Pediatric emergency medicine trisk 1954 1954
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All patients should be given supplemental oxygen. Patients with profuse
secretions, respiratory depression, or impaired mental status should be intubated
and mechanically ventilated. Intubation should be performed as gently as possible
to minimize the risk of arrhythmias.
A decreased metabolic rate produces less carbon dioxide, and usual minute
ventilation would produce respiratory alkalosis, increasing the risk of dangerous
arrhythmias. Therefore, ventilation should begin at approximately one-half the
normal minute ventilation.
Assessment of acid–base status and ventilation in the hypothermic patient is
the subject of considerable confusion. Blood gas machines heat the patient’s
blood sample to 37°C (98.6°F) before measuring pH and gas partial pressures
(thus providing theoretical values if the patient were 37°C [98.6°F]). If the
patient’s actual temperature is provided with the sample, the machine can correct
the values according to the nomogram of Kelman and Nunn ( Table 90.6 shows
one set of guidelines for appropriate correction). However, it is important to
understand two concepts. The first is the ectothermic principle, which relies on
the following aspect of physiology: dissociation of ions and partial pressures of
gases are decreased in cooled blood. In hypothermia, therefore, neutral pH is
higher, whereas “normal” PCO 2 is lower than is encountered at 37°C (98.6°F).
For example, hypoventilation of the hypothermic patient with a pH of 7.5 would
actually induce an undesirable respiratory acidosis. A second, more practical
concept is that if the patient’s blood volume is restored and oxygenation
maintained, acidosis will be corrected spontaneously as the patient is warmed.
Heart rate and rhythm should be monitored continuously and the patient
handled gently to avoid precipitation of life-threatening arrhythmias in an irritable
myocardium. Sinus bradycardia, atrial flutter, and atrial fibrillation are common
but rarely of hemodynamic significance. Spontaneous reversion to sinus rhythm
is the rule when temperature is corrected. It may be difficult to detect pulses in
the hypothermic patient; therefore, it is important to provide chest compressions
until pulseless electrical activity has been ruled out by echocardiography or
arterial BP monitoring. Ventricular fibrillation may occur spontaneously or with
trivial stimulation, especially at temperatures less than 28° to 29°C (82.4° to
84.2°F). Electrical defibrillation is warranted but frequently is ineffective until
core temperature rises. Chest compressions should be initiated and maintained
until the temperature is higher than 30°C (86°F), when defibrillation is more
likely to be effective.
Fluid replacement is essential. Relatively little plasma loss occurs in acute
hypothermia but losses may be great in hypothermia of longer duration. Normal
