Veno-venous perfusion-induced hyperthermia: effect on hemodynamics

R. Vertrees, W. Tao, D. Devo, R. Bmnston, J. Zwischenberger

Research output: Contribution to journalArticle

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Abstract

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 languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number6
StatePublished - 1996

Fingerprint

Induced Hyperthermia
Hemodynamics
hemodynamics
Cardiac Output
fever
cardiac output
Perfusion
Heart Rate
heart rate
Vascular Resistance
stroke
Oxygen
Central Venous Pressure
Venous Pressure
Femoral Vein
Blood pressure
Ventricular Pressure
Analysis of variance (ANOVA)
oxygen
Stroke Volume

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Vertrees, R., Tao, W., Devo, D., Bmnston, R., & Zwischenberger, J. (1996). Veno-venous perfusion-induced hyperthermia: effect on hemodynamics. FASEB Journal, 10(6).

Veno-venous perfusion-induced hyperthermia : effect on hemodynamics. / Vertrees, R.; Tao, W.; Devo, D.; Bmnston, R.; Zwischenberger, J.

In: FASEB Journal, Vol. 10, No. 6, 1996.

Research output: Contribution to journalArticle

Vertrees, R, Tao, W, Devo, D, Bmnston, R & Zwischenberger, J 1996, 'Veno-venous perfusion-induced hyperthermia: effect on hemodynamics', FASEB Journal, vol. 10, no. 6.
Vertrees R, Tao W, Devo D, Bmnston R, Zwischenberger J. Veno-venous perfusion-induced hyperthermia: effect on hemodynamics. FASEB Journal. 1996;10(6).
Vertrees, R. ; Tao, W. ; Devo, D. ; Bmnston, R. ; Zwischenberger, J. / Veno-venous perfusion-induced hyperthermia : effect on hemodynamics. In: FASEB Journal. 1996 ; Vol. 10, No. 6.
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abstract = "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.",
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AB - 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.

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