[The etiology of chronic hypercapnia]

Abstract

Background: The ventilatory and the pressure response to CO2 in patients with advanced thoracic disorders are critically dependent on the mechanics of the lung and the respiratory muscles. Changes in drive, therefore, can not be directly assessed with that method. However during changes as a result of intermittent mechanical ventilation, changes in drive can be assessed, if lung and muscle mechanics remain unaffected. In addition, to study changes in ventilatory drive independently in patients successfully treated by intermittent mechanical ventilation, we determined the recruitment threshold, pCO2RT, of the unloaded ventilatory pump to CO2.

Patients: 16 patients with various disorders (4 COPD, 4 COPD and sleep apnoea, 7 scoliosis, 1 fibrothorax) were studied, 14 during nasal IPPV and 2 during mechanical ventilation via tracheostomy.

Results: After they had been successfully adapted to the ventilator, they were entered into the study. The apnoea threshold in all cases had already been reached during the adaptation period. pCO2AT was determined 32 +/- 5 mm Hg. While the patients were passively ventilated, the inspiratory CO2 was increased every 5 minutes, resulting in a stepwise increase in arterial pCO2 by 3 mm Hg. The recruitment threshold pCO2RT was then defined as the lowest pCO2, which resulted in a deformation of the inspiratory pressure curve by the patients own inspiratory efforts. pCO2RT was reproducible within trials and in different trials with a standard error of 1.2 mm Hg. It was found 6 +/- 4 mm Hg above the pCO2 during spontaneous breathing (p < 0.01) in all patients. pCO2RT decreased from 58 +/- 10 to 47 +/- 4 mm Hg during intermittent IPPV and so did the threshold during CO2 rebreathing, while spontaneous pCO2 decreased from 53 +/- 12 to 42 +/- 5 mm Hg. The slope, reflecting drive was decreased to 0.28 compared to normals but remained unchanged 0.32 (n. s.) during the study. Lung function did not change. A highly significant increase in the indices of maximal inspiratory force was observed (p < 0.002) and as a result a decrease in the inspiratory demand (p < 0.008).

Conclusion: Intermittent IPPV does efficiently suppress phasic respiratory drive via thoracic afferent inhibition and therefore effectively unloads the ventilatory pump. The CO2 threshold is increased in patients with hypercapnic ventilatory failure, probably to minimise the load to the ventilatory muscles. With the increase in inspiratory capacity the pCO2 threshold can be restored to normal by intermittent noninvasive or invasive IPPV.