy, likely due to changes in blood
volume and viscosity.

*Medications: Certain medications, such as corticosteroids and oral contraceptives, can

affect ESR levels.

*Blood viscosity: Changes in blood viscosity can affect the rate at which erythrocytes
settle. For example, dehydration can increase blood viscosity and cause erythrocytes to
settle faster, resulting in an elevated ESR.

*Plasma proteins: Changes in the concentration of plasma proteins, such as fibrinogen,

can affect erythrocyte sedimentation rate.

36/ The concept of erythron; the regula on of red blood cells The erythron refers to the collection of
cells, tissues, and organs involved in the production and regulation of red blood cells
(RBCs). This includes the bone marrow, where RBCs are produced, as well as the kidneys
and liver, which play a role in regulating RBC production.

*The regulation of red blood cells involves a complex feedback mechanism that ensures
the body produces enough RBCs to meet its oxygen-carrying needs. This process is
primarily regulated by a hormone called erythropoietin (EPO), which is produced by the
kidneys in response to low oxygen levels in the blood. When oxygen levels in the blood
decrease, EPO is released into the bloodstream and travels to the bone marrow, where it
stimulates the production of RBCs. As RBCs are produced and oxygen levels in the blood
increase, EPO production decreases, helping to maintain a balance between RBC
production and oxygen-carrying capacity.

Other factors that can affect RBC production include:

*Iron levels: Iron is an essential component of hemoglobin, the protein in RBCs that
carries oxygen. Low iron levels can lead to a decrease in RBC production.

*Vitamin B12 and folate levels: These vitamins are necessary for RBC production, and
deficiencies can lead to anemia.

*Chronic kidney disease: Kidneys play a critical role in regulating RBC production
through the production of EPO. Chronic kidney disease can lead to a decrease in EPO
production and subsequent anemia.

*Hormonal imbalances: Hormones such as testosterone and estrogen can affect RBC
production.

*Blood loss: Acute or chronic blood loss can lead to a decrease in RBC production and
subsequent anemia.
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Overall, the regulation of RBC production is a complex process that involves multiple
factors, including hormones, vitamins, and minerals. The balance between RBC
production and oxygen-carrying capacity is critical for maintaining overall health and
wellbeing.

37/Erythrocytes. The structure, features and func ons of erythrocytes Erythrocytes, or red blood cells, are
the most abundant type of blood cell in the human body. They are specialized cells that
are responsible for carrying oxygen from the lungs to the tissues and removing carbon
dioxide from the tissues to the lungs for exhalation. structure, and functions of
erythrocytes:

*Erythrocytes are biconcave, disc-shaped cells that lack a nucleus and most organelles.
This allows for a larger surface area-to-volume ratio, which facilitates efficient gas
exchange. They are filled with hemoglobin, a protein that binds to oxygen and carries it
throughout the body. Each erythrocyte contains about 270 million hemoglobin
molecules. Erythrocytes have a lifespan of about 120 days, after which they are
removed from circulation and broken down by the spleen and liver.

Structure: The cell membrane of erythrocytes is made up of lipids and proteins and is
highly flexible, allowing the cells to squeeze through narrow capillaries. The cytoplasm
of erythrocytes contains hemoglobin, which makes up about one-third of the cell's
weight. Erythrocytes are formed in the bone marrow, where they go through a series
of developmental stages before being released into circulation.

Functions: Erythrocytes are responsible for transporting oxygen from the lungs to the
tissues and removing carbon dioxide from the tissues to the lungs. They are able to
achieve this function efficiently due to their shape, size, and high hemoglobin content.
The binding and release of oxygen by hemoglobin is facilitated by changes in pH and the
partial pressure of oxygen in the blood. Erythrocytes also play a role in maintaining the
pH balance of the blood by transporting carbon dioxide to the lungs for exhalation.

38/ The amount of erythrocytes and its changes in physiological condi ons. The amount of erythrocytes, or
red blood cells, in the body can vary based on several physiological conditions. The
normal range for erythrocyte count in adult men is 4.5 to 5.5 million cells per microliter
(mcL) of blood, while for adult women, it is 4.0 to 5.0 million cells/mcL.

Changes in erythrocyte count can occur due to various physiological conditions such as :

*High altitude: At high altitudes, there is a lower concentration of oxygen in the air. This
causes the body to produce more erythrocytes to increase the oxygen-carrying capacity
of the blood.

*Exercise: During exercise, the body's oxygen demand increases. This causes the body
to produce more erythrocytes to deliver more oxygen to the muscles.

*Pregnancy: During pregnancy, the body produces more erythrocytes to support the
increased oxygen demand of the growing fetus.

*Blood loss: Acute or chronic blood loss can lead to a decrease in erythrocyte count and
subsequent anemia.

*Kidney disease: Chronic kidney disease can lead to a decrease in erythropoietin

production, a hormone that stimulates erythrocyte production, resulting in anemia.

*Vitamin and mineral deficiencies: Iron, vitamin B12, and folate are essential for
erythrocyte production. Deficiencies in these nutrients can lead to a decrease in
erythrocyte count and anemia.
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*Certain medications: Some medications, such as chemotherapy drugs, can cause a
decrease in erythrocyte count.

39/ Hemolysis; the types of hemolysis. Mechanisms of osmo c hemolysis. Hemolysis is the breakdown of
erythrocytes, or red blood cells, and the release of their contents into the bloodstream.
There are three types of hemolysis: osmotic hemolysis, mechanical hemolysis, and
immune hemolysis.

*Osmotic hemolysis occurs when erythrocytes are placed in a solution that is hypotonic,
meaning it has a lower concentration of solutes than the cytoplasm of the erythrocyte.
Water moves into the erythrocyte due to the concentration gradient, causing it to swell
and potentially burst, leading to hemolysis.

mechanism of osmotic : When erythrocytes are placed in a hypotonic solution, water

moves into the cells due to the concentration gradient. The influx of water causes the
erythrocytes to swell, and their volume increases. The increased volume of erythrocytes
causes an increase in their internal pressure, which can lead to the rupture of the cell
membrane. Once the cell membrane ruptures, hemoglobin is released into the
bloodstream, and the erythrocyte is destroyed.

There are two types of osmotic hemolysis: physiological and pathological. Physiological
osmotic hemolysis occurs during the normal life cycle of erythrocytes, as they are
constantly exposed to hypotonic conditions in the bloodstream. However, the
erythrocytes are able to maintain their integrity due to their unique structure and
membrane properties. Pathological osmotic hemolysis occurs in diseases such as
hereditary spherocytosis, where the erythrocyte membrane is defective, making them
more susceptible to hemolysis in hypotonic conditions. Another example is in sickle cell
disease, where the sickled erythrocytes are more prone to osmotic hemolysis due to
their abnormal shape and membrane properties.

40/ Hemoglobin, its types, amount, composi on, and compounds of hemoglobin Hemoglobin is a protein
found in erythrocytes, or red blood cells, that is responsible for carrying oxygen from the
lungs to the tissues of the body. Hemoglobin also helps transport carbon dioxide from
the tissues back to the lungs, where it is eliminated from the body. There are several
types of hemoglobin :

Hemoglobin A (HbA): This is the most common type of hemoglobin in adult humans,
accounting for about 97% of hemoglobin. HbA is composed of two alpha globin chains
and two beta globin chains.

Hemoglobin A2 (HbA2): This type of hemoglobin accounts for about 2-3% of hemoglobin
and is composed of two alpha globin chains and two delta globin chains.

Hemoglobin F (HbF): This type of hemoglobin is primarily found in fetuses and

newborns, accounting for about 60-80% of hemoglobin at birth. HbF is composed of two
alpha globin chains and two gamma globin chains.

*The amount of hemoglobin in the blood can vary depending on age, sex, and health
status. The normal range for adult males is 13.5-17.5 grams per deciliter (g/dL), and for
adult females, it is 12.0-15.5 g/dL.

*The composition of hemoglobin is primarily protein, with each hemoglobin molecule

consisting of four globin chains (alpha, beta, delta, or gamma) and four heme groups.
The heme group contains an iron atom that binds to oxygen and gives hemoglobin its
characteristic red color.
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 *Hemoglobin can also bind to other compounds, including carbon dioxide and nitric
oxide. When carbon dioxide binds to hemoglobin, it forms carbaminohemoglobin, which
helps transport carbon dioxide from the tissues back to the lungs. When nitric oxide
binds to hemoglobin, it helps regulate blood flow and blood pressure in the body.

Overall, hemoglobin plays a critical role in oxygen transport and carbon dioxide
elimination in the body. The different types of hemoglobin have varying compositions,
with HbA being the most common in adult humans. Hemoglobin can also bind to other
compounds such as carbon dioxide and nitric oxide, which are important for regulating
blood flow and blood pressure in the body.

41/ Criteria for red blood cell satura on by hemoglobin. Colour index, its value and signi cance Red blood cell
saturation by hemoglobin is determined by several criteria, including the oxygen
saturation level of hemoglobin, the concentration of hemoglobin in the erythrocytes, and
the number of erythrocytes in circulation.

*One measure of red blood cell saturation is the color index, which is the ratio of the
amount of hemoglobin to the number of erythrocytes in a given volume of blood. The
color index is calculated by dividing the hemoglobin concentration (in grams per deciliter
or g/dL) by the erythrocyte count (in millions per cubic millimeter or million/mm3). The
normal range for the color index is 0.8-1.0, indicating that the amount of hemoglobin is
roughly proportional to the number of erythrocytes.

*The color index can be used as an indicator of anemia or polycythemia. Anemia is a

condition characterized by a decrease in the number of erythrocytes or a decrease in
hemoglobin concentration, leading to a decreased color index. Polycythemia is a
condition characterized by an increase in the number of erythrocytes or an increase in
hemoglobin concentration, leading to an increased color index.

*The significance of the color index lies in its ability to provide information about the
oxygen-carrying capacity of the blood. A normal color index indicates that the blood has
an adequate amount of hemoglobin to transport oxygen to the tissues. Abnormal color
index values can indicate a range of conditions affecting the erythrocytes or hemoglobin,
and can help guide diagnosis and treatment.

42/ Classi ca on of white blood cells. White blood cells, also known as leukocytes, are a diverse
group of immune cells that play an important role in protecting the body from infections
and diseases. There are five main types of white blood cells, each with their own unique
structure and function:

Neutrophils: These are the most abundant type of white blood cells and are the first line
of defense against infections. They are characterized by their multilobed nucleus and the
presence of small granules in their cytoplasm.

Lymphocytes: These are the second most abundant type of white blood cells and are
responsible for specific immune responses. They include B cells, T cells, and natural
killer cells, each with their own unique role in recognizing and attacking foreign
invaders.

Monocytes: These are large white blood cells with a single kidney-shaped nucleus. They
can differentiate into macrophages and dendritic cells, which play a crucial role in
phagocytosis and antigen presentation, respectively.

Eosinophils: These are specialized white blood cells that are involved in the body's
response to parasitic infections and allergic reactions. They are characterized by their bi-
lobed nucleus and the presence of large granules in their cytoplasm.
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 Basophils: These are the least abundant type of white blood cells and are involved in the
body's response to allergies and parasitic infections. They are characterized by their
multi-lobed nucleus and the presence of large granules in their cytoplasm

43/ The number of leukocytes in peripheral blood in normal state. Physiological changes in the number of cells and
factors that a ect their numbers. The normal number of leukocytes in peripheral blood can vary
depending on a person's age, gender, and overall health status. However, in general, the
normal is 4,000 to 11,000 cells per microliter (mcL) of blood. This number includes all
five main types of white blood cells: neutrophils, lymphocytes, monocytes, eosinophils,
and basophils. The specific number of each type of white blood cell in peripheral blood
can also vary, with neutrophils typically being the most abundant and basophils being
the least abundant. The abnormal levels of leukocytes in peripheral blood, either too
high or too low, can be a sign of an underlying health condition and may require further
medical evaluation. Physiological changes in the number of leukocytes can occur during
certain situations, such as:

*Infection: In response to an infection, the body may produce more white blood cells in
order to fight off the invading pathogen. This can cause a temporary increase in the
number of leukocytes in the blood.

*Exercise: Intense physical activity or exercise can cause a temporary increase in the
number of leukocytes in the blood. This is thought to be due to the release of stress
hormones such as cortisol.

*Pregnancy: The number of leukocytes in the blood can increase during pregnancy due
to the increased demand for immune cells to protect both the mother and developing
fetus.

Factors that can affect the number of leukocytes in the blood include:

*Age: The number of leukocytes in the blood can vary with age, with newborns typically
having higher levels of white blood cells than adults.

*Gender: Females tend to have slightly higher levels of white blood cells in the blood
compared to males.

*Medications: Certain medications, such as steroids or chemotherapy drugs, can affect

the number of leukocytes in the blood.

*Medical conditions: Certain medical conditions, such as autoimmune diseases,

infections, or cancer, can cause an increase or decrease in the number of leukocytes in
the blood.

44/ Leukocyte counts, the methods of its determina on Leukocyte counts are determined by measuring
the number of white blood cells (leukocytes) present in a sample of blood. The most
common methods used to determine leukocyte counts include:

*Automated cell counting: This method uses automated instruments, such as a

hematology analyzer, to count the number of cells in a blood sample. The instrument
counts the cells based on their size, shape, and electrical charge. Automated cell
counting is quick and accurate, and is the most commonly used method for determining
leukocyte counts.

*Manual cell counting: This method involves counting cells under a microscope using a
special chamber called a hemocytometer. The hemocytometer is a glass slide with a grid
etched on it that is used to count cells in a specific volume of blood. Manual cell counting
is more time-consuming and requires more skill than automated cell counting, but it can
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 be useful in situations where automated cell counting is not available or when a more
accurate count is needed.

*Flow cytometry: This method uses a laser-based instrument to analyze the physical and
chemical properties of cells in a blood sample. The instrument can differentiate between
different types of cells based on their size, shape, and surface markers. Flow cytometry
is a highly sensitive method for detecting and quantifying cells, but it is more expensive
and requires specialized equipment and training.

45/ The physiological role of individual forms of leucocytes Leukocytes play a crucial role in the body's
immune system. There are five main types of leukocytes, each with a different
physiological role:

*Neutrophils: Neutrophils are the most abundant type of white blood cell and are the
first responders to infections. They are phagocytic cells that can engulf and destroy
invading pathogens such as bacteria and fungi.

*Lymphocytes: Lymphocytes are involved in the specific immune response and help the
body recognize and remember pathogens that it has previously encountered. There are
two main types of lymphocytes: B cells, which produce antibodies that recognize specific
pathogens, and T cells, which directly attack infected cells and help coordinate the
immune response.

*Monocytes: Monocytes are also phagocytic cells that can engulf and destroy pathogens.
They also play a role in presenting antigens to T cells, which helps activate the immune
response.

