Sudden cardiac death means that the heart and subsequently the circulation stops. Patients with a structural heart disease like coronary heart disease have a higher risk for sudden cardiac death. Around 30% to 50% of all patients with coronary heart disease suffer sudden cardiac death at some stage of their illness. In cardiac arrest the brain lacks blood and oxygen and the patient loses consciousness. After a few minutes of lack of oxygen brain cells begin to be irreversibly damaged. Although potentially lethal, if a patient in cardiac arrest is found and resuscitated early, they may be saved and brain damage prevented. To date about one tenth to a third of successfully resuscitated patients leave hospital to live an independent life again.
One form of therapy that may help to improve these neurologic deficits is called 'therapeutic hypothermia' or 'resuscitative hypothermia'. It is a form of therapy where patients that have been resuscitated after cardiac arrest and are still unconscious after resuscitation are cooled to 33 °C for several hours. Clinical trials have shown that with therapeutic hypothermia the neurologic damage caused by the cardiac arrest may be attenuated. Pathophysiologic studies discovered that therapeutic hypothermia works in many different ways. One way is that it lowers cell metabolism and prevents the production of harmful substances that form during resuscitation and continuously damage the brain cells. Hypothermia may be initiated by different methods like cold drips, cooling pads or cooling catheters.
We have summarized three randomized trials with conventional cooling methods on a total of 383 patients that evaluated the effects of therapeutic hypothermia in patients resuscitated after cardiac arrest in comparison to resuscitated patients treated without therapeutic hypothermia. With conventional cooling methods like cooling blankets or cooling helmets, patients were 55% more likely to leave the hospital without major brain damage. When the results of two additional studies (one study only published as an abstract and another comparing cooling through haemofiltration) were added, this effect remained unchanged. No cooling specific adverse events were reported. One of the limitations of our review is that the majority of patients had a specific form of cardiac arrest, with ventricular fibrillation and ventricular tachycardia as the underlying cardiac rhythm. In summary, there is current evidence supporting the use of conventional cooling to induce mild hypothermia in cardiac arrest survivors within the first hours of resuscitation.
Conventional cooling methods to induce mild therapeutic hypothermia seem to improve survival and neurologic outcome after cardiac arrest. Our review supports the current best medical practice as recommended by the International Resuscitation Guidelines.
Good neurologic outcome after cardiac arrest is hard to achieve. Interventions during the resuscitation phase and treatment within the first hours after the event are critical. Experimental evidence suggests that therapeutic hypothermia is beneficial, and a number of clinical studies on this subject have been published. This review was originally published in 2009.
We performed a systematic review and meta-analysis to assess the effectiveness of therapeutic hypothermia in patients after cardiac arrest. Neurologic outcome, survival and adverse events were our main outcomes. We aimed to perform individual patient data analysis, if data were available, and to form subgroups according to the cardiac arrest situation.
We searched the following databases: the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2001, Issue 7); MEDLINE (1971 to July 2011); EMBASE (1987 to July 2011); CINAHL (1988 to July 2011); PASCAL (2000 to July 2011); and BIOSIS (1989 to July 2011). The original search was performed in January 2007.
We included all randomized controlled trials assessing the effectiveness of therapeutic hypothermia in patients after cardiac arrest, without language restrictions. Studies were restricted to adult populations cooled with any cooling method, applied within six hours of cardiac arrest.
Validity measures, the intervention, outcomes and additional baseline variables were entered into a database. Meta-analysis was only done for a subset of comparable studies with negligible heterogeneity. For these studies, individual patient data were available.
We included four trials and one abstract reporting on 481 patients in the systematic review. The updated search resulted in no new studies to include. Quality of the included studies was good in three out of five studies. For the three comparable studies on conventional cooling methods all authors provided individual patient data. With conventional cooling methods, patients in the hypothermia group were more likely to reach a best cerebral performance categories (CPC) score of one or two (five point scale: 1 = good cerebral performance, to 5 = brain death) during the hospital stay (individual patient data; RR 1.55; 95% CI 1.22 to 1.96) and were more likely to survive to hospital discharge (individual patient data; RR 1.35; 95% CI 1.10 to 1.65) compared to standard post-resuscitation care. Across all studies, there was no significant difference in reported adverse events between hypothermia and control.