Biomedical subjects

O Bauerle

Publications and source records attributed to O Bauerle.

4 recordsLinked to original sources

PubMed1998

Mechanisms by which COPD affects exercise tolerance.

In view of the recent advances in our understanding of the pathophysiology of COPD, we felt that it would be appropriate to examine the contribution of several abnormalities, not hitherto examined, to exercise limitation in this disease. These included: (1) The ability to exceed maximum expiratory flow (determined during forced maneuvers from TLC) during partial expiratory maneuvers. This is referred to as deltaFEV1. (2) Shape of the flow-volume curve (Shape). (3) Susceptibility to develop dynamic hyperinflation (dynamic hyperinflation index, DHI). (4) Ventilatory response to exercise (VEmax/VEpred). Twenty-four COPD patients (FEV1 = 42 +/- 13% pred) underwent symptom-limited progressive exercise. DeltaFEV1, shape, DHI and VEmax/VEpred were determined. All values were normalized to eliminate the effects of age, sex, and body size. Shape had no impact on peak VO2 (r = 0.8). DeltaFEV1 (r = 0.50), DHI (r = 0.50) and VEmax/VEpred (r = 0.46) correlated significantly with peak VO2 with all three exceeding FEV1 (r = 0.43). DHI and deltaFEV1 correlated significantly with each other (r = 0.43) suggesting that the latter exerts its beneficial effects by reducing the tendency to develop DH. We conclude that variability among patients in ventilatory response to exercise and in deltaFEV1 (likely an expression of extent of regional mechanical heterogeneity) contribute importantly to variability of exercise tolerance in COPD.

Aged↗

PubMed1995

Primary pulmonary hypertension in children: clinical characterization and survival.

OBJECTIVES: This study characterized mortality in a group of Mexican children (n = 18, mean [+/- SD] age 9.9 +/- 3 years) with primary pulmonary hypertension and investigated the factors associated with their survival. BACKGROUND: Primary pulmonary hypertension is a progressive, fatal disease of unknown cause. Establishing the diagnosis earlier in life may influence prognosis. METHODS: A dynamic cohort of children with primary pulmonary hypertension were enrolled between December 1977 and May 1991 and followed up through September 1992. Measurements included hemodynamic and pulmonary function variables in addition to demographic data, medical history and response to vasodilator treatment. We also compared the survival estimates of these children with those of our adult patients with primary pulmonary hypertension (n = 42, mean age 27.9 +/- 8.5 years). RESULTS: Baseline mean (+/- SD) pulmonary artery pressure was similar in children and adults (66 +/- 15 vs. 65 +/- 18 mm Hg, p = NS), but a higher cardiac index resulted in a lower mean pulmonary vascular resistance index in children (18 +/- 7 vs. 26 +/- 12 U/m2, p < 0.01). The proportion of patients who had a positive hemodynamic response to vasodilator treatment was higher in children than in adults (41% vs. 25%). Estimated median survival in children was 4.12 years (95% confidence interval [CI] 0.75 to 8.66) and 3.12 years in adults (95% CI 0.5 to 13.25, chi-square log-rank 0.81, p = NS). Elevated right atrial pressure (rate ratio 10.2) and decreased stroke volume index (rate ratio 32.9) were the only significant predictors of mortality (Cox proportional hazards model). CONCLUSIONS: Children with primary pulmonary hypertension have a poor survival expectancy, which does not appear to differ from that in adults with primary pulmonary hypertension. Mortality in childhood primary pulmonary hypertension is also associated with variables that assess right ventricular dysfunction.

Adult↗

PubMed1995

Role of ventilatory response to exercise in determining exercise capacity in COPD.

The progression of chronic obstructive pulmonary disease (COPD) is generally associated with decreased exercise capacity. Differences in forced expired volume in 1 s (FEV1) among patients account for only a fraction of the variability in maximal oxygen consumption (VO2max). We hypothesized that variability in ventilatory response to exercise and in inspiratory mechanics and body mass index contributes importantly to variability in VO2max in this disease. We analyzed the files of 53 patients with established diagnosis of COPD who underwent a recent symptom-limited exercise test. We used inspiratory capacity and maximum inspiratory flow as measures of variability in inspiratory mechanics. The minute ventilation (VE) at the subject's VO2max was divided by the predicted in a normal subject at the same VO2 to obtain a ratio (VE,max/VE,pred). The ventilatory response during exercise provided the best correlation with peak VO2 (r = 0.62). FEV1 and inspiratory capacity also correlated with peak oxygen consumption but not as well as the ventilatory response (r = 0.49 and r = 0.46, respectively). Maximum inspiratory flow and body mass index showed only weak positive correlations (r = 0.23, not significant). The stepwise analysis generated the following equation: VO2max (%predicted) = (77.26 x VE,pred/VE,max) + [0.45 x FEV1 (%predicted)] - 23.66; r = 0.76, P < 0.001. We conclude that variability in the ventilatory response during exercise is one of the main determinants of variability in exercise capacity in COPD patients.

Adult↗

PubMed1994

Survival in primary pulmonary hypertension. Validation of a prognostic equation.

BACKGROUND: The prognosis of patients with primary pulmonary hypertension (PPH) remains a major problem for the planning and assessment of therapeutic interventions. The objectives of this study were (1) to characterize mortality in a Mexican population of patients with PPH and to investigate factors associated with survival and (2) to test the applicability in this population of the prognostic equation proposed by the US National Institutes of Health study on PPH. METHODS AND RESULTS: A dynamic cohort of patients with PPH at our institution were enrolled between June 1977 and August 1991 and prospectively followed at regular intervals through September 1992. Measurements at diagnosis included hemodynamic and pulmonary function variables in addition to information on demographic data and medical history. The response to vasodilator treatment was also analyzed. The estimated median survival of the group was 4.04 years (95% confidence interval, 2.98 to 5.08 years). Variables associated with poor survival (univariate analysis) included an elevated mean right atrial pressure, a decreased cardiac index, and a decreased mixed venous PO2. A reduced forced vital capacity and the absence of vasodilator treatment were also associated with poor survival. A multivariate Cox proportional-hazards regression analysis was used to assess the adjusted hazard ratios, hence the relative contributions of the variables controlling for confounding. Reduced forced vital capacity and cardiac index and increased right atrial pressure were still significantly associated as risk factors for survival in patients with PPH. Survival as computed by the equation correlated with real survival of PPH patients with positive predictive values of 87%, 91%, and 89% at 1, 2, and 3 years, respectively. The equation, however, was relatively unable to predict deaths in our population, in part because of the strict limits of poor prognosis. CONCLUSIONS: Mortality in PPH is largely associated with hemodynamic variables that assess right ventricular function. The proposed prognostic equation had a high sensitivity and a relatively low specificity to predict survival in our PPH population. To improve this specificity it may be necessary to increase the limits of poor prognosis as defined by the equation.

Adult↗