Why the study?
How do ventilatory and mouth occlusion pressure responses to CO2 differ between COPD patients in acute respiratory failure and normal subjects?
How do ventilatory and mouth occlusion pressure responses to CO2 differ between COPD patients in acute respiratory failure and normal subjects?
CO2 drive is a major determinant of respiratory stimulation in many COPD patients with acute respiratory failure.
Blunted CO2 ventilatory response may contribute to hypercapnic failure in COPD; leaves open whether drive impairment is causal or consequential.
The aim of our study was to determine the importance of chemoreceptor stimulation by carbon dioxide in setting the level of ventilation in patients with chronic obstructive pulmonary disease (COPD) in acute respiratory failure. We studied the ventilatory and mouth occlusion pressure (P0.1) responses to CO2 in 25 COPD patients under treatment for episodes of acute respiratory failure, and in 24 normal subjects. Carbon dioxide rebreathing tests were performed in the spontaneously breathing, intubated patients, after arterial blood gases had been quasi-normalized by mechanical ventilation, which allowed us to compare both groups at similar resting arterial carbon dioxide tension (PaCO2) and acid-base status. The slopes of the ventilatory responses were markedly lower in the patients (mean +/- SEM, 1.28 +/- 0.23 versus 12.53 +/- 1.13 l.min-1.kPa-1). The slopes of the P0.1 responses were lower in the patients (0.27 +/- 0.05 versus 0.45 +/- 0.05 kPa.kPa-1), but the absolute P0.1 values were not significantly different from the normals. Increasing PaCO2 from 5.3 to 8 kPa (40 to 60 mmHg) resulted in a mean increase of 34% in ventilation. These results show that CO2 drive is a major determinant of respiratory stimulation in many COPD patients with acute respiratory failure.
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Tardif et al. (1993) studied this question.
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