A prospective evaluation of the electrocardiographic manifestations of hypothermia.

OBJECTIVE: To determine the effects of body temperature, ethanol use, electrolyte status, and acid-base status on the electrocardiograms (ECGs) of hypothermic patients. METHODS: Prospective, two-year, observational study of patients presenting to an urban ED with temperature < or =95 degrees F (< or =35 degrees C). All patients had at least one ECG obtained. Electrocardiograms were interpreted by a cardiologist blinded to the patient's temperature. J-point elevations known as Osborn waves were defined as present if they were at least 1 mm in height in two consecutive complexes. RESULTS: 100 ECGs were obtained in 43 patients. Presenting temperatures ranged between 74 degrees F and 95 degrees F (23.3 degrees C-35 degrees C). Initial rhythms included normal sinus (n = 34), atrial fibrillation (n = 8), and junctional (n = 1). Osborn waves were present in 37 of 43 initial ECGs. Of the six initial ECGs that did not have Osborn waves present, all were obtained in patients whose temperatures were > or =90 degrees F > or =32.2 degrees C). For the entire group, the Osborn wave was significantly larger as temperature decreased (p = 0.0001, r = -0.441). The correlation between temperature and size of the Osborn wave was strongest in six patients with four or more ECGs (range r = -0.644 to r = -0.956, p = 0.001). No correlation could be demonstrated between the height of the Osborn waves and the serum electrolytes, including sodium, chloride, potassium, bicarbonate, BUN, creatinine, glucose, anion gap, and blood ethanol levels. CONCLUSIONS: The presence and size of the Osborn waves in hypothermic patients appear to be a function of temperature. The magnitude of the Osborn waves is inversely correlated with the temperature.

Pharmacologic effects on thermoregulation: mechanisms of drug-related heatstroke.

In summary, a number of pharmacologic agents interfere with the body's ability to maintain normal body temperature during exercise or under conditions of environmental heat stress. Life threatening elevation of body temperature may occur. Regardless of the predisposing cause of heatstroke, the final common pathway is heat injury to tissues causing cell death. Rapid cooling of the patient must take precedence and elucidation of the pathophysiologic disturbance is secondary to the accomplishment of this goal.