*Eosinophils: Eosinophils are involved in the body's response to parasitic infections and
allergic reactions. They release enzymes that can destroy parasites and are involved in
modulating the body's inflammatory response.

*Basophils: Basophils are involved in allergic reactions and release histamine and other
chemicals that contribute to inflammation and swelling.

46/The speci c mechanisms of protec on – immunity:

cell-mediated immunity (T-lymphocytes); b) humoral immunity (B-lymphocytes).

The immune system provides protection against pathogens, such as bacteria, viruses,
fungi, and parasites, through two main mechanisms: cell-mediated immunity and
humoral immunity. Both mechanisms involve the action of specific immune cells, such as
T-lymphocytes and B-lymphocytes. a) Cell-mediated immunity: Cell-mediated immunity
involves the action of T-lymphocytes These cells are responsible for recognizing and
directly attacking infected or abnormal cells. There are several types of T cells, including:

*Helper T cells (Th): These cells recognize and bind to antigens presented on the surface
of infected or abnormal cells by specialized antigen-presenting cells. The Th cells then
activate other immune cells, such as B cells and cytotoxic T cells, to destroy the infected
cells.

*Cytotoxic T cells (Tc): These cells directly recognize and kill infected or abnormal cells.
They are activated by Th cells and use specialized enzymes and proteins to destroy the
targeted cells.

*Memory T cells: These cells are created during an immune response and are responsible
for "remembering" the specific pathogen that caused the response. If the same
pathogen is encountered again in the future, the memory T cells can quickly mount a
response to eliminate the infection. / Cell-mediated immunity is important in providing
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 protection against intracellular pathogens, such as viruses and some bacteria, as well as
against cancer cells.

b) Humoral immunity: Humoral immunity involves the action of B-lymphocytes, also

called B cells. These cells produce and secrete antibodies, which are specialized proteins
that recognize and bind to specific antigens on the surface of pathogens. The antibodies
can then neutralize or eliminate the pathogen by various mechanisms, such as blocking
its ability to infect cells or marking it for destruction by other immune cells. B cells are
activated by Th cells, which recognize and bind to antigens presented by antigen-
presenting cells. Once activated, B cells can differentiate into plasma cells, which are
specialized cells that secrete large amounts of antibodies, or into memory B cells, which
are responsible for "remembering" the specific pathogen and mounting a quick response
in case of future infections. Humoral immunity is important in providing protection
against extracellular pathogens, such as bacteria and parasites, as well as against toxins
produced by some pathogens.

47/ Nonspeci c defense mechanisms:

a) cellular factors (phagocytosis) b) protec ve proper es of the plasma, lymph, etc

Nonspecific defense mechanisms are the first line of defense against pathogens and
include cellular and chemical factors that provide protection against a wide range of
pathogens. a) Cellular factors: One of the main cellular factors of nonspecific defense is
phagocytosis, which is the process by which certain cells, such as neutrophils and
macrophages, engulf and destroy pathogens. Phagocytic cells recognize and bind to
pathogens through specialized receptors on their surfaces and then engulf the pathogen
within a specialized vesicle called a phagosome. The phagosome then fuses with
lysosomes, which contain enzymes that can degrade the pathogen. Other cellular factors
include natural killer (NK) cells, which can directly kill infected or abnormal cells, and
dendritic cells, which are specialized cells that capture and present antigens to other
immune cells to initiate an immune response.

b) Protective properties of the plasma, lymph, etc: The plasma and lymph contain
various protective factors, such as complement proteins, interferons, and antimicrobial
peptides, that can directly attack or inhibit the growth of pathogens. Complement
proteins are a group of proteins that can form a complex on the surface of pathogens,
leading to their destruction by phagocytic cells or by the formation of membrane attack
complexes that can directly lyse the pathogen. Interferons are proteins that can be
produced by infected cells in response to viral infection and can stimulate the immune
response to help eliminate the virus. They can also have direct antiviral effects by
inhibiting viral replication. Antimicrobial peptides are small proteins that can be
produced by various cells, such as epithelial cells and phagocytes, and can directly kill or
inhibit the growth of pathogens.

Overall, these nonspecific defense mechanisms provide a first line of defense against
pathogens and help to limit the spread of infection until a specific immune response can
be mounted.

48/ Changes in leukocyte counts, and factors that cause them. Leukocyte counts can change in response
to various physiological and pathological conditions. Here are some examples of changes
in leukocyte counts and factors that can cause them:

*Infection: During an infection, leukocyte counts may increase due to the activation of
the immune system. This increase is usually due to an increase in neutrophils, but can
also involve an increase in monocytes, lymphocytes, and eosinophils, depending on the
type of infection.
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*Inflammation: Inflammation can also cause an increase in leukocyte counts, especially
neutrophils. This is because neutrophils are the first cells to arrive at the site of
inflammation and are involved in clearing away damaged tissue and invading pathogens.

*Allergic reactions: Allergic reactions can cause an increase in eosinophils and basophils,
which are involved in the immune response to allergens.

*Stress: Stress can cause an increase in leukocyte counts, especially neutrophils and
monocytes, due to the activation of the hypothalamic-pituitary-adrenal (HPA) axis and
the sympathetic nervous system.

*Medications: Certain medications, such as corticosteroids, can cause a decrease in

leukocyte counts, especially lymphocytes.

*Bone marrow disorders: Disorders of the bone marrow, such as leukemia or

myelodysplastic syndrome, can cause abnormal leukocyte counts, either increases or
decreases, due to the production of abnormal cells.

*Autoimmune disorders: Autoimmune disorders can cause an increase in leukocyte

counts, especially lymphocytes and monocytes, due to the activation of the immune
system against the body's own tissues.

49/ Thymus. Autoan gensThe thymus is a specialized organ of the immune system located in
the upper chest, behind the sternum. It plays a critical role in the development and
maturation of T-lymphocytes, which are a type of white blood cell that are involved in
cell-mediated immunity. The thymus is unique in that it contains both developing T-
lymphocytes and epithelial cells. These epithelial cells are involved in the selection and
maturation of T-lymphocytes. They express a variety of self-antigens, which are proteins
that are normally present in the body, as well as other antigens that are not normally
present. During development in the thymus, T-lymphocytes are exposed to these self-
antigens, which helps to ensure that they do not attack the body's own tissues once they
leave the thymus and enter circulation. Autoantigens are self-antigens that are
recognized by the immune system as foreign, leading to an autoimmune response.
Autoantigens can be present in various tissues and organs throughout the body,
including the thymus. In some autoimmune disorders, such as myasthenia gravis and
autoimmune polyendocrine syndrome type 1, autoantibodies are produced against self-
antigens that are normally present in the thymus, leading to dysfunction of the thymus
and the development of autoimmune disease.

50/ Changes in leukocyte counts, and factors that cause them Leukocytes, or white blood cells, are a vital
component of the immune system and play a crucial role in defending the body against
infections and diseases. Changes in leukocyte counts can indicate various conditions or
physiological responses. Here are some factors that can cause alterations in leukocyte
counts:

*Infection: Bacterial, viral, fungal, or parasitic infections can lead to an increase in

leukocyte counts. This increase, known as leukocytosis, is primarily due to the body's
immune response, where white blood cells multiply to combat the invading pathogens.

*Inflammation: Inflammatory conditions, such as autoimmune diseases (e.g.,

rheumatoid arthritis, lupus), allergies, or tissue damage, can cause an increase in
leukocyte counts. Inflammation triggers the release of chemical signals that stimulate
the bone marrow to produce more white blood cells.

*Stress or Physical Exertion: Stressful situations or intense physical exercise can

temporarily increase leukocyte counts. This response is mediated by stress hormones,
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into the bloodstream.

*Medications: Certain medications, such as corticosteroids or medications that stimulate

the immune system, can affect leukocyte counts. Corticosteroids, for example, can cause
a decrease in leukocyte counts by suppressing immune activity.

*Bone Marrow Disorders: Diseases affecting the bone marrow, such as leukemia or
myelodysplastic syndromes, can disrupt the production of white blood cells. This can
lead to decreased leukocyte counts (leukopenia) or abnormal types of white blood cells.

*Radiation or Chemotherapy: Treatment modalities like radiation therapy or

chemotherapy can have an impact on the bone marrow, affecting the production of white
blood cells. This can lead to a decrease in leukocyte counts, increasing the risk of
infections.

*Autoimmune Disorders: Some autoimmune disorders, such as systemic lupus

erythematosus or HIV/AIDS, can cause alterations in leukocyte counts. These conditions
can either lead to an increase or decrease in white blood cell numbers, depending on the
specific disease process.

51/ The concept of an gens and an bodies. An gens and an bodies are two important components of the immune
system, which help to protect the body against harmful pathogens such as bacteria, viruses, and parasites. An an gen is
any substance that can be recognized by the immune system as foreign and poten ally harmful. This can include
proteins, carbohydrates, as well as on the surface of cells that have been infected by a pathogen. When an an gen enters
the body, it is recognized by immune cells such as B-cells and T-cells, which then trigger an immune response to eliminate
the an gen. An bodies, also known as immunoglobulins, are proteins that are produced by B-cells in response to an
an gen. Each an body is designed to recognize and bind to a speci c an gen, like a lock and key. When an an body
binds to an an gen, it can neutralize it by preven ng it from infec ng cells or by marking it for destruc on by other
immune cells such as phagocytes. An bodies can also be produced ar cially and used as treatments for certain
diseases. For example, monoclonal an bodies are laboratory-produced an bodies that are designed to target speci c
an gens, and they can be used to treat cancer, autoimmune diseases, and other condi ons.

52/ General characteris cs of all blood type systems All blood type systems share several general
characteristics:

Inheritance: Blood types are inherited from parents through their genes, which are
passed down from generation to generation.

Antigens: Each blood type system is characterized by the presence or absence of specific
antigens on the surface of red blood cells. These antigens are proteins or sugars that can
be recognized by the immune system and can trigger an immune response.

Antibodies: In response to exposure to foreign antigens, the immune system produces

antibodies that are specific to those antigens. Individuals who lack a particular antigen
will have antibodies against it in their blood.

Compatibility: Blood transfusions and organ transplants must take into account the
compatibility of the donor and recipient blood types. If incompatible blood types are
mixed, the recipient's immune system may attack and destroy the donor blood cells,
leading to serious health problems.

Diversity: There are many different blood type systems, each with multiple variations,
resulting in a wide variety of possible blood types in the human population.

Testing: Blood typing is typically done through laboratory testing of a blood sample,
using specific reagents to detect the presence or absence of antigens and antibodies
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 53/ The classi ca on of blood types by ABO system. The ABO blood group system is the most well-
known and widely used blood type classification system. It is based on the presence or
absence of two antigens (A and B) on the surface of red blood cells, and the presence or
absence of antibodies against these antigens in the plasma. There are four main blood
types in the ABO system:

Type A: Individuals with type A blood have the A antigen on their red blood cells and
produce antibodies against the B antigen in their plasma.

Type B: Individuals with type B blood have the B antigen on their red blood cells and
produce antibodies against the A antigen in their plasma.

Type AB: Individuals with type AB blood have both the A and B antigens on their red
blood cells, and they do not produce antibodies against either antigen in their plasma.

Type O: Individuals with type O blood do not have either the A or B antigen on their red
blood cells, but they produce antibodies against both A and B antigens in their
plasma. / In addition to these four main blood types, the ABO system also includes the
Rh factor, which is another antigen present on the surface of red blood cells. Individuals
who have the Rh factor are classified as Rh-positive (Rh+) and those who do not have
the Rh factor are classified as Rh-negative (Rh-). / Therefore, when blood is typed using
the ABO system, it can be classified as one of eight different blood types: A+, A-, B+, B-,
AB+, AB-, O+, or O-. Understanding an individual's blood type is important for safe blood
transfusions and organ transplants, as transfusing incompatible blood types can cause
serious health problems.

54/ The technique, rules of the ABO blood type determina on system. Requirements for standard sera. The ABO
blood type determination system is typically done through laboratory testing of a blood
sample, using specific reagents to detect the presence or absence of antigens and
antibodies. The following are the general steps and rules for ABO blood type
determination:

Sample collection: A blood sample is collected from the individual being tested using a
sterile needle and tube.

Preparation of reagents: Two types of reagents are required for ABO blood typing: anti-A
and anti-B sera. These are usually commercially available and are standardized to ensure
accuracy and consistency of results.

Mixing the sample with the reagents: A small amount of the individual's blood is mixed
separately with each of the two reagents. The samples are observed for agglutination
(clumping), which indicates the presence of the corresponding antigen on the surface of
the red blood cells.

Interpretation of results: If agglutination occurs in the tube with the anti-A serum, the
individual has type A blood. If agglutination occurs in the tube with the anti-B serum, the
individual has type B blood. If agglutination occurs in both tubes, the individual has type
AB blood. If there is no agglutination in either tube, the individual has type O blood.

Rules for ABO blood type determination: If an individual has type A blood, they have the
A antigen on their red blood cells and will have antibodies against the B antigen in their
plasma. / If an individual has type B blood, they have the B antigen on their red blood
cells and will have antibodies against the A antigen in their plasma. / If an individual
has type AB blood, they have both the A and B antigens on their red blood cells and do
not have antibodies against either antigen in their plasma. /If an individual has type O
blood, they do not have either the A or B antigen on their red blood cells and will have
antibodies against both A and B antigens in their plasma.
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 Requirements for standard sera: Standard sera used in ABO blood typing must be
prepared and stored under specific conditions to maintain their potency and
specificity. / Standard sera should be validated and certified by regulatory authorities
to ensure their quality and consistency. / Standard sera should be used within their
expiration date to ensure accurate results. / Standard sera should be stored according to
the manufacturer's instructions, usually at a temperature of 2-8°C.

55/ Possible errors in blood type determining by the ABO system. While the ABO blood typing system is a
highly accurate and reliable method for determining blood type, errors can occur due to
a variety of factors. Some possible errors that can occur during blood type determination
by the ABO system include:

Technical errors: Errors can occur during the testing process, such as incorrect sample
collection or handling, incorrect reagent preparation, or failure to observe agglutination
correctly.

Contamination: Contamination of the blood sample or reagents can result in incorrect

results. For example, if a blood sample is contaminated with saliva or other fluids, it can
cause false agglutination.

Sample mix-up: Mix-up of samples can occur during sample collection, handling, or
testing, resulting in an individual being assigned an incorrect blood type.

Rare blood types: Rare blood types can be difficult to detect and may require specialized
testing methods. In some cases, individuals with rare blood types may be misclassified
as having a more common blood type.

Interference by medications or transfusions: Certain medications or transfusions can

interfere with blood typing results, making it difficult to accurately determine an
individual's blood type.

Human error: Human error, such as mislabeling or misinterpretation of results, can also
lead to errors in blood typing.

