Aktuelle Abstracts 10.08.2001
Am J Respir Crit Care Med 2001 Jun;163(7):1637-41
Diaphragm activation during exercise in chronic obstructive pulmonary disease.
Sinderby C, Spahija J, Beck J, Kaminski D, Yan S, Comtois N, Sliwinski P
Guy-Bernier Research Center, Maisonneuve-Rosemont Hospital, Department of Medicine, and Ste Justine Research Center, Ste Justine Hospital, Montreal, Quebec, Canada. SINDERBY@COMPUSERVE.COM
Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V E) was 12.2 +/- 1.9 L/min (mean +/- SD) at rest, and increased progressively (p < 0.001) to 31.0 +/- 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 +/- 3% of TLC at end-exercise. Pdi at rest was 9.4 +/- 3.2 cm H(2)O and increased during the first two thirds of exercise (p < 0.001) to plateau at about 13 cm H(2)O. EAdi was 24 +/- 6% of voluntary maximal at rest and increased progressively during exercise (p < 0.001) to reach 81 +/- 7% at end-exercise. In conclusion, dynamic hyperinflation during exhaustive exercise in patients with COPD reduces diaphragm pressure-generating capacity, promoting high levels of diaphragm activation.
PMID: 11401887, UI: 21294707
Am J Respir Crit Care Med 2001 Jun;163(7):1614-8
Physiologic effects of negative pressure ventilation in acute exacerbation of chronic obstructive pulmonary disease.
Gorini M, Corrado A, Villella G, Ginanni R, Augustynen A, Tozzi D
Respiratory Intensive Care Unit, Careggi Hospital, Florence, Italy. firstname.lastname@example.org
To assess the physiologic effects of continuous negative extrathoracic pressure (CNEP), negative pressure ventilation (NPV), and negative extrathoracic end-expiratory pressure (NEEP) added to NPV in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD), we measured in seven patients ventilatory pattern, arterial blood gases, respiratory mechanics, and pressure- time product of the diaphragm (PTPdi) under four conditions: (1) spontaneous breathing (SB); (2) CNEP (-5 cm H(2)O); (3) NPV; (4) NPV plus NEEP. CNEP and NPV were provided by a microprocessor-based iron lung capable of thermistor-triggering. Compared with SB, CNEP improved slightly but significantly Pa(CO(2 ))and pH, and decreased PTPdi (388 +/- 59 versus 302 +/- 43 cm H(2)O. s, respectively, p < 0.05) and dynamic intrinsic positive end-expiratory pressure (PEEPi) (4.6 +/- 0.5 versus 2.1 +/- 0.3 cm H(2)O, respectively, p < 0.001). NPV increased minute ventilation (V E), improved arterial blood gases, and decreased PTPdi to 34% of value during SB (p < 0.001). NEEP added to NPV further slightly decreased PTPdi and improved patient-ventilator interaction by reducing dynamic PEEPi and nontriggering inspiratory efforts. We conclude that CNEP and NPV, provided by microprocessor-based iron lung, are able to improve ventilatory pattern and arterial blood gases, and to unload inspiratory muscles in patients with acute exacerbation of COPD.
PMID: 11401883, UI: 21294703
Am J Respir Crit Care Med 2001 Jun;163(7):1578-83
Defective natural killer and phagocytic activities in chronic obstructive pulmonary disease are restored by glycophosphopeptical (inmunoferon).
Prieto A, Reyes E, Bernstein ED, Martinez B, Monserrat J, Izquierdo JL, Callol L, de LUCAS P, Alvarez-Sala R, Alvarez-Sala JL, Villarrubia VG, Alvarez-Mon M
Department of Medicine CSIC Associated Unit, University of Alcala, Alcala de Henares, Madrid, Spain.
We have investigated both modifications in natural (innate) immunity caused by chronic obstructive pulmonary disease (COPD) and the effects of a glycophosphopeptical immunomodulator (Inmunoferon) treatment on COPD-associated immunoalterations. In a double-blinded clinical trial, 60 patients with COPD received glycophosphopeptical or placebo during 90 consecutive days at oral doses of 3 g/d. Fifty-six sex- and age-matched healthy control subjects were included as a reference group for immunologic parameters. Peripheral blood natural killer (PBNK) cell cytotoxic activity and phagocytic activity of peripheral monocytes/macrophages (Mo/Ma) and polymorphonuclear (PMN) cells were assessed at baseline and then again at the end of treatments. We found both PBNK activity and phagocytic activity to be significantly decreased in patients with COPD compared with levels in healthy volunteers. The treatment with glycophosphopeptical provoked significant stimulatory effects on PBNK cytotoxic activity. This stimulation was not mediated by an increase in CD3(-)CD56(+) NK cells. Further, glycophosphopeptical significantly increased the percentage of monocytes and PMNs that phagocytize Escherichia coli in vitro, as well as increased phagocytic indices. We conclude that peripheral blood cells of patients with COPD show clear defects in natural immunity that are partially rescued by glycophosphopeptical.
