[Modern aspects of cardiogenic shock]

Since the introduction of coronary care units the in-hospital mortality decreased in acute myocardial infarction (AMI), but not the mortality which persisted at about 90% in cardiogenic shock (CS). the definition of CS is based on a cardiac index of greater than 2.2 1/min/m2 and an advancing lactate acidosis with lactate values of about 4.0 mmol/1 which leads to death in most cases by the so-called secondary ventricular fibrillation. Measurements of invasive haemodynamic parameters like cardiac index etc. were superseded by clinical parameters because of methodological problems in clinical routine. Forrester deals with clinical parameters and the pulmonary wedge pressure to separate 4 haemodynamically different subsets in the acute stage of AMI. The treatment of cardiogenic shock uses the manipulation of pre- and/or afterload. Nitrates reduce an increased PCV to normal values because of dilating the capacity vessels (preload) which leads to venous pooling. The cardiac index increases up to 20%. Vasodilators (Na-nitroprusside, phentolamine, prazosin, hydralazine, captopril) also caused an increase of the cardiac index because of afterload reduction. This therapeutic strategy demands exact continuous arterial blood pressure monitoring. A perfusion pressure greater than 80 mm Hg on an average will extend the infarction area in narrowed coronary arteries. Positive inotropic drugs (dopamine, dobutamine, amrinone) increase the contractility of the injured myocardium. From the haemodynamic point of view the best results can be achieved by application of temporary intraaortic counterpulsation (IABP) by reducing afterload and increasing diastolic perfusion of the coronary arteries. Nevertheless IABP is of restricted value because of high rate of pump-dependence.