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Biomedical subjects

K A Webb

Publications and source records attributed to K A Webb.

At least 19 recordsLinked to original sources
PubMed2006

Combined physiological effects of bronchodilators and hyperoxia on exertional dyspnoea in normoxic COPD.

BACKGROUND: Studies examining the physiological interactions of oxygen (O(2)) and bronchodilators (BD) during exercise in chronic obstructive pulmonary disease (COPD) should provide new insights into mechanisms of exercise intolerance. We examined the effects of O(2) and BD, alone and in combination, on dyspnoea, ventilation (e), breathing pattern, operating lung volumes, and exercise endurance. METHODS: In a randomised, double blind, crossover study, 16 patients with COPD (mean (SE) FEV(1) 43(3)% predicted) performed pulmonary function tests and an incremental exercise test, then completed four visits in which they received either nebulised BD (ipratropium 0.5 mg + salbutamol 2.5 mg) or placebo (PL) with either 50% O(2) or room air (RA). After 90-105 minutes the patients performed pulmonary function tests, then breathed RA or O(2) during symptom limited constant load exercise at 75% peak work rate. RESULTS: With BD the mean (SE) increase in inspiratory capacity (IC) was 0.3 (0.1) l (p<0.05) at rest and during exercise, permitting greater tidal volume (Vt) expansion during exercise and a greater peak e. With O(2), e decreased during exercise as a result of decreased breathing frequency (F), with no significant change in IC. During exercise with BD+O(2), IC and Vt increased, F decreased, and e did not change. Dyspnoea decreased with all interventions at a standardised time during exercise compared with PL+RA (p<0.05). Endurance time was significantly (p<0.05) greater with BD+O(2) (10.4 (1.6) min) than with O(2) (8.5 (1.4) min), BD (7.1 (1.3) min) and PL+RA (5.4 (0.9) min). CONCLUSION: By combining the benefits of BD (reduced hyperinflation) and O(2) (reduced ventilatory drive), additive effects on exercise endurance were observed in patients with normoxic COPD.

Bronchodilator Agents↗
PubMed2005

Physiological changes during symptom recovery from moderate exacerbations of COPD.

Acute exacerbations of chronic obstructive disease (AECOPD) are characterised by worsening dyspnoea that is variably prolonged. In this study, physiological changes during moderate AECOPD were examined and the factors associated with dyspnoea resolution over time were determined. In total, 20 patients experiencing an AECOPD were evaluated within 72 h of initial worsening of symptoms (day 0) with pulmonary function testing, metabolic testing and symptom assessment using the dyspnoea domain of the Chronic Respiratory Disease Questionnaire (CRQ). Treatment was optimised and testing was repeated after 7, 14, 30 and 60 days. At day 0, patients were very short of breath (CRQ-dyspnoea mean+/-SEM 2.4+/-0.3) and showed significant airflow obstruction (forced expiratory volume in one second (FEV1) 41+/-3% predicted) and lung hyperinflation (forced residual capacity (FRC) 164+/-7% pred). By day 60 CRQ-dyspnoea improved to 4.6+/-0.5 (some shortness of breath); FRC and residual volume decreased by 5 and 11%, respectively; inspiratory capacity (IC) and slow vital capacity increased by 18 and 17%, respectively; and FEV1 increased by 18% with no change in FEV1/FVC. Total lung capacity did not change during AECOPD, and thus, changes in IC reliably reflected changes in end-expiratory lung volume. In conclusion, moderate acute exacerbation of chronic obstructive pulmonary disease is characterised by worsening airflow obstruction and lung hyperinflation. Improvement of dyspnoea following acute exacerbations of chronic obstructive pulmonary disease was associated with reduction in lung hyperinflation and consequent increase in expiratory flow rates.

Acute Disease↗
PubMed2004

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease.

