Can a saddle pulmonary embolism cause syncope?

Can a Saddle Pulmonary Embolism Cause Syncope?

Yes, saddle pulmonary embolism can definitely cause syncope, and this presentation should be considered a high-risk feature requiring immediate evaluation and treatment. Syncope occurs in saddle PE through multiple mechanisms including acute hemodynamic compromise, right ventricular dysfunction, and neurally-mediated reflex responses.

Epidemiology and Clinical Significance

• Syncope occurs in approximately 19% of all pulmonary embolism cases 1, but the frequency is notably higher in saddle PE specifically
• In patients with saddle PE, syncope is reported in 43% of cases 2, making it one of the most common presenting symptoms alongside dyspnea (72%) 2
• Saddle embolism is an independent predictor of syncope in PE patients (P = 0.044), along with right ventricular dysfunction 3
• Among hospitalized syncope patients, PE prevalence ranges from 1.4% to 17.3% depending on the population studied 4, and pulmonary embolism is frequently underdiagnosed in patients presenting with syncope 4

Pathophysiological Mechanisms

The mechanism of syncope in saddle PE is multifactorial, involving both hemodynamic and neurally-mediated components 4:

Hemodynamic Mechanisms

• Acute increase in pulmonary vascular resistance when >30-50% of the pulmonary arterial bed is occluded 4
• Right ventricular failure with inability to maintain adequate cardiac output against the sudden afterload increase 4
• Rightward septal shift causing diastolic left ventricular dysfunction and further compromising systemic cardiac output 4
• Critical decrease in systemic blood pressure (typically to ≤60 mmHg systolic) causing cerebral hypoperfusion 4

Neurally-Mediated Reflex Component

• Vasovagal reflex activation can occur even in non-massive PE with central artery involvement 5
• This explains why syncope can occur in saddle PE patients without persistent hemodynamic instability or shock 5
• The reflex mechanism may lead to transient profound hypotension and bradycardia disproportionate to the degree of vascular obstruction 4

Clinical Presentation and Risk Stratification

Key Clinical Features

• 94.3% of PE patients with syncope have right ventricular dysfunction on echocardiography, compared to 72.1% without syncope (P = 0.004) 3
• 24.2% of PE patients with syncope have saddle embolism, compared to 10.9% without syncope 3
• Most saddle PE patients present with dyspnea (72%) and syncope (43%), while hypotension is documented in only 14% 2
• Syncope can be the sole presenting symptom of saddle PE, even in the absence of chest pain or dyspnea 6, 7

Important Clinical Pitfall

Syncope in saddle PE does not necessarily indicate massive PE or require thrombolytic therapy. Many patients with saddle PE and syncope remain hemodynamically stable after the initial event and can be managed with standard anticoagulation 2, 5. The presence of syncope reflects the neurally-mediated component and central location of the embolus, not always massive hemodynamic compromise.

Diagnostic Approach

When to Suspect PE in Syncope Patients

Maintain high clinical suspicion for PE even when syncope symptoms are transient or have resolved 1. The European Society of Cardiology guidelines emphasize that:

• Apply clinical decision rules (Wells score, Geneva score) regardless of whether symptoms persist 1
• Obtain D-dimer testing and appropriate imaging even in patients with resolved symptoms if PE is clinically suspected 1
• CTA chest is the diagnostic modality of choice when PE is suspected in syncope patients 4

High-Risk Features Requiring Hospitalization

According to European Heart Journal guidelines, syncope patients should be hospitalized when 4:

• Suspected or known significant heart disease is present
• ECG abnormalities suggest arrhythmic syncope
• Syncope occurred during exercise
• Syncope caused severe injury
• Family history of sudden death exists

Management Implications

Acute Treatment

• Standard anticoagulation with heparin and warfarin is appropriate for most saddle PE patients with syncope 2
• Thrombolytic therapy is reserved for patients with persistent hemodynamic instability (shock, sustained hypotension), not based solely on the presence of syncope 2
• Catheter-directed therapy may be considered in submassive PE with right heart strain and syncope 6
• Treatment should be directed at ameliorating the structural lesion (the PE itself) and its consequences 4

Prognosis

• In-hospital mortality for saddle PE without pre-existing cardiopulmonary disease is relatively low when appropriately treated 2
• No patients with saddle PE died during hospitalization in one series of 14 patients, all managed with standard anticoagulation 2
• Anticoagulation duration (minimum 3 months) should not be shortened based on resolution of symptoms 1

Follow-up Considerations

• Follow-up at 3-6 months is recommended even if symptoms have resolved, to assess for chronic complications 1
• Up to 47% of patients may have reduced maximal aerobic capacity at one year, regardless of whether initial symptoms were transient 1
• Post-PE syndrome with decreased quality of life can occur even after transient initial presentations 1

Key Clinical Pearls

• Syncope + dyspnea in a patient with PE risk factors = saddle PE until proven otherwise 3, 2
• The combination of syncope and right ventricular dysfunction strongly suggests central/saddle PE 3
• Absence of shock does not exclude saddle PE - the neurally-mediated component can cause syncope without persistent hemodynamic collapse 5
• Even transient syncope in PE carries prognostic significance and warrants full anticoagulation and appropriate follow-up 1