‘Lecture Notes’

UNIT - VII

RESPIRATION
CHAPTER 37 Pulmonary Ventilation Page # 4

Pulmonary Circulation,
CHAPTER 38 Page # 20
Pulmonary Edema, Pleural Fluid
Physical Principles of Gas Exchange; Diffusion of
CHAPTER 39 Oxygen & Carbon Dioxide Page # 28
Through the Respiratory Membrane
Transport of Oxygen and Carbon Dioxide
CHAPTER 40 Page # 35
in Blood and Tissue Fluids
CHAPTER 41 Regulation of Respiration Page # 45

Respiratory Insufficiency—Pathophysiology,
CHAPTER 42 Page # 57
Diagnosis, Oxygen Therapy
 CHAPTER 37

Pulmonary Ventilation
 CHAPTER 38

Pulmonary Circulation,
Pulmonary Edema,
Pleural Fluid
 CHAPTER 39

Physical Principles of Gas Exchange;

Diffusion of Oxygen
and Carbon Dioxide
Through the Respiratory Membrane
 CHAPTER 40

Transport of
Oxygen and Carbon Dioxide
in Blood and Tissue Fluids
 CHAPTER 41

Regulation of Respiration
 Brain Stem

• Controls Vital Reflexes like:

BREATHING,
HEART RATE REGULATION,
Midbrain BLOOD PRESSURE CONTROL
SWALLOWING

• Regulating AROUSAL and

maintaining CONSCIOUSNESS
RESPIRATORY PNEUMOTAXIC CENTER
• Superior portion of the pons
CENTER • Nucleus parabrachialis

Inhibits Controls rate and depth of breathing

Control the “switch-off” point of the inspiratory ramp
DORSAL RESPIRATORY GROUP
• Dorsal portion of the medulla
• Nucleus tractus solitarius (NTS) VENTRAL RESPIRATORY GROUP
• Ventrolateral part of the medulla
Inspiration • Nucleus ambiguous
Generation of basic rhythm of respiration
Normal quiet respiration: remain inactive
Inhibits
Inhibits During heavy exercise: both inspiration and expiration
Carotid bodies – Glossopharyngeal nerve (spilling over of extra signals from Dorsal Respiratory Group)
Aortic bodies – Vagus Nerve

Peripheral chemoreceptors More inhibitory impulses to

(Carotids & Aortic bodies)
RAMP Signal
Dorsal Respiratory group
Baroreceptors
Lung receptors Short Inspirationhbjhh
Stimulates Short Expiration mn
↓O2, ↑CO2, ↑ H+
3 Sec 2 Sec Increased frequency of respiration
↓ Bp
Over inflation of lungs (hering breuer reflex)
 RESPIRATORY CENTER

Inspiration
DORSAL RESPIRATORY
Dorsal portion of the Nucleus
GROUP medulla Tractus Solitarius
Generation of basic rhythm of respiration
(Repetitive bursts of inspiratory neuronal action
potentials)

Normal quiet respiration: remain inactive

VENTRAL RESPIRATORY Ventrolateral part of the
Nucleus Ambigus
GROUP medulla
During heavy exercise: both inspiration and expiration

Controls rate and depth of breathing

Superior portion of the
PNEUMOTAXIC CENTER pons
Nucleus Parabrachialis
Control the “switch-off” point of the inspiratory ramp

APNEUSTIC CENTER Promotes sustained and deep inspiration

 CAROTID BODY
&
GLOMUS CELLS
When the partial pressure of oxygen < 60 mmHg

K+ channel closes

Depolarization

Calcium channel open

Ca++ moves inwards

Neurotransmitters are released

(ATP - Predominantly)
(Acetylcholine)

Afferent fiber activation

(Glossopharyngeal & Vagus nerve)

Increased Respiratory Rate

 CHEMICAL CONTROL OF RESPIRATION
Effect of Effect on
Direct effect on
PERIPHERAL BLOOD CONCENTRATION PERIPHERAL CHEMORECEPTORS
CENTRAL CHEMORECEPTORS
on Central Chemoreceptors (Carotid bodies & Aortic bodies)
Can not cross the blood-brain barrier.

