Clinical Physiology of Respiration

Dr. M Qathar RF T
 Contents

Function of the respiratory system

Embryology
Anatomic concepts
Physiologic concepts
Pathology
Clinical : symptoms
physical signs
disease patterns
 Functions of the lung

Respiration: ventilation and gas exchange: O2, CO2, pH,

warming and humidifying
Non-respiratory functions:
synthesis, activation and inactivation of vasoactive
substances, hormones, neuropeptides, eicosanoids,
lipoprotein complexes.
Hemostatic functions (thromboplastin, heparin)
Lung defense: complement activation, leucocyte
recruitment, cytokines and growth factors
Speech, vomiting, defecation, childbirth
 What does the respiratory system consist of?
 Embryology
Embryology : lung development starts from the gut
24 days after conception; diaphragm forms in
cervical region at 3-4 weeks and moves
progressively downwards carrying the phrenic
nerves with; lung lobes are identifiable at 12 weeks;
bronchial tree is completed at 16 weeks and alveoli
and capillaries appear at 24 28 weeks; surfactant
appears at 35 weeks.
Postnatal Alveolarization: intense first 8-10 y
(alveolar buds hyperplastic growth) and
enlargement of all structures throughout
adolescence and early adulthood ( hypertrophic
growth)
 Embryology and disease
Developmental abnormalities: tracheo-
oesophageal fistula, cleft palate, cysts, agenesis,
sequestration, cilia dysfunction and abnormal
structure, diaphragmatic hernias.
Shared nerve supply (Vagus) between respiratory
tract and GI tract Gastro-oesophageal reflux can
increase bronchial secretions (reflexively) and
cause bronchial constriction ( together with
oesophageal spasm).
Diaphragmatic irritation is often experienced as
pain in the cervical region (referred pain) from
where it evolved.
 Anatomy

Surface Anatomy: borders of the pleura

borders of the lung
fissures
lung lobes
Bronchial tree, vascular and nerve supply, lymphatics.
Angle of Louis
Histology, cilia, secretory and immunologic cells.
Thoracic cage
Diaphragm and accessory muscles of breathing
 How is the respiratory system controlled/regulated?
 Physiology

Lung mechanics and Lung functions

Airway resistance
Diffusion :Gas laws ( Graham, alveoalar gas
equation, Charles, Boyle, Dalton, Henry)
Blood gases: PaO2, PaCO2, pH, HCO3, O2 sat
Hemoglobin, dissociation curve, 2,3DPG
Surfactant
Control of Breathing
 Surfactant

Reduces surface tension and therefore elastic recoil,

making breathing easier
Reduces the tendency to pulmonary oedema
Equalises pressure in large and small alveoli
Oxyhemoglobin dissociation curve

Left shift increased HB Right shiftdecreased

affinty for O2 ( release of HB affinity for O2 (
O2 to tissues) release of O2 to tissues)
Alkalosis Acidosis
Hypothermia
Hyperthermia
2,3 DPG
2,3 DPG
COHB
MetHB
 Hypoxia

Anemic hypoxia- HB
CO intoxication- HB availabilty, shifts O2 HB
dissociation curve to the left
Respiratory hypoxia-next slide
R to L extrapulmonary shunting- ASD,VSD,PDA
Circulatory hypoxiacardiac failure, shock-
Ischemic hypoxia- arterial obstruction
Increased O2 requirements- fever, exercise,
thyrotoxicosis
Improper O2 utilization- cyanide, diptheria toxin
 Blood gases: PO2 and PCO2

Hypoxemia Hypercarbia
Hypoventilation Hypoventilation
Diffusion Ventilation / perfusion
Ventilation / perfusion inequality
inequality
AV Shunt
High altitude
 How is the respiratory system affected by disease?
 Pathology

Airway diseases: COPD, asthma, bronchiectasis,

cystic fibrosis, obstructive sleep apnoea
Parenchymal disease: pneumonia, ARDS,
Interstitial lung disease, pneumoconiosis
Pleural disease: pleural effusion, empyema.
Vascular disease: thrombo-embolism, primary
pulmonar hypertension
Neoplastic disease: Bronchus Ca, mesothelioma,
adenoma, carsinoid
 Airway diseases

Causes: atopy, cigarette smoking, infection,

abnormal lung defense
Effect: obstruction to airflow
Mechanism: bronchospasm, inflammation, airway
remodelling, destruction, collapsing airways
Consequences: air flow ( FEV1, PEF); work of
breathing resp muscle fatigue respiratory
failure; PaO2, PaCO2 PHT cor pulmonale
 Parenchymal disease

consolidation - infection - typical/atypical

Oedema - cardiac vs non-cardiac (ARDS)
interstitial lung disease - idiopathic fibrosis,
sarcoidosis, hypersensitivity pneumonitis,
pneumoconiosis
Vascular secondary/primary PHT, cor pulmonale,
pulmonary thrombo-embolism (unexplained
dyspnea); Virchow triade: stasis, coagulability,
blood vessel abnormality, varicose veins,
endothelial dysfunction DVT risk
 Pleural disease

