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.