Acute and Chronic Respiratory Failure Lecture

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MEDICAL UNIVERSITY - PLEVEN

FACULTY OF MEDICINE
DEPARTMENT OF PROPEDEUTICS OF INTERNAL DISEASES

MAIN SYMPTOMS AND SYNDROMS OF LUNG DISEASES.


ACUTE AND CHRONIC RESPIRATORY FAILURE

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Assoc. Prof. P. Glogovska, M.D. PhD
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•January 2020 Critical Reviews in Biotechnology 40(2):1-18
FUNCTIONAL ANATOMY AND PHYSIOLOGY

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http://www.nhlbi.nih.gov/health/health-topics/topics/hlw/system.html
FUNCTIONAL ANATOMY AND PHYSIOLOGY

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PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2021
The major bronchial divisions and the fissures, lobes and segments of the lungs.

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Davidson’s Principles and Practice
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Vascular anatomy of an acinus

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•IJC Heart & Vasculature 9(C)
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DOI:10.1016/j.ijcha.2015.08.002
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https://www.researchgate.net/publication/301845346_Breath_Activity_Detection_Algorithm
https://www.youtube.com/watch?v=9j6BpanhpKY
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https://doctorlib.info/physiology/physiology-2/47.html 15
https://courses.lumenlearning.com/boundless-biology/chapter/breathing/
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Types of Breathing

Types of breathing in humans include eupnea, hyperpnea, diaphragmatic, and


costal breathing; each requires slightly different processes.
Eupnea is normal quiet breathing that requires contraction of the diaphragm and
external intercostal muscles.
Diaphragmatic breathing requires contraction of the diaphragm and is also called
deep breathing.
Costal breathing requires contraction of the intercostal muscles and is also called
shallow breathing.

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https://onepointhealth.com.au/physiotherapy/the-what-why-how-of-diaphragm-breathing/
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Costal breathing is a breathing method
that uses movements of the ribs to drive
both the inhale and the exhale phases of
your breath.

The main muscles used during inhales


are the intercostals, but variations may
also involve the spinal erectors, the
levator costarum, and even the superior
serratus posterior

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The respiratory rate is measured by counting the
number of breaths for one minute through counting
how many times the chest rises.
Adults: 15–18 breaths per minute
Elderly ≥ 65 years old: 12–28 breaths per minute.
Elderly ≥ 80 years old: 10-30 breaths per minute.

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Impaired breathing – changes in

frequency
depth
rhythm and
ventilation per minute

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Abnormal Breathing Patterns
Quantative changes

Apnea
Absence of breathing. (Ap-knee-a)
Eupnea
Normal breathing (Eup-knee-a)
Orthopnea
Only able to breathe comfortable in upright position (such as sitting in chair),
unable to breath laying down, (Or-thop-knee-a)
Dyspnea
Subjective sensation related by patient as to breathing difficulty
Paroxysmal nocturnal dyspnea - attacks of severe shortness of breath that wakes a
person from sleep, such that they have to sit up to catch their breath - common in
patient's with congestive heart failure.
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Quantative changes
Hyperpnea: Increased depth of breathing (Hi-perp-knee-a)
Increased volume with or without and increased frequency (RR), normal
blood gases present.

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Quantative changes
Hyperventilation

Hyperventilation. Increased rate (A) or depth (B), or combination of both.


"Over" ventilation - ventilation in excess of the body's need for CO2 elimination.
Results in a decreased PaCO2, and a respiratory alkalosis.
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Quantative changes
Hypoventilation

Hypoventilation. Decreased rate (A) or depth


(B), or some combination of both.
"Under" ventilation - ventilation that is less
than needed for CO2 elimination, and
inadequate to maintain normal PaCO2. Results
in respiratory acidosis.
Can be a slow rate with normal tidal volumes such that the total minute
ventilation is inadequate.
Can be a normal rate but with such low tidal volumes that air exchange
is only in the dead space and not effective.

