This paper provides an up-to-date review of the management and outcome of accidental hypothermia patients with and without cardiac arrest. The authors reviewed the relevant literature in their specialist field. Summaries were merged, discussed and approved to produce this narrative review. The hospital use of minimally-invasive rewarming for non-arrested, otherwise healthy, patients with primary hypothermia and stable vital signs has the potential to substantially decrease morbidity and mortality for these patients. Extracorporeal life support (ECLS) has revolutionised the management of hypothermic cardiac arrest, with survival rates approaching 100 % in some cases. Hypothermic patients with risk factors for imminent cardiac arrest (temperature <28 °C, ventricular arrhythmia, systolic blood pressure <90 mmHg), and those who have already arrested, should be transferred directly to an ECLS-centre. Cardiac arrest patients should receive continuous cardiopulmonary resuscitation (CPR) during transfer. If prolonged transport is required or terrain is difficult, mechanical CPR can be helpful. Delayed or intermittent CPR may be appropriate in hypothermic arrest when continuous CPR is impossible. Modern post-resuscitation care should be implemented following hypothermic arrest. Structured protocols should be in place to optimise pre-hospital triage, transport and treatment as well as in-hospital management, including detailed criteria and protocols for the use of ECLS and post-resuscitation care. Based on new evidence, additional clinical experience and clearer management guidelines and documentation, the treatment of accidental hypothermia has been refined. ECLS has substantially improved survival and is the treatment of choice in the patient with unstable circulation or cardiac arrest.

Background. A silent polymorphism (+1166 A/C single-nucleotide polymorphism) localized in the 3′-UTR (untranslated region) of the human angiotensin II type-1 r

RGS2 (regulators of G-protein signaling) is a negative regulator of Galphaq protein signaling, which mediates the action of several vasoconstrictors. RGS2-deficient mouse line exhibits a hypertensive phenotype and a prolonged response to vasoconstrictors. To compare RGS2 expression in peripheral blood mononuclear cells (PBMs) and cultured fibroblasts from normotensive subjects and hypertensive patients. PBMs were isolated from 100 controls and 150 essential hypertensives. Additionally, fibroblasts were isolated from skin biopsy of 11 normotensives and 12 hypertensives and cultured up to the third passage. Quantitative mRNA and protein RGS2 expression were performed by real-time quantitative reverse transcriptase-polymerase chain reaction and by immunoblotting, respectively. Free Ca measurement was performed in monolayers of 24-h serum-deprived cells, using FURA-2 AM. Phosphorylation of the extracellular signal-regulated kinases ERK1/2 was measured by immunoblotting. Polymorphism (C1114G) in the 3' untranslated region of the RGS2 gene was investigated by direct sequencing and real-time polymerase chain reaction (PCR). RGS2 mRNA expression was significantly lower in PBM and in fibroblasts from hypertensives, in comparison to normotensives. C1114G polymorphism was associated with RGS2 expression, with the lowest values in GG hypertensives. The 1114G allele frequency was increased in hypertensives compared with normotensives. Angiotensin II-stimulated intracellular Ca increase and ERK1/2 phosphorylation were higher in fibroblasts from hypertensive patients compared with control subjects, and in those with the G allele, independently of the blood pressure status. The angiotensin II-stimulated Ca mobilization and ERK1/2 phosphorylation were negatively correlated with RGS2 mRNA expression. Low expression of RGS2 contributes to increased G-protein-coupled signaling in hypertensive patients. The allele G is associated with low RGS2 expression and blood pressure increase in humans.