Of ions and temperature: The complicated interplay of temperature, fluids, and electrolytes on myocardial function

This article discusses the potential of levosimendan to treat calcium-induced myocardial dysfunction associated with deep hypothermia. Moderate hypothermia (30 to 34°C) usually improves myocardial contractility and stabilizes heart rhythm, but deep hypothermia can cause severe myocardial dysfunction, which is mediated by intracellular calcium overload. In experimental studies, levosimendan appears effective in reversing this. Clinical studies are needed to confirm these findings and to determine whether levosimendan could also be used for accidental hypothermia and perhaps to mitigate diastolic dysfunction under moderate hypothermia. © 2013 BioMed Central Ltd

What is the right temperature to cool post-cardiac arrest patients?

Background: Brain ischemia and reperfusion injury leading to tissue degeneration and loss of neurological function following return of spontaneous circulation after cardiac arrest (CA) is a well-known entity. Two landmark trials in 2002 showed improved survival and neurological outcome of comatose survivors of out-of-hospital cardiac arrest (OHCA) of presumed cardiac origin when the patients were subjected to therapeutic hypothermia of 32 to 34°C for 12 to 24hours. However, the optimal target temperature for these cohorts is yet to be established and also it is not clear whether strict fever management and maintaining near normal body temperature are alone sufficient to improve the outcome. Methods: Objective: The objective is to determine whether a hypothermic goal of a near-normal body temperature of 36°C reduces all-cause mortality compared with a moderate hypothermia of 33°C for the unconscious survivors of OHCA of presumed cardiac origin when subjected randomly to these different targeted temperatures. Design: A multicenter, international, open label, randomized controlled trial. Setting: Thirty-six ICUs in Europe and Australia participated in this study. Participants: Unconscious adults (older than 18years of age) who survived (Glasgow coma scale less than 8) OHCA due to presumed cardiac origin with subsequent persistent return of spontaneous circulation (more than 20minutes without chest compressions). Intervention: The above participant cohorts were randomized to targeted body temperature of either 33°C or 36°C for 36hours after the CA with gradual rewarming of both groups to 37°C (hourly increments of 0.5°C) after the initial 28hours. Body temperatures in both the groups were then maintained below 37.5°C for 72hours after the initial 36hours. Outcomes: Primary outcome measure of all-cause mortality in both the groups at the end of the trial with the secondary outcome measure of all-cause mortality, composite neurological function as evaluated by cerebral performance category scale and modified ranking scale at the end of 180days were studied. Results: Out of the 939 participants, all-cause mortality at the end of the trial was 50% in the 33°C group (225 of 466 patients) compared with 48% in the 36°C group (235 of 473 patients); the hazard ratio with a temperature of 33°C was 1.06 (95% confidence interval (CI) 0.89 to 1.28, P = 0.51). At the end of 180days, 54% of patients in the 33°C group versus 52% in the 36°C group had died or had poor neurological outcome according to cerebral performance category (risk ratio 1.02, 95% CI 0.88 to 1.16, P = 0.78) but the modified ranking scale at the end of 180days was unchanged (52%) in both groups (risk ratio 1.01, 95% CI 0.89 to 1.14, P = 0.87). Conclusions: Maintaining targeted lower normothermia of 36°C had similar outcomes compared with induced moderate hypothermia of 33°C for unconscious survivors of OHCA of presumed cardiac cause

Simulation of propofol anaesthesia for intracranial decompression using brain hypothermia treatment

<p>Abstract</p> <p>Background</p> <p>Although propofol is commonly used for general anaesthesia of normothermic patients in clinical practice, little information is available in the literature regarding the use of propofol anaesthesia for intracranial decompression using brain hypothermia treatment. A novel propofol anaesthesia scheme is proposed that should promote such clinical application and improve understanding of the principles of using propofol anaesthesia for hypothermic intracranial decompression.</p> <p>Methods</p> <p>Theoretical analysis was carried out using a previously-developed integrative model of the thermoregulatory, hemodynamic and pharmacokinetic subsystems. Propofol kinetics is described using a framework similar to that of this model and combined with the thermoregulation subsystem through the pharmacodynamic relationship between the blood propofol concentration and the thermoregulatory threshold. A propofol anaesthesia scheme for hypothermic intracranial decompression was simulated using the integrative model.</p> <p>Results</p> <p>Compared to the empirical anaesthesia scheme, the proposed anaesthesia scheme can reduce the required propofol dosage by more than 18%.</p> <p>Conclusion</p> <p>The integrative model of the thermoregulatory, hemodynamic and pharmacokinetic subsystems is effective in analyzing the use of propofol anaesthesia for hypothermic intracranial decompression. This propofol infusion scheme appears to be more appropriate for clinical application than the empirical one.</p