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Tachypnea
Increased frequency without blood gas abnormality

https://media.lanecc.edu/users/driscolln/RT127/Softchalk/regulation_of_Breathing/regulation_of_Breathing4.html
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Qualitative changes
Kussmaul's Respiration

Kussmaul's respiration.
Increased rate and depth
of breathing over a
prolonged period of time.
In response to metabolic
acidosis, the body's
attempt to blow off CO2 to
buffer a fixed acid such as
ketones. Ketoacidosis is
seen in diabetics.

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Qualitative changes
Cheyne-Stokes respirations
(CSR)

Gradual increase in volume and frequency,


followed by a gradual decrease in volume
and frequency, with apnea periods of 10 -
30 seconds between cycle. Described as a
crescendo - decrescendo pattern.
Characterized by cyclic waxing and waning
ventilation with apnea gradually giving
way to hyperpneic breathing.
Seen with low cardiac output states (CHF)
with compromised cerebral perfusion
Creates lag of CSF CO2 behind arterial
PaCO2 and results in characteristic cycle.
Delayed sensitivity to CO2 changes- during
apnea the CO2 increase above the
threshold for stimulus but the brain is slow
to respond, then it over shoots by
hyperventilating and the signal to reduce
ventilation is slow to be recognized. 29
Qualitative changes
Biot's respiration

Similar to CSR but VT is constant except during apneic periods. Short


episodes of rapid, deep inspirations followed by 10 - 30 second apneic
period. 30
Common symptoms

Dyspnea
Cyanosis
Cough
Expectoration
Hemoptysis
Chest pain

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Broncho pulmonary symptoms and syndromes

Dyspnea (noun)
1. difficult or laboured breathing.
Dyspnea is shortness of breath that is often described as a
feeling of being "hungry for air." Anyone can become dyspneic
with strenuous exercise, and it can also occur as a result of
medical problems like lung or heart disease, obesity, or
anxiety. Dyspnea is uncomfortable and it can even be painful.
Very strenuous exercise, extreme temperatures, obesity and
higher altitude all can cause shortness of breath in a healthy
person. Outside of these examples, shortness of breath is
likely a sign of a medical problem.

Shortness of breath — known medically as dyspnea — is often


described as an intense tightening in the chest, air hunger, 32
difficulty breathing, breathlessness or a feeling of suffocation.
Dyspnea
Causes
Anxiety disorders
Asthma
Pulmonary embolism
Broken ribs
Excess fluid around the heart
Choking
A collapsed lung
Heart attacks
Heart failure
Heart rhythm problems
Anemia
Pneumonia and other respiratory infections
Pregnancy
A severe allergic reaction, anaphylaxis
Sudden blood loss

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N Engl J Med 333:1547–1553, 1995,
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Neurophysiologic basis of dyspnea

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https://thoracickey.com/dyspnea/
Patients may use different terms to describe breathing
discomfort due to various causes. In some instances
these descriptors may be useful in establishing a
differential diagnosis and in assessing the response to
therapy.
Patients with asthma or myocardial ischemia often refer
to “chest tightness.”
Patients with pulmonary edema may suffer a sensation
of “air hunger” or “suffocation.”
Patients with COPD and hyperinflation of the chest
often note an inability to take a deep, satisfying breath.
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Dyspnea - mechanisms

1. Humoral – pCO2+ pO2, shift pH to acid side


2. Neurolegulatory includes impulsion from
chemoreceptors and baroreceptors
3. Central dysfunction of respiratory center or
cortex neurons.

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Dyspnea – clinical types

Respiratory dyspnea
Caused by respiratory diseases
Abnormal ventilation and gas exchange
Hypoxemia and hypercapnia

1.Inspiratory
2.Expiratory
3.Mixed 39
Dyspnea – clinical types

1. Inspiratory – large airway


Depression in suprasternal and supraclavicular fossa,
intercostal space
2. Expiratory small airway
Expiratory time – prolonged; ronchi
3. Mixed - increased RR, shallow breathing
4. Other types
Lung dyspnea
Cardiatic dyspnea
Hematic dyspnea

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Dyspnea – classification according pathogenesis

Cerebral –violation of
respiratory center
Lung – lung diseases
Cardiac dyspnea
Hematic dyspnea – anemra,
acidosis

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Psyhogenic dyspnea
hysteria, panic attacks
paper bag rebreathing

Exclude all other reasons before thinking


about this type of dyspnea!!!!!