This study examined the effects of bronchodilator-induced reductions in lung hyperinflation on breathing pattern, ventilation and dyspnoea during exercise in chronic obstructive pulmonary disease (COPD). Quantitative tidal flow/volume loop analysis was used to evaluate abnormalities in dynamic ventilatory mechanics and their manipulation by a bronchodilator. In a randomised double-blind crossover study, 23 patients with COPD (mean +/- SEM forced expiratory volume in one second 42 +/- 3% of the predicted value) inhaled salmeterol 50 microg or placebo twice daily for 2 weeks each. After each treatment period, 2 h after dose, patients performed pulmonary function tests and symptom-limited cycle exercise at 75% of their maximal work-rate. After salmeterol versus placebo at rest, volume-corrected maximal expiratory flow rates increased by 175 +/- 52%, inspiratory capacity (IC) increased by 11 +/- 2% pred and functional residual capacity decreased by 11 +/- 3% pred. At a standardised time during exercise, salmeterol increased IC, tidal volume (VT), mean inspiratory and expiratory flows, ventilation, oxygen uptake (VO2) and carbon dioxide output. Salmeterol increased peak exercise endurance, VO2 and ventilation by 58 +/- 19, 8 +/- 3 and 12 +/- 3%, respectively. Improvements in peak VO2 correlated best with increases in peak VT; increases in peak VT and resting IC were interrelated. The reduction in dyspnoea ratings at a standardised time correlated with the increased VT. Mechanical factors play an important role in shaping the ventilatory response to exercise in chronic obstructive pulmonary disease. Bronchodilator-induced lung deflation reduced mechanical restriction, increased ventilatory capacity and decreased respiratory discomfort, thereby increasing exercise endurance.

Administration, Inhalation↗
PubMed2001

Dynamic hyperinflation and exercise intolerance in chronic obstructive pulmonary disease.

The role of dynamic hyperinflation (DH) in exercise limitation in chronic obstructive pulmonary disease (COPD) remains to be defined. We examined DH during exercise in 105 patients with COPD (FEV(1) = 37 +/- 13% predicted; mean +/- SD) and studied the relationships between resting lung volumes, DH during exercise, and peak oxygen consumption (VO(2)). Patients completed pulmonary function tests and incremental cycle exercise tests. We measured the change in inspiratory capacity (Delta IC) during exercise to reflect changes in DH. During exercise, 80% of patients showed significant DH above resting values. IC decreased 0.37 +/- 0.39 L or 14 +/- 15% predicted during exercise (p < 0.0005), but with large variation in range. Delta IC correlated best with resting IC, both expressed %predicted (r = -0.50, p < 0.0005). Peak VO(2) (%predicted maximum) correlated best with the peak tidal volume attained (VT standardized as % of predicted vital capacity) (r = 0.68, p < 0.0005), which, in turn, correlated strongly with IC at peak exercise (r = 0.79, p < 0.0005) or at rest (r = 0.75, p < 0.0005). The extent of DH during exercise in COPD correlated best with resting IC. DH curtailed the VT response to exercise. This inability to expand VT in response to increasing metabolic demand contributed importantly to exercise intolerance in COPD.

Aged↗
PubMed2001

Effects of hyperoxia on ventilatory limitation during exercise in advanced chronic obstructive pulmonary disease.

We studied interrelationships between exercise endurance, ventilatory demand, operational lung volumes, and dyspnea during acute hyperoxia in ventilatory-limited patients with advanced chronic obstructive pulmonary disease (COPD). Eleven patients with COPD (FEV(1.0) = 31 +/- 3% predicted, mean +/- SEM) and chronic respiratory failure (Pa(O(2)) 52 +/- 2 mm Hg, Pa(CO(2 ))48 +/- 2 mm Hg) breathed room air (RA) or 60% O(2) during two cycle exercise tests at 50% of their maximal exercise capacity, in randomized order. Endurance time (T(lim)), dyspnea intensity (Borg Scale), ventilation (V E), breathing pattern, dynamic inspiratory capacity (IC(dyn)), and gas exchange were compared. Pa(O(2)) at end-exercise was 46 +/- 3 and 245 +/- 10 mm Hg during RA and O(2), respectively. During O(2), T(lim) increased 4.7 +/- 1.4 min (p < 0.001); slopes of Borg, V E, V CO(2), and lactate over time fell (p < 0.05); slopes of Borg-V E, V E-V CO(2), V E-lactate were unchanged. At a standardized time near end-exercise, O(2) reduced dyspnea 2.0 +/- 0.5 Borg units, V CO(2) 0.06 +/- 0.03 L/min, V E 2.8 +/- 1.0 L/min, and breathing frequency 4.4 +/- 1.1 breaths/min (p < 0.05 each). IC(dyn) and inspiratory reserve volume (IRV) increased throughout exercise with O(2) (p < 0.05). Increased IC(dyn) was explained by the combination of increased resting IRV and decreased exercise breathing frequency (r(2) = 0.83, p < 0.0005). In conclusion, improved exercise endurance during hyperoxia was explained, in part, by a combination of reduced ventilatory demand, improved operational lung volumes, and dyspnea alleviation.