Pleural effusion: alb, LDH, pleural/serum,

cholesterol, glucose, ADA, pH.
exudate: infection, inflammation, neoplastic,
blood ( permeability)
transudate: hypoproteinemia (renal, liver -
oncotic pressure), systemic venous hypertension
( hydrostatic pressure - Heart failure)
Empyema
Chylothorax, pseudo-chylothorax
 Neoplastic disease

Bronchus Ca: squamous, small cell ca, adeno ca, large

cell ca, broncho-alveolar ca
Mesothelioma
Metastatic ca
Rare tumours: lymphoma, malt-lymphoma
Benign tumours
Control and Mechanism of breathing

Alveolar hypoventilation
Sleep-related: central and obstructive sleep apnoea,
Ondines curse
Neuro-muscular diseases: polio, Guillain-Barre
syndrome, myasthenia gravis, resp muscle fatigue,
polimyositis
Chest wall: kyphoscoliosis, rib fractures with flail
chest
Complications of Lung disease

Cor pulmonale
Respiratory failure: ventilatory failure vs oxygenation
failure hypercapnia, acidosis and hypoxaemia
Endstage lung disease
Pneumothorax
 How is disease of the respiratory system recognized?
 Clinical Manifestations

Dyspnea, PND, orthopnea, trepopnea, platypnea

and orthodeoxia.
Cough: productive vs non-productive, volume,
character, blood, post-nasal discharge
Chest pain: ischaemic, pleuritic, chest wall, GE
reflux, tearing of tissue
Constitutional: fever, night sweats, weight loss
RHF: swelling, pain R hypochondrium, abdominal
distention, palpitations
 Dyspnea cont.
Due to:
Airway obstruction
Greater force needed to provide adequate
ventilation
Wheezing sound due to air being forced
through airways narrowed due to constriction
or fluid accumulation
Decreased compliance of lung tissue

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 Signs of dyspnea:

Flaring nostrils
Use of accessory muscles in breathing
Retraction (pulling back) of intercostal spaces

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 Cough

Attempt to clear the lower respiratory passages by

abrupt and forceful expulsion of air
Most common when fluid accumulates in lower
airways

52
 Cough may result from:

Inflammation of lung tissue

Increased secretion in response to mucosal irritation
Inhalation of irritants
Intrinsic source of mucosal disruption such as tumor invasion
of bronchial wall
Excessive blood hydrostatic pressure in pulmonary
capillaries
Pulmonary edema excess fluid passes into airways

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 When cough can raise fluid into pharynx, the cough is
described as a productive cough, and the fluid is sputum.
Production of bloody sputum is called hemoptysis
Usually involves only a small amount of blood
loss
Not threatening, but can indicate a serious
pulmonary disease
Tuberculosis, lung abscess, cancer, pulmonary
infarction.
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 If sputum is purulent, and infection of lung or airway is
indicated.
Cough that does not produce sputum is called a dry,
nonproductive or hacking cough.
Acute cough is one that resolves in 2-3 weeks from onset of
illness or treatment of underlying condition.
Us. caused by URT infections, allergic rhinitis, acute bronchitis,
pneumonia, congestive heart failure, pulmonary embolus, or
aspiration.

55
 A chronic cough is one that persists for more than 3 weeks.
In nonsmokers, almost always due to postnasal drainage
syndrome, asthma, or gastroesophageal reflux disease
In smokers, chronic bronchitis is the most common cause,
although lung cancer should be considered.

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 Cyanosis

When blood contains a large amount of unoxygenated

hemoglobin, it has a dark red-blue color which gives skin a
characteristic bluish appearance.
Most cases arise as a result of peripheral vasoconstriction result is
reduced blood flow, which allows hemoglobin to give up more of
its oxygen to tissues- peripheral cyanosis.
Best seen in nail beds
Due to cold environment, anxiety, etc.

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 Central cyanosis can be due to :
Abnormalities of the respiratory membrane
Mismatch between air flow and blood flow
Expressed as a ratio of change in ventilation (V) to perfusion
(Q) : V/Q ratio
Pulmonary thromboembolus - reduced blood
flow
Airway obstruction reduced ventilation
In persons with dark skin can be seen in
the whites of the eyes and mucous
membranes.
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 Lack of cyanosis does not mean oxygenation is normal!!
In adults not evident until severe hypoxemia is present
Clinically observable when reduced hemoglobin levels reach 5
g/ dl.
Severe anemia and carbon monoxide poisoning give
inadequate oxygenation of tissues without cyanosis
Individuals with polycythemia may have cyanosis when
oxygenation is adequate.

