Abstract
Avalanche patients who are completely buried but still able to breathe are exposed to hypothermia, hypoxia, and hypercapnia
(triple H syndrome). Little is known about how these pathological changes affect brain physiology. The study aim was to investigate
the effect of hypothermia, hypoxia, and hypercapnia on brain oxygenation and systemic and cerebral hemodynamics.
Anesthetized pigs were surface cooled to 28C. Fraction of inspiratory oxygen (FIO2 ) was reduced to 17% and hypercapnia
induced. Hemodynamic parameters and blood gas values were monitored. Cerebral measurements included cerebral perfusion
pressure (CPP), brain tissue oxygen tension (PbtO2 ), cerebral venous oxygen saturation (ScvO2 ), and regional cerebral oxygen saturation
(rSO2). Tests were interrupted when hemodynamic instability occurred or 60 min after hypercapnia induction. ANOVA for
repeated measures was used to compare values across phases. There was no clinically relevant reduction in cerebral oxygenation
(PbtO2 , ScvO2, rSO2) during hypothermia and initial FIO2 reduction. Hypercapnia was associated with an increase in pulmonary
resistance followed by a decrease in cardiac output and CPP, resulting in hemodynamic instability and cerebral
desaturation (decrease in PbtO2 , ScvO2, rSO2). Hypercapnia may be the main cause of cardiovascular instability, which seems to
be the major trigger for a decrease in cerebral oxygenation in triple H syndrome despite severe hypothermia.