Aged↗
PubMed2001

Evaluation of bronchodilator responses in patients with "irreversible" emphysema.

Given the emerging physiological and clinical rationale for pharmacological lung-volume reduction, assessment of volume responses to bronchodilators is likely to be highly relevant in chronic obstructive pulmonary disease (COPD). The authors examined the magnitude of lung-volume reduction after acute bronchodilator treatment in patients with advanced emphysema. Eighty-four stable patients with emphysema (mean+/-SEM forced expiratory volume in one second (FEV1): 32+/-1% predicted) performed spirometry and body plethysmography before and 15-30 min after 200 microg salbutamol. Only irreversible patients with a postbronchodilator change in FEV1 <10% pred were considered in this study. Postsalbutamol, the majority of subjects (83%) had significant improvements in one or more lung volumes: on average, residual volume (RV), functional residual capacity (FRC), inspiratory capacity (IC), forced vital capacity and slow vital capacity changed by -18+/-2, -10+/-1, 8+/-1, 9+/-1 and 7+/-1% pred (p<0.0005 each). Total lung capacity (TLC) decreased 0.12+/-0.04 L (p<0.01). Change in IC reflected change in FRC (r=-0.60, p<0.0005), but more strongly in the 57% of patients with no significant change in TLC (r=-0.93, p<0.0005). The magnitude and frequency of volume responses were greatest in patients with the most severe COPD; for example, RV decreased by 0.51+/-0.09 L (23+/-4% pred) and 0.27+/-0.04 L (14+/-2% pred) in severe and moderate subgroups, respectively. Significant reductions in lung hyperinflation occurred in the absence of a change in forced expiratory volume in one second after low-dose salbutamol in a majority of patients with advanced emphysema; the greatest changes occurred in those with the most severe disease.

Aged↗
PubMed2000

Respiratory sensation during chest wall restriction and dead space loading in exercising men.

We mimicked important mechanical and ventilatory aspects of restrictive lung disorders by employing chest wall strapping (CWS) and dead space loading (DS) in normal subjects to gain mechanistic insights into dyspnea causation and exercise limitation. We hypothesized that thoracic restriction with increased ventilatory stimulation would evoke exertional dyspnea that was similar in nature to that experienced in such disorders. Twelve healthy young men [28 +/- 2 (SE) yr of age] completed pulmonary function tests and maximal cycle exercise tests under four conditions, in randomized order: 1) control, 2) CWS to 60% of vital capacity, 3) added DS of 600 ml, and 4) CWS + DS. Measurements during exercise included cardiorespiratory parameters, esophageal pressure, and Borg scale ratings of dyspnea. Compared with control, CWS significantly reduced the tidal volume response to exercise, increased dyspnea intensity at any given work rate or ventilation, and thus limited exercise performance. DS stimulated ventilation but had minimal effects on dyspnea and exercise performance. Adding DS to CWS further increased dyspnea by 1.7 +/- 0.6 standardized Borg units (P = 0.012) and decreased exercise performance (total work) by 21 +/- 6% (P = 0.003) over CWS alone. Across conditions, increased dyspnea intensity correlated best with decreased resting inspiratory reserve volume (r = -0.63, P < 0.0005). Dyspnea during CWS was described primarily as "inspiratory difficulty" and "unsatisfied inspiration," similar to restrictive disorders. In conclusion, severe dyspnea and exercise intolerance were provoked in healthy normal subjects when tidal volume responses were constrained in the face of increased ventilatory drive during exercise.

Adult↗
PubMed1999

Spirometric correlates of improvement in exercise performance after anticholinergic therapy in chronic obstructive pulmonary disease.

