Effect of Carbon Dioxide on Diaphragmatic Function in Human Beings

Abstract

We studied the effects of acute changes in the partial pressure of arterial carbon dioxide on diaphragmatic contractility and performance in four normal men. To study contractility we measured the ability of the diaphragm to generate pressure at a given level of excitation by determining the relation between the electrical activity of the diaphragm and transdiaphragmatic pressure during a voluntary quasi-isometric inspiratory effort carried out at different levels of end-tidal carbon dioxide. Our results show that contractility was reduced with hypercapnia (when end-tidal carbon dioxide was 7.5 per cent or higher), although hypocapnia (end-tidal carbon dioxide, 3 per cent) had no effect on diaphragmatic contractility. We also studied the development of diaphragmatic fatigue before and during carbon dioxide breathing. Subjects were studied at the same diaphragmatic tension-time index, a value analogous to the more familiar myocardial tension-time index, while the same inspiratory flow was maintained. Electromyographic signs of fatigue appeared at a lower tension-time index during hypercapnia than during normocapnia, indicating that endurance is diminished during hypercapnia. These findings show that acute respiratory acidosis equivalent to an arterial carbon dioxide tension of about 54 mm Hg decreases the contractility and endurance time of the diaphragm in human beings.

Discharge frequencies of parasternal intercostal and scalene motor units during breathing in normal and COPD subjects.

“…Previous attempts to estimate the degree of motor-neuronal activation during breathing have used surface EMG of inspiratory muscles expressed relative to "maximal" values obtained during inhalation to TLC (12)(13)(14). We could have used a similar method to compare the neural drive in COPD patients and control sub- jects.…”

Skeletal muscle dysfunction in COPD: clinical and laboratory observations

“…Acute hypercapnia leads to intracellular acidosis that has marked effects upon muscle cell metabolism, including decreases in ATP, PCr and adenosine nucleotides [64,65]. Furthermore, acute hypercapnia in healthy humans reduces limb muscle and diaphragm contractility [66,67]. Findings from animal studies are conflicting; decreases in PCr and ATP/ADP ratios have been reported in rat muscles exposed to high carbon dioxide levels [68], whereas no differences were found in phosphate metabolite activity between hypercapnic and normocapnic rat diaphragms [69].…”

The diaphragm: contractile properties and fatigue.

“…Hypercapnia impairs diaphragmatic contractility (41) (66). Muscle weakness renders the diaphragm more susceptible to fatigue because it increases the ratio (Pdi breath/Pdi max) by lowering the denominator, whereas the numerator is either unchanged or increased as in obstructive lung disease (39).…”