M Sage, J Wales, J Cooper, I White
M Sage, J Wales, J Cooper, I White. Induced Hypothermia Following Cardiac Arrest And Subsequent Neurological Outcomes: An Audit. The Internet Journal of Neurology. 2010 Volume 13 Number 2.
It is estimated that there are 92 to 189 cases of cardiac arrest per 100,000 inhabitants in industrialised countries each year1,2,3 and 375,000 sudden cardiac arrests in Europe every year4 . Some 14% to 40% have a return of spontaneous circulation (ROSC) and are admitted to hospital and of those only 7% to 30% leave hospital to live an independent life5. Several studies have shown that the use of induced hypothermia can improve rates of survival and level of neurological function following a cardiac arrest5, 6, 7.
Aims and Objective
This audit was conducted to review the cases of cardiac arrest presenting to, or occurring in, St Peter’s Hospital in 2009-10 in order to assess the neurological outcomes of patients who were cooled on the ICU, and to determine whether therapeutic hypothermia should be implemented as standard care following cardiac arrest, or, if not, in which cases it would be most beneficial.
This audit has been based on the findings of two papers, both of which demonstrated a significant improvement in long term neurological outcomes for patients following induced hypothermia. Bernard et al6 studied 77 patients with out of hospital cardiac arrests who were each randomly assigned to care with normothermia or hypothermia (core body temperature reduced to 33°C within 2 hours of the return of spontaneous circulation and maintained at that temperature for 12 hours). Their primary outcome measure was survival to discharge with sufficiently good neurological function to be discharged home or to a rehabilitation facility. Death or discharge to a nursing facility, ie where there was little likelihood of neurological improvement, was considered a poor outcome. They demonstrated that treatment with moderate hypothermia improved outcomes in patients with coma after resuscitation from an out-of-hospital cardiac arrest. Some 49% of their patients treated with hypothermia were considered to have a ‘good’ outcome (ie discharged to home or rehabilitation facility) whilst only 26% of those in the normothermia group had the same outcome
Records were tracked from ICU admissions during 2009-10 using the coding reference for cardiac arrest. These notes were reviewed and the following was recorded: age, gender, location of arrest (in or out of hospital), initial heart rhythm, extent of CPR required, whether the patient was treated with induced hypothermia and how soon following arrest cooling commenced. Patient outcomes were recorded in terms of whether the patient was discharged to their home, a rehabilitation facility, a nursing home or died in hospital. All patients were cooled with the use of the Arctic Sun® 2000 temperature management system (Medivance).
There were 85 patients admitted to the ICU coded as having had a cardiac arrest during the study period. Nine sets of notes were unobtainable and two patients had been miscoded. Consequently 74 patients were eligible to be included in the audit. Of these 74 patients 47 (64%) were male and 27 (36%) female
When studying in and out of hospital arrests combined it is shown that patients who had a VF cardiac arrest and were cooled had a 62% rate of survival, and 58% rate of survival with good neurological outcome. If they had a VF cardiac arrest and were not cooled they had a 20% rate of survival with good neurological outcome.
At rest, the brain uses 20% of total body oxygen consumption in order to allow oxidative phosphorylation of glucose to ATP. Since the brain has a high metabolic rate but a lack of substrate storage (glucose) it is extremely sensitive to hypoxia. In order to protect the brain, autoregulation ensures that cerebral blood flow (CBF) is kept constant when the mean arterial pressure (MAP) is between 50-100 mmHg9. When the MAP drops below 50 mmHg, the CBF initially increases to compensate for hypoxia but in a cardiac arrest scenario this compensation mechanism cannot maintain adequate perfusion pressure and anoxic injury occurs. Damage occurs to neurones with reperfusion of the brain as transmembrane electrochemical gradients are disrupted. Intracellular glutamate levels increase during reperfusion, activating ion channel complexes, causing intracellular shift of calcium. This in turn causes reactive oxygen species to accumulate activating degradative enzymes which contribute to exocytotic cell death and cerebral injury10, 11, 12. Reperfusion injury occurs in two stages13. Initially there is injury at the time of reperfusion itself when reactive oxygen species are released. With current practice it is very difficult to ameliorate this with therapeutic hypothermia because reperfusion remains the priority. The second stage lasts hours to days and is related to transmembrane dysfunction as outlined above. This stage can be targeted by therapeutic hypothermia in its current form.
Induced hypothermia causes cerebral metabolic rate to drop by 7% for every 1°C fall in body temperature14. This reduces cellular metabolism and cerebral oxygen demand15 and confers protection by several other mechanisms; it reduces the production of free radicals16, improves cellular ion handling and pH balance17 and reduces the inflammatory signalling which leads to cell death18. Therapeutic hypothermia is currently advised by the Resuscitation Council (UK) following a cardiac arrest, although the new guidelines recognise the lower level of evidence for its use following a PEA or asystolic arrest19. Its use is contraindicated in severe systemic infection, pre-existing coagulopathy and multiple organ failure20.
This is not a randomised trial; rather it is an audit of practice and outcomes at a single district general hospital in England.
It is important to acknowledge that circumstances of the period before cooling is commenced can vary widely between patients. This audit did not correct for other variables such as time from arrest to commencement of CPR, or time to cooling or for co-morbidities. While all patients admitted were considered to potentially have a favourable outcome, the findings of this audit do not take account of why cooling was not implemented in certain patients. Co-morbidities or contraindications to cooling may have existed, which would have made a favourable outcome less likely regardless of whether or not induced hypothermia was instigated.
Conclusions and recommendations
It was shown that patients who suffer a VF cardiac arrest have a 62% rate of survival if subsequently treated with hypothermia at St Peter’s ICU. This varies only slightly whether the arrest was as an inpatient or out of hospital: 60% and 62% respectively. 92% of the survivors of out of hospital arrests and 100% of the survivors of in-patient VF arrests had a good neurological recovery. Those who are not cooled following a VF arrest have a 20% survival rate overall (25% for out-of-hospital arrests and 20% for inpatient arrests).
This audit was presented at a regional meeting of the Surrey Wide Critical Care Network and was contributory in influencing practice within all Intensive Care Units in this county. It was concluded that it was best practice to treat all patient transferred to ICU post-VF or VT arrest with therapeutic hypothermia.