We wished to determine which resting spirometric parameters best reflect improvements in exercise tolerance and exertional dyspnea in response to acute high-dose anticholinergic therapy in advanced COPD. We studied 29 patients with stable COPD (FEV(1) = 40 +/- 2% predicted [%pred]; mean +/- SEM) and moderate to severe chronic dyspnea. In a double-blind placebo-controlled cross-over study, patients performed spirometry and symptom-limited constant-load cycle exercise before and 1 h after receiving 500 micrograms of nebulized ipratropium bromide (IB) or saline placebo. There were no significant changes in spirometry, exercise endurance, or exertional dyspnea after receiving placebo. In response to IB (n = 58): FEV(1), FVC, and inspiratory capacity (IC) increased by 7 +/- 1%pred, 10 +/- 1%pred, and 14 +/- 2%pred, respectively (p < 0.001), with no change in the FEV(1)/FVC ratio. After receiving IB, exercise endurance time (Tlim) increased by 32 +/- 9% (p < 0.001) and slopes of Borg dyspnea ratings over time decreased by 11 +/- 6% (p < 0.05). Percent change (%Delta) in Tlim correlated best with DeltaIC%pred (p = 0.020) and change in inspiratory reserve volume (DeltaTLC%pred) (p = 0.014), but not with DeltaFVC%pred, DeltaPEFR%pred, or DeltaFEV(1)%pred. Change in Borg dyspnea ratings at isotime near end exercise also correlated with DeltaIC%pred (p = 0.04), but not with any other resting parameter. Changes in spirometric measurements are generally poor predictors of clinical improvement in response to bronchodilators in COPD. Of the available parameters, increased IC, which is an index of reduced resting lung hyperinflation, best reflected the improvements in exercise endurance and dyspnea after IB. IC should be used in conjunction with FEV(1) when evaluating therapeutic responses in COPD.

Administration, Inhalation↗
PubMed1999

Ventilatory assistance improves exercise endurance in stable congestive heart failure.

We postulated that ventilatory assistance during exercise would improve cardiopulmonary function, relieve exertional symptoms, and increase exercise endurance (T(lim)) in patients with chronic congestive heart failure (CHF). After baseline pulmonary function tests, 12 stable patients with advanced CHF (ejection fraction, 24 +/- 3% [mean +/- SEM]) performed constant-load exercise tests at approximately 60% of their predicted maximal oxygen consumption (V O(2)max) while breathing each of control (1 cm H(2)O), continuous positive airway pressure optimized to the maximal tolerable level (CPAP = 4.8 +/- 0.2 cm H(2)O) or inspiratory pressure support (PS = 4.8 +/- 0.2 cm H(2)O), in randomized order. Measurements during exercise included cardioventilatory responses, esophageal pressure (Pes), and Borg ratings of dyspnea and leg discomfort (LD). At a standardized time near end-exercise, PS and CPAP reduced the work of breathing per minute by 39 +/- 8 and 25 +/- 4%, respectively (p < 0. 01). In response to PS: T(lim) increased by 2.8 +/- 0.8 min or 43 +/- 14% (p < 0.01); slopes of LD-time, V O(2)-time, V CO(2)-time, and tidal Pes-time decreased by 24 +/- 10, 20 +/- 11, 28 +/- 8, and 44 +/- 9%, respectively (p < 0.05); dyspnea and other cardioventilatory parameters did not change. CPAP did not significantly alter measured exercise responses. The increase in T(lim) was explained primarily by the decrease in LD- time slopes (r = -0.71, p < 0.001) which, in turn, correlated with the reductions in V O(2)-time (r = 0.61, p < 0.01) and tidal Pes-time (r = 0.52, p < 0.01). in conclusion, ventilatory muscle unloading with PS reduced exertional leg discomfort and increased exercise endurance in patients with stable advanced CHF.

Double-Blind Method↗
PubMed1999

Pulmonary arteriovenous malformation as a cause of severe exertional dyspnoea.

A 48-year-old woman presented to the respiratory clinic with progressive exertional dyspnoea and an abnormal chest radiograph. Examination revealed mucosal telangiectasia and pulmonary angiography confirmed the presence of two pulmonary arterial venous malformations (PAVM). After therapeutic coil embolisation, dyspnoea was markedly improved, and exercise tolerance increased. Comparison of exercise test responses before and after this therapeutic intervention provides new insights into the physiological mechanisms of exertional dyspnoea in this condition.

Arteriovenous Malformations↗
PubMed1998

Qualitative aspects of exertional dyspnea in patients with interstitial lung disease.

