Hemodynamic and cardiometabolic studies in patients with distributive circulatory dysfunctions : with special reference to the effects of the beta-1-adrenoreceptor agonist prenalterol

A total of 49 patients were studied, using invasive hemodynamic techniques with systemic arterial, pulmonary artery and right atrial pressure recordings together with thermodilution cardiac output determinations. Sixteen of the patients were also subjected to cardiometabolic studies, using measurement of coronary sinus blood flow by the continuous thermodilution technique and analyses of oxygen content and lactate concentration in the systemic and coronary circulation. A common denominator in the five investigations was, that a distributive cardiovascular dysequilibrium was either induced (for surgical or anaesthesiological reasons) or already present due to a pathological condition. Thoracic epidural block from T 1 to T 12 induced marked decrease in systemic blood pressure due to vasodilation and impairment of cardiac performance. Prenalterol administration effectively abolished the low blood pressure by its marked inotropic action, having no effect on systemic vascular resistance. Myocardial oxygen consumption changed in parallel with the changes in cardiac work following both thoracic epidural block and prenalterol. Coronary vascular resistance was markedly decreased by the block and was not affected by prenalterol. It is suggested, that the critically low perfusion pressure is the main cause of the coronary vasodilation and that alpha-blockade induced by the thoracic epidural block is of less importance. The combination of a thoracic epidural block from T 1 to T 12 and selective ß1-stimulation with prenalterol was an effective way to modify the cardiovascular response to infrarenal aortic cross clamping. This treatment transferred the patients to a more favourable cardiac function curve and possibly facilitated the redistribution of blood flow in association with clamping. In association with declamping of the infrarenal aorta or the common iliac arteries, volume loading to a slightly elevated left ventricular filling pressure shortly before declamping was an effective way to counteract the expected blood pressure drop. A normal left ventricular filling pressure prior to declamping did not prevent the blood pressure drop following declamping. It is suggested, that mismatching between vascular volume and blood volume is the main cause of declamping hypotension. In patients with low resistance, distributive septic shock caused by gram negative bacteremias and signs of impaired cardiac function, prenalterol effectively reversed the hypotension and improved tissue perfusion by selectively increasing cardiac output. In parallel to the increased cardiac work, an increase in myocardial metabolic demand was demonstrated.digitalisering@umu.s