Paper: Aliverti et al, Chest wall mechanics during pressure support ventilation (Crit Care. 2006;10(2):R54)
INTRODUCTION: During pressure support ventilation (PSV) a part of the breathing pattern is controlled by the patient, and synchronization of respiratory muscle action and the resulting chest wall kinematics is a valid indicator of the patient's adaptation to the ventilator. The aim of the present study was to analyze the effects of different PSV settings on ventilatory pattern, total and compartmental chest wall kinematics and dynamics, muscle pressures and work of breathing in patients with acute lung injury. METHOD: In nine patients four different levels of PSV (5, 10, 15 and 25 cmH2O) were randomly applied with the same level of positive end-expiratory pressure (10 cmH2O). Flow, airway opening, and oesophageal and gastric pressures were measured, and volume variations for the entire chest wall, the ribcage and abdominal compartments were recorded by opto-electronic plethysmography. The pressure and the work generated by the diaphragm, rib cage and abdominal muscles were determined using dynamic pressure-volume loops in the various phases of each respiratory cycle: pre-triggering, post-triggering with the patient's effort combining with the action of the ventilator, pressurization and expiration. The complete breathing pattern was measured and correlated with chest wall kinematics and dynamics. RESULTS: At the various levels of pressure support applied, minute ventilation was constant, with large variations in breathing frequency/ tidal volume ratio. At pressure support levels below 15 cmH2O the following increased: the pressure developed by the inspiratory muscles, the contribution of the rib cage compartment to the total tidal volume, the phase shift between rib cage and abdominal compartments, the post-inspiratory action of the inspiratory rib cage muscles, and the expiratory muscle activity. CONCLUSION: During PSV, the ventilatory pattern is very different at different levels of pressure support; in patients with acute lung injury pressure support greater than 10 cmH2O permits homogeneous recruitment of respiratory muscles, with resulting synchronous thoraco-abdominal expansion.
Paper: Aliverti et al, Effect of salbutamol on lung function and chest wall volumes at rest and during exercise in COPD. Thorax. 2005 Nov;60(11):916-2
BACKGROUND: Inhaled bronchodilators can increase exercise capacity in chronic obstructive pulmonary disease (COPD) by reducing dynamic hyperinflation, but treatment is not always effective. This may reflect the degree to which the abdomen allows dynamic hyperinflation to occur. METHOD: A double blind, randomised, crossover trial of the effect of 5 mg nebulised salbutamol or saline on endurance exercise time was conducted in 18 patients with COPD of mean (SD) age 67.1 (6.3) years and mean (SD) forced expiratory volume in 1 second (FEV1) of 40.6 (15.0)% predicted. Breathing pattern, metabolic variables, dyspnoea intensity, and total and regional chest wall volumes were measured non-invasively by optoelectronic plethysmography (OEP) at rest and during exercise. RESULTS: Salbutamol increased FEV1, forced vital capacity (FVC) and inspiratory capacity and reduced functional residual capacity (FRC) and residual volume significantly. OEP showed the change in resting FRC to be mainly in the abdominal compartment. Although the mean (SE) end expiratory chest wall volume was 541 (118) ml lower (p<0.001) at the end of exercise, the endurance time was unchanged by the bronchodilator. Changes in resting lung volumes were smaller when exercise duration did not improve, but FEV1 still rose significantly after active drug. After the bronchodilator these patients tried to reduce the end expiratory lung volume when exercising, while those exercising longer continued to allow end expiratory abdominal wall volume to rise. The change to a more euvolumic breathing pattern was associated with a lower oxygen pulse and a significant fall in endurance time with higher isotime levels of dyspnoea. CONCLUSIONS: Nebulised salbutamol improved forced expiratory flow in most patients with COPD, but less hyper-nflated patients tried to reduce the abdominal compartmental volume after active treatment and this reduced their exercise capacity. Identifying these patients has important therapeutic implications, as does an understanding of the mechanisms that control chest wall muscle recruitment.
