Cardiovascular responses to an acute volume load in deep hypothermia

Lauri, Timo

doi:10.1093/oxfordjournals.eurheartj.a014915

Cited by 10 publications

(2 citation statements)

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“…Also, Hb concentration changes were unrelated to diuresis, as diuretic output was constant throughout experiments. More likely, changes in Hb concentration were caused by fluctuations in plasma volume by other mechanisms, as has been reported in the time course of surface cooling [48,49] and rewarming [50]. Our findings of temporarily decreased CVP, EDV and ESV during hypothermia support the assumption that plasma volume was reduced in hypothermia and returned to normal during rewarming.…”

Section: Discussionsupporting

confidence: 86%

Post-hypothermic cardiac left ventricular systolic dysfunction after rewarming in an intact pig model

et al. 2010

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IntroductionWe developed a minimally invasive, closed chest pig model with the main aim to describe hemodynamic function during surface cooling, steady state severe hypothermia (one hour at 25°C) and surface rewarming.MethodsTwelve anesthetized juvenile pigs were acutely catheterized for measurement of left ventricular (LV) pressure-volume loops (conductance catheter), cardiac output (Swan-Ganz), and for vena cava inferior occlusion. Eight animals were surface cooled to 25°C, while four animals were kept as normothermic time-matched controls.ResultsDuring progressive cooling and steady state severe hypothermia (25°C) cardiac output (CO), stroke volume (SV), mean arterial pressure (MAP), maximal deceleration of pressure in the cardiac cycle (dP/dtmin), indexes of LV contractility (preload recruitable stroke work, PRSW, and maximal acceleration of pressure in the cardiac cycle, dP/dtmax) and LV end diastolic and systolic volumes (EDV and ESV) were significantly reduced. Systemic vascular resistance (SVR), isovolumetric relaxation time (Tau), and oxygen content in arterial and mixed venous blood increased significantly. LV end diastolic pressure (EDP) remained constant. After rewarming all the above mentioned hemodynamic variables that were depressed during 25°C remained reduced, except for CO that returned to pre-hypothermic values due to an increase in heart rate. Likewise, SVR and EDP were significantly reduced after rewarming, while Tau, EDV, ESV and blood oxygen content normalized. Serum levels of cardiac troponin T (TnT) and tumor necrosis factor-alpha (TNF-α) were significantly increased.ConclusionsProgressive cooling to 25°C followed by rewarming resulted in a reduced systolic, but not diastolic left ventricular function. The post-hypothermic increase in heart rate and the reduced systemic vascular resistance are interpreted as adaptive measures by the organism to compensate for a hypothermia-induced mild left ventricular cardiac failure. A post-hypothermic increase in TnT indicates that hypothermia/rewarming may cause degradation of cardiac tissue. There were no signs of inadequate global oxygenation throughout the experiments.

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Section: Discussionsupporting

confidence: 86%

Post-hypothermic cardiac left ventricular systolic dysfunction after rewarming in an intact pig model

et al. 2010

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“…Several studies on therapeutically induced hypothermia have reported severe stiffness of the left ventricle and acute volume overload during rewarming. [23][24][25] If patients have to be weaned from ECC during refractory diastolic dysfunction with elevated left ventricular filling pressures, acute aggravation of reperfusion pulmonary edema occurs. Our study therefore underlines that prolonged ECMO support can prevent this complication if patients are weaned from ECMO after successful stabilization of cardiopulmonary function.…”

Section: Discussionmentioning

confidence: 99%