Randomized controlled trial
PMID: 11401877, UI: 21294697
Am J Respir Crit Care Med 2001 Jun;163(7):1567-71
Multivariable assessment of the 6-min walking test in patients with chronic obstructive pulmonary disease.
van Stel HF, Bogaard JM, Rijssenbeek-Nouwens LH, Colland VT
Asthmacentre Heideheuvel, Hilversum, The Netherlands. email@example.com
Functional exercise tolerance in patients with chronic obstructive pulmonary disease (COPD) is often assessed by the 6-min walking test (6MWT). To assess if the use of multiple factors adds to walking distance in describing performance in the 6MWT, an exploratory factor analysis was performed on physiological measurements and dyspnea ratings recorded during testing. Eighty-three patients with mild to severe COPD performed repeated 6MWTs before inpatient pulmonary rehabilitation. Factor analysis on 15 variables yielded a stable four-factor structure explaining 78.4% of the total variance. Recorded heart rate variables contributed to factor 1 (heart rate pattern), walking distance, heart rate increase, and decrease contributed to factor 2 (endurance capacity), oxygen desaturation variables contributed to factor 3 (impairment of oxygen transport), and dyspnea and effort variables contributed to factor 4 (perceived symptoms). Walking distance decreased in half of the 53 patients measured posttreatment, but self-perceived change in exercise tolerance improved in 84% and was explained by change in walking distance, by less desaturation, and by less dyspnea (R(2) = 0.55, p = 0.005). Qualitative analysis showed that 29 of 53 patients improved in three or four factors. Performance in the 6MWT can be described with four statistically independent and clinically interpretable factors. Because clinically relevant changes consist of more than only walking distance, assessment of functional exercise tolerance in patients with COPD improves by reporting multiple variables.
PMID: 11401875, UI: 21294695
Am J Respir Crit Care Med 2001 Jun;163(7):1562-6
Lung function 5 yr after lung volume reduction surgery for emphysema.
Gelb AF, McKenna RJ Jr, Brenner M, Epstein JD, Zamel N
Pulmonary Division, Department of Medicine, Lakewood Regional Medical Center, University of California, Los Angeles, California, USA. firstname.lastname@example.org
Current datum more than 2 yr after lung volume reduction surgery (LVRS) for emphysema is limited. This prospective study evaluates pre-LVRS baseline and 5-yr results in 26 symptomatic patients (mean age 67 +/- 6 yr) (mean +/- SD) who underwent bilateral, targeted upper lobe stapled LVRS using video-assisted thoracoscopy. Baseline forced expiratory volume in 1 s (FEV(1)) was 0.7 +/- 0.2 L (mean +/- SD), 29 +/- 10% predicted. Following LVRS, with none lost to follow-up, mortality due to respiratory failure at 0.5, 1, 2, 3, 4, and 5 yr was 4%, 4%, 19%, 31%, 46%, and 58%, respectively. Increase above baseline for FEV(1) > 200 ml and/or FVC > 400 ml at 1, 2, 3, 4, and 5 yr post-LVRS was noted in 73%, 46%, 35%, 27%, and 8% of all patients; decrease in dyspnea grade >/= 1 in 88%, 69%, 46%, 27%, and 15%; and elimination of initial oxygen dependence in 18 patients in 78%, 50%, 33%, 22%, and 0%, respectively. Expiratory airflow improved due to the increase in both lung elastic recoil and small airway intraluminal caliber. Five patients decreased FEV(1) 141 +/- 60 ml/yr and FVC 102 +/- 189 ml/yr over 3.8 +/- 1.2 yr post-LVRS, similar to their pre-LVRS rate of decline. In the 11 patients who survived 5 yr, at 0.5-1.0 yr post-LVRS peak increase in FEV(1) was 438 +/- 366 ml, with a decline of 149 +/- 157 ml the following year and 78 +/- 59 ml/yr over 4.0-4.5 yr. Bilateral LVRS provided palliative clinical and physiological improvement in 9 of 26 patients at 3 yr, 7 at 4 yr, and 2 at 5 yr.
PMID: 11401874, UI: 21294694
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