Paper:Lung Mechanics and Dyspnea during Exacerbations of Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2005 Dec 15;172(12):1510-6
RATIONALE: Exacerbation of chronic obstructive pulmonary disease commonly causes hospitalization. The change in lung mechanics during exacerbation and its relationship to symptoms in spontaneously breathing individuals has not been described. OBJECTIVE: We hypothesized that changes in both airflow and lung volumes would occur during an exacerbation, but that only volume change would relate to symptomatic improvement. METHODS: Lung mechanics and resting dyspnea were recorded in 22 hospitalized patients during recovery from exacerbation. MEASUREMENTS: Spirometry, inspiratory capacity, respiratory system resistance and reactance, tidal breathing patterns, and expiratory flow limitation were recorded after nebulized bronchodilator therapy on the first 3 d after admission, at discharge, and 6 wk postadmission (Day 42). Prebronchodilator measurements were taken on Day 2, at discharge, and on Day 42. MAIN RESULTS: Postbronchodilator inspiratory capacity increased 0.23 +/- 0.07 L by discharge and 0.42 +/- 0.1 L by Day 42, FEV1 rose 0.09 +/- 0.04 and 0.2 +/- 0.05 L at discharge and Day 42, respectively, and FVC increased 0.21 +/- 0.08 and 0.47 +/- 0.09 L at discharge and Day 42 (all p < 0.05). Consistent reduction in dyspnea was seen as the exacerbation resolved. Respiratory system resistance, FEV1/FVC, and expiratory flow limitation were unchanged throughout, indicating that changes in lung volume rather than airflow resistance predominated. CONCLUSIONS: Improvement in operating lung volumes is the principal change seen as a chronic obstructive pulmonary disease exacerbation resolves and increase in inspiratory capacity is a useful guide to a reduction in dyspnea.
Paper: Laude et al, The effect of helium and oxygen on exercise performance in chronic obstructive pulmonary disease: a randomized crossover trial.
RATIONALE: Breathing supplemental oxygen reduces breathlessness during exercise in patients with chronic obstructive pulmonary disease (COPD). Replacing nitrogen with helium reduces expiratory flow resistance and may improve lung emptying. Combining these treatments should be independently effective. OBJECTIVES: Study the effect of changing oxygen or helium concentration in inspired gas during exercise in patients with stable COPD. METHODS: In 82 patients (mean age, 69.7 yr; mean FEV(1), 42.6% predicted), we measured endurance shuttle walking distance, resting and exercise oxygen saturation, and end-exercise dyspnea (Borg scale) while patients breathed Heliox28 (72% He/28% O(2)), Heliox21 (79% He/21% O(2)), Oxygen28 (72% N(2)/28% O(2)), or medical air (79% N(2)/21% O(2)). Gases were administered using a randomized, blinded, crossover design via a face mask and an inspiratory demand valve. RESULTS: Breathing Heliox28 increased walking distance (mean+/-SD, 147+/-150 m) and reduced Borg score (-1.28+/-1.30) more than any other gas mixture. Heliox21 significantly increased walking distance (99+/-101 m) and reduced dyspnea (Borg score, -0.76+/-0.77) compared with medical air. These changes were similar to those breathing Oxygen28. The effects of helium and oxygen in Heliox28 were independent. The increase in walking distance while breathing Heliox28 was inversely related to baseline FEV(1) breathing air. Conclusion: Reducing inspired gas density can improve exercise performance in COPD as much as increasing inspired oxygen. These effects can be combined as Heliox28 and are most evident in patients with more severe airflow obstruction.
Paper: Vogiatzis et al, Patterns of dynamic hyperinflation during exercise and recovery in patients with severe chronic obstructive pulmonary disease.
BACKGROUND: Not all patients with severe chronic obstructive pulmonary disease (COPD) progressively hyperinflate during symptom limited exercise. The pattern of change in chest wall volumes (Vcw) was investigated in patients with severe COPD who progressively hyperinflate during exercise and those who do not. METHODS: Twenty patients with forced expiratory volume in 1 second (FEV(1)) 35 (2)% predicted were studied during a ramp incremental cycling test to the limit of tolerance (Wpeak). Changes in Vcw at the end of expiration (EEVcw), end of inspiration (EIVcw), and at total lung capacity (TLCVcw) were computed by optoelectronic plethysmography (OEP) during exercise and recovery. RESULTS: Two significantly different patterns of change in EEVcw were observed during exercise. Twelve patients had a progressive significant increase in EEVcw during exercise (early hyperinflators, EH) amounting to 750 (90) ml at Wpeak. In contrast, in all eight remaining patients EEVcw remained unchanged up to 66% Wpeak but increased significantly by 210 (80) ml at Wpeak (late hyperinflators, LH). Although at the limit of tolerance the increase in EEVcw was significantly greater in EH, both groups reached similar Wpeak and breathed with a tidal EIVcw that closely approached TLCVcw (EIVcw/TLCVcw 93 (1)% and 93 (3)%, respectively). EEVcw was increased by 254 (130) ml above baseline 3 minutes after exercise only in EH. CONCLUSIONS: Patients with severe COPD exhibit two patterns during exercise: early and late hyperinflation. In those who hyperinflate early, it may take several minutes before the hyperinflation is fully reversed after termination of exercise.