56/ Characteris cs of the Rh-system. The Rh system is a blood group system that refers to the
presence or absence of the Rh antigen on the surface of red blood cells. The Rh system is
named after the Rhesus monkey, in which the antigen was first identified. The following
are some characteristics of the Rh system:

Rh antigens: The Rh system has many antigens, but the most important is the D antigen.
Individuals who have the D antigen on their red blood cells are Rh-positive (Rh+), while
those who do not have the D antigen are Rh-negative (Rh-).

Inheritance: The Rh antigen is inherited from both parents, just like the ABO blood group
antigens. If both parents are Rh+, their offspring have a 75% chance of being Rh+, and
a 25% chance of being Rh-. If one parent is Rh+ and the other is Rh-, their offspring
have a 50% chance of being Rh+ and a 50% chance of being Rh-.

Antibody production: Individuals who are Rh- do not have the D antigen on their red
blood cells, and therefore may develop antibodies against the D antigen if they are
exposed to Rh+ blood. This can happen during pregnancy if the fetus is Rh+ and the
mother is Rh-, or during a blood transfusion if the transfused blood is Rh+. Rh antibodies
can cause a severe immune reaction if Rh+ blood is transfused or during subsequent
pregnancies with an Rh+ fetus.

Clinical significance: The Rh system is important in transfusion medicine and obstetrics.

Blood transfusions must be carefully matched for Rh antigens to prevent an immune
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mother and a Rh+ fetus can cause hemolytic disease of the newborn, a potentially life-
threatening condition in which the mother's Rh antibodies attack the fetal red blood
cells.

Testing: Rh blood typing is usually performed using the same blood sample collected for
ABO blood typing. Commercially available anti-D sera is used to test for the presence of
the D antigen on red blood cells. If agglutination occurs, the individual is Rh+; if there is
no agglutination, the individual is Rh-

57/ The Rh-factor determina on technique. Possible errors in determina on The Rh-factor determination
technique is a laboratory test used to determine the presence or absence of the Rh factor
on the surface of red blood cells. The Rh factor is an antigen found on the surface of red
blood cells that plays a crucial role in determining blood compatibility for transfusions.
The Rh-factor determination technique involves taking a blood sample from the patient
and then testing it for the presence of Rh factor using a series of laboratory tests. The
most common technique used for Rh-factor determination is the indirect antiglobulin test
(IAT), also known as the Coombs test. The IAT involves mixing the patient's blood
sample with a reagent that contains antibodies against the Rh factor. If the Rh factor is
present on the surface of the patient's red blood cells, it will react with the antibodies in
the reagent, causing them to clump together. This clumping, known as agglutination, can
be detected visually or using laboratory equipment. If the patient's blood does not react
with the Rh factor antibodies in the reagent, it is considered Rh-negative. If the patient's
blood does react with the Rh factor antibodies, it is considered Rh-positive. The Rh-
factor determination technique is important in determining blood compatibility for
transfusions, as Rh-negative individuals can develop a dangerous immune response if
they receive Rh-positive blood. This can lead to a condition known as hemolytic disease
of the newborn in pregnant women who are Rh-negative and carrying an Rh-positive
fetus. Overall, the Rh-factor determination technique is a vital laboratory test that helps
ensure the safety and efficacy of blood transfusions.

Possible errors in Rh-factor determination include: Contamination of the blood sample:

Contamination of the blood sample can occur during collection, processing, or testing,
which can lead to inaccurate results. To minimize the risk of contamination, it is
important to follow proper collection and handling procedures.

*Technical errors: Technical errors can occur during the testing process, such as
incorrect pipetting, mixing, or reading of the results. It is important to use calibrated
equipment and follow the testing protocol correctly.

*Human errors: Human errors can occur due to a lack of training, experience, or
attention to detail. It is important for the laboratory staff to be properly trained and to
follow quality control procedures to minimize the risk of human errors.

*False-positive or false-negative results: False-positive results occur when the Rh factor

is detected in a sample that does not actually contain it, while false-negative results
occur when the Rh factor is not detected in a sample that actually contains it. These
errors can occur due to technical errors, human errors, or biological factors such as weak
expression of the Rh factor.

58/ Reasons of the Rh-con ict between mother and fetus. Rh-conflict, also known as Rh incompatibility,
can occur when a Rh-negative mother carries a Rh-positive fetus. This can lead to a
condition known as hemolytic disease of the newborn, in which the mother's immune
system produces antibodies against the Rh factor in the fetus's blood, leading to the
destruction of the fetus's red blood cells.
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The reasons for Rh-conflict between mother and fetus are as follows:

Rh-negative mother carrying a Rh-positive fetus: Rh-conflict occurs when a Rh-negative

mother carries a fetus who has inherited the Rh factor from the father, who is Rh-
positive.

*Sensitization: During pregnancy, the mother's immune system may become sensitized
to the Rh factor in the fetus's blood, resulting in the production of antibodies against it.
This can occur during delivery, miscarriage, or ectopic pregnancy, or any other time
when there is mixing of the mother's and fetus's blood.

*Subsequent pregnancies: If the mother is sensitized during her first pregnancy, her
immune system will remember how to produce antibodies against the Rh factor. If
subsequent pregnancies involve a Rh-positive fetus, the mother's antibodies can cross
the placenta and attack the fetal red blood cells, leading to hemolytic disease of the
newborn.

*Rhesus factor blood transfusions: Rh-conflict can also occur if a Rh-negative person
receives a blood transfusion that contains Rh-positive blood.

*Organ transplantation: Rh-conflict can also occur following an organ transplant from a
donor who is Rh-positive to a recipient who is Rh-negative.

59/ Transfusion of blood. The rules and methods of blood transfusion Blood transfusion is a medical
procedure in which blood or blood components are transferred from one person (the
donor) to another person (the recipient). Blood transfusions are used to treat a wide
range of medical conditions, including anemia, bleeding disorders, and blood cancers.
The process of blood transfusion involves several steps:

*Donor screening: Before a blood transfusion can take place, the donor must undergo a
thorough screening process to ensure that the donated blood is safe for transfusion.
Donors are tested for infectious diseases such as HIV, hepatitis B and C, and syphilis, as
well as other conditions that could make the donated blood unsuitable for transfusion.

*Blood typing: The donor's blood type is determined, and the blood is tested for the
presence of antigens and antibodies that could cause a reaction in the recipient.

*Cross-matching: A small amount of the donor's blood is mixed with the recipient's
blood to check for compatibility and minimize the risk of a transfusion reaction.

*Preparation: Once the donated blood has been screened and matched with the
recipient's blood, it is prepared for transfusion. The blood may be separated into
different components, such as red blood cells, plasma, and platelets, depending on the
recipient's needs.

*Transfusion: The blood or blood components are transfused into the recipient's
bloodstream through an intravenous (IV) line. The transfusion is typically given slowly
at first, with the rate increased gradually if the recipient tolerates the transfusion well.

*Monitoring: The recipient is monitored closely during and after the transfusion for any
signs of a reaction or complication. Vital signs, such as blood pressure, heart rate, and
temperature, are checked regularly.

*Post-transfusion testing: After the transfusion, the recipient is tested for any antibodies
that may have developed in response to the transfused blood.

The rules and methods of blood transfusion include the following:

*Matching blood types: Before a blood transfusion, the blood type of the donor and
recipient must be matched to ensure compatibility. The ABO blood group system, which
includes blood types A, B, AB, and O, and the Rh factor, which can be either Rh-positive
or Rh-negative, are the most important factors in determining blood compatibility.

*Cross-matching: In addition to blood typing, cross-matching is also performed to

ensure compatibility. Cross-matching involves mixing a small amount of the donor's
blood with the recipient's blood to check for any reactions.

*Pre-transfusion testing: Before a blood transfusion, the recipient is tested for any
existing antibodies that could react with the donor's blood. This helps to minimize the
risk of a transfusion reaction.

*Sterility: Blood products must be sterile to avoid the transmission of infectious

diseases. Sterile needles and tubing are used to administer blood transfusions.

*Transfusion reactions: Transfusion reactions can occur due to incompatibility or other

factors, such as bacterial contamination. Symptoms of a transfusion reaction can include
fever, chills, shortness of breath, and hives. If a *transfusion reaction occurs, the
transfusion must be stopped immediately, and appropriate treatment must be
administered.

*Transfusion rates: Blood transfusions are typically given at a slow rate initially, with
the rate increased gradually if the recipient tolerates the transfusion well. This helps to
minimize the risk of a transfusion reaction.

*Monitoring: During and after a blood transfusion, the recipient is monitored for any
signs of a transfusion reaction, such as changes in vital signs, fever, or allergic reactions.

60/ The physiological role and e ect of transfused blood. The physiological role of transfused blood is to
increase the amount of circulating red blood cells, which carry oxygen to the body's
tissues. Blood transfusions can also increase the levels of other blood components, such
as platelets, plasma, and clotting factors, depending on the specific needs of the
recipient.

The effect of transfused blood on the body depends on the type of blood component
being transfused. For example, red blood cells are responsible for carrying oxygen to the
body's tissues, and a blood transfusion can increase the oxygen-carrying capacity of the
blood. This can be particularly important in patients with anemia, a condition in which
the body does not produce enough red blood cells to meet its oxygen needs.

Platelets, which are involved in blood clotting, may be transfused in patients with
bleeding disorders or in those who have undergone surgery. Plasma, which contains
proteins involved in immune function and blood clotting, may be transfused in patients
with clotting disorders or in those who have lost a significant amount of blood.

The physiological effects of transfused blood can also include an increase in blood
volume and blood pressure, which can be important in patients with shock or other
conditions that cause low blood pressure. Transfused blood can also help to replenish
the body's stores of iron and other essential nutrients.

While blood transfusions can be life-saving in many situations, they are not without risk.
Transfusion reactions, infections, and other complications can occur, and the decision to
transfuse blood must be carefully weighed against the potential risks and benefits.

61/ Haemostasis, its types. Vascular-platelet haemostasis, its signi cance : Haemostasis is the physiological
process of stopping bleeding from damaged blood vessels. It involves a series of
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clotting), and proteins in the blood known as clotting factors. The primary goal of
haemostasis is to maintain blood flow within the circulatory system while preventing
excessive bleeding. There are three main types of haemostasis:

Vascular Constriction (Vasoconstriction): When a blood vessel is damaged, the smooth

muscles in its walls contract, causing the vessel to narrow. This constriction helps
reduce blood flow to the injured area, which is an initial response to limit blood loss.
Vasoconstriction is mediated by the release of certain chemicals, such as endothelin,
which act on the smooth muscle cells of the blood vessel walls.

Platelet Plug Formation (Primary Haemostasis): When the inner lining of a blood vessel
is damaged, it exposes the underlying connective tissue and collagen fibers. Platelets in
the blood are activated by this exposure and adhere to the site of injury. Once attached,
they change shape, release chemical signals, and aggregate together to form a platelet
plug. This plug serves as a temporary seal to prevent further bleeding and provides a
surface for subsequent clotting factor activation.

Coagulation (Secondary Haemostasis): Coagulation involves a series of chemical

reactions that result in the formation of a blood clot. Clotting factors, which are proteins
present in the blood, are activated in a cascade-like fashion. This cascade ultimately
leads to the conversion of soluble fibrinogen into insoluble fibrin. Fibrin forms a mesh-
like network that traps blood cells, platelets, and plasma to form a stable blood clot. The
clot reinforces the platelet plug and prevents the escape of blood from the damaged
vessel.

The phases of hemostasis are as follows:

Vascular Phase: This phase involves vasoconstriction, which is the narrowing of blood
vessels at the site of injury. Vasoconstriction helps reduce blood flow to the area and
initiates the formation of a platelet plug.

Platelet Phase (Platelet Plug Formation): In this phase, platelets adhere to the exposed
collagen fibers at the site of injury, forming a platelet plug. This initial plug formation is
temporary and serves as the first step in the clotting process.

Coagulation Phase: Coagulation is the process of blood clot formation. It involves a

complex cascade of reactions in which clotting factors are activated, ultimately leading
to the conversion of fibrinogen (a soluble plasma protein) into fibrin (insoluble threads).
Fibrin forms a meshwork that stabilizes the platelet plug and traps red blood cells to
form a clot.

Clot Retraction: After clot formation, the clot undergoes retraction, which involves the
contraction of platelets and the tightening of the fibrin meshwork. Clot retraction helps
to compact the clot, squeezing out excess fluid and promoting wound closure.

Fibrinolysis: Once tissue repair has begun, the clot is gradually dissolved through a
process called fibrinolysis. Fibrinolysis involves the activation of plasmin, an enzyme that
breaks down fibrin and allows for the gradual dissolution of the clot. This process helps
in the removal of the clot once the healing process is complete.

62/Vascular-platelet haemostasis, its signi cance. Vascular-platelet haemostasis, also known as

primary haemostasis, refers to the initial response in the haemostatic process that
involves the interaction between blood vessel walls and platelets. It plays a crucial role
in controlling bleeding and initiating the formation of a blood clot. The significance of
vascular-platelet haemostasis lies in its ability to rapidly respond to vessel injury and
form a temporary platelet plug. Here are some key points highlighting its significance:
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 Rapid Response: Vascular-platelet haemostasis is the first line of defence against
bleeding. When a blood vessel is damaged, platelets quickly adhere to the exposed
collagen fibers in the vessel wall. This rapid response helps to minimize blood loss and
initiate the clotting process.

Formation of Platelet Plug: The accumulation and activation of platelets at the site of
injury lead to the formation of a platelet plug. The platelet plug acts as a temporary seal
to block the opening in the blood vessel, preventing further bleeding until the
coagulation cascade can generate a stable blood clot.

Initiation of Coagulation: The platelet plug also plays a crucial role in initiating the
coagulation cascade. Activated platelets release chemical signals, such as thromboxane
A2 and ADP, which recruit and activate additional platelets. These activated platelets
provide a surface for the assembly and activation of clotting factors, triggering the
secondary haemostasis or coagulation phase.

Interaction with the Vessel Wall: Platelets not only adhere to the exposed collagen fibers
but also interact with the damaged vessel wall. They release substances like von
Willebrand factor (vWF) and endothelial-derived nitric oxide, which contribute to the
recruitment and activation of additional platelets, enhance platelet aggregation, and
promote vessel constriction.

Regulation of Haemostasis: Vascular-platelet haemostasis is tightly regulated to prevent

excessive clotting or inadequate clot formation. Various factors, including endothelial
cells and antithrombotic molecules, maintain the balance between promoting platelet
activation and aggregation at the site of injury and preventing uncontrolled clot
formation in healthy vessels.

