Veno-venous perfusion-induced hyperthermia: effect on hemodynamics

The therapeutic utility of hyperthermia maybe limited by deleterious effects on hemodynamics, that potentially maybe ameliorated by hyperthermia induced by venovenous perfusion. Swine (49.2±5.2 kg) were divided into 38°C and 43°C Groups (n=6 each) and subjected to jugular-to-femoral vein veno-venous perfusion-induced hyperthermia for 120 minutes. We compared the hemodynamic response at 38°C, 41°C and 43°C in the 43°C Group (one way ANOVA) to the 38°C Group (paired t-test). Variables include: heart rate (HR), arterial blood pressure (MAP), cardiac output (CO), left ventricular filling pressure (LVFP), pulmonary artery pressure (PAP), venous oxygen saturation (SVO₂), central venous pressure (CVP), stroke volume index (SVI), left and right ventricular stroke work index (LVSWI and RVSW1), cardiac work (CW), oxygen delivery (dO₂), and systemic and pulmonary vascular resistance (SVR and PVR). Significant results at p<0.05 are expressed as percent change from baseline: HR increased by 15±11 % at 41°C, 29±15 % at 43°C, MAP increased by 26±7 % at 41°C, 27±9 % at 43°C, CO increased by 49±22 % at 41°C, 59124 % at 43°C, SVR increased by 27±10 % at 41°C, LVSWI increased by 52±7 % at 41°C, CW increased by 39±15 % at 41°C, dO₂ increased by 23±6 % at 43°C, and SvO₂ increased 50±8% at 43°C. We conclude that hyperthermia to 43°C causes significant hemodynamic changes including, increases in HR, MAP, CO. LVSWI, and CW in a temperature-dependent fashion with no decrease in dO₂ or SvO₂. Heating bv venovenous perfusion does not cause an overall cardiac decompensation at 43°C.