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Ventilatory control in two asthmatics resuscitated from respiratory arrest
Australian and New Zealand Journal of Medicine
|June 1, 1984
Summary
Asthma patients revived from attacks showed significantly reduced ventilatory responses to asphyxia. Endogenous opioids may cause this impaired ventilatory control, potentially contributing to sudden asthma death.
Area of Science:
- Pulmonary Medicine
- Neuroscience
- Respiratory Physiology
Background:
- Asthma is a chronic respiratory disease characterized by airway inflammation and hyperresponsiveness.
- Fulminant asthma attacks can lead to respiratory failure and sudden death.
- Chemoreceptor function plays a critical role in regulating breathing.
Observation:
- Two female patients revived from fulminant asthma attacks exhibited significantly blunted ventilatory responses to asphyxia compared to healthy subjects.
- Dopamine-receptor blockade did not improve the depressed ventilatory responses in asthmatic patients.
- Naloxone, an opioid antagonist, reversed the impaired ventilatory responsiveness in one patient, suggesting a role for endogenous opioids.
Findings:
- Asthmatic patients demonstrated significantly lower ventilatory responses to asphyxia (0.70 +/- 0.10 L/min/%SaO2-1 and 0.64 +/- 0.21 L/min/%SaO2-1) compared to normal subjects (1.54 +/- 0.11 L/min/%SaO2-1).
- Ventilatory responses to hypercapnia were in the low normal range for the asthmatic patients.
- Naloxone administration normalized ventilatory responsiveness to asphyxia and hypercapnia in one patient, indicating opioid involvement.
Implications:
- Defective chemoreceptor responses to chemical stimuli may contribute to the pathophysiology of sudden asthma death.
- Endogenous opioids might mediate disorders of ventilatory control in asthma.
- Targeting opioid pathways could offer novel therapeutic strategies for managing severe asthma exacerbations and preventing mortality.