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A 77-year-old woman with a medical history of constipation and small bowel bacterial overgrowth presented to an outpatient endoscopy center for EGD/colonoscopy. Both procedures went well with no complications, however while in the recovery room, the patient became abruptly hypotensive to the 70s/30s mmHg with nausea and chest pain. She was transferred to our center for further care. In our emergency room she was initially normotensive with a heart rate of 113 in atrial fibrillation, but subsequently decompensated, requiring intubation and pressors. An EKG revealed ST elevations in V1 and AVR with diffuse ST depressions, and thus a CODE STEMI was activated. Coronary angiography revealed no significant coronary disease. At this point we had to step back and reconsider the cause for this patient’s ongoing profound shock. Our differential was broad, and included obstructive shock secondary to pulmonary embolism or tamponade, hypovolemic shock secondary to a GI procedural complication, and anaphylactic shock. Bedside echocardiogram ruled out pericardial effusion and acute valvular disease, revealing a hyperdynamic LV with systolic anterior motion of the mitral valve. Pulmonary arteriogram ruled out pulmonary embolus. Right heart catheterization revealed significantly elevated biventricular filling pressures with a cardiac index of 1.3 L/min/m 2 . Given suspicion for an outflow tract obstruction, she was temporized with an esmolol drip, phenylephrine, and IV fluids. Electrical cardioversion was successful, with immediate rise in her blood pressure despite only a modest improvement in her heart rate. This case demonstrates an unusual presentation of atrial fibrillation resulting in severe hemodynamic compromise. Typically, atrial fibrillation with rates in the 110s, as in our patient, does not cause profound hypotension. This was the principle driver of diagnostic uncertainty. A perfect storm of volume depletion from colonoscopy prep, diastolic dysfunction, dynamic left ventricular outflow tract obstruction due to systolic anterior motion of the mitral valve, and loss of atrial systole resulted in profound cardiogenic shock. This obstructive physiology must be kept in mind in patients with cardiogenic shock who do not improve with usual care.

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