To investigate the pathophysiologic mechanisms of ventilator dependence, we took physiologic measurements in 28 patients with COPD and 11 postcardiac surgery (PCS) patients receiving long-term mechanical ventilation during a spontaneous breathing trial, and in 20 stable, spontaneously breathing patients matched for age and disease. After 40 +/- 14 min of spontaneous breathing, 20 of 28 patients with COPD and all 11 PCS patients were judged ventilator-dependent (VD). We found that in the 31 VD patients tidal volume was low (VT: 0.36 +/- 0.12 and 0.31 +/- 0.08 L for COPD and PCS, respectively), neuromuscular drive was high (P(0.1): 5.6 +/- 1. 6 and 3.9 +/- 1.9 cm H(2)O), inspiratory muscle strength was reduced (Pdi(max): 42 +/- 12 and 28 +/- 15 cm H(2)O), and lung mechanics were abnormal, particularly PEEPi (5.9 +/- 3.0 cm H(2)O) and lung resistance (22.2 +/- 9.2 cm H(2)O/L/s) in COPD. The load/capacity balance was altered (Pdi/Pdi(max) and Ppl/Ppl(max) > 0.4) and the effective inspiratory impedance was high (P(0.1)/VT/TI >/= 10 cm H(2)O/L/s). Failure to wean occurred in patients with f/VT > 105 breaths/min/L and 56% of patients with COPD with f/VT < 80 breaths/min/L. Those who failed despite a low f/VT ( < 80 breaths/min/L) either showed ineffective inspiratory efforts, which artificially lowered f/ VT (n = 8), or did not increase breathing frequency (n = 5), but P(0.1) and P(0.1)/VT/TI were as high as in other VD patients. In the 31 VD patients, Pa(CO(2)) increased during the weaning trial (+12.3 +/- 8.0 mm Hg). We conclude that in the presence of a high drive to breathe, the imbalance between increased work load and reduced inspiratory muscle strength causes respiratory distress and CO(2) retention. Noninvasive measurements (breathing pattern, P(0.1), P(0.1)/ VT/TI) may give better insight into weaning failure useful in clinical decision-making, particularly in patients with COPD not showing rapid shallow breathing (56% in this study).
The effect of high altitude (HA) on exercise-induced diaphragm fatigue in normal subjects was examined.Eight normal subjects completed an incremental exercise test at sea level (SL) and at 3,325 m. Before (baseline), during, and after exercise (recovery), maximal transdiaphragm pressure (Pdi,sniff), breathing pattern, and diaphragmatic effort (PTPdi) were measured. Arterialized blood lactate was measured at baseline and during recovery.At maximal exercise (WRmax) Pdi,sniff fell to 72% and 61% of baseline at SL and HA respectively, recovering to baseline in 60 min at SL, and >60 min at HA. At the 5th min of recovery, circulating lactate was six-fold and seven-fold baseline at SL and HA, respectively. The time course of circulating lactate recovery was as for Pdi,sniff. To conclude, in normal subjects hypoxia-related effects, and not an increase in diaphragm work, hastens exercise-induced diaphragm fatigue and delays its recovery at high altitude compared to sea level. Eur Respir J 2001; 17: 674±680.
To investigate the physiologic effects of proportional assist ventilation (PAV) in difficult-to-wean, mechanically ventilated patients with advanced COPD, we measured in eight ICU patients the breathing pattern, neuromuscular drive (P0.1), lung mechanics, and inspiratory muscle effort (PTPdi and PTPpl) during both spontaneous breathing (SB) and ventilatory support with PAV, CPAP, and CPAP + PAV (in random sequence). PAV (volume assist [VA] and flow assist [FA]) was set as follows: dynamic lung elastance and inspiratory pulmonary resistance were measured during SB; then VA and FA were set to counterbalance the elastic and resistive loads exceeding the normal values, respectively, the inspiratory muscles bearing a normal elastic and resistive workload. CPAP was set close to dynamic intrinsic PEEP (8.3 +/- 3.4 cm H2O). We found significant reductions in P0.1 and PTPdi during both CPAP (-45 and -37%, respectively) and PAV (-50 and -48%, respectively). However, only the combination of PAV and CPAP brought P0.1 (1.69 +/- 0.97 cm H2O) and PTPdi (100 +/- 68 cm H2O. s) within normal values, and ameliorated the breathing pattern compared with SB (tidal volume: 0.69 +/- 0.33 versus 0.33 +/- 0.14 L; breathing frequency, 14.6 +/- 4.6 versus 21.0 +/- 6.5 breaths/min, respectively), without generating ineffective inspiratory efforts. We conclude that in difficult-to-wean COPD patients, (1) PAV improves ventilation and reduces both P0.1 and inspiratory muscle effort; (2) the combination of PAV and CPAP can unload the inspiratory muscles to values close to those found in normal subjects.
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