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Background: Acute asthma exacerbations commonly lead to hyperventilation-induced hypocapnia (low arterial CO2 levels). While mild hypocapnia is frequent, extreme hypocapnia (PaCO2 ≤10 mmHg) causing coma is rare. This case highlights a life-threatening instance of severe hypocapnia in an asthma patient, complicated by anxiety-related hyperventilation and management challenges related to oxygen therapy.
Case presentation: A 43-year-old man with a history of bronchial asthma presented to the emergency department with flu-like symptoms and acute shortness of breath. On arrival, he was normoxic, but he subsequently developed marked hyperventilation accompanied by carpopedal spasm and a state of unresponsiveness. Arterial blood gas analysis, while on supplemental oxygen, revealed profound respiratory alkalosis, with a pH of 7.75, PaCO2 of 10 mmHg, and PaO2 of 237 mmHg. Management consisted of cautious oxygen titration, controlled rebreathing to gradually restore carbon dioxide levels, light sedation to alleviate hyperventilation, and correction of electrolyte imbalances. Neuroimaging excluded intracranial pathology. The patient’s neurological status improved within hours, leading to complete recovery without the need for invasive mechanical ventilation.
Discussion: Asthma exacerbations complicated by severe hypocapnia present a unique and often underrecognized therapeutic dilemma. Although oxygen is essential to prevent hypoxemia, excessive administration may further lower PaCO2, exacerbate cerebral vasoconstriction, and impair perfusion. Anxiety-related hyperventilation can further amplify these effects, potentially leading to transient cerebral dysfunction. Prompt recognition of extreme hypocapnia, careful modulation of oxygen delivery, and physiologically guided ventilation are essential to restore cerebral and systemic homeostasis.
Conclusion: This case emphasizes the need to recognize extreme hypocapnia as a potential cause of coma in asthma exacerbations, especially when anxiety-driven hyperventilation is involved. With timely supportive care and careful ventilatory management, balancing oxygen therapy and CO2 control, full neurological recovery and clinical stability were achieved.