A 72 year old female with history of chronic atrial fibrillation not on anticoagulation was brought to the emergency department (ED) after she was found gasping for breath. She was found to have undetectable blood pressure by Emergency Medical System and the electrocardiogram revealed atrial fibrillation with rapid ventricular response (RVR). Multiple attempts of electrical cardioversion were unsuccessful in restoring normal sinus rhythm en route to the ED. On initial evaluation in the ED, she was unresponsive with blood pressure (BP) of 107/48 mm Hg, pulse 160/minute, respiratory rate 15/minute, and oxygen saturation 99% on bag and mask ventilation. Physical examination revealed irregularly irregular heart rate in 170s but clear bilateral breath sounds. No jugular venous distension was noted. She was intubated and started on Cardizem drip following which her BP dropped to 54/43 mm Hg and she was started on pressor support. Pertinent labs included troponin 0.04 ng/mL, WBC 7700/mm3, hemoglobin 14 g/dL, platelets 183000/mm3 and D-dimer 11809 ng/ml. Bedside echocardiogram revealed severely dilated right ventricle with severely decreased systolic function and moderate to severe tricuspid regurgitation. CT chest showed large volume diffuse bilateral pulmonary emboli with a large saddle embolus. Shortly afterwards, she developed cardiac arrest with Pulseless electrical activity (PEA) and was successfully resuscitated. She was started on tissue plasminogen activator (tPA) infusion, however she continued to develop recurrent episodes of PEA. Cardiosurgery consultation deemed surgical embolectomy to be futile. Her family opted for no more resuscitation efforts and she passed away from subsequent PEA.
Discussion:
Pulmonary embolism (PE) may have varied presentation ranging from asymptomatic to hemodynamic collapse with obstructive shock. Atypically, it may present as new onset atrial fibrillation (AF) masquerading the diagnosis of PE. Relation between PE and AF is two-way. PE can cause AF due to right atrial strain from increased pulmonary vascular resistance whereas AF can cause PE due to thrombus formation in right atrium. Massive PE, defined as presenting with systolic BP <90 mm Hg, is the second most common cause of sudden death and has mortality rate of 30-60%. Majority of these deaths occur during first few hours of care. Hence it is very important to diagnose these patients early and administer proper timely thrombolytic therapy.
Conclusions:
PE can masquerade as AF and diagnosis can be missed or delayed, especially in those with prior history of AF. Hence, it is crucial to have low threshold of suspicion for PE in patients presenting with respiratory distress and worsening AF.