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Organ blood flow and O 2 transport during hypothermia (27°C) and rewarming in a pig model
Author(s) -
Valkov Sergei,
Mohyuddin Rizwan,
Nilsen Jan Harald,
Schanche Torstein,
Kondratiev Timofei V.,
Sieck Gary C.,
Tveita Torkjel
Publication year - 2018
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep087205
Subject(s) - hypothermia , anesthesia , medicine , blood flow , accidental hypothermia , hemodynamics , cardiology
New FindingsWhat is the central question of this study? Absence of hypothermia‐induced cardiac arrest is a strong predictor for a favourable outcome after rewarming. Nevertheless, detailed knowledge of preferences in organ blood flow during rewarming with spontaneous circulation is largely unknown.What is the main finding and its importance? In a porcine model of accidental hypothermia, we find, despite a significantly reduced cardiac output during rewarming, normal blood flow and O 2 supply in vital organs owing to patency of adequate physiological compensatory responses. In critical care medicine, active rewarming must aim at supporting the spontaneous circulation and maintaining spontaneous autonomous vascular control.Abstract The absence of hypothermia‐induced cardiac arrest is one of the strongest predictors for a favourable outcome after rewarming from accidental hypothermia. We studied temperature‐dependent changes in organ blood flow and O 2 delivery ( D O 2 ) in a porcine model with spontaneous circulation during 3 h of hypothermia at 27°C followed by rewarming. Anaesthetized pigs ( n = 16, weighing 20–29 kg) were randomly assigned to one of two groups: (i) hypothermia/rewarming ( n = 10), immersion cooled to 27°C and maintained for 3 h before being rewarmed by pleural lavage; and (ii) time‐matched normothermic (38°C) control animals ( n = 6), immersed for 6.5 h, the last 2 h with pleural lavage. Regional blood flow was measured using a neutron‐labelled microsphere technique. Simultaneous measurements of D O 2and O 2 consumption ( V ̇ O 2 ) were made. During hypothermia, there was a reduction in organ blood flow,V ̇ O 2and D O 2 . After rewarming, there was a 40% reduction in stroke volume and cardiac output, causing a global reduction in D O 2 ; nevertheless, blood flow to the brain, heart, stomach and small intestine returned to prehypothermic values. Blood flow in the liver and kidneys was significantly reduced. Cerebral D O 2andV ̇ O 2returned to control values. After hypothermia and rewarming there is a significant lowering of D O 2owing to heart failure. However, compensatory mechanisms preserve O 2 transport, blood flow andV ̇ O 2in most organs. Nevertheless, these results indicate that hypothermia‐induced heart failure requires therapeutic intervention.