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The beneficial hemodynamic effects of afterload reduction by sodium nitroprusside during rewarming from experimental
Brage Håheim1, Timofey Kondratiev1, Erik Sveberg Dietrichs2
1Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037 Tromsø, Norway.
Insights
Rewarming from hypothermia causes cardiac dysfunction. Reducing systemic vascular resistance with sodium nitroprusside improved cardiac output and stroke volume but did not fully restore function, indicating a need for inotropic support.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Rewarming from hypothermia induces cardiac dysfunction (HCD) and increased systemic vascular resistance (SVR).
- Previous treatments combined inotropic support and vasodilation.
- This study investigates arterial dilation's isolated effect on cardiac function during hypothermia rewarming.
Purpose of the Study:
- To evaluate the isolated effect of arterial vasodilation using sodium nitroprusside (SNP) on cardiac function during rewarming from hypothermia.
- To determine if reducing systemic vascular resistance (SVR) alone can alleviate hypothermia-induced cardiac dysfunction (HCD).
Main Methods:
- A rat model was used to induce HCD via 4 hours of hypothermia (15°C) followed by rewarming.
- Left ventricular (LV) function was assessed using a conductance catheter.
- Preload recruitable stroke work (PRSW) measured LV contractility, and SVR was pharmacologically adjusted using SNP.
Main Results:
- Both groups showed reduced stroke volume (SV) and cardiac output (CO) post-rewarming.
- SNP-treated rats exhibited significantly increased SV and CO compared to controls during rewarming.
- Reduced SVR, mean arterial pressure, and end-systolic pressure were observed in the SNP group, while PRSW remained similarly reduced in both groups.
Conclusions:
- Rewarming from hypothermia significantly increases SVR.
- Pharmacological reduction of SVR positively impacts CO and SV during HCD.
- SVR reduction alone is insufficient to fully address HCD; additional inotropic support is necessary.
Background:
Rewarming from hypothermia is associated with depressed cardiac function, known as hypothermia-induced cardiac dysfunction (HCD), and increased systemic vascular resistance (SVR). Previous studies on pharmacological treatment of HCD have demonstrated beneficial effects when using drugs with the combined effects; cardiac inotropic support and peripheral vasodilation. The presented study aims to investigate the isolated effects of arterial dilatation on cardiac functional variables during rewarming from hypothermia using sodium nitroprusside (SNP).
Methods:
We utilized a rat model designed to induce HCD following 4 h at 15 °C and rewarming. To study effects on left ventricular (LV) functional variables in response to afterload reduction by SNP during rewarming a conductance catheter was used. Index of LV contractility, preload recruitable stroke work (PRSW), was obtained with inferior vena cava occlusions at 37 °C before and after hypothermia. Pressure signals from a catheter in the left femoral artery was used to pharmacologically adjust SVR.
Results:
After rewarming both animal groups showed significant reduction in both SV and CO as a manifestation of HCD. However, compared to saline controls, SV and CO in SNP-treated animals increased significantly during rewarming in response to afterload reduction displayed as reduced SVR, mean arterial- and end-systolic pressures. The cardiac contractility variable PRSW was equally reduced after rewarming in both groups.
Conclusion:
When rewarming the present model of HCD a significant increase in SVR takes place. In this context, pharmacologic intervention aimed at reducing SVR show clear positive results on CO and SV. However, a reduction in SVR alone is not sufficient to fully alleviate CO during HCD, and indicate the need of additional inotropic support.
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