63/Coagula on haemostasis, its phases, mechanism, signi cance Coagulation haemostasis, also known as
secondary haemostasis, refers to the process of blood clot formation that occurs
following the initial platelet plug formation in the haemostatic response. It involves a
complex cascade of interactions between various clotting factors, resulting in the
conversion of soluble fibrinogen into insoluble fibrin, which forms a stable blood clot.
Coagulation haemostasis consists of three main phases: initiation, amplification, and
propagation.

Initiation Phase:begins when there is tissue damage and exposure of the blood to tissue
factor, also known as factor III. TF is normally present on the surface of cells outside the
bloodstream, such as cells in the subendothelial tissue. When vascular injury occurs, TF
is exposed to blood, leading to its interaction with factor VIIa. This interaction forms the
TF-VIIa complex, which initiates the coagulation cascade.

Amplification Phase: In the amplification phase, the TF-VIIa complex activates factors IX
and X, leading to the formation of the tenase complex. The tenase complex consists of
activated factor IX (IXa), activated factor VIII (VIIIa), calcium ions, and phospholipids
present on the platelet surface. The tenase complex activates factor X, converting it to
its active form, factor Xa. Factor Xa plays a central role in the coagulation cascade as it
acts as a protease enzyme that cleaves prothrombin.

Propagation Phase: The propagation phase involves the conversion of prothrombin to

thrombin. Thrombin is a key enzyme in the coagulation cascade and has multiple
functions. It converts fibrinogen, a soluble plasma protein, into insoluble fibrin strands.
Fibrin strands form a mesh-like network that entraps blood cells, platelets, and plasma
components to create a stable blood clot. Thrombin also amplifies the coagulation
process by activating factors V, VIII, and XI, leading to further thrombin generation and
propagation of the clotting cascade.
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 **Significance of Coagulation Haemostasis:

Formation of Stable Blood Clot: Coagulation haemostasis plays a vital role in the
formation of a stable blood clot. The conversion of fibrinogen into fibrin creates a
meshwork that strengthens the platelet plug, stabilizes the clot, and prevents further
bleeding.

Limitation of Blood Loss: By forming a stable blood clot, coagulation haemostasis helps
to limit blood loss from the site of injury. It acts as a long-term solution to seal the
damaged blood vessel and prevent excessive bleeding.

Wound Healing: The formation of a blood clot through coagulation haemostasis provides
a scaffold for subsequent steps in the wound healing process. The clot acts as a
protective barrier, allowing cells involved in tissue repair to migrate to the injury site
and initiate the healing process.

Prevention of Infection: The fibrin network formed during coagulation can help prevent
the entry of pathogens into the wound site, reducing the risk of infection.

Regulation of Clot Formation: Coagulation haemostasis is tightly regulated to maintain

the delicate balance between preventing excessive clotting (thrombosis) and promoting
appropriate clot formation. Various regulatory mechanisms, including anticoagulant
proteins and inhibitors, help prevent clotting from spreading beyond the site of injury.

64/Modern concepts about the main factors involved in coagula on haemostasis – coagulants (plasmic, platelet,
leukocy c, ssue) In modern concepts of coagulation haemostasis, the main factors involved
can be broadly categorized into plasmic coagulants, platelet coagulants, leukocytic
coagulants, and tissue factors. These factors work together in a complex network to
initiate and regulate the coagulation cascade. these factors:

Plasmic Coagulants: Plasmic coagulants refer to the clotting factors found in the plasma,
which are primarily produced by the liver. These factors are numbered using Roman
numerals (I to XIII) and are involved in various stages of the coagulation cascade.
plasmic coagulants include:

*Fibrinogen (Factor I): Fibrinogen is a soluble plasma protein that is converted into
insoluble fibrin during clot formation. Fibrin provides the structural framework for the
blood clot.

*Prothrombin (Factor II): Prothrombin is a precursor protein that is converted into its
active form, thrombin, during the coagulation cascade. Thrombin plays a central role in
converting fibrinogen to fibrin and amplifying the coagulation process.

*Factors VII, VIII, IX, X.10: These factors, along with calcium ions and phospholipids,
form the tenase and prothrombinase complexes that activate factor X and convert
prothrombin to thrombin.

*Factors V.5 and XIII: These factors contribute to the stabilization of the fibrin clot.
Factor V is an essential cofactor in the prothrombinase complex, while factor XIII cross-
links fibrin strands, making the clot more stable.

Platelet Coagulants: Platelets play a critical role in haemostasis. They contain granules
that store and release various coagulation factors upon activation. Key platelet
coagulants include:

*Platelet Factor 3: PF3 is a phospholipid present on the surface of activated platelets. It

provides a surface for the assembly and activation of coagulation factors, promoting
clotting.
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 *von Willebrand Facton : vWF is a protein that mediates the adhesion of platelets to the
damaged vessel wall. It also stabilizes factor VIII in the plasma and enhances platelet
aggregation.

Leukocytic Coagulants: Although leukocytes (white blood cells) are primarily associated
with the immune response, they also contribute to haemostasis. Neutrophils and
monocytes release coagulant substances, such as DNA and histones, that promote clot
formation and stability.

Tissue Factors: Tissue factors, also known as extrinsic factors, are not present in the
blood but are exposed upon tissue damage. The main tissue factor involved in
coagulation is Tissue Factor (TF), also called Factor III. TF interacts with Factor VII to
initiate the coagulation cascade.

65/An coagulants, their types, mechanisms of ac on, signi cance. Anticoagulants are medications that
reduce blood clot formation, a process known as coagulation. They are commonly used in
the treatment and prevention of various conditions, such as deep vein thrombosis (DVT),
pulmonary embolism (PE), atrial fibrillation, and stroke. Anticoagulants work by
interfering with different steps of the blood clotting process, ultimately preventing the
formation of clots or reducing their size. There are several types of anticoagulants,
including:

Heparin: Heparin is a naturally occurring anticoagulant that can be administered

intravenously or subcutaneously. It works by enhancing the activity of antithrombin III,
a protein that inhibits clotting factors such as thrombin and factor Xa. Heparin has a
rapid onset of action but requires close monitoring due to its potential side effects and
the need for frequent dose adjustments.

Low Molecular Weight Heparin: LMWHs, such as enoxaparin and dalteparin, are derived
from heparin but have a smaller molecular size. They have a longer duration of action
and can be given subcutaneously, allowing for once- or twice-daily dosing. LMWHs also
enhance the activity of antithrombin III, leading to inhibition of thrombin and factor Xa.

Warfarin: Warfarin is an oral anticoagulant that interferes with the synthesis of vitamin
K-dependent clotting factors (II, VII, IX, and X) in the liver. It takes several days to
reach its full effect and requires regular monitoring of the International Normalized
Ratio (INR) to maintain the desired level of anticoagulation. Warfarin has numerous
drug and food interactions and necessitates caution due to its narrow therapeutic
window.

Direct Oral Anticoagulant: DOACs, including dabigatran, rivaroxaban, apixaban, and

edoxaban, are newer oral anticoagulants that directly inhibit specific clotting factors.
Dabigatran directly inhibits thrombin (factor IIa), while rivaroxaban, apixaban, and
edoxaban target factor Xa. DOACs have a more predictable anticoagulant effect, do not
require regular monitoring, and have fewer drug and food interactions compared to
warfarin.

The significance of anticoagulants lies in their ability to prevent and treat

thromboembolic disorders. They help to prevent blood clots from forming in arteries or
veins, reducing the risk of complications such as heart attack, stroke, or pulmonary
embolism. Anticoagulants are particularly important in conditions where there is an
increased risk of clot formation, such as atrial fibrillation, mechanical heart valves, and
after major orthopedic surgeries. However, it is crucial to use anticoagulants judiciously,
as they can increase the risk of bleeding, and their dosing and monitoring require careful
consideration to balance efficacy and safety.
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 66/Plasmins and brinolysis, its mechanisms, signi cance Plasmin is an enzyme that plays a role in the
process of fibrinolysis, which is the natural breakdown of blood clots. Fibrinolysis helps
to maintain normal blood flow and prevent the formation of excessive or unwanted blood
clots. Plasmin acts by degrading fibrin, the protein meshwork that forms the structure of
a blood clot. the mechanisms of plasmins and fibrinolysis in more detail:

*Plasminogen activation: Plasminogen, an inactive precursor, is converted into plasmin

through the action of plasminogen activators. There are two primary types of
plasminogen activators involved in fibrinolysis:

Tissue-type plasminogen activator: t-PA is primarily synthesized and released by

endothelial cells lining blood vessels. It binds to fibrin within the blood clot, converting
plasminogen into plasmin at the site of clot formation. This localized activation ensures
that plasmin primarily acts on the fibrin meshwork and limits systemic effects.

Urokinase-type plasminogen activator : u-PA is produced by various cells, including

endothelial cells and certain immune cells. Unlike t-PA, u-PA can bind directly to
plasminogen and convert it into plasmin both within and outside of the clot. u-PA-
mediated activation of plasminogen occurs in a more widespread manner.

*Conversion of plasminogen to plasmin: Plasminogen has several lysine-binding sites,

which can interact with lysine residues present on fibrin. Plasminogen activators,
particularly t-PA, bind to fibrin and plasminogen simultaneously, localizing plasminogen
activation to the clot surface. This binding induces conformational changes in
plasminogen, enabling its cleavage by the plasminogen activator. Plasminogen is cleaved
at a specific site, resulting in the formation of plasmin, the active enzyme.

*Action of plasmin: Once formed, plasmin acts as a potent proteolytic enzyme, capable
of degrading fibrin and other clotting factors:

Fibrin degradation: Plasmin cleaves fibrin strands within the blood clot, leading to the
breakdown of the clot structure. Plasmin breaks the peptide bonds within the fibrin
molecule, resulting in the generation of smaller fragments called fibrin degradation
products (FDPs) or fibrin split products. These fragments are then cleared from the
circulation.

Degradation of other clotting factors: Plasmin also degrades other proteins involved in
clot formation, including fibrinogen (the soluble precursor of fibrin), factors V and VIII
(which contribute to clot stability), and factors XIII (which cross-links fibrin). This
degradation further weakens and disrupts the clot.

*Regulation of fibrinolysis: Fibrinolysis is regulated by several mechanisms to prevent

excessive clot breakdown or uncontrolled bleeding:

Plasminogen activator inhibitors :PAIs, such as plasminogen activator inhibitor-1

(PAI-1), are present in the blood and can inhibit the activity of plasminogen activators.
They help regulate the intensity and duration of fibrinolysis by limiting excessive plasmin
generation.

Alpha-2-antiplasmin: Alpha-2-antiplasmin is a protein that rapidly binds to plasmin,

inactivating it and preventing the uncontrolled degradation of fibrin and other clotting
factors. The significance of plasmin and fibrinolysis includes:

Clot dissolution: Fibrinolysis helps to dissolve blood clots, promoting the restoration of
blood flow in affected blood vessels. This process is essential in preventing blockages
and maintaining vascular patency.
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Regulation of clot formation: Fibrinolysis serves as a counterbalance to the clotting
process, preventing excessive clot formation. It helps to maintain a delicate balance
between clotting and fibrinolysis to ensure appropriate hemostasis.

Tissue repair: Fibrinolysis plays a role in tissue remodeling and repair. Once a clot has
fulfilled its purpose in preventing bleeding, fibrinolysis helps to remove the clot and
allow for the regeneration of healthy tissue.

Thrombolytic therapy: The understanding of fibrinolysis and the use of plasminogen

activators has led to the development of thrombolytic therapy. Thrombolytic agents,
such as recombinant tissue plasminogen activator (rt-PA), can be administered in certain
cases, such as acute myocardial infarction or ischemic stroke, to rapidly dissolve blood
clots and restore blood flow.

67/The role of the vascular wall in the regula on of coagula on hemostasis and brinolysis The vascular wall
plays a critical role in the regulation of coagulation hemostasis and fibrinolysis. It
provides a dynamic interface between the blood and the underlying tissues, actively
participating in maintaining hemostatic balance. Here are the key aspects of the vascular
wall's involvement:

Endothelial cells: The endothelial cells lining the blood vessels are central to regulating
coagulation and fibrinolysis. They possess anticoagulant and profibrinolytic properties
that help prevent excessive clot formation and promote clot dissolution:

Anticoagulant properties: Endothelial cells produce and release molecules such as

heparin-like molecules, thrombomodulin, and tissue factor pathway inhibitor (TFPI).
These molecules inhibit the activity of clotting factors and coagulation enzymes,
including thrombin, thereby reducing clotting potential.

Profibrinolytic properties: Endothelial cells synthesize and release tissue-type

plasminogen activator (t-PA), the primary activator of plasminogen in the fibrinolytic
pathway. t-PA binds to fibrin within the clot, converting plasminogen into plasmin,
promoting clot breakdown.

Surface properties: The negatively charged surface of endothelial cells repels clotting
factors, preventing their activation and limiting clot formation.

Endothelial cell-derived factors: Endothelial cells secrete various factors that modulate
coagulation and fibrinolysis:

Nitric oxide (NO): NO is a potent vasodilator produced by endothelial cells. It helps

maintain blood flow and prevents platelet activation and aggregation.

Prostacyclin (PGI2): PGI2 is another vasodilator released by endothelial cells. It inhibits

platelet activation and aggregation and acts as an anticoagulant by reducing platelet
adhesion to the vascular wall.

Von Willebrand factor (vWF): Endothelial cells release vWF, a glycoprotein that mediates
platelet adhesion to damaged endothelium and plays a role in clot formation.

Endothelial cell integrity: An intact endothelial cell layer provides a physical barrier that
prevents exposure of the underlying procoagulant components, such as collagen and
tissue factor. When the endothelium is damaged, the exposure of these components
triggers clot formation and activates the coagulation cascade.

Regulation of inflammatory response: Endothelial cells also contribute to the regulation

of the inflammatory response, which can influence coagulation and fibrinolysis.
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Inflammation can lead to endothelial dysfunction and a procoagulant state by promoting
the release of proinflammatory cytokines and adhesion molecules.

Overall, the vascular wall and its endothelial cells actively participate in maintaining a
delicate balance between coagulation hemostasis and fibrinolysis. The anticoagulant and
profibrinolytic properties of the endothelium, along with the secretion of regulatory
factors, help prevent excessive clot formation and promote the dissolution of formed
clots. Endothelial cell integrity is crucial in maintaining hemostatic balance, and
disruption of the endothelial barrier can lead to dysregulated coagulation and thrombotic
disorders.

68/The physiological role of platelets. Platelets, also known as thrombocytes, are small, disc-
shaped blood cells that play a vital physiological role in hemostasis, which is the process
of preventing and stopping bleeding. Here are the key physiological roles of platelets:

Formation of platelet plugs: When there is injury or damage to a blood vessel, platelets
are among the first responders to the site. They adhere to the exposed collagen fibers
and other components of the damaged vessel wall, forming a platelet plug. Platelet
adhesion is mediated by the interaction between platelet surface receptors, such as
glycoprotein Ib (GPIb), and von Willebrand factor (vWF) in the damaged area.