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Key points in the assessment are:

Duration and onset of breathlessness. Patients


often underestimate the duration of
symptoms”inquiring about exercise tolerance over a
period of time is a useful way of assessing duration
and progression
Severity of breathlessness. Assess the level of
handicap and disability by asking about effects on
lifestyle, work, and daily activities

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Key points in the assessment
Exacerbating factors.
Ask about rest and exertion, nocturnal symptoms, and body
position.
The timing of nocturnal breathlessness may provide clues to the
likely cause: left ventricular failure causes breathlessness after a
few hours of sleep, and resolves after about 45 minutes;
asthma tends to occur later in the night; laryngeal inspiratory stridor
causes noisy breathlessness of very short duration (<1 min); and
Cheyne“Stokes apnoea result in breathlessness that is recurrent
and clears each time in less than 30 sec.
Orthopnoea is suggestive of left ventricular failure or diaphragm
paralysis, although it is also common in many chronic lung
diseases.
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Associated symptoms, such as cough, haemoptysis,
chest pain, wheeze, stridor, fever, loss of appetite and
weight, ankle swelling, and voice change. Wheeze may
occur with pulmonary oedema, pulmonary embolism,
bronchiolitis, and anaphylaxis, in addition to asthma
and COPD
Personal and family history of chest disease
Lifetime employment, hobbies, pets, travel, smoking,
illicit drug use, medications
Examination of the cardiovascular and respiratory
systems 46
Is the dyspnoea related only to exertion?
How far can the patient walk at a normal pace on
the level?
This may take some skill to elicit, as few people
note their symptoms in this form, but a brief
discussion about what they can do in their daily
lives usually gives a good estimate of their mobility.
Is there variability in the symptom?

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https://www.youtube.com/watch?v=O4lcEKBMTMg
Orthopnea

Orthopnea –
severe shortness of
breath
Orthopnea is the
symptom
of dyspnea
(shortness of
breath) that occurs
when a person is
lying flat 48
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Cyanosis

Cyanosis is characterized by bluish discoloration


of skin and mucous membranes.
Cyanosis is usually a sign of an underlying
condition rather than being a disease in itself.
The most common symptoms of the condition are
bluish discoloration of the lips, fingers, and toes.

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Central
Peripherial
Differential cyanosis

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http://www.medicinehack.com/
Symptoms of central cyanosis

This is manifested by bluish or purple discoloration of tongue


and lips and mucous membranes of the mouth.
It is seen in diseases of the heart or lungs and in abnormal
haemoglobin conditions like methemoglobin and
sulfhemoglobin etc. Here cyanosis is caused due to
desaturation of central arterial blood due to diseases of the
heart and lungs.
This deoxygenated venous blood instead of going to the lungs
for oxygenation moves to the general blood circulation of the
body leading to symptoms of cyanosis.
Usually central cyanosis is accompanied with features of
peripheral cyanosis.
There may be other features like breathlessness, shortness of
breath, bluish or purple discolouration of the oral mucous
membranes, rapid and shallow breathing etc.
The hands and feet are usually normal temperature or warm.
They may be cold if there is concomitant peripheral cyanosis. 53
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Symptoms of peripheral cyanosis

This is caused by decreased blood circulation in the


peripheral organs and limbs. This may occur due to
stasis or stagnation of blood and excessive
extraction of oxygen from the blood making it
deoxygenated and manifesting as cyanosis.
The affected areas turn bluish or purple and are
cold to touch. It is commonly seen in the nail beds.
The condition resolves with gentle warming. There
is no bluing of the mucous membrane of the mouth.
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Age and onset of cyanosis