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 Pain

Originates in pleurae, airways or chest wall

Inflammation of the parietal pleura causes sharp or stabbing
pain when pleura stretches during inspiration
Usually localized to an area of the chest wall, where a pleural
friction rub can be heard
Laughing or coughing makes pain worse
Common with pulmonary infarction due to embolism

60
 Inflammation of trachea or bronchi produce a central chest
pain that is pronounced after coughing
Must be differentiated from cardiac pain
High blood pressure in the pulmonary circulation can cause
pain during exercise that often mistaken for cardiac pain
(angina pectoris)

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 Hemoptysis

Upper airway: nasopharyngeal, GIT

Tracheobronchial: neoplasm, bronchitis,
bronchiectasis, trauma, foreign body
Parenchyma: pneumonia, lung abscess, TB,
mycetoma, SLE, Wegeners, Goodpasture, lung
contusion
Primary vascular disease: AV malformations,
pulmonary embolism, pulmonary venous pressure
Others: Systemic coagulopathy, anticoagulants,
pulmonary endometriosis
 Massive hemoptysis

100 250 ml blood per day

Causes: most frequently PTB and bronchiectasis
Rx: maintain oxygenation and prevent blood
spilling into unaffected regions, avoid
asphyxiation
Suppress cough
Invasive management: double lumen
endotracheal tube or balloon catheter to seal off
site of bleeding, mechanical ventilation, laser
phototherapy, embolotherapy, resection
 Respiratory system

signs of respiratory distress,

hyperinflation,
consolidation,
pleural effusion,
pneumothorax,
sup vena cava obstruction
 Physical signs
General: Cyanosis, anaemia, jaundice, oedema,
lymphadenopathy, clubbing
Respiratory examination:
1. Observation
2. Palpation
3. Percussion
4. Auscultation
 Clubbing
The selective bulbous enlargement of the end of a digit
(finger or toe).
Usually painless
Commonly associated with diseases that cause decreased
oxygenation
Lung cancer
Cystic fibrosis
Lung abscess
Congenital heart disease

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 Auscultation

Intensity of breath sounds: N, or absent

Character of breath sounds: N or bronchial breathing/
amphoric breathing
Intensity of vocal sounds: (one-one, 99)N,
(bronchophony) or or nasal ( aegophony)
Whispering pectoriloquy ( 66)
Adventitious sounds: ronchi, creps, rubs, clicks.
 APPLICATION OF ADVENTITIOUS LUNG SOUNDS
Lung sounds Possible mechanism Characteristics Causes
Wheezes Rapid airflow through obstructed High-pitched; most Asthma, congestive heart
airways caused by often occur during failure, bronchitis
bronchospasm, mucosal edema exhalation

Stridor Rapid airflow through obstructed High-pitched; often Croup, epiglottitis,

airway caused by inflammation occurs during postextubation
inhalation

Crackles
Insp & exp Excess airway secretions moving Coarse and often clear Bronchitis, respiratory
with airflow with cough infections

Early insp Sudden opening of proximal Scanty, transmitted to Bronchitis, emphysema,

bronchi mouth; not affected by asthma
cough

Late insp Sudden opening of peripheral Diffuse, fine; occur Atelectasis, pneumonia,
airways initially in dependent pulmonary edema,
regions fibrosis
Abnormality Initial Inspection Palpitation Percussion Ausculation Possible
impression causes
Acute airways Appears acutely Use of Reduced Increased Expiratory Asthma,
obstruction ill accessory expansion resonance wheezing bronchitis
muscles
Chronic airways Appears Increased Reduced Increased Diffuse reduction Chronic
obstruction chronically ill antero-posterior expansion resonance in breath sounds; bronchitis,
diameter, use of early inspiratory emphysema
accessory crackles
muscles

Consolidation May appear Inspiratory lag Increased Dull note Bronchial breath Pneumonia,
acutely ill fremitus sounds; crackles tumor

Pneumothorax May appear Unilateral Decreased Increased Absent breath Rib fracture, open
acutely ill expansion fremitus resonance sounds wound
Pleural effusion May appear Unilateral Absent fremitus Dull note Absent breath Congestive heart
acutely ill expansion sounds failure

Local bronchial Appears acutely Unilateral Absent fremitus Dull note Absent breath Mucous plug
obstruction ill expansion sounds

Diffuse intersitial Often normal Rapid shallow Often normal; Slight decrease in Late inspiratory Chronic exposure
fibrosis breathing increased resonance crackles to inorganic dust
fremitus

Acute upper Appears acutely Laboured Often normal Often normal Inspiratory or Epiglottitis,
airway ill breathing expiratory stridor croup, foreign
obstruction or both body aspiration
 Diagnostic procedures

XRC, CT scan, MRI scan

Lung functions
Blood
Blood gases
Sputum, cilia function
Bronchoscopy, biopsy
Nuclear medicine
 How can disease of the respiratory system be treated
or prevented?
 Treatment/prevention

Patient education
Immunization
Medication: antibiotics, bronchodilators, anti-
inflammatory drugs,diuretics, anti-coagulants
Ventolators
Physiotherapy
Surgery
Why do you have to know all this?

Because so that you can one day say:

Trust me, I am your doctor!