PULMONARY EMBOLISM
Pulmonary embolism (PE) occurs when a thrombus—most commonly originating in the deep veins of the lower limbs—travels to and lodges within the pulmonary arterial circulation. This sudden obstruction disrupts pulmonary blood flow, impairs gas exchange and increases strain on the right side of the heart.
Pulmonary embolism exists on a spectrum ranging from small, clinically silent emboli to massive embolism causing cardiovascular collapse and sudden death. The pathophysiology of PE is unique in that symptoms arise not only from impaired oxygenation but also from acute haemodynamic compromise, particularly of the right ventricle.
What You Need to Know
Pulmonary embolism occurs when thrombotic material, most commonly originating from the deep veins of the lower limbs, lodges within the pulmonary arterial circulation. The immediate physiological consequence is disruption of normal ventilation–perfusion matching. Alveoli distal to the embolus continue to receive air but are no longer perfused with blood, creating areas of dead space ventilation. Although ventilation may appear adequate, oxygen transfer into the bloodstream is inefficient, leading to hypoxaemia that is often disproportionate to clinical findings on lung examination.
Several interrelated pathophysiological processes explain the acute presentation of pulmonary embolism:
Ventilation–perfusion mismatch, where ventilated alveoli are not perfused, reducing effective gas exchange
Sudden increase in pulmonary vascular resistance, caused by mechanical obstruction and reflex vasoconstriction
Acute strain on the right ventricle, which is poorly adapted to abrupt rises in afterload
The increase in pulmonary vascular resistance has profound cardiovascular consequences. The right ventricle is designed to pump blood into a low-pressure, highly compliant pulmonary circulation. When resistance rises suddenly, as in pulmonary embolism, the ventricle may be unable to generate sufficient pressure to maintain forward flow. Acute right ventricular dilation can occur, impairing contractility and reducing right-sided output. As pulmonary blood flow falls, left ventricular preload decreases, leading to a drop in cardiac output and systemic hypotension.
The severity of haemodynamic compromise depends on the size and location of the embolus, the presence of pre-existing cardiopulmonary disease, and the patient’s ability to compensate. Small emboli may primarily cause hypoxaemia and pleuritic symptoms, while large or multiple emboli can precipitate acute right heart failure, shock, and sudden collapse. This combination of respiratory and circulatory dysfunction explains why pulmonary embolism can range from mild and insidious to rapidly life-threatening.
Beyond the Basics
Formation and Embolisation of Thrombi
Most pulmonary emboli originate from thrombi that form in the deep veins of the lower limbs or pelvis. Thrombus formation is promoted by the interaction of venous stasis, endothelial injury, and a hypercoagulable state, a combination often referred to as Virchow’s triad. Reduced blood flow during prolonged immobility, direct vessel injury from surgery or trauma, and systemic conditions that increase clotting tendency such as malignancy, pregnancy, or inherited coagulation disorders all increase the likelihood of venous thrombosis.
Once a thrombus detaches, it is carried through the venous circulation to the right side of the heart and then ejected into the pulmonary arterial system. The physiological impact depends on both the size of the embolus and its location. Small emboli lodged in distal branches may cause limited haemodynamic disturbance, while large emboli or multiple emboli obstructing central pulmonary arteries can abruptly compromise pulmonary blood flow and cardiovascular stability.
Ventilation–Perfusion Mismatch and Hypoxaemia
Obstruction of pulmonary blood flow creates a characteristic ventilation–perfusion mismatch. Alveoli distal to the embolus remain ventilated but are no longer perfused, meaning air reaches regions of lung that cannot participate in gas exchange. This dead space ventilation increases the proportion of wasted breaths and reduces overall oxygen transfer into the bloodstream.
Compensatory mechanisms can worsen this mismatch. Blood is redirected toward non-obstructed regions of lung, but reflex vasoconstriction in response to local hypoxia and inflammatory mediators alters normal flow patterns. Carbon dioxide diffuses more readily than oxygen and may initially remain normal or even fall because patients hyperventilate in response to hypoxaemia and anxiety. Oxygenation, however, is more severely affected, explaining why hypoxaemia can be marked even when chest imaging appears relatively unremarkable.
