Drive and Performance of the Ventilatory Apparatus in Chronic Obstructive Lung Disease

Lourenço, Ruy V.; Miranda, Joseph M.

doi:10.1056/nejm196807112790201

Cited by 109 publications

(50 citation statements)

References 19 publications

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“…This pattern is consistent with a previous study by LOURENÇO and MIRANDA [22] showing that the Edi response to carbon dioxide tension (PCO 2 ) is remarkably low in hypercapnic COPD patients. Contrasting evidence, however, was given in a brief report by GRIBBIN et al [14].…”

supporting

confidence: 93%

“…To our knowledge, only a few studies [14,15,21,22] have dealt with Edi measurement of chemoresponsiveness to carbon dioxide in patients with COPD. In previous papers, we have thoroughly criticized the use of either surface or oesophageal EMG recording to assess respiratory drive in humans [9,15,19,[33][34][35][36].…”

Section: Discussionmentioning

confidence: 99%

“…Contrasting evidence, however, was given in a brief report by GRIBBIN et al [14]. On the other hand, in many relevant papers [8,10,14,22], the study group and the control group were not · · · · ^^ accurately matched for age and pulmonary mechanics. This shortcoming needs to be stressed because in assessing the relative importance of factors which affect the respiratory response to exogenous CO 2 stimulation, differentiation of diminished carbon dioxide responsiveness of central origin from that due to mechanical impairment is an important issue of clinical relevance.…”

mentioning

confidence: 95%

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Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Scano¹,

Spinelli²,

Duranti³

et al. 1995

Eur Respir J

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C Ca ar rb bo on n d di io ox xi id de e r re es sp po on ns si iv ve en ne es ss s i in n C CO OP PD D p pa at ti ie en nt ts s w wi it th h a an nd d w wi it th ho ou ut t c ch hr ro on ni ic c h hy yp pe er rc ca ap pn ni ia a G. Scano*, A. Spinelli*, R. Duranti*, M. Gorini**, F. Gigliotti**, P. Goti*, J. Milic-Emili † Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia. G. Scano, A. Spinelli, R. Duranti, M. Gorini, F. Gigliotti, P. Goti, J. Milic-Emili. ©ERS Journals Ltd 1995. ABSTRACT: To ascertain whether and to what extent the reduced ventilatory response to a hypercapnic stimulus in chronic obstructive pulmonary disease (COPD) patients depends on a blunted chemoresponsiveness of central origin or to mechanical impairment, we studied two groups of COPD patients without (group A) and with (group B) chronic hypercapnia, but with similar degrees of airway obstruction and hyperinflation.The study was performed on 17 patients (9 normocapnic and 8 hypercapnic). Six age-matched normal subjects (group C) were also studied as a control. During a CO 2 rebreathing test, ventilation (VE), mouth occlusion pressure (P0.1), and the electromyographic activity of diaphragm (Edi) were recorded and then plotted against end-tidal carbon dioxide tension (PCO 2 ).Inspiratory muscle strength was significantly lower in the hypercapnic group (group B) compared to normocapnic group (A), and in these groups compared to the control group (C). Both patient groups exhibited significantly lower ∆VE/∆PCO 2 than the control group. In hypercapnics, ∆P0.1/∆PCO 2 was significantly lower than in normocapnics and control group, whilst mouth occlusion pressure as % of maximal inspiratory pressure ∆P0.1(%MIP)/∆PCO 2 did not differ significantly among the three groups. ∆Edi/∆PCO 2 increased from C to A. At a PCO 2 of 8.65 kPa, VE was similar in the normocapnic and control group, but lower in hypercapnics; Edi was similar in hypercapnic and control group; but greater in normocapnics. P0.1(%MIP) did not differ significantly among groups.Although these data seem to suggest that CO 2 chemoresponsiveness was normal in hypercapnic and increased in normocapnic COPD patients, the lower VE at a PCO 2 of 8.65 kPa casts doubts about the adequacy of chemoresponsiveness in the hypercapnic group. In the latter, the reduced P0.1 response in face of normal P0.1(MIP) and Edi responses to carbon dioxide stimulation could suggest an impairment in inspiratory muscle function. Mechanical impairment and inadequate chemoresponsiveness are both likely to contribute to the low ventilatory response to CO 2 stimulation in chronic hypercapnic COPD patients. Eur Respir J., 1995, 8, 78-85

