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.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology