Respiratory response to arm elevation in patients with chronic airflow obstruction

We have shown that patients with chronic airflow obstruction (CAO) complain of disabling dyspnea when performing seemingly trivial tasks with unsupported arms. Surprisingly little is known about the metabolic and ventilatory responses to unsupported upper extremity activity even though some of the muscles of the upper torso and shoulder girdle are used to perform simple and complex everyday tasks as well as partake in ventilation. To determine the effect of simple arm elevation in 20 patients with CAO we studied their lung function, VO2, VCO2, and VE, with arms down at the side (AD), during 2 min with arms extended forward up to shoulder level (AE), and during recovery. To determine the pattern of ventilatory muscle recruitment we also measured endoesophageal (Ppl), gastric (Pg), and transdiaphragmatic (Pdl) pressures. In five of the patients the electromyographic signal (EMG) of the sternocleidomastoid (Sm) muscle was recorded and analyzed in its time domain (amplitude) and power spectrum density (median frequency). Within 30 s of arm elevation VO2, VCO2, and VE rose and remained elevated for 1 min after the arms were lowered. The increase in VE resulted from increases in respiratory rate and minimal rise in tidal volume (VT). With AE, FEV1 decreased by 5% (p less than 0.02) but FRC increased by 2% (p less than 0.05). Peak inspiratory pressure (Pimax) dropped from 54 +/- 4 to 48 +/- 4 cm H2O (p less than 0.005); Pdimax remained unchanged. Immediately after raising the arms Pgi, inspiratory swing in Pdi (delta Pdi), end-expiratory Ppl, and end-expiratory Pg increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of unsupported arm exercise on ventilatory muscle recruitment in patients with severe chronic airflow obstruction

We have proposed that unsupported arm exercise alters ventilatory muscle recruitment and precipitates dyspnea in patients with severe chronic airflow obstruction (CAO). To test this hypothesis, we studied 11 patients with CAO during symptom-limited, unsupported arm exercise (UAE) and compared it with supported arm cycling (SAE). During each exercise period, we recorded endoesophageal (PpI), gastric (Pg), and transdiaphragmatic (Pdi) pressures along with heart rate, respiratory rate, and endurance time. Expired gas was collected to determine oxygen uptake (VO2) and minute ventilation (VE). Exercise endurance was shorter for UAE than for SAE (210 +/- 114 versus 270 +/- 120 s, p less than 0.05), even though peak exercise heart rate (113 +/- 5 versus 122 +/- 7 beats/min, p less than 0.05), VO2 (5.9 +/- 0.5 versus 7.1 +/- 0.8 ml/kg/min, p less than 0.05) and VE (16.5 +/- 1.2 versus 19.8 +/- 1.3 L/min, p less than 0.05) were lower for UAE. Mean (+/- SD) values for changes in pleural (delta PpI) and gastric (delta Pg) pressures during either type of arm exercise were significantly greater than at rest (p less than 0.02). In eight of 11 patients during UAE, the changes between end-inspiratory and end-expiratory transdiaphragmatic pressure (delta Pdi) were observed to develop in a similar pattern. In these patients, end-inspiratory Pg was more positive and end-inspiratory PpI was less negative during UAE than during SAE (p less than 0.02). In addition, PpI at end expiration was markedly positive when performing UAE (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory response during arm elevation in isolated diaphragm weakness.

Upper extremity exercise is associated with a significant metabolic and ventilatory cost that is particularly evident in patients with severe chronic airflow obstruction. In these patients abnormal ventilatory muscle recruitment has been hypothesized to relate to impaired diaphragm function resulting from hyperinflation. Similar data have never been reported in patients with isolated diaphragm weakness but without airflow obstruction or hyperinflation, a group that would ideally define the role of diaphragm function during arm elevation (AE). We prospectively studied 15 patients with isolated diaphragm weakness of varying severity (Pdi(sniff), 31.74 +/- 3.75 cm H(2)O) as contrasted with eight normal subjects (Pdi(sniff), 111. 77 +/- 13.35 cm H(2)O) of similar age. Patients with diaphragm weakness demonstrated significant lung volume restriction with normal DL(CO)/VA. There was no difference in resting oxygen consumption (V O(2)), carbon dioxide production (V CO(2)), minute ventilation (V E), and tidal volume (VT) between the two groups; however, a borderline difference in resting breathing frequency (f(b)) (p = 0.056) was evident. Both groups demonstrated a rise in V O(2), V CO(2), and V E during 2 min of AE anteriorly. Normal subjects demonstrated a statistically significant rise in VT but a statistically insignificant rise in f(b) during AE. In contrast, patients with diaphragm weakness demonstrated a statistically significant rise in f(b) during AE but a statistically insignificant rise in VT. In patients the observed rise in VT directly correlated with baseline Pdi(sniff) (r = 0.59, p = 0.02) and Pdi(max) (r = 0.81, p = 0.002). Both groups demonstrated a rise in Pdi during AE. The rise in Pdi during AE directly correlated to Pdi(sniff) in the patients (r = 0.69, p = 0.004). Observed end-expiratory Ppl rose during arm elevation in both the patient group and in the normal control group, but no evidence of a differential response to AE was found. In those patients with greater diaphragm weakness (Pdi(sniff) < 30 cm H(2)O), abnormal respiratory muscle function (lesser rise in Pdi) and a lesser increase in VT during AE were more evident. These data highlight the importance of diaphragm function in determining the metabolic and respiratory muscle response to arm elevation.     

