The Effect of Hypothermia "Dose" on Vasopressor Requirements and Outcome After Cardiac Arrest

University of Southern California, Department of Internal Medicine, United States.
Resuscitation (Impact Factor: 4.17). 06/2012; 84(2). DOI: 10.1016/j.resuscitation.2012.06.011
Source: PubMed


OBJECTIVES: We evaluated the association between TH use and "dose" and cumulative vasopressor and inotrope requirement, survival, and neurologic outcome. BACKGROUND: Therapeutic hypothermia (TH) improves outcome after cardiac arrest, but may increase vasopressor and inotrope requirements. METHODS: Chart review of in- and out-of-hospital cardiac arrests between 1/1/2005 and 3/15/2010. Data included demographic information, category of post-cardiac arrest illness severity ((I) awake, (II) coma (not following commands but intact brainstem responses)+mild cardiopulmonary dysfunction (SOFA [Sequential Organ Failure Assessment] cardiac+respiratory score<4), (III) coma+moderate-severe cardiopulmonary dysfunction (SOFA cardiac+respiratory score≥4), and (IV) coma without brainstem reflexes), cumulative vasopressor index (CVI), inotrope use, survival, and neurologic outcome. The "dose" of TH (hours*temperature below threshold) was calculated using thresholds of ≤34°C and ≤35°C. Data were analyzed using descriptive statistics, Student's t-test, Wilcoxon test, and chi-squared analysis. Linear and logistic regression evaluated the effect of hypothermia "dose" on total CVI, survival and neurologic outcome. RESULTS: Among 361 comatose patients, 233 (65%) received TH. Vasopressor administration (measured by CVI) was higher in normothermic subjects (60.2% vs. 46.4%; p=0.016). Using a 34°C threshold, SOFA respiratory subscore and PEA arrest predicted total CVI. Using a 35°C threshold, severity of coma, SOFA respiratory subscore, PEA arrest and use of inotropic agents in addition to vasopressors predicted total CVI. Initial motor examination predicted survival and neurologic outcome, while TH "dose" did not. CONCLUSIONS: TH delivery is not associated with vasopressor requirement. TH "dose" is not associated with total CVI, survival, or good outcome. Vasopressor or inotropic requirement should not contraindicate TH use.

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    ABSTRACT: /st>Therapeutic hypothermia, used primarily for protective effects after hypoxia, improves oral and gastric mucosal microvascular oxygenation (μHbO2) during additional haemorrhage. Therefore, we questioned whether hypothermia likewise improves μHbO2 during hypoxic challenges. Since both hypothermia and hypoxia reduce cardiac output (e.g. by myofilament Ca(2)(+) desensitization), and modulate vasomotor tone via K(+)ATP channels, we hypothesized that the Ca(2+) sensitizer levosimendan and K(+)ATP channel blocker glibenclamide would support the cardiovascular system. /st>The effects of mild hypothermia (34°C) on μHbO2 during hypoxia were analysed in a cross-over study on five anaesthetized dogs and compared with normothermia (37.5°C) and hypoxia. During hypothermia, but before hypoxia, glibenclamide (0.2 mg kg(-1)) or levosimendan (20 µg kg(-1)+0.25 µg kg(-1) min(-1)) was administered. Systemic haemodynamic variables, gastric and oral mucosal microvascular oxygenation (reflectance spectrophotometry), and perfusion (laser Doppler flowmetry) were recorded continuously. Data are presented as mean (sem), P<0.05. /st>Hypoxia during normothermia reduced gastric μHbO2 by 27 (3)% and oral μHbO2 by 28 (3)% (absolute change). During hypothermia, this reduction was attenuated to 16 (3)% and 13 (1)% (absolute change). This effect was independent of microvascular flow that did not change during hypoxia and hypothermia. Additional administration of levosimendan during hypothermia restored reduced cardiac output but did not change flow or μHbO2 compared with hypothermia alone. Glibenclamide did not exert any additional effects during hypothermia. /st>Hypothermia attenuates the decrease in μHbO2 during additional hypoxic challenges independent of systemic or regional flow changes. A reduction in cardiac output during hypothermia is prevented by Ca(2)(+) sensitization with levosimendan but not by K(+)ATP channel blockade with glibenclamide.
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