↑H+ Most potent direct effect Changes in hydrogen ion concentration in the Minor effect
blood have considerably less effect in
stimulating the Central chemoreceptors
Can easily cross blood brain barrier
Minor effect
Strong potent effect after conversion to H+
7 times ↓ effect than direct effect on
↑CO2 Mild direct effect Co2 → H2CO3 → H + HCO3 central chemo receptors

This effect last for only 1-2 days due to 5 times ↑ speed of effect than effect on
neutralization of H+ by HCO3- central chemo receptors
via renal compensation
Most potent effect
Effect starts at < 100mmHg
↓O2 No direct effect
Effects peripheral chemoreceptors which Max effect at 30 – 60 mm Hg
will then send impulses to respiratory centre
Chronic Breathing of Low Oxygen
Stimulates Respiration Even More
(Acclimatization in mountaineers)
 AT HIGH ALTITUDE
ACCLIMATIZATION

O2
↓ Stimulation of Respiration
(Because of less oxygen
in air)

↓
CO2
(Because of increased Inhibition of Respiration
respiratory rate) (This effect last for only 1-2 days)
 EFFECT OF
EXERCISE
On RESPIRATION

Brain
At the same time Metabolism increases
Transmitting collateral impulses into
motor impulses to the brain stem ↓O2, ↑CO2, ↑ H+
the exercising respiratory centre
muscles (Normal to slight change
An “anticipatory” in concentration)
stimulation of
respiration at the
onset of exercise

Final adjustment of respiration

Required to keep the oxygen, carbon dioxide,
and hydrogen ion concentrations of the body
Sudden increase in respiration fluids as nearly normal as possible
 Different factors effecting respiration Effect of brain edema on respiratory center
Brain concussion (trauma)
Voluntary control of respiration
Respiration can be controlled voluntarily and that one Brain edema
can hyperventilate or hypoventilate
Raised ICP

Compression of brainstem
Effect of irritant on airways
Irritant Compression of blood vessels supplying brain stem

Pulmonary irritant receptors Treatment: hypertonic saline (mannitol)

Epithelium of the trachea, bronchi, and bronchioles Anesthetics

Primary function is to depress cerebral cortex
Cough bronchoconstriction (asthma) But some also depress respiratory centres (pentobarbital)
“J receptors” Narcotics have more effect on respiratory centres
Engorgement of pulmonary capillaries And less effect on cerebral cortex
(pulmonary edema)
Periodic breathing
J receptors in the alveolar walls (In disease conditions)
(juxtaposition to the pulmonary capillaries) are stimulated The person breathes deeply for a short interval and then
breathes slightly or not at all for an additional interval, with the
Feeling of breathlessness cycle repeating itself over and over
 When a person over-breathes
Cheyne-Stokes (Increase in depth and rate of respiration)
Breathing
thus blowing off too much carbon dioxide from the pulmonary blood
while at the same time increasing blood oxygen,

it takes several seconds before the changed pulmonary blood can be

transported to the brain and inhibit the excess ventilation.

Delay causes over ventilation

over-ventilated blood having low carbon dioxide finally reaches the

brain respiratory center,
the center becomes depressed to an excessive amount.
(and results into decrease in depth and rate of respiration)

Then the opposite cycle begins.

That is, carbon dioxide increases and oxygen decreases in the alveoli.

Again, it takes a few seconds before the brain can respond to these
new changes. When the brain does respond, the person breathes
hard once again and the cycle repeats.
CAUSES:
Severe Cardiac Failure
Brain Damage
A long delay Severe Cardiac Failure: A long delay occurs
Increased negative feedback gain
for transport of blood from the lungs to the brain.
in the respiratory control areas.
occurs for transport of blood from the lungs to the brain.
 OBSTRUCTIVE SLEEP APNEA

Cause
“repeated episodes of interrupted breathing during sleep”
Relaxation of these muscles during sleep causes the pharynx to completely close so that air cannot flow into the lungs

Risk
• Older • Increased fat deposition in the soft tissues of the • Large tongue • Enlarged tonsils
Factors
pharynx compressing pharynx • Shapes of the palate that greatly
• Obesity increase resistance to the flow of air to
• Nasal obstruction
the lungs during inspiration
Events Period of no breathing Stimulation of respiration
Snoring (apnea) Repeated
Followed by
becoming (decreases in po2 and episodes of
Sudden attempts to breathe snoring
louder increases in pco2) apnea
(loud snorts & gasps)
Symptoms
• Sympathetic activity • Pulmonary and systemic hypertension
• Excessive daytime drowsiness
• High heart rates • Elevated risk for cardiovascular disease
Treatment • Uvulopalatopharyngoplasty • Tracheostomy • (CPAP)
(surgery to remove excess • Adenoidectomy
(create an opening in the Nasal ventilation with
fat tissue at the back of Remove enlarged tonsils
trachea to bypass the continuous positive airway
the throat ) or adenoids
obstructed airway during sleep pressure
“CENTRAL” SLEEP APNEA

damage to the central

respiratory centers or
abnormalities of respiratory
neuromuscular apparatus
 CHAPTER 42

Respiratory Insufficiency—
Pathophysiology,
Diagnosis,
Oxygen Therapy
 Causes of
respiratory diseases

Some respiratory diseases Others result from abnormalities abnormal blood transport of
result from inadequate of diffusion through the gases between the lungs
ventilation. pulmonary membrane and tissues.