Cyanosis that occurs due to a congential or birth defect of the


heart usually begins at birth or within the first few years of life.
In heart failure, lung embolism, pneumonia or acute severe attack
of asthma, the cyanosis may have a sudden or abrupt onset as the
patient “begins to turn blue” due to lack of oxygen.
On the other hand patients with chronic obstructive lung disease
or COPD often develop cyanosis gradually over many years.
Patients with a long history of COPD or asthma or other lung
diseases are prone to develop cyanosis

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https://www.slideshare.net/GirishJain10/cyanosis-ppt-by-dr-girish-jain-63579536
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https://www.quora.com/What-are-the-types-of-cyanosis 59
COUGH

Cough is the most frequent symptom of respiratory disease. It is


caused by stimulation of sensory nerves in the mucosa of the
pharynx, larynx, trachea and bronchi.
Acute sensitisation of the normal cough reflex occurs in a number of
conditions.
It is typically induced by changes in air temperature or exposure to
irritants such as cigarette smoke or perfumes.
Coughing is an important defensive reflex that enhances clearance
of secretions and particulates from the airways and protects from
aspiration of foreign materials occurring as a consequence of
aspiration or inhalation of particulate matter, pathogens,
accumulated secretions, postnasal drip, inflammation, and mediators
associated with inflammation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415124/
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The explosive quality of a normal cough is lost in patients with
respiratory muscle paralysis or vocal cord palsy. Paralysis of a
single vocal cord gives rise to a prolonged, low-pitched,
inefficient ‘bovine’ cough accompanied by hoarseness.
Coexistence of an inspiratory noise (stridor) indicates partial
obstruction of a major airway (e.g. laryngeal oedema, tracheal
tumour, scarring, compression or inhaled foreign body) and
requires urgent investigation and treatment.
Types of cough
Productive – cough with phlegm
Non productive – dry, does not contain phlegm
Sputum production is common in patients with acute or
chronic cough, and its nature and appearance can provide
clues to the aetiology

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Cough reflex is constituted by:
1. Rapidly Adapting Receptors (RAR)
2. Slowly Adapting Stretch Receptors (SARs)
3. C-Fibers

Impulses from stimulated cough


receptors traverse an afferent pathway
via the vagus nerve to a ‘cough
center’ in the medulla, which itself
may be under some control by higher
cortical centers. The cough center
generates an efferent signal that
travels down the vagus, phrenic, and
spinal motor nerves to expiratory
musculature to produce the cough.

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https://pharmaceutical-journal.com/article/ld/case-based-learning-cough

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Cough - causes

Viral infection
Bronchitis, pneumonia,
tbc
Colds
Smoking
Allergies
GERD
Postnasal drip
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Cough - causes

Acute sinusitis (nasal and sinus infection)


Bronchiectasis (a chronic lung condition in which abnormal
widening of bronchial tubes inhibits mucus clearing)
Bronchiolitis(especially in young children)
Chronic sinusitis
COPD
Coronavirus disease 2019 (COVID-19)
Croup (especially in young children)
Cystic fibrosis
Emphysema
Heart failure
Laryngitis
Lung cancer
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Cough - causes

Medications called angiotensin-converting enzyme (ACE) inhibitors


Neuromuscular diseases that weaken the coordination of upper
airway and swallowing muscles
Pulmonary embolism (blood clot in an artery in the lung)
Respiratory syncytial virus (RSV) — especially in young children
Sarcoidosis (collections of inflammatory cells in the body)

https://www.mayoclinic.org/symptoms/cough/basics/causes/sym-20050846
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Haemoptysis
Haemoptysis means the coughing of blood in the sputum.
It should never be dismissed without very careful evaluation of the
patient. The potentially serious significance of blood in the sputum is well
known, and fear often leads patients not to mention it: a specific question
is always necessary.
Is there any blood in the sputum?
Is it fresh or altered?
How often has it been seen, and for how long?
Blood may be coughed up alone, or sputum may be bloodstained.
It is sometimes difficult for the patient to describe whether or not the blood
has o
riginated from the chest or whether it comes from the gums or nose, or
even from the stomach. They should always be asked about associated
conditions such as epistaxis (nosebleeds), or the subsequent
development of melaena (altered blood in the stool), which occurs in the
case of upper gastrointestinal bleeding. Usually, however, it is clear that
the blood originates from the chest, and this is an indication for further
investigation. https://aspergillosis.org/haemoptysis/ 69
COUGH - Clinical assessment

