Hypothermia in cardiogenic shock

Cardiogenic shock is a state of inadequate systemic tissue perfusion, despite adequate left ventricular filling pressure. It is caused by extensive myocardial damage and appears to be aggravated by a systemic inflammatory response [1–4]. The result is hypotension with metabolic acidosis and often a fatal outcome. The condition affects approximately 5% of the patients with myocardial infarction, and carries a dismal prognosis if it prevails after reperfusion.

Therapeutic hypothermia has several properties of potential benefit in cardiogenic shock: Experiments with isolated myofibrils, papillary muscles and cross-circulated hearts have demonstrated that mild hypothermia increases myocardial contractility [5–7]. In the in vivo heart, mild hypothermia has been found to increase stroke volume and cardiac output [6, 8].

The increase in contractility is considered to be mediated by an increased myofilament sensitivity to existing Ca²⁺, without a corresponding increase in myocardial oxygen consumption [9]. Moreover, hypothermia reduces the metabolic rate with 5 to 7%/°C [10, 11], thereby reducing the demand on the circulation from the peripheral tissues. In an experimental setting, it also has the ability to reduce infarct size if applied prior to reperfusion [12, 13].

In dog-based and porcine-based models of cardiogenic shock secondary to ischemia, therapeutic hypothermia has improved hemodynamic and metabolic parameters, and reduced mortality [14, 15]. No randomized controlled trials of therapeutic hypothermia in cardiogenic shock in humans exist, but case series indicate that the effects observed in animal experiments can be reproduced [16–19].

In conclusion, therapeutic hypothermia is a promising treatment option for patients in cardiogenic shock that warrants further investigation.