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Objective: To analyze the acid-base balance during heatstroke., Design: Retrospective study., Setting: Heatstroke Center, Makkah, Saudi Arabia., Patients: Hundred nine consecutive heatstroke patients (mean age 55 +/- 12 years) with rectal temperature from 40 to 43.4 degrees C following exposure to hot weather., Intervention: Arterial blood gases collected prospectively and analyzed using 95% confidence limits established by controlled experimental studies. Severity of heatstroke on admission assessed by Simplified Acute Physiology Score and Organ System Failure score., Results: Metabolic acidosis was the predominant acid-base change followed by respiratory alkalosis (81 and 55% of the patients, respectively). The prevalence of metabolic acidosis (but not respiratory alkalosis) was significantly associated with the degree of hyperthermia: 63, 95 and 100% at 41, 42 and 43 degrees C, respectively (p < 0.0001). Patients with metabolic acidosis had a large anion gap (24 +/- 5). Arterial partial pressure of oxygen (PaO2), systolic blood pressure and Organ System Failure score were similar with or without metabolic acidosis. Although the acute physiology score was higher in patients with, than without, metabolic acidosis (15.7 +/- 3.7 vs 9.8 +/- 4.4, p < 0.001), there was no significant difference in neurologic morbidity and mortality (7.9 vs 1.1%, 5.6 vs 0%, p = 0.776 and 0.581, respectively)., Conclusion: We conclude that metabolic acidosis is the predominant response in heatstroke.

Objective: To determine whether nitric oxide (NO) production is increased in heat stroke (HS) patients., Design: A prospective analysis of nitrite and nitrate (NO2*/NO3) levels in ten HS patients was performed at the HS center in Makkah, Saudi Arabia., Methods: Plasma (NO2*/NO3) levels were determined spectrophotometrically before cooling (0 time), and at 6, 12, and 24 h post-cooling., Results: The mean level of NO in the ten HS victims before cooling was significantly higher than in eight control patients (35.6+/-37.0 vs. 3.0+/-4.2 micromol/l; p<0.01). The levels were higher in non-survivors than in survivors. NO also correlated positively with the Acute Physiology and Chronic Health Evaluation II score (r = 0.72, p<0.018). There was no correlation between the NO level before cooling and blood pressure, rectal temperature, or cooling time., Conclusion: HS is associated with excessive NO production, the magnitude of which is proportional to the severity of illness. NO may be an important mediator and integral part of the pathophysiological processes resulting in HS and may be a central factor linking the neurological and cardiovascular abnormalities observed in HS.