This case report highlights that central chemoreceptor function can be permanently damaged by bulbar poliomyelitis, leading to chronic hypoventilation and heart failure that may be unmasked by sedatives years later.
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Alerts clinicians to sedative risk in bulbar polio survivors; leaves open causal role in late hypoventilation and heart failure.
A 41-year-old slender female who had led an active life presented with heart failure. Some months later she became comatose with severe hypercapnia and hypoxemia following a mild sedative and antihistaminic. Studies demonstrated normal respiratory and cardiac mechanics, a normal peripheral and an absent central chemoreceptor response. Ventilatory response to exercise was normal. Hypercapnia and hypoxemia were reversed by voluntary hyperventilation and became more severe during sleep. We suggest that central chemoreceptor function was damaged by bulbar poliomyelitis 20 years earlier. Overt cardio-respiratory failure did not become evident until the respiratory center had been further depressed by recent alcohol consumption and sedatives at night
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Solliday et al. (2009) studied this question.
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