We compared qualitative and quantitative aspects of perceived exertional dyspnea in patients with interstitial lung disease (ILD) and normal subjects and sought a physiological rationale for their differences. Twelve patients with ILD [forced vital capacity = 64 +/- 4 (SE) %predicted] and 12 age-matched normal subjects performed symptom-limited incremental cycle exercise tests with measurements of dyspnea intensity (Borg scale), ventilation, breathing pattern, operational lung volumes, and esophageal pressures (Pes). Qualitative descriptors of dyspnea were selected at exercise cessation. Both groups described increased "work and/or effort" and "heaviness" of breathing; only patients with ILD described "unsatisfied inspiratory effort" (75%), "increased inspiratory difficulty" (67%), and "rapid breathing" (58%) (P < 0.05 patients with ILD vs. normal subjects). Borg-O2 uptake (VO2) and Borg-ventilation slopes were significantly greater during exercise in patients with ILD (P < 0.01). At peak exercise, when dyspnea intensity and inspiratory effort (Pes-to-maximal inspiratory pressure ratio) were similar, the distinct qualitative perceptions of dyspnea in patients with ILD were attributed to differences in dynamic ventilatory mechancis, i.e., reduced inspiratory capacity, heightened Pes-to-tidal volume ratio, and tachypnea. Factors contributing to dyspnea intensity in both groups were also different: the best correlate of the Borg-VO2 slope in patients with ILD was the resting tidal volume-to-inspiratory capacity ratio (r = 0.58, P < 0.05) and in normal subjects was the slope of Pes-to-maximal inspiratory pressure ratio over VO2 (r = 0.60, P < 0. 05).

Aged↗
PubMed1998

General exercise training improves ventilatory and peripheral muscle strength and endurance in chronic airflow limitation.

We studied the impact of a 6-wk supervised, multimodality endurance exercise training program (EXT) on strength and endurance of ventilatory and peripheral muscles in patients with chronic airflow limitation (CAL), and determined whether potential improvements contributed to relief of exertional breathlessness (B) and perceived leg effort/discomfort (LE), respectively. Twenty breathless patients with stable CAL (FEV1 = 41 +/- 3% predicted; mean +/- SEM) were tested at 6-wk intervals at baseline, after a nonintervention control period (pre-EXT), and post-EXT. Measurements included: pulmonary function tests (PFTs), maximal inspiratory/expiratory pressures (MIP, MEP), inspiratory muscle endurance (V(LIM)), quadriceps strength and endurance, exercise endurance, and submaximal cycle exercise with cardioventilatory and symptom responses. Measurements at baseline and pre-EXT were identical. Post-EXT, PFTs did not change; exercise endurance measured on the treadmill, cycle ergometer, arm ergometer, and by 6-min walk distance increased 40 +/- 8%, 43 +/- 10%, 12 +/- 5%, and 34 +/- 9%, respectively (p < 0.05); quadriceps strength increased 21 +/- 5% (p < 0.01); MIP and MEP increased 29 +/- 11% and 27 +/- 11%, respectively (p < 0.05); V(LIM) increased almost threefold (p < 0.05). At isotime near end-exercise, B, LE, carbon dioxide production (VCO2), oxygen consumption (VO2), ventilation, and breathing frequency (F) all fell after EXT (p < 0.05): deltaB correlated with deltaF (r = 0.58, p < 0.01). Increased MIP and V(LIM) did not correlate with improved breathlessness or exercise endurance. Similarly, changes in quadriceps strength and endurance did not correlate with changes in LE or exercise endurance. In conclusion, general nonspecific EXT improved ventilatory and peripheral muscle function in severe CAL, but such improvements did not appear to contribute significantly to reduced exertional symptoms and enhanced exercise performance.

Aged↗
PubMed1998

Measurement of symptoms, lung hyperinflation, and endurance during exercise in chronic obstructive pulmonary disease.

Changes in lung hyperinflation, dyspnea, and exercise endurance are important outcomes in assessing therapeutic responses in chronic obstructive pulmonary disease (COPD). Therefore, we studied the reproducibility of Borg dyspnea ratings, inspiratory capacity (IC; to monitor lung hyperinflation), and endurance time during constant-load symptom-limited cycle exercise in 29 patients with COPD (FEV1 = 40 +/- 2% predicted; mean +/- SEM). Responsiveness was also studied by determining the acute effects of nebulized 500 micrograms ipratropium bromide (IB) or saline placebo (P) on these measurements. During each of four visits conducted over an 8-wk period, spirometry and exercise testing were performed before and 1 h after receiving IB or P (randomized, double-blinded). Highly reproducible measurements included: endurance time (intraclass correlation R = 0.77, p < 0.0001); Borg ratings and IC at rest, at a standardized exercise time (STD), and at peak exercise (R > 0.6, p < 0.0001); and slopes of Borg ratings over time, oxygen consumption (V O2), and ventilation (R > 0.6, p < 0.0001). Responsiveness was confirmed by finding a significant drug effect for: change (Delta) in endurance time (p = 0.0001); DeltaBorgSTD and DeltaBorg-time slopes (p < 0.05); and DeltaIC at rest, at STD, and at peak exercise (p = 0.0001). With all completed visits, DeltaBorgSTD correlated better with DeltaICSTD than any other resting or exercise parameter (n = 115, r = -0.35, p < 0.001). We concluded that Borg dyspnea ratings, and measurements of IC and endurance time during submaximal cycle exercise testing are highly reproducible and responsive to change in severe COPD.

