To investigate the mechanisms underlying ventilator-dependence in patients with chronic obstructive pulmonary disease (COPD), and to assess the effects of the combination of positive end-expiratory pressure (PEEP) and pressure-support ventilation (PSV) on inspiratory muscle effort, we investigated respiratory mechanics in eight ventilator-dependent COPD patients. The patients' breathing pattern, lung mechanics, diaphragmatic effort (PTPdi), diaphragmatic tension-time index (TTdi), and arterial blood gases were measured during both spontaneous breathing (SB) and ventilatory assistance consisting of PSV alone (15, 20, and 25 cm H2O) and PSV combined with a PEEP of 5 cm H2O (reducing PSV to 10, 15, and 20 cm H2O, respectively, to maintain equivalent inspiratory pressure). The different levels of ventilatory support were delivered in a randomized sequence. Maximal inspiratory (MIP), esophageal (PpImax) and transdiaphragmatic (Pdi(max)) pressures and respiratory drive (P(0.1)) were measured at the beginning of the procedure during SB. We found a high P(0.1) (6.1 +/- 1.7 cm H2O), which seemed to rule out an impairment of respiratory-center output. Apparently, inspiratory muscle strength was compatible with successful weaning (38.5 +/- 8.8, 50.9 +/- 9.7, and 51.8 +/- 9.5 cm H2O for MIP, PPImax and Pdi(max), respectively). However, abnormal respiratory mechanics (particularly an intrinsic positive end-expiratory pressure (PEEPi) of 8.3 +/- 1.9 cm H2O and pulmonary resistance 24.7 +/- 9.5 cm H2O/L/s imposed an excessive load on the inspiratory muscles, as indicated by a high PTPdi (499 +/- 122 cm H2O x s). Increasing levels of PSV progressively and significantly unloaded the patients' inspiratory muscles, although at pressures above 20 cm H2O uncoupling occurred between patient and ventilator respiratory frequency. Application of PEEP during PSV improved ventilatory assistance by further reducing the inspiratory effort (by 17% on average) and by ameliorating patient-ventilator interaction. We conclude that the excessive mechanical load, and in particular the high PEEPi, is the major determinant of ventilator-dependence in COPD patients. Application of PEEP improves the efficiency of PSV in unloading these patients' inspiratory muscles, and can sometimes improve patient-ventilator interaction.

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.

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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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During the early phases of an acute exacerbation, patients with COPD and acute respiratory failure had an imbalance between the decreased capacity of the respiratory muscles to generate pressure and the increased respiratory load. This imbalance was similar to that recorded in patients with COPD and chronic ventilatory failure. In both groups, the imbalance was associated with rapid shallow breathing. Among the mechanical constraints to ventilation, only PEEPi,dyn was different between acute and chronic patients with ventilatory failure.

The aim of this study was to determine whether it is possible using ear-oximetry to prescribe the correct oxygen flow rates during exercise in chronic obstructive pulmonary disease (COPD) patients on long-term oxygen therapy (LTOT).Twenty COPD patients on LTOT, with exercise desaturation breathing oxygen at resting flow rates, performed a series of 6-min treadmill walking tests, with a progressive increase in oxygen flows until oxygen saturation measured by ear-or pulse-oximetry (Sp,O 2 ) was above 90%. The exercise studies were repeated the next day, saturation being measured both noninvasively by ear-oximetry (Sp,O 2 ) and invasively by CO-oximeter (Sa,O 2 ). The exercise studies continued until both Sa,O 2 and Sp,O 2 were above 90%. Reproducibility and agreement of the results were analysed according to Bland and Altman.Sp,O 2 was significantly lower than Sa,O 2 by, on average, 0.7% (p<0.004). Sp,O 2 reproducibility between the two days was good. The invasive and noninvasive oxygen flow prescriptions agreed in only 10 subjects; in six subjects ear-oximetry overestimated the oxygen supply (p<0.0005), whilst in four subjects it underestimated (p<0.01).Contingency table analysis with coded raw data for the values of the sixth minute (that of the deepest desaturation) showed poor agreement between CO-and pulseoximetry (Chi-squared p<0.003). However, theoretically, if the Sp,O 2 target had been raised to 93%, there would have been hardly any underestimations of Sa,O 2 p=NS).We concluded that noninvasive measurement of oxygen saturation is not adequate for estimating arterial saturation in chronic obstructive pulmonary disease. We suggest, as a working solution, that a new cut-off limit of 93% oxygen saturation measured by pulse oximetry should be used as the value below which exercise-induced desaturation should be corrected in order to allow oxygen to be properly prescribed during activities of daily life.