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CURRENT ISSUEMINERVA ANESTESIOLOGICA

A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care

Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 2,036

Frequency: Monthly

ISSN 0375-9393

Online ISSN 1827-1596

 

Minerva Anestesiologica 2010 August;76(8):653-6

    CASE REPORTS

Systolic anterior motion causing hemodynamic instability and pulmonary edema during bleeding

Cavallaro F., Marano C., Sandroni C., Dell’Anna A.

Intensive Care Unit, Catholic University School of Medicine; Agostino Gemelli Hospital, Rome, Italy

Systolic anterior motion (SAM) of mitral valve is the prolapse of a mitral leaflet into the left ventricle outflow tract (LVOT) during systole, causing LVOT obstruction and mitral valve regurgitation. We report the case of a patient who developed SAM-induced hemodynamic instability during bleeding with a clinical picture resembling pulmonary edema. A 77-year-old woman was admitted to our emergency room for abdominal bleeding in polycystic renal disease. Upon arrival, she was normotensive, despite being anuric and acidotic. After infusion of fluids and packed red blood cells (total 3 680 mL in 6 hours) she developed atrial fibrillation and clinical and radiological signs of pulmonary edema. Sedation and non-invasive ventilation brought to immediate severe hypotension. A transesophageal echocardiogram showed an “empty” hypertrophic hypercontractile left ventricle, SAM with LVOT obstruction (intraventricular gradient 154 mmHg) and moderate-to-severe mitral regurgitation. With further fluid infusion hemodynamic stability and sinus rhythm were recovered. SAM, LVOT obstruction and mitral regurgitation disappeared. SAM is a rare but dangerous cause of hemodynamic instability. It has been described in patients with and without left ventricular hypertrophy, in presence of hypovolemia and sympathetic stimulation. In our case it presented with a misleading clinical picture of pulmonary edema simulating fluid overload in an actually hypovolemic patient. In fact, SAM-associated mitral regurgitation together with diastolic dysfunction and tachycardia induced a pulmonary edema whose treatment worsened hypovolemia and precipitated LVOT obstruction and hypotension. Further fluid infusion was resolutive. Echocardiography was fundamental for diagnosis and treatment.

language: English


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