Hypoxic respiratory failure: ventilation and chest wall inspiratory muscle function in severe COPD

<bold>Background:</bold> Type 1 respiratory failure is hypoxia with PaO₂ < 60mmHg without hypercapnia in patients with respiratory distress. To elucidate the impact of hypoxic respiratory failure in severe COPD, we examined ventilation and respiratory muscle function during sustained hypoxia. <bold>Methods:</bold> Fine-wire EMG was implanted in parasternal intercostal (PARA) muscles of severe COPD (N=7, FEV₁ 0.87L 32%pred). We measured airflow, SpO₂, ETCO₂ and PARA EMG activity during room air followed by 20 min isocapnic hypoxia (SpO₂ ~80%). We report 4 min room air (BASE), sustained hypoxia: 2 min after reaching SpO₂ 80% (PEAK) and final 4 min (PLATEAU), and 4 min room air (RECOVERY). <bold>Results:</bold> Minute ventilation (V_I) increased from BASE-PEAK then decreased to PLATEAU (p<0.01). Changes in V_I were related to tidal volume and mean inspiratory flow (p<0.05), without changes in respiratory timing. Peak PARA EMG showed marked increase from BASE-PEAK followed by significant decline with sustained hypoxia (p<0.05). <bold>Conclusions:</bold> In severe COPD, hypoxic respiratory failure elicited a transient and fleeting ventilatory pattern with marked depression in breathing with sustained hypoxia. Significant recruitment of chest wall muscle was noted during acute hypoxia, however, abated in a temporal manner with sustained desaturation. Loss of ventilation and chest wall respiratory muscles poses a risk of hypoxic respiratory deterioration in severe COPD. <fig><object-id>erj;64/suppl_68/PA1668/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig>