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Near-Fatal Asthma

By Mark D. Siegel, MD, FCCP

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Pathophysiology

Most asthma deaths result from asphyxia before patients reach the hospital.25 Mucus plugging and diffuse bronchoconstriction and airway edema wreak havoc on lung mechanics and gas exchange. Increased airway resistance promotes hyperinflation and air trapping. Compliance may decrease as total lung capacity is approached, although this is inconsistent.5

Gas exchange abnormalities are almost universal.5,26-28 Hypoxia results from ventilation/perfusion mismatch and hypoventilation as respiratory failure ensues. The PaCO2 may be low, normal, or high, depending on the severity of obstruction and the patient's ability to ventilate.26 Factors promoting hypercapnia include ventilation/perfusion mismatch, increased dead space, increased CO2 production, and relative hypoventilation, the latter resulting from an increased work of breathing, disordered mechanics, and respiratory muscle fatigue. Importantly, even patients destined to develop respiratory failure may be hypocapnic at first. Hypercapnia generally ensues as ventilatory failure progresses.

In some patients, wide pleural pressure swings can result in pulsus paradoxicus, which correlates well with disease severity.5,27,29 Factors promoting pulsus paradoxicus include (1) increased left ventricular afterload during vigorous inhalation and (2) inadequate left ventricular filling due to right ventricular dilation, which causes intraventricular septal shift, decreased pulmonary blood flow, and external compression of the heart by the hyperinflated lungs

Pulsus paradoxicus may be absent in patients who are fatiguing and cannot generate large negative pleural

 


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