Comparison Between Two Pharmacologic Strategies to Alleviate Rewarming Shock: Vasodilation vs. Inodilation.

Brage Håheim,Erik Sveberg Dietrichs,Torkjel Tveita,Timofei Kondratiev

doi:10.3389/fmed.2020.566388

Brage Håheim, Erik Sveberg Dietrichs + Show 2 more

Open Access

https://doi.org/10.3389/fmed.2020.566388

Copy DOI

Abstract

Rewarming from hypothermia is often challenged by coexisting cardiac dysfunction, depressed organ blood flow (OBF), and increased systemic vascular resistance. Previous research shows cardiovascular inotropic support and vasodilation during rewarming to elevate cardiac output (CO). The present study aims to compare the effects of inodilatation by levosimendan (LS) and vasodilation by nitroprusside (SNP) on OBF and global oxygen transport during rewarming from hypothermia. We used an in vivo experimental rat model of 4 h 15°C hypothermia and rewarming. A stable isotope-labeled microsphere technique was used to determine OBF. Cardiac and arterial pressures were monitored with fluid-filled pressure catheters, and CO was measured by thermodilution. Two groups were treated with either LS (n = 7) or SNP (n = 7) during the last hour of hypothermia and throughout rewarming. Two groups served as hypothermic (n = 7) and normothermic (n = 6) controls. All hypothermia groups had significantly reduced CO, oxygen delivery, and OBF after rewarming compared to their baseline values. After rewarming, LS had elevated CO significantly more than SNP (66.57 ± 5.6/+30% vs. 54.48 ± 5.2/+14%) compared to the control group (47.22 ± 3.9), but their ability to cause elevation of brain blood flow (BBF) was the same (0.554 ± 0.180/+81 vs. 0.535 ± 0.208/+75%) compared to the control group (0.305 ± 0.101). We interpret the vasodilator properties of LS and SNP to be the primary source to increase organ blood flow, superior to the increase in CO.

Highlights

Clinical presentation of accidental hypothermia and rewarming is associated with hypotension, hypoperfusion, and vital organ injury [1, 2]
At 30◦C during rewarming (30◦CRW), all three groups, independent of intervention, showed depressed mean arterial pressure (MAP), cardiac index (CI), cardiac output (CO), and Heart rate (HR) when compared to 37◦CBL
systemic vascular resistance (SVR) was reduced in both sodium nitroprusside (SNP) and LS groups compared to the control

Summary

Introduction

Clinical presentation of accidental hypothermia and rewarming is associated with hypotension, hypoperfusion, and vital organ injury [1, 2]. Coined rewarming shock, this unstable hemodynamic state [3,4,5] contributes to the lethality of 28–35% in accidental hypothermia patients [6, 7]. Clinical experience and experimental studies have identified hypothermia-induced cardiac dysfunction and elevated systemic vascular resistance (SVR) as fundamental mechanisms [5, 8]. Experimental studies are needed to improve our understanding of rewarming shock and identify possible pharmacological treatment options

Objectives

Methods

Results

Discussion

Conclusion