Platelet activation and aggregation: Upon adhesion, platelets become activated and
undergo a series of biochemical changes. They release granules containing various
molecules, including ADP (adenosine diphosphate), thromboxane A2, and serotonin.
These molecules recruit and activate additional platelets, leading to platelet aggregation
and the formation of a stable plug at the site of injury.

Release of clotting factors: Activated platelets also release clotting factors such as
platelet factor 3 (PF3), which serves as a crucial surface for the activation of the
coagulation cascade. PF3 aids in the conversion of prothrombin to thrombin, a key
enzyme involved in clot formation.

Support of coagulation cascade: Platelets provide a surface for the assembly and
activation of various components of the coagulation cascade. They promote the
conversion of fibrinogen to fibrin by facilitating the action of thrombin. The fibrin strands
then form a mesh that stabilizes the platelet plug, leading to the formation of a blood
clot.

Regulation of blood vessel integrity: Platelets also contribute to maintaining the integrity
of blood vessels. They release substances, such as endothelial growth factors and
vascular endothelial growth factor (VEGF), that stimulate the repair and regeneration of
the endothelial lining following vascular injury.

Immune response and inflammation: Platelets are involved in immune responses and
inflammation. They can interact with immune cells and release various proinflammatory
molecules, such as chemokines and cytokines, which play a role in the recruitment and
activation of immune cells.

1/ Circulatory system, its major func ons. The circulatory system, also known as the
cardiovascular system, is a complex network of organs, vessels, and tissues that
transport blood, oxygen, and nutrients to various parts of the body. The circulatory
system consists of the heart, blood vessels (arteries, veins, and capillaries), and blood.

*The heart is a muscular organ that pumps blood throughout the body. It has four
chambers: the right atrium, right ventricle, left atrium, and left ventricle. Blood enters
the right atrium from the body and is pumped into the right ventricle, which then pumps
the blood to the lungs for oxygenation. The oxygenated blood returns to the heart and
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 enters the left atrium, which pumps it into the left ventricle. The left ventricle then
pumps the oxygen-rich blood to the rest of the body through the arteries.

*The arteries are blood vessels that carry oxygen-rich blood away from the heart and
towards the body's organs and tissues. As the arteries branch out into smaller blood
vessels called arterioles, they eventually lead to the smallest blood vessels, the
capillaries. Capillaries are where oxygen and nutrients are exchanged with the body's
tissues and waste products are removed.

*After the exchange of gases and nutrients at the capillaries, the blood then flows back
towards the heart through the veins. The veins are blood vessels that carry oxygen-
depleted blood back to the heart, where it can be oxygenated again. The process of
circulation is continuous and vital for the body's survival.

2/ Morpho-func onal characteris cs of the myocardium, cardiomyocytes, cardiac conduc ve system The
myocardium is the muscular tissue of the heart that is responsible for the contraction of
the heart and the circulation of blood throughout the body. The myocardium is composed
of specialized cardiac muscle cells called cardiomyocytes.

Cardiomyocytes are unique in their structure and function. They are smaller than skeletal
muscle cells and have a single nucleus. They are also branched, with intercalated discs
that allow for the transmission of electrical signals between cells. Cardiomyocytes have
a high density of mitochondria, which produce energy for the contraction of the heart.
They also contain specialized structures called T-tubules and sarcoplasmic reticulum,
which are involved in the regulation of calcium ions, a key factor in the contraction of
cardiac muscle.

The cardiac conductive system is a specialized network of cells that controls the
electrical impulses that regulate the heartbeat. It consists of the sinoatrial node (SA
node), atrioventricular node (AV node), bundle of His, and Purkinje fibers. The SA node,
located in the right atrium, initiates the heartbeat by generating an electrical impulse.
This impulse is then transmitted to the AV node, located at the junction between the
atria and ventricles. The AV node slows down the impulse before transmitting it to the
bundle of His, which branches into the Purkinje fibers. The Purkinje fibers then transmit
the impulse to the ventricles, causing them to contract and pump blood out of the heart.

In summary, the myocardium is composed of specialized cardiac muscle cells called

cardiomyocytes, which are responsible for the contraction of the heart. The cardiac
conductive system is a specialized network of cells that controls the electrical impulses
that regulate the heartbeat. Together, these structures work to ensure the efficient and
coordinated contraction of the heart, which is essential for the circulation of blood
throughout the body.

3/ Physiological proper es of the myocardium, and their characteris cs. The myocardium, or the heart
muscle, has several physiological properties that are essential for its proper function.
properties of the myocardium and their characteristics:

*Excitability: refers to the ability of the myocardium to respond to an electrical stimulus.

This property is due to the presence of specialized cardiac muscle cells called pacemaker
cells, which generate electrical impulses that spread throughout the myocardium and
cause the heart to contract.

*Conductivity: refers to the ability of the myocardium to conduct electrical impulses.

This property is due to the presence of specialized cardiac muscle cells called conduction
fibers, which are responsible for transmitting electrical signals from the pacemaker cells
to the rest of the myocardium.
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 *Contractility: refers to the ability of the myocardium to contract and generate force.
This property is due to the presence of specialized proteins called myofilaments, which
slide past each other to shorten the length of the cardiac muscle cells and generate
force.

*Automaticity: refers to the ability of the myocardium to generate spontaneous electrical

impulses without external stimulation. This property is due to the presence of
pacemaker cells, which are capable of generating electrical impulses even in the absence
of external stimuli.

*Elasticity: refers to the ability of the myocardium to return to its original shape after
being stretched. This property is essential for the proper filling of the heart chambers
during the relaxation phase of the cardiac cycle.

These properties of the myocardium work together to ensure the efficient and
coordinated contraction of the heart, which is essential for the circulation of blood
throughout the body. Any abnormalities in these properties can lead to various
cardiovascular disorders and conditions

4/ The excitability of cardiac muscle, the ac on poten al of typical cardiomyocytes. The excitability of cardiac
muscle refers to the ability of cardiac cells to generate an action potential in response to
an electrical stimulus. The action potential is a complex electrochemical process that
underlies the contraction of cardiac muscle cells.

The action potential of typical cardiomyocytes can be divided into five phases:

*Resting phase: At rest, the membrane potential of the cardiomyocyte is around -90mV,
which is maintained by the balance of ion concentrations inside and outside the cell.

*Depolarization phase: When an electrical stimulus is applied, the membrane potential

becomes less negative, which triggers the opening of voltage-gated sodium channels.
This allows sodium ions to rush into the cell, leading to a rapid depolarization of the
membrane potential.

*Initial repolarization phase: Once the membrane potential reaches around +30mV, the
sodium channels close, and potassium channels begin to open. This allows potassium
ions to flow out of the cell, leading to a partial repolarization of the membrane potential.

*Plateau phase: At this stage, the membrane potential becomes relatively stable due to
the balance of inward and outward currents. The inward current is carried by calcium
ions, which enter the cell through voltage-gated calcium channels, while the outward
current is carried by potassium ions, which continue to flow out of the cell.

*Final repolarization phase: After a prolonged plateau phase, the calcium channels close,
and the potassium channels remain open, leading to a rapid repolarization of the
membrane potential to its resting state.

The action potential of cardiomyocytes is longer and more complex than that of skeletal
muscle cells, allowing for greater contractile force and sustained contractions necessary
for the pumping action of the heart. The proper regulation of the action potential is
essential for the proper function of the heart and any abnormalities in this process can
lead to various cardiovascular disorders and conditions.

5/ Refractoriness of myocardium and its rela on to the phases of the ac on poten al of myocardiocytes, and its rela on
to contrac bility Refractoriness of the myocardium refers to the inability of cardiac cells to
respond to a new stimulus during a certain period of time after an action potential has
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been generated. This period of time is known as the refractory period, and it plays a
crucial role in the regulation of the contraction of the heart.

*The refractory period is divided into two phases: the absolute refractory period and the
relative refractory period. During the absolute refractory period, the cell is completely
unresponsive to any new stimulus, regardless of its strength or duration. This phase
occurs during the initial depolarization phase and the early part of the repolarization
phase of the action potential. During the relative refractory period, the cell is partially
repolarized and can respond to a strong stimulus but requires a greater depolarizing
current than usual to generate an action potential.

The refractory period is essential for the proper regulation of the contraction of the
heart. It ensures that the heart muscle cells have enough time to fully relax before being
stimulated again, allowing for proper filling of the heart chambers and efficient pumping
of blood. Any abnormalities in the refractory period can lead to arrhythmias and other
cardiovascular disorders.

The refractory period is also closely related to the contractility of the myocardium.
During the plateau phase of the action potential, the calcium ions enter the cell and bind
to the contractile proteins, triggering the contraction of the cardiac muscle cells. The
duration of the plateau phase is closely related to the refractory period, and any
abnormalities in this phase can lead to changes in the contractility of the myocardium.
For example, a prolonged plateau phase can lead to increased contractility, while a
shortened plateau phase can lead to decreased contractility.

In summary, the refractoriness of the myocardium is essential for the regulation of the
contraction of the heart, and it is closely related to the phases of the action potential of
cardiomyocytes and the contractility of the myocardium. Any abnormalities in the
refractory period can have serious consequences for the function of the heart and can
lead to various cardiovascular disorders and conditions.

6/ Premature beats, their origin, types of extrasystoles. Premature beats, also known as premature
contractions or extrasystoles, are abnormal heartbeats that occur earlier than expected
in the cardiac cycle. They can originate from various locations in the heart, including the
atria, ventricles, and specialized conducting tissues.

There are two main types of extrasystoles:

*Atrial premature beats (APBs): These occur when the electrical impulse that triggers
the heartbeat originates from an area in the atria other than the sinoatrial node (the
natural pacemaker of the heart). APBs can cause a premature contraction of the atria,
leading to a sensation of fluttering in the chest or palpitations.

*Ventricular premature beats (VPBs): These occur when the electrical impulse that
triggers the heartbeat originates from an area in the ventricles. VPBs can cause a
premature contraction of the ventricles, which can be felt as a skipped beat or
palpitation. VPBs can be more serious than APBs as they can lead to more severe
arrhythmias.

Extrasystoles can also be classified based on their timing in the cardiac cycle. They can
occur during diastole (the relaxation phase of the heart cycle), or during systole (the
contraction phase of the heart cycle). Extrasystoles that occur during diastole are called
premature ventricular contractions (PVCs) or premature atrial contractions (PACs),
depending on where they originate. Extrasystoles that occur during systole are called
premature ventricular beats (PVBs) or premature atrial beats (PABs).
 In summary, premature beats or extrasystoles are abnormal heartbeats that occur
earlier than expected in the cardiac cycle. They can originate from various locations in
the heart and can be classified based on their timing in the cardiac cycle and their origin.
It is important to note that while some extrasystoles may be harmless, others can be a
sign of underlying cardiovascular conditions and should be evaluated by a healthcare
professional.

7/ Automa sm of the heart, the ac on poten al of atypical cardiomyocytes sinoatrial node Automatism refers to
the ability of certain specialized cells in the heart to generate spontaneous electrical
impulses that can trigger the contraction of the heart muscle. The most important of
these cells are located in the sinoatrial (SA) node, which is the natural pacemaker of the
heart.

The SA node is a group of specialized cardiomyocytes located in the right atrium of the
heart. These cells have the ability to generate action potentials spontaneously, without
the need for external stimulation. The action potential of the SA node cells is
characterized by a slow depolarization phase, which is driven by a unique ion channel
called the funny current (If). The depolarization eventually reaches the threshold for
firing an action potential, triggering a rapid depolarization phase driven by the influx of
calcium ions.

The action potential of the SA node cells differs from that of typical cardiomyocytes in
several ways. For example, the depolarization phase is slower, and the action potential is
shorter in duration. Additionally, the resting membrane potential of SA node cells is
more positive than that of typical cardiomyocytes, making them more likely to fire
spontaneously.

The automaticity of the SA node cells is regulated by the autonomic nervous system,
which can modulate the rate and rhythm of the heartbeat. Specifically, the sympathetic
nervous system can increase the rate of firing of the SA node cells, while the
parasympathetic nervous system can slow it down.

In summary, automatism of the heart refers to the ability of specialized cells in the
heart, such as those in the SA node, to generate spontaneous electrical impulses that
can trigger the contraction of the heart muscle. The action potential of atypical
cardiomyocytes in the SA node is characterized by a slow depolarization phase driven by
the funny current, followed by a rapid depolarization phase driven by the influx of
calcium ions. The automaticity of the SA node cells is regulated by the autonomic
nervous system.

8/ Centres of automa city, their mutual rela onship, the gradient of automa city. In addition to the sinoatrial
(SA) node, which is the primary pacemaker of the heart, there are several other
specialized cells in the heart that can generate spontaneous electrical impulses and
contribute to the overall automaticity of the heart. These cells are referred to as
subsidiary pacemakers or centers of automaticity.

Some examples of centers of automaticity in the heart include the atrioventricular (AV)
node, the Purkinje fibers, and certain cells in the myocardium of the atria and ventricles.
These centers of automaticity have different intrinsic firing rates and can act as backup
pacemakers if the SA node fails.

The mutual relationship between the different centers of automaticity in the heart is
complex and involves a number of factors, including the intrinsic firing rates of each
center, their location within the heart, and the influence of the autonomic nervous
system. Generally, the centers of automaticity in the heart are arranged in a hierarchical
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 fashion, with the SA node being the dominant pacemaker and the other centers serving
as backup pacemakers.

The gradient of automaticity refers to the gradual increase in intrinsic firing rate from
the center of automaticity with the slowest firing rate to the center with the fastest
firing rate. The SA node has the highest intrinsic firing rate, followed by the AV node, the
Purkinje fibers, and the cells in the myocardium of the atria and ventricles.

In normal conditions, the SA node sets the pace for the rest of the heart, and the other
centers of automaticity remain dormant. However, if the SA node fails or becomes
compromised, the other centers of automaticity can take over and drive the heartbeat.
This can result in a variety of arrhythmias, including sinus bradycardia (when the
heartbeat is slower than normal), sinus tachycardia (when the heartbeat is faster than
normal), and various forms of heart block (when the electrical impulses are delayed or
blocked between different parts of the heart).

9/ Conduc vity of myocardium, the excita on conduc on rate and a signi cance of its changes. The conductivity
of the myocardium refers to its ability to conduct electrical impulses throughout the
heart, allowing for coordinated contraction of the cardiac muscle. The primary pathway
for electrical conduction in the heart is the cardiac conduction system, which includes
the sinoatrial (SA) node, the atrioventricular (AV) node, the bundle of His, the left and
right bundle branches, and the Purkinje fibers.

