Heat stress : characteristics, pathophysiology and avoidable mistakes

In August 2003 an exceptional heatwave was recorded in Europe. The authors would like to describe 6 patients for which the intensivist was called as a consultant. All patients had a skin temperature >40 degrees C, central nervous system impairment, severe hyponatremia [124.7 mEq/l+/-5.6 (range 117-130)] and severe metabolic acidosis [BE -6.28 mEq/l+/-3.55 (range -9.5-0), HCO3- 17.75 mEq/l+/-3.25 (range 13.4-21.9)]. All patients had decreased platelet count and coagulation abnormalities. Two patients were hypertensive, 4 hypotensive. The heat stress due to the hot environment is characterized by systemic inflammatory response (as in severe sepsis) and hemodynamic impairment (as in hypovolemic shock). The association between hypovolemia and altered microcirculation leads to cell energy failure with metabolic lactic acidosis. The energy failure may induce structural irreversible damage of mitochondria. It is possible to differentiate, during energy failure, the irreversible or reversible condition by volume loading and vasoactive drugs challenge tests. In fact, if the hemodynamic correction is associated with normalization of SvO2 with disappearance of metabolic acidosis, this suggests hemodynamic impairment with intact mitochondrial function. In contrast, if the hemodynamic improvement with normalization of SvO2 is associated and acidosis persists, this suggests irreversible structural mitochondrial damage. The threshold between reversibility and irreversibility is likely time dependent, as suggested by biochemical consideration and by 2 large randomized studies on hemodynamic treatment. The comparative analysis of these 2 studies suggests that the time of intervention may lead to significant differences in mortality. In these patients time is essential.