Aged↗
PubMed1997

Qualitative aspects of exertional breathlessness in chronic airflow limitation: pathophysiologic mechanisms.

We compared qualitative aspects of the sensory experience of exertional breathlessness in normal subjects and in patients with chronic airflow limitation (CAL) and sought a physiologic rationale for these. Twelve patients (66 +/- 2 yr of age, mean +/- SEM) with severe CAL (FEV1 = 37 +/- 5% predicted) and 12 age-matched normal subjects (FEV1 = 103 +/- 5% predicted) were studied. Perceived inspiratory difficulty (BorgIN), inspiratory effort (esophageal pressure expressed as a fraction of maximal esophageal pressure at isovolume [Pes/PImax]), breathing pattern, and operational lung volumes (end-expiratory/inspiratory lung volumes [EELV/EILV]) were measured during symptom-limited incremental cycle exercise testing and compared at a standard VO2 of 50% predicted maximum in normal subjects and in patients with CAL. Qualitative descriptors of breathlessness were selected immediately after exercise. Breathlessness was qualitatively different between normal subjects and patients with CAL. Both normal subjects and patients with CAL chose descriptors of increased "work/effort" and "heaviness" of breathing; however, only patients with CAL consistently chose descriptors denoting "increased inspiratory difficulty" (75%), "unsatisfied inspiratory effort" (75%), and "shallow breathing" (50%). Stepwise regression analysis identified the ratio of Pes/PImax to VT/predicted VC as the strongest correlate of standardized BorgIN (n = 24, r = 0.86, p < 0.001). This latter measurement, which reflects the relationship between effort and ventilatory output, correlated strongly with dynamic EELV/TLC at isotime (r = 0.78, p < 0.001). In conclusion, the qualitatively discrete respiratory sensations of exertional inspiratory difficulty peculiar to patients with CAL may have their origins in thoracic hyperinflation and the resultant disparity between inspiratory effort and ventilatory output.

Aged↗
PubMed1997

Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation.

The mechanisms of exertional dyspnea relief in response to supplemental oxygen (O2) in chronic airflow limitation (CAL) are not precisely known and are likely multifactorial. To explore factors contributing to the relief of dyspnea after oxygen administration, 11 patients with severe CAL (FEV1.0 = 39 +/- 3% predicted, mean +/- SEM) and mild hypoxemia (resting PaO2 = 74 +/- 2 mm Hg) breathed room air (RA) and 60% O2 during exercise at approximately 50% of their maximal incremental exercise capacity. Breathlessness ratings (Borg scale), endurance time, respiratory drive (change in mouth occlusion pressure over the first 0.1 s of inspiration, P0.1), ventilation (VE), breathing pattern, operational lung volumes, gas exchange, and metabolic parameters were compared during RA and 60% O2. PaO2 at exercise cessation during RA and 60% O2 was 65 +/- 3 mm Hg and 226 +/- 12 mm Hg, respectively (p < 0.001). With 60% O2, the mean of individual Borg/time slopes fell significantly (p < 0.05) by 23 +/- 12% and was associated with a 35 +/- 11% increase (p < 0.01) in endurance time (r = -0.64, p < 0.05). During 60% O2, slopes of P0.1 and lactate over time also fell significantly (p < 0.05), whereas delta PaCO2/time did not change significantly. At a standardized time near end-exercise, Borg, VE, and P0.1 changed during 60% O2 by -0.8 +/- 0.3 (p < 0.05), -4.1 +/- 2.0 L/min (p = 0.07), and -1.3 +/- 0.5 cm H2O/s (p < 0.05), respectively. Slopes of Borg/VE, Borg/lactate, and VE/lactate were essentially superimposable during tests on RA and O2: Borg, lactate, and VE all fell proportionally during hyperoxia. In patients with CAL and mild exercise hypoxemia, relief of exertional breathlessness during hyperoxia is explained by reduced ventilatory demand in association with reduced blood lactate levels.