*The excitation conduction rate refers to the speed at which electrical impulses are
conducted through the heart. The rate of conduction can be affected by a number of
factors, including the health of the conduction system, the presence of scar tissue or
other abnormalities in the heart tissue, and the influence of the autonomic nervous
system.

Changes in the excitation conduction rate can have significant implications for the
function of the heart. For example, if the rate of conduction is too slow, this can lead to
bradycardia, which is characterized by a slow heart rate and can cause symptoms such
as dizziness, fatigue, and fainting. If the rate of conduction is too fast, this can lead to
tachycardia, which is characterized by a rapid heart rate and can cause symptoms such
as palpitations, shortness of breath, and chest pain.

Changes in the excitation conduction rate can also increase the risk of arrhythmias,
which are abnormal heart rhythms that can be life-threatening. For example, if the
conduction rate is too slow, this can increase the risk of atrioventricular block, a
condition in which the electrical impulses are blocked between the atria and ventricles.
If the conduction rate is too fast, this can increase the risk of ventricular tachycardia or
ventricular fibrillation, which can lead to sudden cardiac arrest.

In summary, the conductivity of the myocardium is essential for the coordinated

contraction of the heart, and changes in the excitation conduction rate can have
significant implications for heart function and the risk of arrhythmias.

10/ Contrac on of myocardium, features of mechanism in comparison with the mechanism of skeletal muscle bers

the contraction of myocardium is a complex process that is essential for the proper
function of the heart. It is initiated by the depolarization of cardiomyocytes, which leads
to the release of calcium ions and the initiation of excitation-contraction coupling. The
process of myocardial contraction is highly coordinated and regulated by various factors
to ensure efficient pumping of blood through the heart.

The mechanism of myocardial contraction differs from that of skeletal muscle fibers in
several important ways :
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*Calcium entry: In skeletal muscle, calcium ions enter the cell from the sarcoplasmic
reticulum to initiate contraction. In contrast, in myocardial cells, calcium ions enter the
cell from both the extracellular space and the sarcoplasmic reticulum. This results in a
slower and more sustained contraction compared to skeletal muscle.

*Intercalated discs: Myocardial cells are connected to each other by specialized

structures called intercalated discs, which allow for rapid and efficient propagation of
electrical signals. Skeletal muscle fibers do not have intercalated discs, and electrical
signals are propagated more slowly through the extracellular space.

*Energy utilization: Myocardial cells rely primarily on aerobic metabolism, with a rich
supply of mitochondria to generate ATP for contraction. Skeletal muscle fibers also rely
on aerobic metabolism, but can switch to anaerobic metabolism during high-intensity
exercise.

*Regulation: The contraction of myocardial cells is regulated by the autonomic nervous

system, which can increase or decrease heart rate and contractility. Skeletal muscle
fibers are mainly under voluntary control and are regulated by the somatic nervous
system.

*All-or-none response: Skeletal muscle fibers can exhibit graded responses, with greater
force generated by recruitment of more muscle fibers. Myocardial cells exhibit an all-or-
none response, meaning that they either contract fully or not at all.

Overall, the mechanism of myocardial contraction is optimized for efficient pumping of

blood through the heart, with slower and more sustained contractions compared to
skeletal muscle. The unique features of myocardial cells, including intercalated discs and
regulation by the autonomic nervous system, allow for coordinated and synchronized
contraction of the heart.

11/ Heart valve apparatus, the func on of each valve. The heart valve apparatus consists of four valves
that help to regulate blood flow through the heart. The four valves are the tricuspid
valve, the pulmonary valve, the mitral valve, and the aortic valve. Each valve has a
specific function and location within the heart:

*Tricuspid valve: The tricuspid valve is located between the right atrium and right
ventricle. Its function is to prevent the backflow of blood from the right ventricle into the
right atrium during ventricular contraction.

*Pulmonary valve: The pulmonary valve is located between the right ventricle and the
pulmonary artery. Its function is to prevent the backflow of blood from the pulmonary
artery into the right ventricle during diastole.

*Mitral valve: The mitral valve is located between the left atrium and left ventricle. Its
function is to prevent the backflow of blood from the left ventricle into the left atrium
during ventricular contraction.

*Aortic valve: The aortic valve is located between the left ventricle and the aorta. Its
function is to prevent the backflow of blood from the aorta into the left ventricle during
diastole.

The opening and closing of the heart valves are controlled by pressure gradients and
changes in the electrical potential across the heart's chambers. When the heart
contracts, pressure within the ventricles increases, causing the tricuspid and mitral
valves to close, preventing backflow of blood into the atria. This also creates pressure
gradients that cause the pulmonary and aortic valves to open, allowing blood to be
ejected from the ventricles into the pulmonary and systemic circulations, respectively.
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When the ventricles relax during diastole, the pressure within the ventricles decreases,
causing the pulmonary and aortic valves to close, preventing backflow of blood into the
ventricles.

12/ Cardiac cycle and its phases. The cardiac cycle refers to the sequence of events that occur
during one complete heartbeat. The cardiac cycle is divided into two main phases:
systole and diastole. Within each phase, there are several subphases that reflect the
different stages of the heart's contraction and relaxation. The phases of the cardiac cycle
are as follows:

*Atrial systole: The atria contract, forcing blood through the tricuspid and mitral valves
and into the ventricles. This phase accounts for approximately 20% of ventricular filling.

*Isovolumic contraction: The ventricles begin to contract, increasing the pressure within
the ventricles. This phase occurs while all the heart valves are closed, and the volume of
blood within the ventricles remains constant.

*Rapid ejection: The pressure within the ventricles surpasses the pressure in the
pulmonary and aortic arteries, and the semilunar valves open, allowing blood to be
ejected into the pulmonary and systemic circulations.

*Reduced ejection: As the ventricles continue to contract, the rate of blood ejection
slows down.

*Isovolumic relaxation: The ventricles relax, and the pressure within them decreases. All
the heart valves are closed, and the volume of blood within the ventricles remains
constant.

*Rapid filling: The pressure within the ventricles falls below that of the atria, and the
tricuspid and mitral valves open, allowing blood to flow from the atria into the ventricles.

*Diastasis: The rate of filling slows as the ventricles continue to relax.

*Atrial systole (again): The atria contract, forcing any remaining blood into the
ventricles.

The duration of the cardiac cycle varies depending on heart rate, with the cycle
becoming shorter at higher heart rates. The cardiac cycle plays a critical role in
maintaining proper blood flow through the heart and the rest of the circulatory system,
and disruptions to the cardiac cycle can lead to various cardiovascular disorders.

13/ Blood pressure in chambers of a heart. Blood pressure in the chambers of the heart varies
throughout the cardiac cycle, with pressure increasing during systole (contraction) and
decreasing during diastole (relaxation). The pressure in each chamber of the heart
depends on various factors, including the volume of blood present in the chamber, the
strength of the heart's contractions, and the resistance to blood flow in the circulatory
system.

During systole, blood pressure increases in the left ventricle as it contracts to eject blood
into the aorta and throughout the body. At its peak, the pressure in the left ventricle can
reach around 120-140 mmHg. Blood pressure in the right ventricle also increases during
systole as it contracts to eject blood into the pulmonary artery and into the lungs.
However, the pressure in the right ventricle is much lower than that of the left ventricle,
typically peaking at around 25-30 mmHg. During diastole, blood pressure in the left
ventricle drops as it relaxes and begins to fill with blood. The pressure in the left
ventricle during diastole is around 5-12 mmHg. Blood pressure in the right ventricle also
drops during diastole as it relaxes and begins to fill with blood from the superior and
 inferior vena cava. The pressure in the right ventricle during diastole is typically around
2-8 mmHg.

Overall, the pressure changes in the heart during the cardiac cycle help to ensure that
blood is pumped efficiently through the circulatory system, supplying oxygen and
nutrients to the body's tissues and organs. Abnormalities in blood pressure within the
heart can be indicative of various cardiovascular disorders, such as hypertension or
heart failure.

14/ The amount of blood ow, systolic and minute cardiac outputs, addi onal volumes and capaci es. The amount
of blood flow, systolic and minute cardiac outputs, and additional volumes and capacities
are important parameters that relate to the functioning of the cardiovascular system.
Let's explore each of these factors:

*Blood Flow: Blood flow refers to the volume of blood circulated through the blood
vessels within a specific period of time. It is typically expressed in milliliters per minute
(ml/min). The overall blood flow in the body depends on factors such as heart rate,
stroke volume, and the resistance encountered in the blood vessels. Blood flow is crucial
for delivering oxygen, nutrients, and hormones to the body's tissues and removing waste
products.

*Systolic Cardiac Output: Systolic cardiac output represents the volume of blood pumped
out by the heart in each contraction or systole. It is the product of stroke volume (the
volume of blood ejected with each heartbeat) and heart rate. Systolic cardiac output is
important because it reflects the ability of the heart to pump blood effectively. It is
typically expressed in milliliters per beat or liters per minute (L/min).

*Minute Cardiac Output: Minute cardiac output, also known as cardiac output or total
cardiac output, represents the volume of blood pumped by the heart in one minute. It is
calculated by multiplying the heart rate (number of beats per minute) by the stroke
volume (volume of blood ejected per beat). Minute cardiac output provides an indication
of the overall efficiency of the cardiovascular system in delivering blood to the body's
tissues. It is typically expressed in liters per minute (L/min).

*Additional Volumes and Capacities: In the context of the respiratory system, there are
several additional volumes and capacities that describe different aspects of lung
function. These include:

*Inspiratory Reserve Volume (IRV): The inspiratory reserve volume is the additional
volume of air that can be forcibly inhaled after a normal inhalation. It represents the
maximum amount of air that can be inhaled beyond the tidal volume.

*Expiratory Reserve Volume (ERV): The expiratory reserve volume is the additional
volume of air that can be forcibly exhaled after a normal exhalation. It represents the
maximum amount of air that can be exhaled beyond the tidal volume.

*Residual Volume (RV): The residual volume is the volume of air that remains in the
lungs after a maximal exhalation. It is necessary to keep the lungs inflated and maintain
gas exchange even during the expiratory phase.

*Total Lung Capacity (TLC): Total lung capacity is the maximum volume of air that the
lungs can hold. It is the sum of all lung volumes, including tidal volume, inspiratory
reserve volume, expiratory reserve volume, and residual volume.

15/ Regula on of heart ac vity: myogenic, neural, humoral regula on The myogenic regulation of the heart
is the intrinsic ability of cardiac muscle cells to generate and conduct electrical impulses
spontaneously, which results in the rhythmic contraction of the heart.
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The pacemaker cells in the sinoatrial node (SA node) located in the right atrium of the
heart generate electrical impulses spontaneously, initiating the cardiac cycle. These cells
are specialized cardiomyocytes that have a unique set of ion channels that allow for the
spontaneous generation of action potentials, unlike the rest of the cardiac cells.

The electrical impulses generated by the SA node cells spread throughout the atria,
causing them to contract and pump blood into the ventricles. The impulses then travel to
the atrioventricular (AV) node, where the impulses are delayed briefly to allow the atria
to empty fully and the ventricles to fill with blood. After the delay, the impulses are
conducted to the bundle of His, which divides into the left and right bundle branches that
conduct the impulses through the Purkinje fibers, causing the ventricles to contract and
pump blood out of the heart.

*The myogenic regulation of the heart is influenced by various factors, including the
autonomic nervous system, circulating hormones, and the balance of ions such as
sodium, potassium, and calcium inside and outside the cells. For example, the
sympathetic nervous system can increase the heart rate and force of contraction, while
the parasympathetic nervous system can decrease the heart rate and force of
contraction.

Overall, the myogenic regulation of the heart ensures that the heart beats at an
appropriate rate and force to meet the body's metabolic demands, and any disruption in
this mechanism can lead to various cardiac arrhythmias or other cardiovascular
disorders.

*The neural regulation of the heart refers to the control of the heart rate and force of
contraction by the autonomic nervous system. The two branches of the autonomic
nervous system that regulate heart activity are the sympathetic nervous system and the
parasympathetic nervous system.

The sympathetic nervous system activates the heart rate and force of contraction by
releasing norepinephrine onto beta-1 adrenergic receptors in the heart. Norepinephrine
activates a signaling pathway that increases the intracellular concentration of cyclic
AMP, which leads to the phosphorylation of ion channels and proteins involved in the
cardiac action potential. These changes lead to an increase in the heart rate,
contractility, and conduction velocity of the heart.

In contrast, the parasympathetic nervous system reduces the heart rate and force of
contraction by releasing acetylcholine onto muscarinic receptors in the heart, primarily
the M2 receptor. Acetylcholine activates a signaling pathway that decreases the
intracellular concentration of cyclic AMP, leading to the dephosphorylation of ion
channels and proteins involved in the cardiac action potential. These changes lead to a
decrease in the heart rate, contractility, and conduction velocity of the heart.

*The neural regulation of the heart is also influenced by reflexes that originate from
various organs, including the lungs, blood vessels, and baroreceptors in the heart itself.
These reflexes modulate the activity of the autonomic nervous system, helping to
maintain homeostasis in the body.

Overall, the neural regulation of the heart plays a critical role in maintaining the normal
rhythm and function of the heart, and any disruption in this mechanism can lead to
various cardiac arrhythmias or other cardiovascular disorders.

*Humoral regulation of heart activity involves the control of heart rate and contractility
through chemical signals in the blood. The primary mechanisms of humoral regulation of
the heart include the actions of the sympathetic and parasympathetic nervous systems,
as well as several hormones.
*The sympathetic nervous system is responsible for increasing heart rate and
contractility through the release of the hormone epinephrine (also known as adrenaline)
and norepinephrine. These hormones bind to beta-adrenergic receptors on the surface of
cardiac cells, triggering a cascade of intracellular events that result in increased calcium
ion influx and stronger contractions.

*The parasympathetic nervous system, on the other hand, decreases heart rate and
contractility through the release of acetylcholine. Acetylcholine binds to muscarinic
receptors on the surface of cardiac cells, which decreases the activity of the sinoatrial
(SA) node, the heart's natural pacemaker.

*Several hormones also play a role in humoral regulation of the heart. For example, the
hormone atrial natriuretic peptide (ANP) is released from the atria of the heart in
response to increased blood volume or pressure. ANP acts to decrease heart rate and
contractility, as well as promote vasodilation and the excretion of sodium and water
from the body.

Another hormone, angiotensin II, acts to increase heart rate and contractility, as well as
promote vasoconstriction and the retention of sodium and water in the body.
Angiotensin II is produced by the renin-angiotensin-aldosterone system, which is
activated in response to low blood pressure or volume.

Overall, the humoral regulation of heart activity is a complex interplay between the
sympathetic and parasympathetic nervous systems, as well as several hormones that act
to modulate heart rate, contractility, and vascular tone.