How long has the cough been present? A cough lasting a few
days following a cold has less significance than one lasting
several weeks in a middle-aged smoker, which may be the first
sign of a malignancy.
Is the cough worse at any time of day or night?
A dry cough at night may be an early symptom of asthma, as
may cough that comes in spasms lasting several minutes.
Is the cough aggravated by anything, for example dust, pollen
or cold air? The increased reactivity of the airways seen in
asthma, and in some normal people for several weeks after
viral respiratory infections, may present in this way. Severe
coughing, whatever its cause, may be followed by vomiting.

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CHEST PAIN
Many lung disorders can cause chest pain

Pulmonary embolism. This occurs when a blood clot becomes


lodged in a lung (pulmonary) artery, blocking blood flow to lung
tissue.
Pleurisy. If the membrane that covers your lungs becomes inflamed,
it can cause chest pain that worsens when you inhale or cough.
Collapsed lung. The chest pain associated with a collapsed lung
typically begins suddenly and can last for hours, and is generally
associated with shortness of breath. A collapsed lung occurs when air
leaks into the space between the lung and the ribs.
Pulmonary hypertension. This condition occurs when you have high
blood pressure in the arteries carrying blood to the lungs, which can
produce chest pain.
Trauma, fractures of the ribs https://www.mayoclinic.org/diseases-conditions/chest-pain/symptoms-causes/syc-20370838

Tumours 71
Parietal – chest wall, pleura

Etiology - trauma, fractures of the ribs, pleurisy,


pneumothorax PTE
Pleuritic chest pain is characterized by sudden and
intense sharp, stabbing, or burning pain in the chest
when inhaling and exhaling. It is exacerbated by deep
breathing, coughing, sneezing, or laughing. When
pleuritic inflammation occurs near the diaphragm, pain
can be referred to the neck or shoulder

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Visceral pain

Heart, pericardium, main vessles


Pain arising from the heart may present as either ‘‘typical
cardiac pain’’ or ‘‘atypical chest pain’’. The former is described
as a central heavy or crushing pain that may radiate to the jaw,
neck, shoulder, or arm
Pericarditis commonly presents as chest pain described as
midline and sharp. The pain is made worse by movement and
breathing whereas sitting up and leaning forward may relieve it.
The pain my radiate to the back, neck, or left shoulder and is
associated with dyspnoea, tiredness, and fever.
Eoesophagus and mediastinum organs Esophageal spasms
are painful contractions within the muscular tube connecting
your mouth and stomach (esophagus). Esophageal spasms
can feel like sudden, severe chest pain that lasts from a few
minutes to hours. Some people may mistake it for heart pain 73
Chest pain - central

Angina pectoris
Myocardial infarction
Pericarditis
Myocarditis
Mitral valve prolaps

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Chest pain - central
Aorta
Aneurism
Dissecting aortic aneurysm
Esophagus
Esophagitis
Esophageal spasm
Mallory-Weiss syndrome
PTE
Mediastinum
Tracheitis
Tumor
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Chest pain - peripheral

Lung, pleura
Pulmonary infarction
pneumonia
pneumothorax
malignancy
tuberculosis
Connective tissue diseases

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Chest pain - peripheral

Sceletal, muscular

osteoarthritis
Costochondral (Tietze's syndrome)
Contusion/fracture of ribs
Trauma/ disease of the intercostal muscles
Epidemic myalgia (Bornholm disease)

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Chest pain - peripheral

Neural

discopathy
Herpes zoster

Psycho emotional, anxiety


Extrathoracic
Cervicoarthritis, / discopathy
Cholecystitis
Gastritis/Ulcer disease
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Emergency Medicine Journal (EMJ) - An acute care journal by BMJ
Respiratory physiology

