Neurological injury after cardiac arrest – setting a case of prolonged re-warming into a developing research context

Hypothermia is both a reversible precipitant of cardiac arrest and a well-established neuroprotective mechanism. In 1975, Greipp et al. demonstrated induced hypothermia to be a safe, reproducible therapy to support complex cardiac and neurological surgery without cardiopulmonary bypass [1]. National Institute for Health and Care Excellence (NICE) guidance currently supports an active cooling strategy for comatose survivors of cardiac arrest, both in and out of the hospital, to maintain a core body temperature of 32–34 °C for 12–24 h after cardiac arrest to minimise brain injury [2]. However, if accidental hypothermia has precipitated a cardiac arrest, active rewarming will instead be required to restore circulation. In this issue of Anaesthesia Reports, Grewal and Thomas describe a case of prolonged cardiac arrest in a patient with accidental hypothermia who achieved a good neurological outcome with active re-warming [3]. In this accompanying editorial, we consider the current evidence for temperature control interventions in the context of cardiac arrest. Oxygen delivery and demand imbalance results in varying degrees of hypoxic tissue injury. A temperature reduction of 10 °C can reduce neurological oxygen demand by 50–75% [4]. Therefore, a subsequent reduction in blood flow (and oxygen delivery)may be similarly toleratedwithminimal tissue damage. Survival rates following cardiac arrest have remained largely unchanged in the last decade despite best efforts with a considerable proportion of patients succumbing to secondary brain injury as opposed to the original primary cardiac insult [5, 6]. As a result, interest in employing the protective effects of hypothermia developed, in an attempt to prolong the safe ischaemic time of the brain during cardiac arrest. This interest was further fuelled by numerous case reports involving patients submerged in icy water, buried in avalanches or trapped in crevasses. These patients achieved good neurological outcomes after slow rewarming despite prolonged arrest times [7–9]. Grewal and Thomas’ case describes a rare example of this phenomenon in an urban setting [3]. During cardiac arrest, there is a sudden, massive drop in oxygen delivery. To avoid or minimise hypoxic tissue damage, increased delivery or reduced demand is required. Conventional cardiopulmonary resuscitation, comprising chest compressions and artificial ventilation, aims to maintain oxygen delivery. However, manual chest compressions produce, at best, only 20–30% of the usual cardiac output [10]. Mechanical compression devices, such as the Lund University Cardiopulmonary Assist System (LUCAS , Stryker Medical, Portage, USA), represent a major recent advancement in cardiac arrest management. They provide consistent high-quality chest compressions for prolonged periods, as demonstrated in Grewal and Thomas’ case [3]. Additionally, they can be applied in transit, improving the safety of transfers to specialist intervention centres such as those providing primary percutaneous coronary intervention (PPCI) or extracorporeal membrane oxygenation (ECMO).