16/ Myogenic mechanisms of regula on of heart ac vity: a) the Frank-Starling law and the e ect of Anrep; b)
Chronoinotropic dependency (the Bowditch «staircase») Myogenic mechanisms of regulation of heart
activity refer to the inherent ability of cardiac muscle cells to modulate their own
contraction strength and heart rate.

a) The Frank-Starling law and the effect of Anrep are two related myogenic mechanisms
that regulate the strength of cardiac contractions. The Frank-Starling law states that the
strength of cardiac contractions is directly proportional to the initial length of the cardiac
muscle fibers. In other words, the greater the volume of blood filling the heart during
diastole (the relaxation phase), the greater the force of the subsequent systolic
(contraction) phase. This mechanism helps to ensure that the cardiac output matches
the venous return, optimizing the heart's efficiency.

The Anrep effect is a related mechanism that describes how the strength of cardiac
contractions can increase in response to increased afterload (resistance to blood flow).
When the heart is exposed to an increased workload, such as during exercise, the Anrep
effect causes a temporary increase in contractility, independent of changes in preload
(volume of blood in the heart at the end of diastole).

b) Chronoinotropic dependency, also known as the Bowditch "staircase" phenomenon, is

a myogenic mechanism that regulates heart rate. It describes the phenomenon where
the strength of cardiac contractions and heart rate are positively correlated; that is, an
increase in contractility is accompanied by an increase in heart rate. This mechanism is
thought to be due to the interaction between intracellular calcium ion levels and the
activity of ion channels involved in regulating the pacemaker potential of the SA node.

Overall, myogenic mechanisms of regulation of heart activity help to maintain the

optimal balance of cardiac output and vascular resistance, ensuring efficient delivery of
oxygen and nutrients to the body's tissues.

17/Humoral mechanisms of regula on of a heart: e ect of Ca++, K+ , Na+ ; b) role of hormones; c) e ect of metabolites.
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 Humoral mechanisms of regulation of the heart refer to the regulation of heart activity
through the action of chemical messengers, including ions, hormones, and metabolites.

a) The levels of various ions, such as Ca++, K+, and Na+, can have significant effects on
the regulation of the heart. For example, an increase in extracellular Ca++ levels can
lead to increased contractility of the heart muscle, while an increase in extracellular K+
levels can lead to a decrease in heart rate and contractility. Similarly, changes in Na+
levels can affect the depolarization of cardiac cells, which can impact the timing and
strength of contractions.

b) Hormones also play a crucial role in the humoral regulation of the heart. For example,
the hormone epinephrine (also known as adrenaline) released by the adrenal gland in
response to stress or exercise can increase heart rate and contractility by binding to
beta-adrenergic receptors in the heart. Other hormones, such as norepinephrine,
angiotensin II, and atrial natriuretic peptide, can also affect heart rate, contractility, and
vascular tone.

c) Metabolites can also have an impact on the regulation of the heart. For example, high
levels of lactate, a byproduct of anaerobic metabolism, can lead to acidosis, which can
decrease the strength of cardiac contractions. Additionally, changes in the levels of
oxygen and carbon dioxide in the blood can affect the pH of the blood, which can also
have an impact on cardiac function.

Overall, humoral mechanisms of regulation of the heart involve a complex interplay of

ions, hormones, and metabolites that act to modulate heart rate, contractility, and
vascular tone in response to various physiological and environmental factors.

18/ Intracardiac re exes as a form of intracardial regula on, the structure of their re ex arcs. Intracardiac
reflexes are a form of reflex regulation that occurs within the heart itself. They are
responsible for maintaining proper cardiac function by controlling heart rate, rhythm,
and contractility. The reflex arc of intracardiac reflexes involves three main
components: the sensory receptor, the afferent nerve fiber, and the effector organ. The
sensory receptor is located within the heart and detects changes in the mechanical or
chemical environment of the cardiac tissue. The afferent nerve fiber transmits the
sensory information from the receptor to the central nervous system. The effector organ,
in turn, receives signals from the central nervous system and carries out the appropriate
response.

The specific structure of the reflex arc can vary depending on the type of intracardiac
reflex. However, one common example is the atrial reflex. In this reflex, stretching of the
atrial walls due to an increase in blood volume activates stretch receptors called atrial
volume receptors. These receptors send signals through afferent nerve fibers to the
nucleus tractus solitarius in the brainstem. The brainstem, in turn, sends signals through
efferent nerve fibers to the heart, causing a decrease in heart rate and contractility. This
helps to reduce the volume of blood entering the heart and maintain proper cardiac
output.

Overall, intracardiac reflexes play an important role in regulating cardiac function and
ensuring proper blood flow throughout the body.

19/ Extracardiac regula on of cardiac ac vity. Central mechanisms of regula on of a heart. In addition to
intracardiac reflexes, cardiac activity is also regulated by extracardiac mechanisms,
including both central and peripheral mechanisms.

*The central mechanisms of regulation of the heart involve the autonomic nervous
system, which is divided into the sympathetic and parasympathetic branches. The
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 sympathetic branch is responsible for increasing heart rate and contractility, while the
parasympathetic branch is responsible for slowing down heart rate and decreasing
contractility.

*The sympathetic nervous system releases norepinephrine, which binds to beta-

adrenergic receptors on cardiac muscle cells, leading to an increase in heart rate and
contractility. On the other hand, the parasympathetic nervous system releases
acetylcholine, which binds to muscarinic receptors on cardiac muscle cells, leading to a
decrease in heart rate and contractility.

*The autonomic nervous system is controlled by higher brain centers, such as the
medulla oblongata and hypothalamus. These areas receive input from various sensory
receptors throughout the body, as well as from emotional and cognitive centers in the
brain. They then modulate autonomic output to the heart and other organs based on the
body's needs.

Other central mechanisms of regulation of the heart include hormonal regulation, such
as the release of epinephrine and norepinephrine from the adrenal glands, and the renin-
angiotensin-aldosterone system, which regulates blood volume and pressure. Overall,
extracardiac regulation of cardiac activity involves a complex interplay between central
and peripheral mechanisms. These mechanisms work together to maintain proper
cardiac function and ensure adequate blood flow throughout the body.

20/Re ex regula on of heart ac vity from di erent re ex zones:a)re ex of aor c arch (re ex of Zion)b)re ex from the
hollow veins convergence site (Bainbridge re ex);c) caro d sinus re ex (Hering re ex); d)ocular-cardiac re ex (Aschner-
Danini re ex Reflex regulation of heart activity involves the activation of reflexes from
various reflex zones in the body. Here are some examples of reflexes that can affect
heart activity:

a) Reflex of aortic arch (Reflex of Zion): The aortic arch reflex is a reflex that is initiated
by stretch receptors located in the aortic arch. When blood pressure increases, the
stretch receptors are activated, and afferent signals are sent to the medulla oblongata in
the brainstem. The medulla oblongata then sends efferent signals to the heart, which
causes a decrease in heart rate and contractility. This reflex helps to regulate blood
pressure and maintain proper blood flow to the body.

b) Reflex from the hollow veins convergence site (Bainbridge reflex): The Bainbridge
reflex is a reflex that is initiated by stretch receptors located in the walls of the atria,
specifically at the junction of the superior and inferior vena cava. When blood flow into
the atria increases, the stretch receptors are activated, and afferent signals are sent to
the medulla oblongata in the brainstem. The medulla oblongata then sends efferent
signals to the heart, which causes an increase in heart rate and contractility. This reflex
helps to maintain proper blood flow to the body.

c) Carotid sinus reflex (Hering reflex): The carotid sinus reflex is a reflex that is initiated
by baroreceptors located in the carotid sinus, which is a dilated portion of the carotid
artery. When blood pressure increases, the baroreceptors are activated, and afferent
signals are sent to the medulla oblongata in the brainstem. The medulla oblongata then
sends efferent signals to the heart, which causes a decrease in heart rate and
contractility. This reflex helps to regulate blood pressure and maintain proper blood flow
to the brain.

d) Ocular-cardiac reflex (Aschner-Danini reflex): The ocular-cardiac reflex is a reflex that

is initiated by stimulation of the eyeballs. When pressure is applied to the eyeballs,
afferent signals are sent to the medulla oblongata in the brainstem. The medulla
oblongata then sends efferent signals to the heart, which causes a decrease in heart rate
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 and contractility. This reflex is used in clinical settings to help slow down the heart rate
in patients with certain heart conditions.

Overall, reflex regulation of heart activity from different reflex zones helps to maintain
proper cardiac function and ensure adequate blood flow throughout the body.

21/ Conduc on of excita on along the heart, its peculiari es The conduction of excitation along the
heart involves a coordinated series of electrical impulses that trigger the contraction of
the cardiac muscle cells. The process starts with the sinoatrial node, which is the natural
pacemaker of the heart located in the right atrium. The SA node generates electrical
impulses spontaneously, which then travel through the atrial muscle cells, causing them
to contract and propel blood into the ventricles. The electrical impulses then reach the
atrioventricular node, which is located in the junction between the atria and the
ventricles. The AV node serves as a gatekeeper, delaying the electrical impulses to allow
time for the atria to empty their contents into the ventricles before the ventricles
contract. This delay is essential for proper coordination of the heart's pumping action.
After passing through the AV node, the electrical impulses travel down the His-Purkinje
system, a specialized network of cells that rapidly conducts the impulses through the
ventricular muscle cells. This rapid conduction ensures that the ventricles contract
simultaneously and forcefully, effectively pumping blood out of the heart and into the
circulatory system.

Overall, the conduction of excitation along the heart is a highly coordinated process that
ensures efficient and effective pumping of blood throughout the body. Any disruptions in
this process can lead to irregular heart rhythms or arrhythmias, which can be dangerous
and even life-threatening.

The conduction of excitation along the heart has several peculiarities that make it unique
compared to other types of muscle conduction:

Specialized conduction system: Unlike skeletal muscle, which is controlled by the

somatic nervous system, the heart has a specialized conduction system consisting of the
SA node, AV node, and His-Purkinje system. This system ensures that the heart contracts
in a coordinated manner, allowing for efficient pumping of blood.

Automaticity: The SA node has the ability to generate its own electrical impulses
spontaneously, without external stimulation. This property of automaticity allows the
heart to continue beating even in the absence of external input.

Electrical coupling: Cardiac muscle cells are electrically coupled to each other through
gap junctions, allowing for rapid transmission of electrical impulses across the heart.
This property ensures that the electrical impulses generated by the SA node and
conducted through the heart are rapidly propagated, resulting in synchronous
contraction of the heart muscle.

Refractory period: Cardiac muscle cells have a longer refractory period compared to
skeletal muscle cells. This means that once a cardiac muscle cell has been stimulated
and contracted, it cannot be immediately re-stimulated. This property helps prevent
tetanic contractions of the heart, which could be dangerous or even fatal.

Autonomic regulation: The heart is regulated by the autonomic nervous system, which
can increase or decrease heart rate and contractility. This allows the heart to respond to
changing physiological demands, such as during exercise or stress.

Overall, the peculiarities of the conduction of excitation along the heart ensure that the
heart can function effectively as a pump, supplying oxygen and nutrients to the body's
tissues.
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22/ The dipole theory of the origin of ECG. The dipole theory of the origin of the electrocardiogram
(ECG) is a model that explains how the electrical activity of the heart produces the ECG
waveform. According to this theory, the heart can be represented as a dipole,. In the
case of the heart, the dipole consists of the depolarization and repolarization currents
that flow through the heart during the cardiac cycle. As the depolarization wave spreads
through the atria and ventricles, it generates an electrical field that can be detected on
the surface of the body by electrodes placed on the skin. The ECG waveform is created by
the summation of the electrical potentials generated by the dipole as it moves through
the heart. The amplitude and direction of the ECG waveform are determined by the
orientation and strength of the dipole, as well as the location and orientation of the
electrodes. The dipole theory of the origin of the ECG is a useful model for understanding
the basic principles of electrocardiography, and it has been used to develop more
advanced methods for analyzing the ECG waveform. However, it is important to note that
the dipole model is a simplification of the complex electrical activity that occurs during
the cardiac cycle, and it does not fully capture all of the nuances of the ECG signal.

23/ The principles of ECG recording. Types of leads for ECG recording ECG (electrocardiogram) recording is
a medical test that records the electrical activity of the heart. The principles of ECG
recording are as follows:

*Placement of Electrodes: Electrodes are placed on the skin at specific locations to

record the electrical activity of the heart. The standard placement includes six limb leads
and six precordial leads.

*Amplification of Signals: The electrical activity of the heart is very small and needs to
be amplified to be recorded. The ECG machine amplifies the signals from the electrodes
and records them on paper or on a computer screen.

*Calibration: The ECG machine needs to be calibrated to ensure that the recordings are
accurate. This is done by recording a standard voltage signal, which is usually 1 millivolt
(mV), to ensure that the machine is measuring accurately.

*Recording of Waves: The electrical activity of the heart produces a pattern of waves
that can be seen on the ECG. These waves are labeled P, Q, R, S, and T waves. Each wave
represents a different stage of the cardiac cycle.

*Analysis of Waveforms: The ECG recording is analyzed to identify any abnormalities or

irregularities in the electrical activity of the heart. This can help diagnose conditions
such as arrhythmias, heart attacks, and other cardiac disorders.

*Interpretation: The ECG recording is interpreted by a medical professional, such as a

cardiologist or electrocardiograph technician, who can identify any abnormalities and
make a diagnosis based on the recorded data.

Overall, the principles of ECG recording involve the accurate placement of electrodes,
amplification of signals, calibration of the ECG machine, recording of waves, analysis of
waveforms, and interpretation of the results by a medical professional.

There are three types of leads used in ECG recording:

*Limb Leads: Limb leads are placed on the limbs, specifically on the arms and legs, and
are used to record the electrical activity of the heart in the frontal plane. There are three
limb leads on each arm and leg, making a total of six limb leads. These are labeled as
Lead I, II, III, aVR, aVL, and aVF.

*Chest (Precordial) Leads: Chest leads are placed on the chest and are used to record
the electrical activity of the heart in the horizontal plane. There are six chest leads,
labeled V1 to V6. These leads provide a more detailed view of the electrical activity of
the heart and are especially useful for detecting abnormalities in the ventricles.

*Augmented Leads: Augmented leads are also called unipolar leads and are used to
record the electrical activity of the heart in the frontal plane. They are derived from the
limb leads and measure the voltage difference between one limb lead and the center
point between the other two limb leads. There are three augmented leads, labeled aVR,
aVL, and aVF.

In total, the standard 12-lead ECG recording involves placement of six limb leads, six
chest leads, and three augmented leads. The specific placement of the electrodes may
vary depending on the patient's condition and the purpose of the ECG recording.

24/ The origin of the waves, intervals and segments of ECG The waves, intervals, and segments of an
electrocardiogram (ECG or EKG) are related to the electrical activity of the heart during a
cardiac cycle. Here is a brief explanation of the origin of each component:

*P wave: The P wave is the first wave of the ECG and represents the depolarization of
the atria. The electrical impulse generated in the sinoatrial (SA) node spreads
throughout the atria, causing them to contract and pump blood into the ventricles.