Paper: Vogiatzis et al, Skeletal muscle adaptations to interval training in patients with advanced COPD. (Chest 2005)
STUDY OBJECTIVES: To investigate the response to interval exercise (IE) training by looking at changes in morphologic and biochemical characteristics of the vastus lateralis muscle, and to compare these changes to those incurred after constant-load exercise (CLE) training. DESIGN: Randomized, controlled, parallel, two-group study (IE vs CLE training). SETTING: Multidisciplinary, outpatient, hospital-based, pulmonary rehabilitation program. PATIENTS: Nineteen patients with stable advanced COPD (mean +/- SEM FEV1, 40 +/- 4% predicted). INTERVENTIONS: Patients (n = 10) assigned to IE training exercised at a mean intensity of 124 +/- 15% of baseline peak exercise capacity (peak work rate [Wpeak]) with 30-s work periods interspersed with 30-s rest periods for 45 min/d. Patients (n = 9) allocated to CLE training exercised at a mean intensity of 75 +/- 5% Wpeak for 30 min/d. Patients exercised 3 d/wk for 10 weeks. MEASUREMENTS AND RESULTS: Needle biopsies of the right vastus lateralis muscle were performed before and after rehabilitation. After IE training, the cross-sectional areas of type I and IIa fibers were significantly increased (type I before, 3,972 +/- 455 microm2; after, 4,934 +/- 467 microm2 [p = 0.004]; type IIa before, 3,695 +/- 372 microm2; after, 4,486 +/- 346 microm2 [p = 0.008]), whereas the capillary-to-fiber ratio was significantly enlarged (from 1.13 +/- 0.08 to 1.24 +/- 0.07 [p = 0.013]). Citrate synthase activity increased (from 14.3 +/- 1.4 to 20.5 +/- 4.2 micromol/min/g), albeit not significantly (p = 0.097). There was also a significant improvement in Wpeak (by 19 +/- 5%; p = 0.04) and in lactate threshold (by 17 +/- 5%; p = 0.02). The magnitude of changes in all the above variables was not significantly different compared to that incurred after CLE training. During training sessions, however, ratings of dyspnea and leg discomfort, expressed as fraction of values achieved at baseline Wpeak, were significantly lower (p < 0.05) for IE training (73 +/- 9% and 60 +/- 8%, respectively) compared to CLE training (83 +/- 10% and 87 +/- 13%, respectively). CONCLUSIONS: High-intensity IE training is equally effective to moderately intense CLE training in inducing peripheral muscle adaptations; however, IE is associated with fewer training symptoms.
Paper: Aliverti et al, Breath-by-breath assessment of alveolar gas stores and exchange. J Appl Physiol. (2004 Apr;96(4):1464-9)
The volume of O(2) exchanged at the mouth during a breath (Vo(2,m)) is equal to that taken up by pulmonary capillaries (Vo(2,A)) only if lung O(2) stores are constant. The latter change if either end-expiratory lung volume (EELV), or alveolar O(2) fraction (Fa(O(2))) change. Measuring this requires breath-by-breath (BbB) measurement of absolute EELV, for which we used optoelectronic plethysmography combined with measurement of O(2) fraction at the mouth to measure Vo(2,A) = Vo(2,m) - (DeltaEELV x Fa(O(2)) + EELV x DeltaFa(O(2))), and divided by respiratory cycle time to obtain BbB O(2) consumption (Vo(2)) in seven healthy men during incremental exercise and recovery. To synchronize O(2) and volume signals, we measured gas transit time from mouthpiece to O(2) meter and compared Vo(2) measured during steady-state exercise by using expired gas collection with the mean BbB measurement over the same time period. In one subject, we adjusted the instrumental response time by 20-ms increments to maximize the agreement between the two Vo(2) measurements. We then applied the same total time delay (transit time plus instrumental delay = 660 ms) to all other subjects. The comparison of pooled data from all subjects revealed r(2) = 0.990, percent error = 0.039 +/- 1.61 SE, and slope = 1.02 +/- 0.015 (SE). During recovery, increases in EELV introduced systematic errors in Vo(2) if measured without taking DeltaEELV x Ca(O(2))+EELV x DeltaFa(O(2)) into account. We conclude that optoelectronic plethysmography can be used to measure BbB Vo(2) accurately when studying BbB gas exchange in conditions when EELV changes, as during on- and off-transients.
Paper: Aliverti et al, Regional chest wall volumes during exercise in chronic obstructive pulmonary disease. (Thorax. 2004 Mar;59(3):210-6.)
