Therapeutic hypothermia after cardiac arrest

PURPOSE OF REVIEW: Patients who are successfully resuscitated following cardiac arrest often have a significant medical condition termed postresuscitation disease. This includes myocardial stunning, metabolic abnormalities and neurologic injury from global ischemia. There are no clinical signs or diagnostic tests for 24-72 h to distinguish patients who will and will not recover neurologic function. RECENT FINDINGS: Therapeutic hypothermia had been advocated for decades as a treatment to improve neurologic outcome after cardiac arrest. The early studies focused on moderate hypothermia, which was associated with complications and was not clearly beneficial. Over the past decade, studies have focused on mild hypothermia with target temperatures of 32-34 degrees C. Two recent multicentered, randomized, controlled trials have demonstrated improved neurologic outcome with mild therapeutic hypothermia applied to comatose survivors after cardiac arrest compared with a normothermic control group. SUMMARY: As a result of these studies the International Liaison Committee on Resuscitation recommends that 'Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32 degrees C to 34 degrees C for 12 to 24 hours when the initial rhythm was ventricular fibrillation'. Mild therapeutic hypothermia should also be considered for patients with in-hospital arrest and asystole and pulseless electrical activity who are comatose after return of spontaneous circulation.     

Therapeutic hypothermia after cardiac arrest

OVERVIEW: Irreversible brain damage and death are common outcomes after cardiac arrest, even when resuscitation is initially successful. Chances for both survival and a good neurologic outcome are improved when mild hypothermia is induced shortly after reperfusion. Unfortunately, this treatment is often omitted from advanced cardiac life support protocols. The authors discuss the efficacy of therapeutic hypothermia, indications and contraindications for its use, various induction methods, associated complications and adverse effects, and nursing care specific to patients undergoing this procedure.     

Therapeutic hypothermia after cardiac arrest.

Recent evidence supports the use of therapeutic hypothermia after cardiac arrest. This article reviews recent published studies and describes the pathophysiology of hypothermia. Nurses need to understand the physiology of hypothermia to provide care for patients receiving therapeutic hypothermia. A suggested protocol is included to help manage the care of these patients.     

Influence of mild therapeutic hypothermia on the inflammatory response after successful resuscitation from cardiac arrest

Purpose

Although animal studies document conflicting data on the influence of hypothermia on cytokine release in various settings, no data exist if hypothermia affects the inflammatory response after successful cardiopulmonary resuscitation.

Materials and Methods

Arrest- and treatment-related variables of 71 patients were documented, and serum samples were analyzed for levels of interleukin 6, tumor necrosis factor-α, C-reactive protein, and procalcitonin immediately after hospital admission and after 6, 24, and 120 hours. At day 14, patients were dichotomized in those with good and bad neurological outcome.

Results

Regardless of outcomes, interleukin 6 levels were significantly elevated by the use of hypothermia (n = 39). The rate of bacterial colonization was significantly higher in hypothermic patients (64.1 vs 12.5 %; P < .001). On the contrary, procalcitonin levels were, independent of the use of hypothermia, only significantly elevated in patients with bad neurological outcome. Hypothermic patients showed a strong trend to reduced mortality. However, there was no influence on neurological recovery.

Conclusions

In this observational study, hypothermia influenced the inflammatory response after cardiopulmonary resuscitation and lead to a higher rate of bacterial colonization without altering ultimate neurologic recovery.     

Therapeutic hypothermia and vasopressor dependency after cardiac arrest

Objective

Clinical trials of therapeutic hypothermia (TH) after cardiac arrest excluded patients with persistent hemodynamic instability after return of spontaneous circulation (ROSC), and thus equipoise may exist regarding use of TH in these patients. Our objective was to determine if TH is associated with worsening hemodynamic instability among patients who are vasopressor-dependent after ROSC.