Right Ventricular Strain and Haemodynamic Instability
Pulmonary embolism produces a sudden rise in pulmonary vascular resistance due to both mechanical obstruction and vasoconstriction of the remaining pulmonary vasculature. The right ventricle, which is adapted to pump against a low-resistance system, is poorly equipped to respond to abrupt increases in afterload. Acute dilation occurs as the ventricle struggles to eject blood, stretching myocardial fibres beyond their optimal length and reducing contractile efficiency.
As right ventricular output falls, less blood reaches the left side of the heart. Reduced pulmonary venous return lowers left ventricular preload, leading to a fall in cardiac output and systemic blood pressure. In severe embolism, this cascade results in hypotension and shock. Right ventricular ischaemia may also develop because elevated intraventricular pressure reduces coronary perfusion, further impairing contractility and accelerating haemodynamic collapse.
Pulmonary Infarction and Inflammatory Response
In some cases, embolic obstruction leads to pulmonary infarction, particularly when bronchial arterial supply is insufficient to compensate for the loss of pulmonary arterial flow. Infarcted lung tissue becomes inflamed and may bleed into surrounding airspaces, producing pleuritic chest pain and haemoptysis. This pain is typically sharp and worsens with inspiration because the parietal pleura becomes involved.
Beyond local tissue injury, pulmonary embolism triggers a systemic inflammatory response. Release of inflammatory mediators promotes bronchoconstriction and increases alveolar–capillary permeability. These changes narrow airways and allow fluid to leak into alveolar spaces, further impairing ventilation and diffusion of oxygen across the alveolar–capillary membrane.
Gas Exchange and Acid–Base Disturbances
Early in pulmonary embolism, patients often hyperventilate due to hypoxaemia, pain, and sympathetic activation. This leads to excessive elimination of carbon dioxide and development of respiratory alkalosis. Arterial carbon dioxide levels may be low despite significant respiratory distress.
As disease severity increases or haemodynamic compromise develops, compensatory mechanisms may fail. Reduced cardiac output leads to inadequate tissue perfusion, forcing cells to rely on anaerobic metabolism and generating lactic acid. Metabolic acidosis may then emerge, signalling systemic hypoperfusion and a more severe physiological disturbance. The evolution from respiratory alkalosis to mixed or metabolic acidosis reflects progression from primarily respiratory impairment to combined respiratory and circulatory failure.
Clinical Connections
Pulmonary embolism often presents abruptly, reflecting the sudden disruption of pulmonary perfusion and right ventricular loading conditions. Common features include acute onset dyspnoea, pleuritic chest pain from pleural irritation, tachypnoea, tachycardia, and hypoxaemia that appears disproportionate to chest examination findings. Larger emboli may produce syncope, hypotension, or collapse as right ventricular output falls and left ventricular preload drops. The clinical picture can vary widely, which is why unexplained respiratory or haemodynamic deterioration should always prompt consideration of PE.
Certain findings increase concern for haemodynamic significance and impending right ventricular failure:
Sudden hypoxaemia with clear lung fields, suggesting ventilation–perfusion mismatch rather than alveolar disease
Persistent tachycardia or hypotension, indicating reduced cardiac output
Syncope or near-syncope, reflecting abrupt limitation of cerebral perfusion
Diagnosis is guided by clinical probability and confirmed with imaging, most commonly CT pulmonary angiography, which directly visualises intravascular thrombus and assesses clot burden. Ancillary findings such as right ventricular dilation on imaging or echocardiography support risk stratification. Management centres on prompt anticoagulation to prevent further thrombus propagation and allow endogenous fibrinolysis. In high-risk presentations with shock or sustained hypotension, thrombolysis or surgical or catheter-directed intervention may be required to rapidly reduce pulmonary vascular obstruction. Continuous reassessment of oxygenation, haemodynamics, and signs of right ventricular strain is essential, as deterioration can occur quickly when compensatory mechanisms fail.
Concept Check
Why does pulmonary embolism cause ventilation–perfusion mismatch rather than airway obstruction?
How does pulmonary embolism increase right ventricular afterload?
Why can pulmonary embolism lead to hypotension and shock despite normal lung mechanics?
Why is hypoxaemia often disproportionate to chest imaging findings in PE?
How does hyperventilation affect acid–base balance in early pulmonary embolism?