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supporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

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Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Scano¹,

Spinelli²,

Duranti³

et al. 1995

Eur Respir J

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“…On the other hand, the differences become less extent in occlusion pressure response, and the values of slopes are 0.64± 0.32 and 0.48± 0.29 cmH2 0 mmHg ', respectively (p >0.05). The differences in both slopes might be due to the fact that ventilatory response could no longer represent an accurate respiratory drive in COPD patients due to mechanical impairments (Eldridge and Davis 1959; Lourenco and Miranda 1968;Gelb et al 1977). …”

Section: Resultsmentioning

confidence: 99%

Effect of chlormadinone acetate, a synthetic progesterone, on restoring impaired load compensation in chronic obstructive pulmonary disease.

Kimura

Tatsumi

Kuriyama

et al. 1986

Tohoku J. Exp. Med.

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“…The relationship between the arterial carbon dioxide tension (Pa,CO 2 ) and indices of airway obstruction or ventilation-perfusion mismatch, such as the forced expiratory volume in one second (FEV1) or physiological dead space/tidal volume ratio (VD/VT), is weak [6,7]. An excessive load on the respiratory muscles [8], alterations in respiratory timing and pattern [9,10], and a decreased central inspiratory drive [11] have also been proposed, but it is difficult to demonstrate if these are primary or secondary mechanisms.…”

mentioning

confidence: 99%

Functional outcome of patients with chronic obstructive pulmonary disease and exercise hypercapnia

Simard¹,

Maltais²,

Leblanc³

1995

Eur Respir J

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F Fu un nc ct ti io on na al l o ou ut tc co om me e o of f p pa at ti ie en nt ts s w wi it th h c ch hr ro on ni ic c o ob bs st tr ru uc ct ti iv ve e p pu ul lm mo on na ar rySixteen stable COPD patients (13 males and 3 females, aged 60±5 yrs, mean±SD) who had previously undergone pulmonary function tests and progressive exercise testing with arterial blood sampling at rest and maximal capacity, entered the study. At first evaluation (E1), subjects were normocapnic at rest (arterial carbon dioxide tension (Pa,CO 2 ): 4.9-5.7 kPa, (37-43 mmHg)) and all presented exercise-induced hypercapnia (end-exercise Pa,CO 2 >5.7 kPa (43 mmHg) with a minimal 0.5 kPa (4 mmHg) increase from resting value). The subjects were re-evaluated 24-54 months later (34±8 months) (second evaluation (E2)).At E2, forced expiratory volume in one second (FEV1) had decreased from 42±13 to 38±15% of predicted values, and mean resting Pa,CO 2 had increased from 5.2±0.3 to 5.7 + 0.4 kPa. Maximal exercise capacity (Wmax) decreased between E1 and E2 from 76±30 to 56±22 W. Even if Wmax was lower at E2, end-exercise Pa,CO 2 was higher than at E1 (6.6±0.8 vs 6.4±0.5 kPa). At E2, eight subjects presented resting hypercapnia (group H), whilst the others remained normocapnic (Group N). Group H subjects had higher Pa,CO 2 , at Wmax than Group N and lower Wmax than Group N at E2. Group H and N were not significantly different for physiological dead space/tidal volume ratio (VD/VT), FEV1, lung volumes and transfer factor of the lungs for carbon monoxide (TL,CO), both at E1 and E2.In half of the patients studied, exercise hypercapnia was a step in the progression of COPD towards resting hypercapnia, and was associated with severe exercise limitation. During exercise, patients who responded to a deterioration in their lung function by increasing minute ventilation remained normocapnic at rest, whilst those who did not increase their ventilation developed chronic hypercapnia at rest during the 2-4 year follow-up period.

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Drive and Performance of the Ventilatory Apparatus in Chronic Obstructive Lung Disease

Cited by 109 publications

References 19 publications

Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Effect of chlormadinone acetate, a synthetic progesterone, on restoring impaired load compensation in chronic obstructive pulmonary disease.

Functional outcome of patients with chronic obstructive pulmonary disease and exercise hypercapnia

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