*QRS complex: The QRS complex is a series of waves that represents the depolarization
of the ventricles. The Q wave is the first negative deflection and represents the initial
depolarization of the interventricular septum. The R wave is the first positive deflection
and represents the depolarization of the main mass of the ventricles. The S wave is the
negative deflection that follows the R wave and represents the final depolarization of the
ventricles.

*T wave: The T wave represents the repolarization of the ventricles. After the ventricles
contract, they need to relax and prepare for the next cycle. The electrical charge of the
ventricles returns to baseline during the repolarization phase, and this is represented by
the T wave.

*PR interval: The PR interval is the time between the start of the P wave and the start of
the QRS complex. It represents the time it takes for the electrical impulse to travel from
the SA node to the ventricles via the atrioventricular (AV) node.

*ST segment: The ST segment is the period between the end of the S wave and the
beginning of the T wave. It represents the time when the ventricles are depolarized but
not yet repolarized. Any deviation from the normal baseline of the ST segment can
indicate myocardial ischemia or injury.

*QT interval: The QT interval is the time from the start of the Q wave to the end of the T
wave. It represents the total time it takes for the ventricles to depolarize and then
repolarize. Abnormalities in the QT interval can indicate certain cardiac conditions, such
as arrhythmias and electrolyte imbalances.

Overall, the waves, intervals, and segments of the ECG provide valuable information
about the electrical activity of the heart and can help diagnose various cardiac
conditions.

25/ The principles of ECG analysis The analysis of an electrocardiogram (ECG or EKG) involves
several principles that allow healthcare professionals to interpret the electrical activity
of the heart. the key principles of ECG analysis:

*Identify the standard lead placement: The standard lead placement involves placing the
ECG electrodes on specific parts of the body to capture the electrical activity of the heart
from different angles. The standard lead placement includes the limb leads (I, II, III,
aVR, aVL, and aVF) and the precordial leads (V1-V6).

*Determine the heart rate: The heart rate can be calculated by measuring the time
between two R waves (known as the R-R interval) and using the following formula:
heart rate (beats per minute) = 60 / R-R interval (in seconds).

*Assess the rhythm: The rhythm of the ECG refers to the regularity of the electrical
activity of the heart. A regular rhythm has consistent intervals between R waves, while
an irregular rhythm has varying intervals between R waves. An irregular rhythm may
indicate a cardiac arrhythmia.

*Evaluate the P wave: The P wave represents the electrical activity of the atria. The P
wave should be upright and consistent in shape and duration. Abnormalities in the P
wave can indicate atrial enlargement or conduction abnormalities.

*Analyze the QRS complex: The QRS complex represents the electrical activity of the
ventricles. The QRS complex should be narrow and consistent in shape and duration.
Abnormalities in the QRS complex can indicate ventricular conduction abnormalities or
other cardiac conditions.

*Assess the ST segment and T wave: The ST segment and T wave represent the
repolarization of the ventricles. The ST segment should be at baseline, and the T wave
should be upright and consistent in shape and duration. Abnormalities in the ST segment
and T wave can indicate myocardial ischemia or injury.

*Consider other factors: Other factors that can affect ECG analysis include patient age,
medications, electrolyte imbalances, and other medical conditions. These factors should
be taken into account when interpreting the ECG.

Overall, the principles of ECG analysis involve assessing the various components of the
ECG to identify abnormalities and diagnose cardiac conditions. ECG analysis requires
knowledge and expertise, and should be performed by a trained healthcare professional.

26/ The dependence of the electrocardiographic wave al tude from their projec on on the axis of the lead. The
electrocardiographic (ECG) wave altitude (amplitude) is dependent on the projection of
the wave on the axis of the lead. The ECG leads are electrodes placed at specific
locations on the body that record the electrical activity of the heart from different
angles, resulting in different wave projections.

The ECG waves are represented as positive or negative deflections from the baseline,
with the amplitude of the wave reflecting the strength of the electrical signal. The
direction of the deflection (upward or downward) depends on the orientation of the
wave relative to the axis of the lead.

For example, in Lead II, the electrode is placed on the right leg and the positive
electrode is on the left arm. The axis of the lead runs from the right leg to the left arm,
resulting in a positive deflection for waves that are oriented in a direction toward the left
arm (such as the P wave) and a negative deflection for waves that are oriented in a
direction away from the left arm (such as the Q wave).

In contrast, Lead aVR has a negative electrode on the right arm and a positive electrode
on the left leg. The axis of the lead runs from the right arm to the left leg, resulting in a
positive deflection for waves that are oriented in a direction toward the right arm (such
as the Q wave) and a negative deflection for waves that are oriented in a direction away
from the right arm (such as the P wave).
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 Overall, the altitude (amplitude) of the ECG wave is dependent on the projection of the
wave on the axis of the lead. The direction and amplitude of the deflection depend on the
orientation of the wave relative to the axis of the lead, and different leads capture
different aspects of the electrical activity of the heart.

27/ The concept of electrical axis of the heart. Its horizontal, ver cal and intermediate posi on. Methods of
determina on.

The electrical axis of the heart is a concept used to describe the overall direction of the
electrical activity of the heart during the cardiac cycle. It is represented by a vector that
reflects the sum of the electrical forces generated by the heart.

The electrical axis of the heart can be described in terms of its horizontal, vertical, and
intermediate positions.

Horizontal electrical axis : This refers to the direction of the electrical forces in the
frontal plane, which is a vertical plane that divides the body into front and back halves.
The normal range for the horizontal electrical axis is between -30 and +90 degrees. A
horizontal electrical axis that deviates from this range may indicate a conduction
abnormality or other cardiac condition.

Vertical electrical axis : This refers to the direction of the electrical forces in the sagittal
plane, which is a vertical plane that divides the body into left and right halves. The
normal range for the vertical electrical axis is between -30 and +90 degrees. A vertical
electrical axis that deviates from this range may indicate a conduction abnormality or
other cardiac condition.

Intermediate electrical axis : This refers to the direction of the electrical forces in the
transverse plane, which is a horizontal plane that divides the body into upper and lower
halves. The normal range for the intermediate electrical axis is between -30 and +90
degrees. A deviation from this range may indicate a conduction abnormality or other
cardiac condition.

The electrical axis of the heart can be determined using several methods, including :

*The Einthoven triangle method: This method uses the three standard limb leads (I, II,
and III) to calculate the electrical axis of the heart in the frontal plane.

*The Cabrera method: This method uses six unipolar limb leads (aVR, aVL, aVF, and
three augmented limb leads) to calculate the electrical axis of the heart in the frontal
plane.

*The Lewis lead method: This method uses a single lead placed on the fifth intercostal
space at the mid-clavicular line to calculate the electrical axis of the heart in the frontal
plane.

*The Frank vectorcardiogram method: This method uses a combination of multiple leads
to calculate the electrical axis of the heart in all three planes (frontal, sagittal, and
transverse).

Overall, the electrical axis of the heart is an important concept in the interpretation of
electrocardiograms and can provide valuable information about cardiac function and
potential abnormalities.

28/ Methods of long-term ECG recording during normal living ac vity. The concept of Holter monitoring. Long-term
ECG recording during normal living activity is often used to diagnose and monitor cardiac
conditions that may be difficult to detect during a standard ECG. There are several
methods of long-term ECG recording, including:
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 *Holter monitoring: Holter monitoring is a continuous ECG recording that lasts for 24-48
hours. The patient wears a small portable device that records the ECG signals from two
to three leads. The device is then returned to the healthcare provider who downloads the
data and analyzes it for abnormalities.

*Event recording: Event recording involves wearing a small device that can record the
ECG signals for a longer period of time, typically up to 30 days. The device can be
activated by the patient when they experience symptoms, allowing for a more targeted
recording of any abnormal heart activity.

*Mobile cardiac telemetry: This is a newer technology that involves wearing a small
device that continuously records ECG signals and transmits the data to a monitoring
center. The data can be reviewed in real-time by healthcare providers who can alert the
patient if any abnormal activity is detected.

*Implantable loop recorder: This is a small device that is implanted under the skin of the
chest and can record ECG signals for up to three years. The device is often used for
patients who have infrequent or unpredictable symptoms.

Overall, long-term ECG recording during normal living activity can provide valuable
information about cardiac function and potential abnormalities. The choice of method
depends on the specific needs of the patient and the suspected condition being
evaluated.

Holter monitoring is a non-invasive diagnostic test that involves the continuous

recording of the heart's electrical activity (ECG) over a period of 24-48 hours. The test is
named after its inventor, Norman Holter, who developed the first portable ECG recorder
in the 1940s.

During a Holter monitor test, the patient wears a small, battery-operated device that is
attached to the chest by electrodes. The device continuously records the ECG signals
from two to three leads, which are stored on a digital recorder. The patient is instructed
to carry on with their normal daily activities, including sleeping, eating, and exercising,
while wearing the device.

After the monitoring period is complete, the device is returned to the healthcare provider
who downloads the data and analyzes it for any abnormal heart activity. The data can
reveal information about heart rate, rhythm, and other indicators of cardiac function.

Holter monitoring is often used to diagnose and monitor various cardiac conditions,
including arrhythmias, palpitations, and syncope (fainting). It can also be used to
evaluate the effectiveness of certain medications or treatments for cardiac conditions.

Overall, Holter monitoring is a safe and non-invasive diagnostic test that can provide
valuable information about cardiac function and potential abnormalities during a
patient's normal daily activities.

29/ Sound e ects in the heart. The origin of heart sounds. The principle of the method of phonocardiography (PCG). The
heart produces a variety of sound effects that can be heard using a stethoscope. These
sound effects are generated by the movement of blood through the heart's chambers and
valves, and can provide important information about the heart's function and any
potential abnormalities. The two main sound effects produced by the heart are:

*Heart sounds: Heart sounds are the sounds produced by the opening and closing of the
heart's valves. There are two main heart sounds: S1 and S2.
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*S1 (also known as the "lub" sound) is produced by the closure of the mitral and
tricuspid valves at the beginning of systole (contraction of the ventricles). S1 is typically
louder at the apex (bottom) of the heart.

*S2 (also known as the "dub" sound) is produced by the closure of the aortic and
pulmonary valves at the end of systole. S2 is typically louder at the base (top) of the
heart.

*Murmurs: Murmurs are abnormal heart sounds that can indicate a problem with the
heart's valves or other structures. Murmurs are often described as a whooshing or
swishing sound, and can be heard between S1 and S2 (systolic murmurs) or between S2
and S1 (diastolic murmurs). Murmurs can be caused by a variety of conditions, including
valve disorders, congenital heart defects, and infections.

In addition to heart sounds and murmurs, there are other sound effects that can be
heard in certain cardiac conditions, such as pericardial friction rubs (a creaking or
scratching sound caused by inflammation of the pericardium) and gallops (additional
heart sounds caused by abnormal blood flow patterns).

Overall, sound effects in the heart can provide important diagnostic information about
the heart's function and any potential abnormalities

*Heart sounds are the sounds produced by the opening and closing of the heart's valves
during the cardiac cycle. The two main heart sounds, S1 and S2, are caused by the
closure of the heart's valves at specific points in the cycle.

S1, or the "lub" sound, is produced by the closure of the mitral and tricuspid valves at
the beginning of systole (when the ventricles contract). This sound is typically louder at
the apex (bottom) of the heart and is associated with the onset of ventricular
contraction.

S2, or the "dub" sound, is produced by the closure of the aortic and pulmonary valves at
the end of systole (when the ventricles relax). This sound is typically louder at the base
(top) of the heart and is associated with the end of ventricular contraction.

The timing and intensity of heart sounds can provide important information about the
heart's function and any potential abnormalities. For example, a loud S1 sound may
indicate a stiff or thickened heart valve, while a soft or absent S2 sound may indicate a
problem with the aortic or pulmonary valve.

In addition to S1 and S2, there are other heart sounds that can be heard in certain
conditions. For example, a third heart sound (S3) may be heard in patients with
congestive heart failure, while a fourth heart sound (S4) may be heard in patients with
hypertrophic cardiomyopathy.

Overall, heart sounds are an important diagnostic tool that can provide valuable
information about the heart's function and any potential abnormalities.

*Phonocardiography (PCG) is a non-invasive diagnostic tool that records the sound

vibrations produced by the heart using a specialized microphone called a
phonocardiogram. The principle of the method of phonocardiography involves recording
and analyzing the various sound components produced by the heart during the cardiac
cycle.

During a phonocardiogram, the microphone is placed over the chest to detect the sounds
produced by the heart. The sound waves are then amplified and recorded on a graph,
which allows healthcare providers to analyze the timing and intensity of the various
heart sounds.

The different components of the phonocardiogram correspond to different events during

the cardiac cycle. For example, the first heart sound (S1) is represented by a sharp spike
on the graph, while the second heart sound (S2) is represented by a broader spike.
Murmurs and other abnormal sounds can also be detected and analyzed using
phonocardiography.

Phonocardiography is often used in combination with other diagnostic tools, such as

echocardiography and electrocardiography, to provide a more comprehensive evaluation
of the heart's function and any potential abnormalities. It can be particularly useful in
diagnosing valve disorders and other structural abnormalities of the heart.

Overall, the principle of the method of phonocardiography involves recording and

analyzing the sound vibrations produced by the heart during the cardiac cycle to provide
valuable diagnostic information about the heart's function and any potential
abnormalities.

30/ Mechanical manifesta ons of the heart The mechanical manifestations of the heart refer to the
physical movements and contractions of the heart that are necessary to pump blood
throughout the body. The heart is a muscular organ that consists of four chambers : the
right atrium, the right ventricle, the left atrium, and the left ventricle.

The mechanical manifestations of the heart are controlled by a complex network of

electrical signals that regulate the timing and strength of the heart’s contractions.
During each cardiac cycle, the heart undergoes a series of mechanical events that are
necessary to pump blood efficiently and effectively.

The mechanical events of the heart include :

*Atrial systole: The contraction of the atria, which pushes blood into the ventricles.

*Ventricular systole: The contraction of the ventricles, which pumps blood out of the
heart and into the arteries.

*Atrial and ventricular diastole: The relaxation of the atria and ventricles, which allows
blood to flow into the heart from the veins.

The mechanical manifestations of the heart can be measured and evaluated using
various diagnostic tools, such as echocardiography and cardiac catheterization. These
tests can provide important information about the heart's function, including its ability
to pump blood efficiently, the presence of any structural abnormalities, and the effects of
various diseases or conditions on the heart's performance.

Overall, the mechanical manifestations of the heart are essential to maintaining the
body's circulatory system and delivering oxygen and nutrients to the body's tissues and
organs.
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