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Thermoregulation constitutes one of the most important homeostatic systems of the human body. The human thermoregulatory system is highly complex and intertwined with other regulatory homeostatic systems. Different evolutionary adaptations have evolved to ensure a well-regulated body temperature, encompassing simple behavioural (e.g., seeking shelter, going underground) as well as physiological changes (e.g., vasodilatation, sweating). However, when the heat, cold or other stimuli cause a disruption in the thermoregulatory state and our adaptations can no longer cope with the additional stress, the body enters a pathological state. In such instances other measures must be undertaken. In medicine there are several pathological states associated with disruptions in temperature homeostasis. Consequently, these patients have to be, in broad terms, thermoregulated. Speaking specifically, the most common application of thermoregulation is therapeutic temperature management. A prominent example is the utilisation of this technique in post-cardiac arrest patients, who remain comatose after resuscitation. This technique has been in use for almost 20 years since the first major reports on its benefits in improving out-of-hospital cardiac arrest and in-hospital cardiac arrest survival as well as improving neurological outcome. Recently, the findings from one of the biggest targeted temperature international and multicentre trials to date have been published (TTM2 trial; https://ttm2trial.org/). The study surprisingly showed no difference in mortality between patients after out of hospital cardiac arrest, who underwent normo- or hypothermia. Consequently, we might need to re-evaluate certain guidelines, recommendations, and perspectives. The aim of the current review is to present an overview of targeted temperature management in the field of intensive care medicine and cardiac arrest.

Background. Treatment of combined beta blocker and calcium channel blocker intoxication remains challenging due to a profound and treatment-resistant circulatory collapse. Along with standard therapy (calcium, glucagon, mechanical ventilation, vasopressors), two novel approaches are increasingly being reported as successful: hyperinsulinemic euglycemia and intravenous lipid emulsion. Case Report. Our patient: a 66-year-old Caucasian male who ingested approximately 450 mg of bisoprolol, 300 mg of amlodipine, 200 mg of doxazosin and smaller amounts of nifedipine, torasemide, acetysaliclic acid and ibuprofen in a suicide attempt. The patient was hypotensive and bradycardic on admission with left-ventricular ejection fraction estimated at 10-15%. By combining standard therapy (intubation, mechanical ventilation, vasopressors, calcium and glucagon) and new therapies (hyperinsulinemic euglycemia and intravenous lipid emulsions) in a stepwise approach we normalized systolic function and treated bradycardia within 2 hours of admission. However, severe hypotension persisted requiring extremely high doses of norepinephrine (14 mcg/kg/min) and vasopressin (0.03 U/min) to maintain his blood pressure over the following three days. He was discharged home after prolonged in-hospital treatment and rehabilitation (62 days) and extensive physical and psychiatric rehabilitation. Why should an emergency physician be aware of this? Aggressive medical therapy including hyperinsulinemic euglycemia, intravenous lipid emulsions and high doses of norepinephrine could be considered for multidrug intoxication with a predominant clinical picture of beta blocker and calcium channel blocker intoxication in patients presenting with severe hemodynamic compromise.

Objectives. To evaluate independent predictors of 30-day mortality in patients with severe sepsis or septic shock. Background. Severe sepsis and septic shock are associated with increased mortality. Admission APACHE II score is the gold standard for assessing prognosis in critically ill, but several other predictors of mortality have been evaluated. Methods. We retrospectively evaluated clinical and laboratory data in adult patients with severe sepsis or septic shock as predictors of 30-day mortality. Results. Thirty-day mortality was 62.7%. Nonsurvivors in comparison to survivors were significantly more likely to be trea-ted with noradrenalin, renal replacement therapy, mechanically ventilated, to have suffered a fungal infection, had lower admission arterial pH, increased admission Acute Physiology, Age, Chronic Health Evaluation (APACHE) II score and a higher peak lactate level (5.6 ± 6.2 vs 3.1 ± 1.75, p=0.021). Binary logistic regression demonstrated that only peak in-hospital serum lactate level was a significant independent predictor of 30-day mortality (OR 1.367, 95% CI 1.041 to 1.795, p=0.025). Conclusion. Only peak in-hospital lactate significantly and independently predicts 30-day mortality in severe sepsis or septic shock medical patients.