Abstract
While the induction of mild hypothermia (MH) has become the guideline therapy to attenuate hypoxic brain injury after out-of-hospital cardiopulmonary resuscitation, the cardiac effects of hypothermia are controversially discussed. A positive inotropic effect of hypothermia has been demonstrated by numerous research groups in in-vitro models, whereas contradictory effects of hypothermia have been reported in in-vivo models. 10 female pigs were anesthetized and catheterized with a conductance-catheter, a Swan-Ganz catheter and a right atrial pacemaker. A vena cava occlusion balloon and a cooling catheter for induction of mild hypothermia were introduced via the femoral veins. With MH heart rate and whole body oxygen consumption decreased, while lactate levels remained normal. Cardiac output, left ventricular volumes, peak systolic and end-diastolic pressure and dP/dt(max) did not change significantly. Changes in dP/dt(min) and the time constant of isovolumetric relaxation demonstrated impaired active relaxation. In addition, MH prolonged the systolic and shortened the diastolic time interval. The analysis of pressure-volume data, generated from transient vena-cava-occlusion, revealed increased end-systolic and end-diastolic stiffness, indicating positive inotropy and reduced end-diastolic distensibility. Positive inotropy was preserved during pacing, while diastolic function was further impaired. Conclusion: Mild hypothermia provides a positive inotropic effect and reduces the whole body oxygen consumption. The diastolic function is impaired, which, however, is compensated for by decreased spontaneous heart rate. These data suggest that the induction of mild hypothermia might be a new treatment option for refractory acute heart failure.
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