Fundamental Tests of
Pulmonary Performance

Blood PO2 Blood PCO2 pH

 OBSTRUCTIVE LUNG DISEASE RESTRICTIVE LUNG DISEASE

Increased airway resistance Reduction in lung compliance

Pathophysiology making it difficult to exhale air which is the ability of the lungs to
efficiently. expand and contract
Bronchoconstriction
Parenchymal lung diseases
Asthma, chronic bronchitis
pulmonary fibrosis, sarcoidosis
Airway inflammation
Chest wall abnormalities
Diseases Bronchitis
scoliosis, obesity
Mucus production
Neuromuscular diseases
chronic obstructive pulmonary disease
muscular dystrophy, kyphoscoliosis
(COPD)
Total lung capacity (TLC)
Residual volume (RV)
Forced expiratory volume in 1 sec (FEV1)
Functional vital capacity (FVC)

FEV1/FVC Normal /

Peak expiratory flow rate (PEFR) Normal

EMPHYSEMA Smoke

partial paralysis of the cilia

stimulation of excess mucus secretion Inhibition of the alveolar macrophages
of the respiratory epithelium

excess mucus inflammatory edema infection

obstruction of the airway

Smoke
entrapment of air
Inflammation
overstretching
Activates immune cells
destruction of alveolar walls
(50 to 80%) Proteolytic enzymes

Loss of collapse
+ greatly decreases diffusing ventilation-perfusion mismatch pulmonary
elastic recoil (exhalation) capacity of the lung V/Q hypertension

increases airway resistance

hypoventilation
(greatly increased work of breathing) Hypoxia, hypercapnia
death
EMPHYSEMA

NORMAL
 PNEUMONIA
PNEUMONIA

Any
Any inflammatory
inflammatory condition
condition of
of the
the lung
lung in
in which
which some
some or
or all
all of
of the
the alveoli
alveoli are
are filled
filled with
with fluid
fluid and
and blood
blood cells
cells

Infection
[Bacteria (Pneumococcal) / Virus]

Inflammation

Increased permeability

Fluid and even red and white blood cells leak out of the blood into the alveoli

Alveoli are filled with fluid and cellular debris

(consolidation on X-ray / CT scan)

Decrease surface area of the respiratory membrane

Decreased ventilation-perfusion ratio

Hypoxemia (low blood oxygen)

Hypercapnia (high blood carbon dioxide)
 Atelectasis
Collapse of the alveoli
Airway obstruction
Lack of “surfactant”
Tumor (Respiratory distress syndrome
Mucus plug

Air entrapped beyond the block is absorbed Newborn premature babies

If the lung is rigid (fibrotic tissue) Decrease in surfactant production

Lung tissue is pliable Cannot collapse
Absorption of air from the alveoli
Collapse of the alveoli Very negative pressures within the alveoli Increased surface tension
Pulling out of fluid from pulmonary capillaries into the
alveoli
Alveolar edema Increased tendency of collapse
Vasoconstriction

Always increases the resistance to blood flow through the

pulmonary vessels of the collapsed lung

Blood flow through the atelectatic lung is greatly reduced

Most of the blood is routed through the ventilated lung

The overall ventilation-perfusion ratio is only moderately compromised,

So the aortic blood has only mild oxygen desaturation
ASTHMA In an allergic person

Allergen
Contractile hypersensitivity of
the bronchioles in response to IgE antibodies
foreign substances in the air
IgE antibodies attached to mast cells

On 2nd exposure to allergen

Allergen is attached to IgE antibodies which were previously attached to mast cells

