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Cooling after successful resuscitation in cardiac surgery patients
© Vollroth et al.; licensee BioMed Central Ltd. 2013
Received: 5 November 2012
Accepted: 12 September 2013
Published: 23 September 2013
Despite many years of intensive research sudden cardiac death is one of the most common causes of death all over the world. The European Resuscitation Council (ERC) recommends the use of moderate therapeutic hypothermia for 12–24 hours to improve neurological outcome. However, the beneficial effect of this therapy on outcomes for cardiac surgery patients with In- Hospital- Resuscitation (IHR) has not been well studied.
The purpose of this single center analysis was to investigate our first experience in a non – selected IHR population, where hypothermia was induced independent from initial heart rhythm disturbance.
A total of 20 resuscitated patients who were treated in our institution between January 2010 and December 2011 formed the study cohort.
In all patients post- resuscitation course was significantly prolonged with severe low cardiac output syndrome in six patients (30%). Overall four patients (20%) sustained septicemia with the need for high dose inotropic support. The 30 day mortality was 30% (six of twenty). However, stroke with severe neurological impairment appeared in only four patients (20%) after resuscitation with subsequent therapeutic hypothermia.
With our observation study we could demonstrate the benefits for neurological outcome due to therapeutic hypothermia in cardiac surgery patients after successful resuscitation. However post- resuscitation treatment should focus on sufficient therapeutic strategies to avoid the distinctive short term morbidity and mortality.
Despite many years of intensive research, sudden cardiac death is one of the most common causes of death in the United States and Europe . The European Resuscitation Council (ERC) and the International Liaison Committee on Resuscitation (ILCOR) recommend the use of moderate therapeutic hypothermia for 12–24 hours to improve neurological outcome in patients who survive Out- Of- Hospital Resuscitation (OHR) due to ventricular fibrillation. Based on two randomized trials and one meta-analysis, survivors of OHR have been treated with hypothermia in several European centers since 2003 [2, 3]. However, the beneficial effect of this therapy for other heart rhythm disorders and for patients who survived In- Hospital Resuscitation (IHR) has not been well studied. In 2005 the ERC issued the edition of guidelines for resuscitation included an explicit section on the resuscitation concept for cardiac surgery patients after cardiac surgery . This paper encouraged many clinicians in cardiac surgery centers to evaluate their patients more carefully for therapeutic hypothermia after resuscitation.
The purpose of our single center analysis was to investigate our first experience in a non – selected post cardiac surgery patient population, where hypothermia was induced independent from initial heart rhythm disturbance.
All heart rhythm disorders (ventricular fibrillation, pulse less electrical activity, and asystole)
Age: 18–80 years
An interval of maximum 60 min from collapse to return of spontaneous circulation
Stable hemodynamic parameters with moderate inotropic support
Response of verbal commandos after successful resuscitation
Age: ≤18 and ≥ 80 years
An interval of more than 60 minutes of resuscitation
Highly inotropic support
Terminal illness that preceded the arrest
Preoperative characteristics of all 20 hypothermia treated patients
70 ± 11.6
Reason for CPR: ASY/VF
40 % (8)/60% (12)
29 ± 3.2
3.1 ± 0.6
48.8 ± 17
1.7 ± 1.4
History of stroke
Indication for cardiac surgery and perioperative data of all 20 patients undergoing hypothermia after IHR
Duration of surgery
219.9 ± 84.7 min
Duration of CPB
97.3 ± 85.5 min
Aortic clamp time
60.4 ± 49.4 min
In accordance to the above defined criteria in 8 patients (40%) asystole was the reason for resuscitation and subsequent hypothermia. Ventricular fibrillation causes cardiac arrest in 12 patients (60%). In all patients hypothermia was applied as soon as feasible by intravascular cooling with the COOLGARD 3000 Thermal Regulation System (Zoll Intravascular temperature management, Chelmsford, MA, USA). The patients were cooled down to a target body core temperature of 32–33°C.
Our goal was to reach the target temperature within 2 hours after successful resuscitation. Therapeutic hypothermia was maintained for 24 hours and the patients were then re- warmed with a rate of 0.35°C/ h to a target temperature of 37°C. After re- warming sedation was stopped to evaluate neurological status.
Intensive care treatment was in relation to international ICU standards. All patients were deeply sedated by intravenous administration of methohexital or midazolam and sufentanyl. When clinically appropriate, the patients received neuromuscular blocker intravenously using pancoronium.
Follow-up was 100% completed. Data included patient’s demographics, indication for surgery and early outcome (30 days). The resuscitation and hypothermia data were registered in standardized protocols. Continuous variables are expressed as means ± standard deviations throughout the manuscript.
Between 2010 and 2011 a total of 20 patients underwent therapeutic hypothermia after IHR. In twelve patients (60%) ventricular fibrillation caused cardiac arrest with subsequent resuscitation, whereas asystole was causal in eight patients (40%). In all patients post- resuscitation course was significantly prolonged and included low cardiac output syndrome in six patients (30%). Acute renal failure was observed in nine patients (45%). Respiratory failure with the need for tracheotomy occurred in 10 patients (50%). Stroke with severe neurological impairment appeared in only four patients (20%) after therapeutic hypothermia. Overall four patients (20%) sustained septicemia with the need for high inotropic support. In five patients (25%) gastro- intestinal bleeding prolonged the post- resuscitation progress.
Postoperative course and short-term mortality
30 day mortality
Low cardiac output
Postop myocardial infarction
Acute renal failure
We herein report our first single center results of in- hospital resuscitated patients treated with therapeutic hypothermia after previous cardiac surgery. Due to post- resuscitation brain damage as the leading cause of death, the prognosis and patients neurological outcome remains often poor. Two prospective randomized trials and various retrospective analysis supported that therapeutic hypothermia after ventricular fibrillation cardiac arrest improves neurologic outcome [1, 2, 5]. Nevertheless, this therapeutic benefit has not been finally demonstrated in patients with return of circulation from non- shockable rhythms and in patients after in- hospital resuscitation . In our study we observed patients after previous cardiac surgery resuscitated from cardiac arrest due to shockable and non- shockable arrhythmia who were treated with therapeutic hypothermia to a body core temperature between 32 and 33°C for a period of 24 hours.
Our results demonstrate that IHR in cardiac surgery patients lead to severe peri- and post morbidities. However, in order to previously published data we could demonstrate a significant improvement in neurological outcome [7, 8]. Stroke with severe neurological impairment was diagnosed in only four patients after successful resuscitation with subsequent hypothermia. Due to previous cardiac surgery, low- cardiac- output syndrome with subsequent multi organ failure causes death in all deceased patients. With our study we could underline the benefits for neurological outcome due to therapeutic hypothermia independently from initial arrhythmia. However, hemodynamic and respiratory failure seems to be more challenging after IHR in cardiac surgery patients.
The use of therapeutic hypothermia in resuscitated cardiac- surgery patients is associated with improved neurologic outcome independently from initial heart rhythm disturbance. However, post resuscitation care should focus on sufficient cardio- pulmonary treatment strategies to avoid the distinctive short term mortality.
Written consent was obtained from the patients for publication of this report.
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