Acute respiratory failure - etiology, pathogenesis, compensatory mechanisms, and clinical manifestations.
Acute respiratory failure is a life-threatening condition in which the respiratory system fails to maintain adequate gas exchange, resulting in:
- PaO₂ < 60 mmHg (hypoxemia), and/or
- PaCO₂ > 50 mmHg (hypercapnia),
- with pH < 7.35 (if acute).
Classification
Etiology
Type I (hypoxemic) —impaired oxygenation
- ARDS (acute respiratory distress syndrome).
- Severe pneumonia.
- Pulmonary edema (cardiogenic or non-cardiogenic).
- Pulmonary embolism.
- Severe asthma or COPD exacerbation.
Type II (hypercapnic) —impaired ventilation
- COPD exacerbation (most common).
- Neuromuscular disorders (myasthenia gravis, Guillain-Barré).
- CNS depression (sedative overdose, brainstem injury).
- Chest wall disorders (severe kyphoscoliosis, obesity hypoventilation).
Pathogenesis
Type I (hypoxemic)
- Ventilation-perfusion (V/Q) mismatch (e.g., pneumonia, edema).
- Diffusion impairment (e.g., fibrosis, edema).
- Shunt (e.g., alveolar collapse in ARDS).
Type II (hypercapnic)
- Alveolar hypoventilation → reduced CO₂ elimination.
- Causes: decreased respiratory drive, neuromuscular weakness, increased airway resistance.
Compensatory mechanisms
- Increased respiratory rate and depth (hyperventilation in early stages).
- Activation of sympathetic nervous system → tachycardia, vasoconstriction → maintain oxygen delivery.
- In chronic CO₂ retention (COPD): renal compensation → increased bicarbonate reabsorption.
Clinical manifestations
General symptoms
- Dyspnea (most common).
- Use of accessory respiratory muscles.
- Cyanosis (especially in hypoxemic type).
- Tachypnea (early), bradypnea (late or CNS cause).
Neurological
- Restlessness, anxiety.
- Confusion, headache (due to hypercapnia).
- Somnolence → coma (severe hypercapnia).
Cardiovascular
- Tachycardia.
- Hypertension (early), hypotension (late, shock).
Summary table