Mast cell degranulation

• Histamine
• Bradykinin Total lung capacity (TLC)
• Eosinophilic chemotactic factor
• Slow reacting substance of anaphylaxis Residual volume (RV)
Forced expiratory volume in 1 sec (FEV 1)
• Localized edema (bronchiolar walls)
• Secretion of thick mucus (bronchiolar lumens) Functional vital capacity (FVC)
• Spasm of the bronchiolar smooth muscle
FEV1/FVC
Airway resistance increases greatly Peak expiratory flow rate (PEFR)
Dyspnea, or “air hunger,” (Wheezing)
TUBERCULOSIS
Tuberculous infection (lungs)

If untreated (3%)
Invasion of the infected tissue by
macrophages The walling-off process fails
“walling off” (tubercle)
Tubercle bacilli spread throughout the lungs

Large abscess Reduced total Abnormal Reduced Increased “work”

Cavities Fibrosis Respiratory membrane Ventilation-perfusion ratio Vital capacity Of breathing
Surface area
 HYPOXIA Effect of Oxygen therapy
(Classification) • Deficiency of oxygen in the atmosphere
100 % effective
Inadequate oxygenation
extrinsic reasons Extremely effective for hypoxia
• Hypoventilation (neuromuscular disorders)
Not effective for hypercapnia
• Hypoventilation caused by increased airway resistance or
decreased pulmonary compliance
Pulmonary disease • Abnormal alveolar ventilation-perfusion ratio Highly effective
(physiologic dead space or physiologic shunt)
• Diminished respiratory membrane diffusion
Venous-to-arterial
• Right-to-left” cardiac shunts Effective to some extent
shunts
• Anemia or abnormal hemoglobin
Inadequate oxygen • General circulatory deficiency Very small effect
transport to the tissues
• Localized circulatory deficiency (e.g. Coronary vessels) (In the form of dissolved oxygen)
by the blood
• Tissue edema
• Poisoning of cellular oxidation enzymes
• Diminished cellular metabolic capacity for using oxygen, No measurable benefit
Inadequate tissue
because of toxicity, vitamin deficiency, or other factors
capability of using oxygen
Cyanide poisoning, (cytochrome oxidase is completely blocked)
Beriberi (vitamin b deficiency) oxidative enzymes deficiencies
 CYANOSIS

Deoxygenated hemoglobin
(5gm/100 ml of blood)

Intense dark blue – purple color

Anemia
Polycythemia vera
Not enough hemoglobin
Excess of hemoglobin can
for
become deoxygenated
5gm/100 ml of blood
Cyanosis
Cannot be cyanosed
 HYPOXIA • Deficiency of oxygen in the atmosphere Hypercapnia
(Classification) No Hypercapnia
Inadequate oxygenation
extrinsic reasons • Hypoventilation (neuromuscular disorders) Hypercapnia

• Hypoventilation caused by increased airway resistance or decreased

Some Hypercapnia
pulmonary compliance
develops initially
Pulmonary disease • Abnormal alveolar ventilation-perfusion ratio but is resolved
(physiologic dead space or physiologic shunt) with
hyperventilation
• Diminished respiratory membrane diffusion

Venous-to-arterial shunts • Right-to-left” cardiac shunts Hypercapnia

• Anemia or abnormal hemoglobin No Hypercapnia

Inadequate oxygen transport • General circulatory deficiency Hypercapnia
to the tissues by the blood • Localized circulatory deficiency (e.g. Coronary vessels)
No Hypercapnia
• Tissue edema
• Poisoning of cellular oxidation enzymes
• Diminished cellular metabolic capacity for using oxygen, because of
Inadequate tissue capability
toxicity, vitamin deficiency, or other factors No Hypercapnia
of using oxygen
Cyanide poisoning, (cytochrome oxidase is completely blocked)
Beriberi (vitamin b deficiency) oxidative enzymes deficiencies
 Dyspnea

• Hypercapnia

• To a much less extent, hypoxia

• Increased work requirement ventilation

• State of mind
(neurogenic dyspnea or emotional dyspnea)
Carbon dioxide levels Symptoms

Dyspnea
60 to 75mm Hg
Breathing rapidly

The person becomes lethargic

80 to 100mm Hg and sometimes even semi-
comatose

120 to 150mm Hg Anesthesia and death

 resuscitator
Resuscitator
This apparatus forces air through the mask or
endotracheal tube into the lungs of the patient during
the positive-pressure cycle of the resuscitator and then
usually allows the air to flow passively out of the lungs
during the remainder of the cycle.

Tank Respirator
(the “Iron-Lung”)
Tank Respirator (the “Iron-Lung”)

the leather diaphragm moves inward, positive pressure

develops around the body and causes expiration

as the diaphragm moves outward, negative pressure causes

inspiration.