The act of respiration engages the following


three processes:
Transfer of oxygen across the alveolus
Transport of oxygen to the tissues
Removal of carbon dioxide from blood into the
alveolus and then into the environment

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https://www.adamondemand.com/AODHome/AODProductDetails/UnderstandingthePhysiologyoftheRespiratorySystem

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Definition
Respiratory failure is a syndrome in which the
respiratory system fails in one or both of its gas
exchange functions: oxygenation and carbon dioxide
elimination.
Lungs are unable to provide
An abequate supply of O2
And/or remove CO2 efficiency

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Classification

Acute – minutes to hours ( asthma attack,


pneumonia)
Subacute – days to weeks (pneumonia, chronic
bronchitis)
Chronic – months to years

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Pathophysiology

Respiratory failure can arise from an abnormality in any of the


components of the respiratory system, including
the airways,
alveoli,
central nervous system (CNS),
peripheral nervous system, respiratory muscles,
and chest wall.
Patients who have hypoperfusion secondary to cardiogenic,
hypovolemic, or septic shock often present with respiratory
failure.
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Classification

Type 1 hypoxia without hypercapnia Respiratory Failure


PaO2 < 60 mmHg
Low oxygen in the air and/or
PaCO2 > 50 mmHg
Ventilation/perfusion mismatch (in otherwise healthy
individuals breathing
Pneumonia, lung edema room air)

Type 2 hypoxia with hypercapnia


Reduced breathing effort
Increased resistance to breathing
Increased area of the lung that is not
available to gas exchange

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Respiratory failure etiology

Disturbances of lung function


Ventilation
Perfusion
V/P
Diffusion – alveolar capillary membrane

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Respiratory failure etiology
Extra lung disturbances

Nervous regulations – brain


stroke, trauma, tumour, drugs)
Respiratory muscles –
myasthenia poliomyelitis
Chest respiratory movements
fractures, chest wall
Blood circulation – cardiac failure,
anemia
https://www.nhlbi.nih.gov/health-topics/respiratory-failure
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https://www.mdnxs.com/topics-2/pulmonary-and-critical-care/respiratory-failure/
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Hypoxemia – clinical manifestations

Hypotonoa
Pulmonary hypertension
Polycytemia
Tachicardia
Impairment of consiousness
From confusion to coma

https://www.medindia.net/patientinfo/hypoxemia.htm 90
RF – clinical manifestations of II type hypoxemia with hypercapnia

Changes of consciousness – sopor, coma,


confusion, excitement
CO2 – warm periphery, amplified pulsations,
flapping tremor
Bronchial obstruction – wheezws, prolonged
expiration, puffy lips
Co pulmonale – peripherial oedema, JVP,
hepatomegaly, ascites. 91
RF
Respitatory system - clinical manifestations

Cyanosis, dyspnea, hypoxemia, hypercapnia


Increased pressure in pulmonary artery
KVS
Increased blood pressure, tachicardia, pulmonary
hypertension
Collapse, periphery vasodilatation

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RF clinical manifestations

Central nervous system


Hypercapnia – headache, inversion of sleep, cerebral
oedema, myotonic twitching, coma.
Euphoria, disorientation, visual disturbances.

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RF clinical manifestations

Gastrointestinal system Ulcer – stomach and


duodenum, bleeding, sweats, sialorrhea, CL
Kidneys - retension of water , HCO3
Erythropoesis – Er, Hb

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Bibliography
Hutchinson's Clinical Methods. 22nd edition. By Michael Swash and
Michael Glynn. Saunders Ltd, 2007
Duale Reihe Anamnese und Klinische Untersuchung. Middeke M,
Füeßl HS. Thieme, 2010
Bates Guide to Physical Examination and History Taking. 10th
edition. Lippincott Williams & Wilkins, 2008
Google images
Davidson's Principles and Practice of Medicine 21st Ed
Encyclopedia Britannica

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