What is the typical effect of a pulmonary embolus (PE) on pulmonary capillary wedge pressure, mean pulmonary artery pressure, central venous pressure, and dead space/tidal volume ratio?

Pulmonary Embolism and Hemodynamic Changes

A pulmonary embolus is associated with an increase in dead space/tidal volume ratio, not a decrease. 1, 2, 3

Hemodynamic Changes in Pulmonary Embolism

Pulmonary Capillary Wedge Pressure

• Pulmonary capillary wedge pressure typically remains normal or may decrease slightly in acute pulmonary embolism as the obstruction occurs at the arterial level, not affecting the post-capillary pressure 2, 3
• The European Society of Cardiology notes that in acute PE, particularly massive PE, the primary hemodynamic issue is increased pulmonary vascular resistance rather than elevated wedge pressure 1

Mean Pulmonary Artery Pressure

• Mean pulmonary artery pressure increases in pulmonary embolism due to the abrupt increase in pulmonary vascular resistance resulting from vascular obstruction 2, 3
• The European Society of Cardiology states that when more than 30-50% of the pulmonary arterial bed is occluded, there is a significant increase in pulmonary arterial pressure 3
• This increase in pressure is caused by both anatomical obstruction and hypoxic vasoconstriction in the affected areas 3

Central Venous Pressure

• Central venous pressure typically increases in pulmonary embolism due to right ventricular failure from acute pressure overload 2, 3
• The American Heart Association notes that right ventricular dilation and dysfunction occur as a result of increased pulmonary vascular resistance, leading to elevated right atrial pressure (central venous pressure) 1, 3

Dead Space/Tidal Volume Ratio

• Dead space/tidal volume ratio increases (not decreases) in pulmonary embolism due to ventilation/perfusion mismatching 1, 4
• Areas of lung that are ventilated but not perfused (due to embolic obstruction) contribute to increased physiologic dead space 4, 5
• The European Society of Cardiology confirms that PE causes ventilation/perfusion mismatching with some lung units being overventilated relative to perfusion (increased dead space) 1, 4

Pathophysiological Mechanisms

• The abrupt increase in pulmonary vascular resistance results in right ventricular dilation and dysfunction, altering the contractile properties through the Frank-Starling mechanism 2, 3
• Prolonged right ventricular contraction leads to leftward bowing of the interventricular septum, causing desynchronization of the ventricles and impeded left ventricular filling 2, 3
• This cascade can ultimately lead to reduced cardiac output and contribute to systemic hypotension in severe pulmonary embolism 2, 3
• Inflammatory response triggered by thromboemboli in the pulmonary vasculature can contribute to secondary hemodynamic destabilization 24-48 hours after acute PE 6

Common Pitfalls

• Mistaking pulmonary hypertension for systemic hypertension when interpreting hemodynamic changes in PE 2
• Failing to recognize that increased dead space/tidal volume ratio is a characteristic finding in PE due to areas of lung that are ventilated but not perfused 4, 5
• Overlooking that central venous pressure typically increases rather than decreases in PE due to right ventricular failure 2, 3
• Not appreciating that pulmonary capillary wedge pressure usually remains normal or slightly decreased despite elevated pulmonary arterial pressure 1, 3