• K H Scholz.
• Abteilung Kardiologie und Pneumologie, Georg-August-Universität Göttingen. kscholz1@gwdg.de
• Herz. 1999 Oct 1;24(6):448-64.

AbstractCardiogenic shock is a state of inadequate tissue perfusion due to cardiac dysfunction, which is most commonly caused by acute myocardial infarction. The pathophysiology of cardiogenic shock is characterized by a downward spiral: ischemia causes myocardial dysfunction, which, in turn, augments the ischemic damage and the energetical imbalance. With conservative therapy, mortality rates for patients with cardiogenic shock are frustratingly high reaching more than 80%. Additional thrombolytic therapy has not been shown to significantly improve survival in such patients. Emergency cardiac catheterization and coronary angioplasty, however, seem to improve the outcome in shock-patients, which most probably is due to rapid and complete revascularization generally reached by angioplasty. In addition to interventional therapy with rapid coronary revascularization, the use of mechanical circulatory support may interrupt the vicious cycle in cardiogenic shock by stabilizing hemodynamics and the metabolic situation. Different cardiac assist devices are available for cardiologists and cardiac surgeons: 1. intraaortic balloon counterpulsation (IABP), 2. implantable turbine-pump (Hemopump), 3. percutaneous cardiopulmonary bypass support (CPS), 4. right heart, left heart, or biventricular assist devices placed by thoracotomy, and 5. intra- and extrathoracic total artificial hearts. Since percutaneous application is possible with IABP, Hemopump and CPS, these devices are currently used in interventional cardiology. The basic goals of the less invasive intraaortic balloon counterpulsation (IABP; Figure 1) are to stabilize circulatory collapse, to increase coronary perfusion and myocardial oxygen supply, and to decrease left ventricular workload and myocardial oxygen demand (Figure 2). Since the advent of percutaneous placement, IABP has been used by an increasing number of institutions (Figure 3). In addition to cardiogenic shock, the system may be of use in a variety of other indications in the catheterization laboratory and intensive care unit, including weaning from percutaneous cardiopulmonary bypass, in ischaemic left ventricular failure, in unstable angina, in high risk PTCA, and in prophylactic support in patients with myocardial infarction and successful revascularization. Animal experimental data showed that IABP may improve success of thrombolysis and recent clinical data suggest that survival is enhanced and transfer for revascularization is facilitated when patients with myocardial infarction and cardiogenic shock undergo thrombolysis and IABP rather than thrombolysis alone. A lot of studies had demonstrated before, that combined use of counterpulsation and revascularization therapy (i.e. coronary bypass surgery or angioplasty) may improve prognosis in patients with myocardial infarction complicated by cardiogenic shock (Table 1). In such patients, early treatment with IABP is most important: Multivariate analysis identified early IABP-support with a duration of shock to IABP-treatment of > or = 4 hours as an independent predictor of a positive short-term outcome. In shock-patients with postinfarction ventricular septal defect, IABP provides a marked hemodynamic improvement, and a significant decrease in shunt-flow (Figure 5). However, despite initial stabilization with IABP, such patients need immediate surgical repair of the septal defect to avoid hemodynamic deterioration. The rate of complications related to percutaneous IABP was significantly attenuated by employing catheters of reduced size. Using 9.5-F catheters, a long duration of counterpulsation emerged as the most significant factor associated with complications. In our hospital, those patients with 9.5-F catheters in whom counterpulsation did not exceed 48 hours had a low complication rate of 3.9%. The Hemopump is a catheter-mounted transvalvular left ventricular assist device intended for surgical placement via the femoral artery (Figures 6 and 7). (ABSTRACT TRUNCATED)

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