Does shunting occur with large pulmonary embolism (PE)?

Shunting in Large Pulmonary Embolism

Yes, shunting occurs in large pulmonary embolism through two distinct mechanisms: intrapulmonary arteriovenous shunting from ventilation-perfusion mismatch, and right-to-left intracardiac shunting through a patent foramen ovale (PFO) when present.

Primary Mechanism: Intrapulmonary Shunting

The European Society of Cardiology identifies intrapulmonary arteriovenous shunting as a key pathophysiological factor contributing to hemodynamic collapse in acute PE. 1 This occurs when:

• Obstructed pulmonary arteries create zones of high ventilation-perfusion (V/Q) mismatch, while compensatory overflow in non-obstructed capillary beds creates relative overperfusion with lower V/Q ratios 1, 2
• The resulting ventilation-perfusion mismatch is the primary mechanism of hypoxemia in PE, amplified by low mixed venous oxygen from reduced cardiac output 2

Secondary Mechanism: Right-to-Left Intracardiac Shunting

In approximately one-third of patients with large PE, right-to-left shunting through a patent foramen ovale can be detected by echocardiography. 1 This occurs when:

• Increased right ventricular afterload and right atrial pressure from massive PE creates an inverted pressure gradient between the right and left atrium 1, 3
• The elevated right atrial pressure exceeds left atrial pressure, forcing deoxygenated blood through the PFO directly into systemic circulation 3, 2

Clinical Significance and Risk Stratification

The presence of PFO in patients with massive PE dramatically increases morbidity and mortality:

• 5.9-fold increased risk of ischemic stroke compared to PE patients without PFO 1, 3
• 2.4-fold increased mortality risk 1, 3
• 15-fold increased risk of peripheral arterial embolism 1, 3
• 33% incidence of silent brain infarcts versus only 2% in PE patients without PFO 1, 3

Diagnostic Approach

The American College of Cardiology recommends screening for PFO in massive or submassive PE using echocardiography with agitated saline bubble study. 3 Key diagnostic features include:

• Severe hypoxemia refractory to supplemental oxygen should raise immediate suspicion for right-to-left shunting 2
• Paradoxical worsening of hypoxemia with increasing positive end-expiratory pressure (PEEP) is pathognomonic for intracardiac shunting 4
• Adding bubble study to routine transthoracic echocardiography increases detection of impending paradoxical embolism (thrombus trapped within PFO) 1, 3

Management Implications

When intracardiac shunting is identified, aggressive therapeutic options must be considered:

• Surgical embolectomy may result in the lowest stroke rate for impending paradoxical embolism (thrombus visible in PFO), particularly when intracardiac thrombus is identified 1, 3
• Thrombolysis may be associated with highest mortality compared to surgery or medical treatment with heparin in this specific scenario 1, 3
• Catheter-based techniques should be considered as an alternative to surgery when appropriate 1, 3

Critical Pitfalls to Avoid

Do not treat refractory hypoxemia with aggressive PEEP escalation when intracardiac shunt is present or suspected:

• Increasing airway pressures worsens right-to-left shunting by further elevating right atrial pressure 4
• Airway pressure release ventilation (APRV) should be considered as it decreases shunt fraction, improves V/Q matching, and decreases right atrial pressure 4
• Management should aim to decrease pulmonary vascular resistance through definitive PE treatment (thrombolysis, embolectomy) while minimizing intrathoracic pressures 4

The paradoxical phenomenon where PFO may serve as a "pop-off valve" preventing acute right ventricular failure must be balanced against the severe risks of paradoxical embolism and intractable hypoxemia. 5 This dual nature makes early detection and aggressive management essential in massive PE with suspected shunting.