Case Presentation: A 47-year-old female with no significant medical history, however, a strong family history of venous thromboembolism presented to the hospital after a witnessed episode of syncope. On presentation she was hemodynamically stable, saturating well on room air and in no active distress. Initial workup revealed elevation of troponin, BNP, and d-dimer. Electrocardiogram showed signs of right heart strain. Computed tomography angiogram of chest revealed large bilateral panlobar central and peripheral acute pulmonary emboli including saddle embolus with findings concerning for right ventricular strain. Patient was started on heparin drip for management. In the emergency department she again had another syncopal episode and suffered a pulseless electrical activity cardiac arrest from which she was unable to be resuscitated.
Discussion: Syncope in Acute pulmonary embolism (APE) is incompletely understood, but can occur secondary to transient drop in cardiac output, fatal arrhythmias in the setting of acute right heart failure, vasovagal reflex and hemodynamically unstable dysrhythmia (such as bradycardia or tachycardia). Management and risk stratification of APE typically depends on stratification tools such as the PE severity index (PESI) or on clinical guidelines that include markers of hemodynamic instability or right ventricular dysfunction. Hemodynamic instability is defined in terms of blood pressure (SBP <90 mm Hg) or presence of shock. Syncope is not included in common stratification guidelines despite reported frequent association with mortality in observational datasets. Our patient was hemodynamically stable on presentation despite presenting with syncope with associated right ventricular dysfunction. Presence of syncope in APE may have grave prognosis, as the patients might soon become hemodynamically unstable depending on the mechanism of syncope. In some cases, syncope can be brief, and the occluded pulmonary vasculature can undergo partial adaptation resulting in stabilization of blood pressure and can sometimes obscure impending clinical decompensation. Decision to initiate thrombo lytic therapy is controversial, and a multidisciplinary team approach is necessary.
Conclusions: It can be challenging to diagnose APE in a patient presenting with syncope and it can be even more challenging to risk stratify and decide on management options when APE is identified. Syncopal presentation of APE should be considered as a high-risk possible criterion because of possibility of sudden decline in clinical course, and consideration should be given to triage to an area where rescue strategies including thrombolysis are readily available.