Annabel H. Nickol

Corticospinal control of respiratory muscles in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) face an increased respiratory load and in consequence have an elevated respiratory drive. We used transcranial magnetic stimulation (TMS) to investigate associated changes in corticospinal excitability both at rest and during voluntary facilitation at different levels of inspiratory effort. Diaphragm and abdominal motor thresholds were significantly lower in COPD than healthy controls, but the quadriceps response was the same. In patients there was a significant increase in diaphragm response from rest during 20% inspiratory efforts but no further increase with greater efforts. In controls there was a further stepwise increase at 40% and 60% of inspiratory effort. The cortical silent period was significantly shorter in COPD. Using paired stimulation to study intracortical inhibitory and excitatory circuits we found significantly less excitability of intracortical facilitatory circuits in patients at long (>7 ms) interstimulus intervals. These results suggest that there is a ceiling effect in motor control output to the respiratory muscles of patients with COPD.

A quick and easy method of measuring the hypercapnic ventilatory response in patients with COPD

BACKGROUNDnHypercapnic ventilatory response (HCVR) techniques have not previously been adequately validated in patients with chronic obstructive pulmonary disease (COPD). We have tested the hypothesis that end-tidal PCO(2) may be used to test the HCVR in COPD during non-steady-state rebreathing, despite the fact that large (arterial-end-tidal) PCO(2) differences (P(a-et)CO(2)) exist during air breathing.nnnMETHODSnEight patients and 11 healthy volunteers underwent steady-state HCVR testing and non-steady-state rebreathing HCVR testing, using Pa and PetCO(2).nnnRESULTSnIn COPD patients, PetCO(2) was lower than PaCO(2) by a constant amount throughout steady-state HCVR, but equalised with PaCO(2) during non-steady-state HCVR. Consequently there were no differences in HCVR slope using either method (steady-state p=0.91; rebreathing p=0.73), or HCVR intercept in rebreathing (p=0.68) whether PaCO(2) or PetCO(2) was used. The steady-state HCVR intercept using PetCO(2) was greater than that using PaCO(2) (p=0.02). In healthy volunteers PetCO(2) equalised with PaCO(2) during steady-state HCVR, but was progressively greater than PaCO(2) during non-steady-state. Consequently, there was no difference in HCVR slope (p=0.21) or intercept (p=0.46) whether PaCO(2) or PetCO(2) was used. During non-steady-state there was a P(a-et)CO(2) difference in slope (p=0.03) and intercept (p=0.04).nnnCONCLUSIONSnIn COPD patients non-steady-state HCVR using PetCO(2) is well tolerated, which is as accurate as PaCO(2). HCVR slope may be derived using PetCO(2) during steady-state testing, though there may be errors in intercept compared to use of PaCO(2). In healthy volunteers PetCO(2) may be used to estimate PaCO(2) during steady-state but not rebreathing HCVR.