Circulation. 2008;117:686-697
doi: 10.1161/CIRCULATIONAHA.106.613596
doi: 10.1161/CIRCULATIONAHA.106.613596
(Circulation. 2008;117:686-697.)
© 2008 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Cardiogenic Shock
Current Concepts and Improving Outcomes
From The Leon H. Charney Division of Cardiology, Cardiovascular Clinical Research Center, New York University School of Medicine, New York, NY.
Correspondence to Judith S. Hochman, MD, New York University School of Medicine, 530 First Ave, SKI-9R, New York, NY 10016. E-mail Judith.Hochman@nyumc.org
Key Words: cardiovascular diseases • myocardial infarction • outcomes research • shock
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Cardiogenic shock (CS) occurs in
5% to 8% of patients hospitalized with ST-elevation myocardial infarction (STEMI). Recent research has suggested that the peripheral vasculature and neurohormonal and cytokine systems play a role in the pathogenesis and persistence of CS. Early revascularization for CS improves survival substantially. New mechanical approaches to treatment are available, and clinical trials are feasible even in this high-risk population. Most importantly, hospital survivors have an excellent chance for long-term survival with good quality of life. This review will outline the causes, pathophysiology, and treatment of CS with a focus on CS complicating myocardial infarction (MI.) The case will be made for viewing CS as a serious disorder with a high early death rate, but one that is treatable and that, if approached aggressively, can result in full recovery.
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Diagnosis and Causes |
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CS is a state of end-organ hypoperfusion due to cardiac failure. The definition of CS includes hemodynamic parameters: persistent hypotension (systolic blood pressure <80 to 90 mm Hg or mean arterial pressure 30 mm Hg lower than baseline) with severe reduction in cardiac index (<1.8 L · min–1 · m–2 without support or <2.0 to 2.2 L · min–1 · m–2 with support) and adequate or elevated filling pressure (eg, left ventricular [LV] end-diastolic pressure >18 mm Hg or right ventricular [RV] end-diastolic pressure >10 to 15 mm Hg). The diagnosis is usually made with the help of pulmonary artery (PA) catheterization; however, Doppler echocardiography may also be used to confirm elevation of LV filling pressures.1 Hypoperfusion may
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