RT Book, Section A1 Serrao, Gregory A1 Bier, Benjamin A1 Gidwani, Umesh A2 Fuster, Valentin A2 Narula, Jagat A2 Vaishnava, Prashant A2 Leon, Martin B. A2 Callans, David J. A2 Rumsfeld, John S. A2 Poppas, Athena SR Print(0) ID 1202456766 T1 Circulatory and Cardiogenic Shock T2 Fuster and Hurst's The Heart, 15e YR 2022 FD 2022 PB McGraw-Hill Education PP New York, NY SN 9781264257560 LK accesscardiology.mhmedical.com/content.aspx?aid=1202456766 RD 2024/10/12 AB Chapter SummaryThis chapter describes the pathophysiology, assessment, classification, and management of cardiogenic shock (see Fuster and Hurst’s Central Illustration). The pathophysiology of cardiogenic shock involves a maladaptive compensatory cycle triggered by acute reduction in cardiac output. All etiologies initiate a physiologic cascade rooted in three main pathways: (1) increase in left ventricular end diastolic pressure, (2) reduction of blood pressure, and (3) triggering of inflammatory responses. If left uninterrupted, the compensatory cycle will lead to progressive cardiac dysfunction and ultimately death. A thorough assessment of the patient with suspected cardiogenic shock is necessary to confirm diagnosis and inform treatment decisions, and involves physical examination, ultrasonography, laboratory studies, invasive hemodynamics, and coronary angiography, as appropriate. Cardiogenic shock with predominant left ventricular failure is more common than isolated right ventricular failure, and etiology can be categorized as primary, obstructive, or valvular. Etiology of cardiogenic shock with predominant right ventricular failure is usually primary or obstructive, often related to acute pulmonary embolism of hemodynamic significance. Concurrent left ventricular failure and right ventricular failure is relatively common among causes of cardiogenic shock and the underlying etiology is primary, obstructive, electrical, or structural. Treatment for cardiogenic shock depends on etiology, and may involve a combination of vasoactive agents (pressors and inotropes), treatment of myocardial ischemia and revascularization as appropriate, and mechanical circulatory support (e.g. intra-aortic balloon pump counterpulsation, percutaneous left ventricular assist device, and/or extracorporal membrane oxygenation) as needed.