Aged↗
PubMed1996

Mechanisms of relief of exertional breathlessness following unilateral bullectomy and lung volume reduction surgery in emphysema.

STUDY OBJECTIVE: To explore mechanisms of relief of exertional breathlessness following surgery to reduce thoracic gas volume in patients with emphysema. MATERIALS AND METHODS: We studied 8 patients with emphysema (FEV1 = 39 +/- 3% predicted; residual volume [RV] = 234 +/- 12% predicted; mean +/- SEM) who were severely breathless despite optimal pharmacotherapy and who underwent unilateral bullectomy for giant bullae (greater than one third hemithorax); 4 of these also had ipsilateral lung reduction (pneumectomy). Pulmonary function and cycle exercise performance (n = 6) were evaluated before and 13 +/- 3 weeks after surgery. Chronic breathlessness was measured with the Baseline Dyspnea Index and the Medical Research Council dyspnea scale. Exertional breathlessness was measured using Borg ratings at a standardized work rate (BorgSTD). RESULTS: FEV1, FVC, and maximal inspiratory pressures increased postsurgery by 29 +/- 7% (p < 0.05), 24 +/- 10% (p = 0.06), and 39 +/- 12% (p < 0.01), respectively. Plethysmographic total lung capacity, RV, and functional residual capacity fell by 14 +/- 2%, 30 +/- 4%, and 18 +/- 3%, respectively (p < 0.001). All measures of chronic breathlessness improved significantly (p < 0.05). During exercise at a standardized work rate, BorgSTD fell 45% (p < 0.05), end-expiratory lung volume (EELV) fell 22% (p < 0.01), and breathing frequency (F) fell 25% (p = 0.08). By multiple stepwise regression analysis, 99% (p = 0.007) of the variance in symptom relief (delta BorgSTD) was explained by the combination of decreased ratio of the end-expiratory lung volume to total lung capacity, decreased F, and diminished mechanical constraints on tidal volume (tidal volume to vital capacity ratio). CONCLUSION: Reduced exertional breathlessness at a given workload after volume reduction surgery was attributed to a combination of reduced thoracic hyperinflation, reduced F, and reduced mechanical constraints on lung volume expansion.

Dyspnea↗
PubMed1995

Breathlessness during induced lung hyperinflation in asthma: the role of the inspiratory threshold load.

The effects of the inspiratory threshold load (ITL) on breathlessness and ventilatory mechanics during acute bronchoconstriction were studied by comparing responses to continuous positive airway pressure (CPAP) and inspiratory positive airway pressure (IPAP) in 12 asthmatic subjects after methacholine bronchoprovocation to a maximum change (delta) in FEV1 of 50%. At maximum response, "optimal CPAP" (CPAPOPT) was selected as the level of CPAP providing maximum subjective improvement in breathlessness. Spirometry, breathing pattern, esophageal pressure (Pes), and operational lung volumes were monitored. At maximum response, FEV1 decreased by 54 +/- 3% (mean +/- SEM) (p < 0.001), dynamic end-expiratory volume (EELVdyn) increased 66 +/- 8%, by 1.4 +/- 0.2 L (p < 0.001), and subjects reported severe breathlessness (Borg Scale = 5.6 +/- 0.8). CPAPOPT (5.3 +/- 0.6 cm H2O) significantly (p < 0.001) reduced breathlessness (delta Borg Scale = -3.0 +/- 0.5) and did not cause further dynamic hyperinflation. CPAPOPT reduced peak inspiratory Pes by 27% (p < 0.001), the tension-time index (TTI) for the inspiratory muscles by 27% (p < 0.01), and the inspiratory work rate per liter of ventilation by 14% (p < 0.05). During CPAPOPT, the delivered extrinsic positive end-expiratory pressure (PEEPe) (6.4 +/- 0.4 cm H2O) was strongly related (p < 0.001) to the measured ITL (6.9 +/- 1.0 cm H2O) at maximum response. Responses to IPAP of the same magnitude as CPAP OPT at maximum response were similar to those during CPAPOPT, except that IPAP did not counteract ITL or reduce breathlessness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