Cooling the body presumably also reduces overall metabolic workload and demand on the heart. There seems to be a direct cardioprotective effect as well. Following reperfusion, the acidic pH caused by tissue ischemia is rapidly corrected, and the Na+/Ca++ pump is activated, causing a rapid influx of calcium into the cells, which causes irreversible cell damage and myocardial stunning.²³ One animal study found that hypothermia reduced myocardial injury by preventing intracellular Ca++ overload at reperfusion via inhibition of the Na+/Ca++ exchanger.²³ Another animal study found hypothermia significantly improved immediate myocardial salvage and long-term left ventricular remodeling after infarct reperfusion.²⁴

CRITICAL DECISION

Who should get therapeutic hypothermia?

Traditionally, cooling has been restricted to victims of ventricular fibrillation cardiac arrest, and this was reflected in both the 2005 and 2010 guidelines from the European Resuscitation Council (ERC) and the American Heart Association (AHA). Increasingly, however, cooling is being successfully applied to other rhythms. Bernard reports a 7% to 17% favorable outcome at hospital discharge for asystole or pulseless electrical activity (PEA) depending on when and where the cooling took place, while Testori reports an odds ratio of 1.84 for good neurologic outcome when these patients were cooled.^25,26 This appears to be especially true when the time interval from collapse to return of spontaneous circulation is brief.²⁷

Given that the prognosis is so poor after cardiac arrest, it is reasonable to attempt hypothermia on all adult patients with cardiac arrest, regardless of presenting rhythm.

CRITICAL DECISION

When should induction of therapeutic hypothermia begin?

The current recommendation for cooling is that it begin after return of spontaneous circulation, but the ideal timing of induction has not yet been clearly established. Results of some animal studies have suggested that the earlier therapeutic hypothermia is instituted the better, and that delayed hypothermia might have no benefit, a finding that is supported in at least one recent clinical trial.^25,28,29

CRITICAL DECISION

What methods can be used to induce therapeutic hypothermia?

The best method of therapeutic hypothermia has not been determined, and none is endorsed by the AHA or the ERC.^2,30 Ice-cold intravenous infusions, ice packs, cooling blankets, noninvasive surface cooling devices, and endovascular cooling have all been used.^{2,8-11,17-19,30,31} The location of cooling and the expense or complexity of the equipment ultimately will dictate what method is used. If cooling is initiated in the field, ice packs and cold saline are the simplest and least expensive. In a monitored environment, endovascular cooling at a rate of 1.1°C (2°F) per hour provides more precise control and may prevent the overshoot sometimes seen with surface cooling, but whether this affects outcome is unknown.^30,32,33

CRITICAL DECISION

How should therapeutic hypothermia be maintained?