From the Guidelines
Syncope in pulmonary embolism occurs through several interconnected mechanisms, primarily involving obstruction of pulmonary blood flow by emboli, which increases pulmonary vascular resistance and right ventricular afterload, leading to right ventricular dysfunction and decreased left ventricular filling, resulting in reduced cardiac output and cerebral perfusion, as noted in the 2020 European Society of Cardiology guidelines 1. The mechanisms of syncope in pulmonary embolism are complex and multifactorial. Key factors include:
- Obstruction of pulmonary blood flow by emboli, increasing pulmonary vascular resistance and right ventricular afterload
- Right ventricular dysfunction and decreased left ventricular filling, resulting in reduced cardiac output and cerebral perfusion
- Hypoxemia from ventilation-perfusion mismatch, further compromising oxygen delivery to the brain
- Neurally-mediated reflexes, including the Bezold-Jarisch reflex, triggering paradoxical vasodilation and bradycardia when the right ventricle is strained, exacerbating the drop in blood pressure
- Arrhythmias, particularly tachyarrhythmias, developing due to right heart strain and hypoxemia, further compromising cardiac output These mechanisms often occur simultaneously, with the severity of syncope correlating with the extent of pulmonary vascular obstruction and the patient's cardiopulmonary reserve, as discussed in the 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care 1. In massive pulmonary embolism, mechanical obstruction can be so severe that it causes near-complete circulatory collapse, as noted in the 2000 European Society of Cardiology guidelines on diagnosis and management of acute pulmonary embolism 1. The most critical aspect of managing syncope in pulmonary embolism is prompt recognition and treatment of the underlying condition, with a focus on restoring pulmonary blood flow and preventing further clot propagation, as emphasized in the 2020 European Society of Cardiology guidelines 1.
From the Research
Mechanisms of Syncope in Pulmonary Embolism (PE)
The mechanisms of syncope in pulmonary embolism (PE) are complex and multifactorial. Some possible mechanisms include:
- Vaso-vagal mechanism: Syncope in non-massive pulmonary embolism may be due to a vaso-vagal mechanism that can lead to a reduction of arterial blood pressure when central artery thrombosis is involved 2.
- Reduction in systolic and/or diastolic blood pressure: Patients with syncope have significant reductions in systolic and/or diastolic blood pressure, which can lead to a decrease in cardiac output and ultimately result in syncope 2.
- Obstruction of blood flow: Pulmonary embolism can cause obstruction of blood flow in the lungs, leading to a decrease in oxygenation of the blood and a subsequent decrease in cardiac output, which can result in syncope 3, 4.
- Right heart failure: Pulmonary embolism can also cause right heart failure, which can lead to a decrease in cardiac output and ultimately result in syncope 5.
Clinical Characteristics of Patients with Syncope and PE
Patients with syncope and PE often have similar clinical characteristics to those without syncope, including:
- Respiratory failure: Patients with syncope and PE may experience respiratory failure, which can worsen the prognosis 5.
- Arterial hypotension: Patients with syncope and PE may also experience arterial hypotension, which can decrease cardiac output and worsen the prognosis 5.
- Right heart failure: Right heart failure is a common complication of PE and can lead to syncope 5.
Prognostic Significance of Syncope in PE
The prognostic significance of syncope in PE is not well established. Some studies suggest that syncope is a predictor of major bleeding events in patients with PE 6, while others suggest that syncope does not seem to determine a poor prognosis 5. Further research is needed to fully understand the prognostic significance of syncope in PE.