Cardiac Index During Therapeutic Hypothermia: Which Target Value Is Optimal?

Abstract

Mild therapeutic hypothermia is now recognized as standard therapy in patients resuscitated from out-ofhospital cardiac arrest (OHCA), and is recommended in comatose patients suff ering from cardiac arrest related to ventricular fi brillation (VF) [1]. In these patients, maintaining an adequate tissue oxygen delivery (DO 2 ) is crucial. However, during hypothermia, clinical signs of hypo perfusion such as cold, clammy skin and delayed capillary refi ll are not reliable and monitoring devices must, therefore, be used to measure or estimate the cardiac index (CI). However, there are no recommendations regarding the target value of CI in the hypo thermic patient. In this article, the authors attempt to provide clinicians with some rationale to guide their therapy for the management of CI in patients treated with mild therapeutic hypothermia. M ild therapeutic hypothermiaNeurologic outcome and survival rates are improved in patients treated with mild therapeutic hypothermia [2,3]. Th e reason for the improved survival is probably related to the preservation of cerebral function. During mild therapeutic hypothermia, clinical data demonstrate that heart rate is signifi cantly reduced, an eff ect that usually improves left ventricular (LV) fi lling [4] . Whereas CI usually decreases with hypothermia, mild therapeutic hypothermia exerts positive inotropic eff ects in isolated human and pig myocardium. Th e phenomenon of increased inotropism during mild therapeutic hypothermia is not associated with increased sarcoplasmic reticulum Ca 2+ -content or increased Ca 2+ -transients [5] . Moreover, recent studies using animal species and in humans have provided accumulating evidence suggesting that mild therapeutic hypothermia may also improve cardiac performance [5,6]. Th erefore, the higher survival rates may also be related to positive hemodynamic eff ects of cooling in patients already suff ering from cardiac disease. Furthermore, a study about the hemodynamic eff ects of mild therapeutic hypothermia in 20 consecutive patients admitted in cardio genic shock after successful resuscitation from OHCA showed that these patients seemed to benefi t from mild therapeutic hypothermia in terms of myocardial performance, catecholamine usage, and survival when compared to a historic control group of matched patients treated without hypothermia [7]. Moreover, animal studies have shown that, in myocardial infarction, hypothermia decreases oxygen consumption and in farct size [8]. Th e positive inotropic eff ect of mild therapeutic hypothermia measured by systolic func tion has also been demonstrated in in vivo studies [5,9 ] an d can be measured echocardiographically by the signifi cant increase in ejection fraction (EF) and the augmented contraction velocity measured by pulse contour analysis. However, as shown by Lewis et al., increasing the heartrate (HR) under hypothermic conditions has a neg ative impact on LV contractility [9]. Although systolic performance is clearly improved at all temperature steps investigated, pronounced hyp...

Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

“…26 This also implies that SVO 2 as a marker of cardiac output may not be as reliable at lower temperatures, corresponding to the weaker correlations between SVO 2 and CI seen in the TTM33 group. 27 However, overall levels of lactate were higher in the TTM33 group suggesting that the metabolic supply and demands may be slightly imbalanced at 33°C, but interestingly lactate concentrations remained elevated during rewarming. Multiple mechanisms may contribute to increased lactate during cooling as fat metabolism increases and lactate clearance may be impaired; the latter may partly be explained by reduced liver flow during cooling.…”

Therapeutic hypothermia for stroke: Where to go?

“…In contrast, others have reported an increase in mean arterial pressure accompanying decreases in body temperature as a result of greater systemic vascular resistance from hypothermiainduced peripheral vasoconstriction (Giraud et al, 2013;Polderman, 2009). However, these haemodynamic changes caused by therapeutic hypothermia did not adversely affect neurological outcomes.…”

“…However, there were no significant differences in blood glucose level or insulin requirements in patients subjected to hypothermia (Clark et al, 2009;Tokutomi et al, 2004). Diuresis during hypothermia is due to increased venous return caused by vasoconstriction, leading to atrial natriuretic peptide activation and a decrease in the level of antidiuretic hormone (Giraud et al, 2013). Hypothermia can also affect bowel function by promoting ileus and delaying gastric emptying (Nunnally et al, 2011).…”