The effect of hypothermia "dose" on vasopressor requirements and outcome after cardiac arrest.
ABSTRACT 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.
- [show abstract] [hide abstract]
ABSTRACT: Hospital mortality was examined in all patients successfully resuscitated from a witnessed out-of-hospital cardiac arrest due to ventricular fibrillation over a 1-yr period. Variables independently predictive of hospital mortality were a history of congestive heart failure before cardiac arrest, the time between collapse and initiation of CPR, and the time between collapse and restoration of circulation. The latter time was not related to either patient age or clinical history. Thus, hospital mortality was predetermined by prehospital factors, some of which can be changed.Critical Care Medicine 12/1985; 13(11):927-9. · 6.12 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: This study investigated the effect of prolonged cardiac arrest and subsequent cardiopulmonary resuscitation on left ventricular systolic and diastolic function. Cardiac arrest from ventricular fibrillation results in cessation of forward blood flow, including myocardial blood flow. During cardiopulmonary resuscitation, myocardial blood flow remains suboptimal. Once the heart is defibrillated and successful resuscitation achieved, reversible myocardial dysfunction, or "stunning," may occur. The magnitude and time course of myocardial stunning from cardiac arrest is unknown. Twenty-eight domestic swine (26 +/- 1 kg) were studied with both invasive and noninvasive measurements of ventricular function before and after 10 or 15 min of untreated cardiac arrest. Contrast left ventriculograms, ventricular pressures, cardiac output, isovolumetric relaxation time (tau) and transthoracic Doppler-echocardiographic studies were obtained. Twenty-three of 28 animals were successfully resuscitated and postresuscitation data obtained. Left ventricular ejection fraction showed a significant reduction 30 min after resuscitation (p < 0.05). Regional wall motion analysis revealed diffuse, global left ventricular systolic dysfunction. Left ventricular end-diastolic pressure increased significantly in the postresuscitation period (p < 0.05). Isovolumetric relaxation time (tau) was significantly increased over baseline by 2 h after resuscitation (p < 0.05). Similar findings were noted with the Doppler-echocardiographic analysis, including a reduction in fractional shortening (p < 0.05), a reduction in mitral valve deceleration time (p < 0.05) and an increase in left ventricular isovolumetric relaxation time at 5 h after resuscitation (p < 0.05> By 24 h, these invasive and noninvasive variables of systolic and diastolic left ventricular function had begun to improve. At 48 h, all measures of left ventricular function had returned to baseline levels. Myocardial systolic and diastolic dysfunction is severe after 10 to 15 min of untreated cardiac arrest and successful resuscitation. Full recovery of this postresuscitation myocardial stunning is seen by 48 h in this experimental model of ventricular fibrillation cardiac arrest.Journal of the American College of Cardiology 08/1996; 28(1):232-40. · 14.09 Impact Factor
- Intensive Care Medicine 08/1996; 22(7):707-10. · 5.26 Impact Factor