Pathophysiology ofHemodynamic Stress and Cardiac Injury

Acute PE increases pulmonary vascular resistance, partly owing to hypoxic vasoconstriction. In patients without prior cardiopulmonary disease, the mean pulmonary artery pressure can double to approx 40 mmHg. A further doubling of pulmonary artery pressure may occur in patients with chronic thromboembolic pulmonary hypertension (11).

Right ventricular enlargement owing to pressure overload causes a leftward shift of the interventricular septum, a manifestation of interventricular dependence that leads to reduced left ventricular (LV) preload and decreased cardiac output. RV contraction continues even after the left ventricle starts relaxing at end systole. The interventricular septum flattens during systole and then bulges toward the left ventricle, with paradoxical septal motion that distorts the normally circular LV cavity. There is diastolic LV impairment, owing to septal displacement, reduced LV distensibility, and impaired LV filling during diastole.

Increased RV afterload can cause RV dilatation, hypokinesis, tricuspid regurgitation with annular dilatation ofthe tricuspid valve, and ultimately RV failure. While this pathological process evolves, most patients maintain a normal systemic arterial pressure for 12-48 h and may give the impression of being "hemodynamically stable." Then, often abruptly, systemic arterial hypotension resistant to supportive medical therapy and cardiac arrest may ensue (12).

Increased RV wall tension and oxygen demand, combined with reduced coronary perfusion and oxygen supply, may cause RV myocardial ischemia. As RV wall stress increases, cardiac ischemia may develop because increased RV pressure compresses the right coronary artery, diminishes subendocardial perfusion, and limits myocardial oxygen supply (13). This setting provides the substrate for abnormal release of cardiac biomarkers.

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