Pathophysiology, diagnosis, and treatment of infarction-related cardiogenic shock

Abstract

Cardiogenic shock is characterized by inadequate tissue perfusion due to cardiac dysfunction, and it is often caused by acute myocardial infarction. The mortality rate in patients with cardiogenic shock is still very high (i.e., 50-60%). The pathophysiology of cardiogenic shock involves a vicious spiral circle: ischemia causes myocardial dysfunction, which in turn aggravates myocardial ischemia. Myocardial stunning and/or hibernating myocardium can enhance myocardial dysfunction, thus, worsening the cardiogenic shock. Low perfusion pressures with global ischemia leads to multiorgan dysfunction. Ischemia and reperfusion can result in systemic inflammation or within the first few days sepsis due to the translocation of bacteria or bacterial toxins from the intestines, which can result in increased mortality. The key to an optimal treatment of cardiogenic shock patients is a structured approach: (1) rapid diagnosis and prompt initiation of therapy to increase blood pressure and augment cardiac output with subsequently improved perfusion. (2) Rapid coronary revascularization is of critical importance. Using this approach, mortality can be reduced. In many hospitals, initial stabilization is achieved by intraaortic balloon counterpulsation (IABP). However, evidence for improved survival from randomized studies on the use of IABP in combination with PCI is lacking. (3) In order to achieve adequate perfusion, dobutamine and sometimes in combination with norepinephrine might be necessary. Recent studies have shown that the calcium sensitizer levosimendan in cardiogenic shock can be a useful addition to medical therapy. In this overview, epidemiology, pathophysiology, and guideline-oriented treatment strategies for cardiogenic shock are presented.