Methods

We performed a prospective observational study in vasopressor-dependent post-cardiac arrest patients. Inclusion criteria were age >17, non-trauma cardiac arrest, comatose after ROSC, and persistent vasopressor dependence. The decision to initiate TH (33–34 °C) was made by the treating physician. We measured cumulative vasopressor index (CVI) and mean arterial pressure (MAP) every 15 min during the first 6 h after ROSC. The outcome measures were change in CVI (primary outcome) and MAP (secondary outcome) over time. We graphed median CVI and MAP over time for the treated and not treated cohorts, and used propensity adjusted repeated measures mixed models to test for an association between TH induction and change in CVI or MAP over time.

Results

Seventy-five post-cardiac arrest patients were included (35 treated; 40 not treated). We observed no major differences in CVI or MAP over time between the treated and not treated cohorts. In the mixed models we found no statistically significant association between TH induction and changes in CVI or MAP.

Conclusion

In patients with vasopressor-dependency after cardiac arrest, the induction of hypothermia was not associated with a decrease in mean arterial pressure or increase in vasopressor requirement.     

Clinical application of mild therapeutic hypothermia after cardiac arrest

OBJECTIVE: Postresuscitative mild hypothermia lowers mortality, reduces neurologic impairment after cardiac arrest, and is recommended by the International Liaison Committee on Resuscitation. The European Resuscitation Council Hypothermia After Cardiac Arrest Registry was founded to monitor implementation of therapeutic hypothermia, to observe feasibility of adherence to the guidelines, and to document the effects of hypothermic treatment in terms of complications and outcome. DESIGN: Cardiac arrest protocols, according to Utstein style, with additional protocols on cooling and rewarming procedures and possible adverse events are documented. SETTING: Between March 2003 and June 2005, data on 650 patients from 19 sites within Europe were entered. PATIENTS: Patients who had cardiac arrest with successful restoration of spontaneous circulation were studied. MEASUREMENTS AND MAIN RESULTS: Of all patients, 462 (79%) received therapeutic hypothermia, 347 (59%) were cooled with an endovascular device, and 114 (19%) received other cooling methods such as ice packs, cooling blankets, and cold fluids. The median cooling rate was 1.1 degrees C per hour. Of all hypothermia patients, 15 (3%) had an episode of hemorrhage and 28 patients (6%) had at least one episode of arrhythmia within 7 days after cooling. There were no fatalities as a result of cooling. CONCLUSIONS: Therapeutic hypothermia is feasible and can be used safely and effectively outside a randomized clinical trial. The rate of adverse events was lower and the cooling rate was faster than in clinical trials published.     

Long-term neurological outcome after cardiac arrest and therapeutic hypothermia

Aim of the studyTo analyse the neurological status of survivors after cardiac arrest (CA) treated with hypothermia.MethodsWe prospectively included all patients with CA treated with hypothermia at intensive care units (ICU) in two university hospitals and one regional hospital. All adult survivors at 6 months after CA, n = 48, were invited for neurological follow-up and 43 accepted. History, clinical status, ability testing and questionnaires were administered to screen for difficulties, including Assessment of Motor and Process Skills, Neurobehavioral Cognitive Status Examination, Frontal Lobe Assessment Battery, EQ-VAS quality of life scale, Skåne Sleep Index, Hospital Anxiety and Depression Rating Scale, Self-reported Montgomery and Åstrand Depression Rating Scale, Global Deterioration Scale, Rivermead Behavioural Memory Test, and the Cerebral Performance Categories (CPC).ResultsNo patient was found to be in a chronic vegetative state and all patients were living at home, one with extensive help. Thirty-six patients were in CPC1 at follow-up, and some degree of neurological sequelae was found in 40 patients, but was mild in all but 3. Three patients had no subjective complaints, nor could any deficits be detected. Initial defects improved over-time. Short-term memory loss, executive frontal lobe dysfunction along with mild depression and sleep rhythm disturbances were the most common findings.ConclusionsMild cognitive impairment is common following hypothermia-treated cardiac arrest but has little effect on activities of daily living or quality of life.     

Mild induced hypothermia and survival after out-of-hospital cardiac arrest

Background

Mild induced hypothermia (MIH) was introduced for post cardiac arrest care in Sweden in 2003, based on two clinical trials. This retrospective study evaluated its association with 30-day survival after out-of-hospital cardiac arrest (OHCA) in a Swedish community from 2003 to 2015.