A condition in which the respiratory system fails to maintain adequate gas exchange, leading to hypoxaemia (low oxygen levels) and/or hypercapnia (high carbon dioxide levels).
What are the two main types of respiratory failure?
Type 1 (Hypoxaemic) Respiratory Failure: Low oxygen (PaO₂ < 8 kPa or 60 mmHg) with normal or low CO₂.
Type 2 (Hypercapnic) Respiratory Failure: High CO₂ (PaCO₂ > 6 kPa or 45 mmHg) with or withoutlow oxygen.
In conditions like pneumonia, pulmonary embolism, or COPD, ventilation and perfusion are imbalanced, leading to areas where oxygenation is impaired but blood flow continues, reducing overall oxygenation.
What conditions cause a right-to-left shunt and how does it contribute to hypoxaemia?
Right-to-left shunts occur when deoxygenated blood bypasses the lungs and mixes with oxygenated blood, leading to persistent hypoxaemia. Causes include:
Congenital heart defects (e.g., Tetralogy of Fallot, Eisenmenger syndrome).
Severe ARDS with collapsed alveoli.
Why does diffusion limitation lead to hypoxaemia?
In diseases like pulmonary fibrosis, thickened alveolar membranes slow oxygen diffusion into the blood, especially during exercise when oxygen demand is high.
What are the main causes of hypercapnia?
Alveolar Hypoventilation – Primary mechanism.
Increased Dead Space Ventilation – Leads to inefficient CO₂ clearance.
Respiratory Muscle Fatigue – Failure of muscles to maintain ventilation.
What conditions cause alveolar hypoventilation leading to hypercapnia?
Severe COPD (air trapping and muscle fatigue reduce ventilation).
How does increased dead space ventilation contribute to hypercapnia?
Conditions like severe COPD and pulmonary embolism cause areas of lung ventilation with poor perfusion, leading to inefficient CO₂ removal.
Why does respiratory muscle fatigue lead to hypercapnia?
In conditions like acute exacerbations of COPD or severe pneumonia, increased work of breathing over time weakens the muscles, reducing effective ventilation and causing CO₂ retention.
What are the clinical consequences of acute hypoxaemia?
Dyspnoea (shortness of breath)
Cyanosis (bluish skin, especially lips/fingertips)
Tachycardia (fast heart rate)
Confusion, agitation, or restlessness
Arrhythmias (irregular heartbeats)
Lactic acidosis (anaerobic metabolism due to oxygen deficiency)
Loss of consciousness, seizures, or coma in severe cases
What are the clinical consequences of chronic hypoxaemia?
Pulmonary hypertension (due to prolonged vasoconstriction of pulmonary arteries)
Right heart failure (cor pulmonale)
Polycythaemia (increased red blood cell production as compensation)
Chronic hypoxaemia stimulates the kidneys to release erythropoietin (EPO), which increases red blood cell production to enhance oxygen transport. This can lead to hyperviscosity of blood, increasing the risk of thrombosis.
What are the clinical consequences of acute hypercapnia?
What are the clinical consequences of chronic hypercapnia?
Morning headaches (CO₂ retention overnight)
Fatigue, sleepiness (CO₂ narcosis)
Tremors and muscle weakness
Desensitization of central CO₂ chemoreceptors (leading to reliance on hypoxic drive for breathing)
Worsening respiratory acidosis (pH disturbance affecting enzymes and organ function)
Why does chronic hypercapnia lead to a shift in respiratory drive?
Normally, ventilation is driven by CO₂ levels. In chronic hypercapnia (e.g., COPD), chemoreceptors become desensitised, and the body relies more on hypoxaemia to trigger breathing (hypoxic drive).
What are the life-threatening complications of combined hypoxaemia and hypercapnia?