BACKGROUND: Dynamic hyperinflation of the lungs impairs exercise performance in chronic obstructive pulmonary disease (COPD). However, it is unclear which patients are affected by dynamic hyperinflation and how the respiratory muscles respond to the change in lung volume. METHODS: Using optoelectronic plethysmography, total and regional chest wall volumes were measured non-invasively in 20 stable patients with COPD (mean (SD) forced expiratory volume in 1 second 43.6 (11.6)% predicted) and dynamic hyperinflation was tracked breath by breath to test if this was the mechanism of exercise limitation. Resting ventilation, breathing pattern, symptoms, rib cage and abdominal volumes were recorded at rest and during symptom limited cycle ergometry. Pleural, abdominal, and transdiaphragmatic pressures were measured in eight patients. RESULTS: End expiratory chest wall volume increased by a mean (SE) of 592 (80) ml in 12 patients (hyperinflators) but decreased by 462 (103) ml in eight (euvolumics). During exercise, tidal volume increased in euvolumic patients by reducing end expiratory abdominal volume while in hyperinflators tidal volume increased by increasing end inspiratory abdominal and rib cage volumes. The maximal abdominal pressure was 22.1 (9.0) cm H(2)O in euvolumic patients and 7.6 (2.6) cm H(2)O in hyperinflators. Euvolumic patients were as breathless as hyperinflators but exercised for less time and reached lower maximum workloads (p<0.05) despite having better spirometric parameters and a greater expiratory flow reserve. CONCLUSIONS: Dynamic hyperinflation is not the only mechanism limiting exercise performance in patients with stable COPD. Accurate measurement of chest wall volume can identify the different patterns of respiratory muscle activation during exercise.
Paper: Dellaca et al, Detection of expiratory flow limitation in COPD using the forced oscillation technique. (Eur Respir J. 2004 Feb;23(2):232-40)
Expiratory flow limitation (EFL) during tidal breathing is a major determinant of dynamic hyperinflation and exercise limitation in chronic obstructive pulmonary disease (COPD). Current methods of detecting this are either invasive or unsuited to following changes breath-by-breath. It was hypothesised that tidal flow limitation would substantially reduce the total respiratory system reactance (Xrs) during expiration, and that this reduction could be used to reliably detect if EFL was present. To test this, 5-Hz forced oscillations were applied at the mouth in seven healthy subjects and 15 COPD patients (mean +/- sD forced expiratory volume in one second was 36.8 +/- 11.5% predicted) during quiet breathing. COPD breaths were analysed (n=206) and classified as flow-limited if flow decreased as alveolar pressure increased, indeterminate if flow decreased at constant alveolar pressure, or nonflow-limited. Of these, 85 breaths were flow-limited, 80 were not and 41 were indeterminate. Among other indices, mean inspiratory minus mean expiratory Xrs (deltaXrs) and minimum expiratory Xrs (Xexp,min) identified flow-limited breaths with 100% specificity and sensitivity using a threshold between 2.53-3.12 cmH2O x s x L(-1) (deltaXrs) and -7.38- -6.76 cmH2O x s x L(-1) (Xexp,min) representing 6.0% and 3.9% of the total range of values respectively. No flow-limited breaths were seen in the normal subjects by either method. Within-breath respiratory system reactance provides an accurate, reliable and noninvasive technique to detect expiratory flow limitation in patients with chronic obstructive pulmonary disease.
Paper: Dellaca et al, Noninvasive detection of expiratory flow limitation in COPD patients during nasal CPAP. (Eur Respir J. 2006 May;27(5):983-91)
The difference between mean inspiratory and expiratory respiratory reactance (delta(rs)) measured with forced oscillation technique (FOT) at 5 Hz allows the detection of expiratory flow limitation (EFL) in chronic obstructive pulmonary disease (COPD) patients breathing spontaneously. This aim of this study was to evaluate whether this approach can be applied to COPD patients during noninvasive pressure support. Delta(rs) was measured in seven COPD patients subjected to nasal continuous positive airway pressure (CPAP) at 0, 4, 8 and 12 cmH2O in sitting and supine positions. Simultaneous recording of oesophageal pressure and the Mead and Whittenberger (M-W) method provided a reference for scoring each breath as flow-limited (FL), non-flow-limited (NFL) or indeterminate (I). For each patient, six consecutive breaths were analysed for each posture and CPAP level. According to M-W scoring, 47 breaths were FL, 166 NFL and 51 I. EFL scoring using FOT coincided with M-W in 94.8% of the breaths. In the four patients who were FL in at least one condition, delta(rs) was reduced with increasing CPAP. These data suggest that the forced oscillation technique may be useful in chronic obstructive pulmonary disease patients on nasal pressure support by identifying continuous positive airway pressure levels that support breathing without increasing lung volume, which in turn increase the work of breathing and reduce muscle effectiveness and efficiency.