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  • Meeting abstract
  • Open Access

Hypothermia in cardiogenic shock

  • 1
Critical Care201216 (Suppl 2) :A21

  • Published:


  • Infarct Size
  • Metabolic Acidosis
  • Papillary Muscle
  • Cardiogenic Shock
  • Filling Pressure

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 [14]. 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 [57]. 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 [1619].

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

Authors’ Affiliations

Department of Cardiology, Lund University, Skane University Hospital, Sweden


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