Mnemonic

Pulmonary Embolism Physiology

A memory aid for the physiological consequences of pulmonary embolism.

Expansion

Increased dead space, hypoxaemia from mismatch, and right ventricular strain

Expansion

Respiratory effects

  • Alveolar dead space rises, since alveolar units are ventilated but not perfused
  • Hypoxaemia from redistribution of flow to other units, creating low V/Q areas; also from atelectasis (loss of surfactant in the affected zone) and, in severe cases, right to left shunting through a patent foramen ovale
  • Hyperventilation from J receptor and reflex stimulation, so carbon dioxide is typically low

Cardiovascular effects

  • Mechanical obstruction plus hypoxic and mediator-driven vasoconstriction raise pulmonary vascular resistance
  • Right ventricular strain and dilatation; the thin-walled right ventricle tolerates acute pressure loading poorly
  • Septal shift impairs left ventricular filling, so cardiac output falls and obstructive shock ensues

Pulmonary infarction occurs in only about 10 to 15 per cent, because the bronchial circulation maintains tissue viability; it is commoner with small peripheral emboli and with pre-existing cardiac or lung disease.