Future Treatment of Acute Cardiac Collapse - A Role for Percutaneous Circulatory Assist Devices

1.1 Acute cardiac collapse Patients with cardiogenic shock and cardiac arrest still have a very poor prognosis despite recent improvements in treatment algorithms. Acute coronary ischemia and myocardial infarction (AMI) is the most frequent cause of cardiogenic shock and cardiac arrest. Improved survival has been shown for patients with AMI treated with urgent coronary revascularization. Also, improved pre-hospital logistics and cooling after successful resuscitation has shown possible benefit for cardiac arrest patients. However, a large proportion of patients with AMI and acute cardiac collapse do not survive until hospital discharge. These represent a group where current treatment options are often unsuccessful. This far, advances in pharmacological treatment have produced various substances with theoretical and hemodynamic promise but clinical effects have been scarce. The use of vasopressors and inotropes generally has failed to show effect on mortality in cardiogenic shock and cardiac arrest. Recently a large clinical trial showed no effect of intravenous medication on survival for cardiac arrest victims (Figure 1). Lately, more thought provoking data have emerged indicating a possible negative effect of vasopressor therapy on cardiac and cerebral perfusion during circulatory collapse and resuscitation. Clinical reports have further suggested a possible relationship between the use of adrenaline like drugs and increased mortality in patients with acute myocardial infarction and shock. Mechanical support with intra-aortic balloon pump (IABP) counter pulsation therapy has been routinely used for several years in cardiogenic shock but the clinical usefulness is currently being strongly questioned. In cardiac arrest, optimally performed chest compressions are critical for successful re-establishment of intrinsic pulse giving rhythm (Figure 2). Mechanical compression-decompression devices have also shown impressive hemodynamic effects experimentally but a benefit compared with conventional chest compressions has not been found in clinical trials. Both IABP and the compression-decompression devices have been associated with bleeding complications. The mechanisms behind refractory cardiogenic shock and cardiac arrest may be many and are yet not clearly defined. It seems clear however, that with the pharmacological and