Abstract

We present five patients (4 females, 1 male, age range 62–79 yrs) with severe hypotension aggressively treated and who had persistent shock. The clinical setting included 2 pts following SVT, 2 pts postoperatively, and 1 pt with hemorrhagic shock. The initial evaluation suggested aortic dissection, cardiac tamponade, acute mitral regurgitation, cardiac contusion or cardiogenic shock. A transthoracic echo was performed and was nondiagnostic. The transesophageal echocardiogram (TEE) clearly ruled out these causes of shock and established the diagnosis of provokable hypertrophic obstructive cardiomyopathy (HOCM) with systolic anterior motion of the mitral valve (SAM), increased left ventricular outflow tract velocity and mitral regurgitation. None of the patients had asymmetric septal hypertrophy or positive family history for HOCM and only one had a history of hypertension. During the echo study, vasopressors were discontinued and serially IV fluid, IV beta blocker followed by IV alpha constrictors were used stepwise until the SAM and outflow tract obstruction resolved. The systolic blood pressure (SBP), pulse (P) were recorded and Cardiac Output (CO) and Index (CI) were noted with a Swan-Ganz catheter before and after the therapeutic intervention and TEE: SBP (mmHg) P(BPM) co (1/m) cl(l/m/m 2 ) PreinteNention (mean) 89 109 3.3 1.6 Postintervention (mean) 137 99 5.3 2.7 We conclude that TEE is a valuable tool in patients with shock to establish the cause of hypotension of undetermined etiology. Elucidating the pathophysiology of severe hypotension by TEE can profoundly affect the management of these patients by correctly redirecting therapy. In patients with severe hypotension who do not respond to vasopressors the diagnosis of provokable HOCM should be considered and a TEE performed. The TEE is valuable not only to diagnose this unusual condition but also to assist in titrating therapy.

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