Intro to Lung function and Gaseous Exchange Flashcards
How Ventilation and Perfusion Are Achieved in Normal Lungs
Ventilation: Movement of air in and out of the lungs, driven by pressure changes during breathing.
Inspiration: Diaphragm contracts → thoracic volume increases → intrapulmonary pressure drops → air enters lungs.
Expiration: Diaphragm relaxes → thoracic volume decreases → air is pushed out.
Controlled by the respiratory centers in the medulla and pons.
Perfusion: Blood flow to the alveoli via the pulmonary capillaries.
The right ventricle pumps deoxygenated blood to the lungs via the pulmonary arteries.
Gas exchange occurs at the alveolar-capillary membrane.
Ventilation/Perfusion (V/Q) Matching:
Ideally, ventilation and perfusion are matched (V/Q ≈ 0.8).
Mismatch (e.g., pulmonary embolism or COPD) impairs gas exchange.
Describe the physiological basis of respiratory failure: type 1 and type 2
Respiratory failure: Inability of the lungs to maintain adequate oxygenation and/or remove carbon dioxide.
Type 1 (Hypoxemic) Respiratory Failure:
Low PaO₂ (< 8.0 kPa), normal or low PaCO₂.
Causes:
V/Q mismatch (e.g., pneumonia, pulmonary embolism)
Shunting (e.g., ARDS)
Diffusion defects (e.g., pulmonary fibrosis)
Type 2 (Hypercapnic) Respiratory Failure:
Low PaO₂ + high PaCO₂ (> 6.0 kPa).
Causes:
Alveolar hypoventilation (e.g., COPD, neuromuscular disease)
CNS depression (e.g., overdose)
Chest wall abnormalities
Describe the role of lung surfactants and pleural fluid in lung compliance
Lung Compliance: The ability of the lungs to expand (ΔV/ΔP).
Surfactant:
Secreted by Type II alveolar cells.
Reduces surface tension within alveoli, preventing collapse (atelectasis).
Increases lung compliance and reduces the work of breathing.
Deficiency (e.g., in preterm neonates) leads to neonatal respiratory distress syndrome.
Pleural Fluid:
Thin fluid in the pleural cavity between visceral and parietal pleura.
Lubricates and reduces friction during breathing.
Creates surface tension that keeps lungs adhered to chest wall, aiding expansion.
Describe the physiological mechanisms of coughing, mucous production and breathlessness
Coughing:
Protective reflex to clear irritants or secretions.
Triggered by stimulation of cough receptors (e.g., in trachea, bronchi).
Sequence: Deep inspiration → closure of glottis → contraction of expiratory muscles → sudden opening of glottis → forceful expulsion of air.
Mucous Production:
Produced by goblet cells and submucosal glands in airways.
Traps dust, microbes, and pollutants.
Cleared via mucociliary escalator (cilia push mucus up toward the throat).
Breathlessness (Dyspnea):
Sensation of difficulty breathing.
Can be due to:
Increased work of breathing (e.g., asthma, fibrosis)
Impaired gas exchange (e.g., pneumonia)
Abnormal neural perception (e.g., anxiety)
Describe lung function tests and their application in recognising obstructive and restrictive lung disease
Spirometry:
Measures volumes and flow rates of air.
Key values:
FVC (Forced Vital Capacity)
FEV1 (Forced Expiratory Volume in 1 sec)
FEV1/FVC ratio
Obstructive Lung Disease (e.g., asthma, COPD):
FEV1↓, FVC normal or ↓ slightly
FEV1/FVC ratio < 70%
Airflow limitation due to narrowed airways.
Restrictive Lung Disease (e.g., pulmonary fibrosis, scoliosis):
FVC↓, FEV1↓ proportionally
FEV1/FVC ratio normal or increased
Due to reduced lung expansion/compliance.
Other Tests:
Peak Expiratory Flow Rate (PEFR): Monitors asthma control.
Gas diffusion tests: Assess alveolar-capillary exchange (e.g., DLCO test).
Body plethysmography: Measures total lung volumes and resistance.
Define Asthma
Asthma is a chronic inflammatory disease of the airways characterized by:
Reversible airway obstruction
Bronchial hyperresponsiveness
Airway inflammation and mucus overproduction
Triggers:
Allergens, cold air, exercise, infections, pollutants.
Symptoms:
Wheezing, breathlessness, chest tightness, and coughing (often worse at night or early morning).
Pathophysiology:
Inflammation leads to narrowing of airways.
Smooth muscle contraction and mucosal edema worsen airflow limitation.
Airway remodeling may occur in chronic cases.
Treatment:
Bronchodilators (e.g., salbutamol)
Anti-inflammatory agents (e.g., inhaled corticosteroids)