A comparison of the ventilatory responses to exercise of elderly and younger humans.

Elderly adults are assumed to have an exaggerated ventilatory response to exercise. This study sought to examine this assumption by comparing the steady-state ventilatory and gas exchange responses of a group of elderly and younger humans. Steady-state ventilatory responses to moderate cycle ergometer exercise were measured in 14 elderly (71.0 +/- 1.3, mean +/- SEM years) and 14 younger (21.8 +/- 0.7 years) subjects. Compared with the younger group, the elderly had a significantly higher VE, VCO2, and VO2 at all work rates. In addition, delta VE/delta VCO2 was significantly higher for the elderly than for the younger subjects (31.07 +/- 1.34 vs 27.16 +/- 1.01, respectively; p less than .03), but the intercept with the ventilation axis was significantly lower (0.81 +/- 0.97 1.min-1 vs 4.15 +/- 0.77 1.min-1, respectively; p less than .015). Consequently, the VE-VCO2 relationships of the two groups crossed and the ventilatory equivalent for CO2 was similar for both groups. Thus, in these elderly subjects, the steeper delta VE/delta VCO2 was misleading because it was not associated with a greater ventilatory equivalent for CO2. In summary, although the ventilatory response of these elderly subjects to a given work rate was greater than that of the younger subjects, this was secondary to a greater metabolic requirement and cannot therefore be considered exaggerated. Furthermore, the data suggest that delta VE/delta VCO2 may be an inappropriate index of the ventilatory response to exercise in the elderly.     

The role of exercise ventilation in clinical evaluation and risk stratification in patients with chronic heart failure

BACKGROUND: Patients with chronic heart failure (CHF) are characterised by an increased ventilatory response to exercise. The role of exercise ventilation in the risk stratification and evaluation of patients with CHF has not yet been established. AIM: To examine the relationship between exercise ventilation indices and clinical parameters of CHF and to assess the prognostic value of the ventilatory response to exercise. METHODS: The study group consisted of 87 patients with CHF (72 males, mean age 58 years) with a mean left ventricular ejection fraction of 32%. Ten patients were in NYHA class I, 38 - in NYHA class II, 34 - in NYHA class III, and 5 - in NYHA class IV. The control group consisted of 20 patients without CHF (13 males, mean age 58 years, mean LVEF - 61%). All studied subjects underwent maximal exercise test with gas-exchange measurement. The following parameters were analysed: peak exercise oxygen consumption [peak VO(2) (ml/kg/min)], VE-VCO(2) index [a coefficient of linear regression analysis depicting an association between ventilation (VE) and carbon dioxide production (VCO(2)) during exercise] and VE/VCO(2) ratio at peak exercise to VE/VCO(2) ratio while at rest (VE/VCO(2 peak/rest)). RESULTS: Ventilatory response indices were significantly higher in patients with CHF compared with controls: VE-VCO(2) - 37.9+/-11.1 vs 27.1+/-4.1; VE-VCO(2 peak/rest) - 0.89+/-0.14 vs 0.75+/-0.10 (p<0.001). In CHF patients a significant positive correlation between ventilatory response parameters and NYHA class (VE-VCO(2) - r=0.52; VE/VCO(2 peak/rest) - r=0.47) and a negative correlation with peak VO(2) (VE-VCO(2) - r=-0.52; VE/VCO(2 peak/rest) - r=-0.49) were noted (p<0.0001 for all correlations). No correlation was found between ventilatory parameters and echocardiographic variables or CHF aetiology. During the follow-up period lasting at least 12 months, 17 (22%) patients died. In the univariate Cox model, NYHA class III-IV, decreased peak VO(2) and increased VE-VCO(2) and VE/VCO(2 peak/rest) values were significantly associated with the risk of death. The multivariate analysis revealed that VE/VCO(2 peak/rest) > or =1.0 was the adverse prognostic factor, independent of peak VO(2) (p=0.02) and NYHA class (p=0.01). The Kaplan-Meier analysis showed that prognosis during the 18-month follow-up period in patients with enhanced exercise ventilation was worse than in the remaining patients (59% survival in patients with VE/VCO(2 peak/rest) > or =1.0 59% vs 91% survival in patients with VE/VCO(2 peak/rest) <1.0, p=0.001). CONCLUSIONS: In patients with stable CHF simple exercise ventilation parameters may provide important clinical and prognostic information.     

Impaired glucose tolerance worsens exercise capacity and ventilatory response to exercise in patients with chronic heart failure

BACKGROUND: There is increasing evidence for the importance of peripheral abnormalities in the pathogenesis and progression of heart failure (HF). Recently, glucose and insulin metabolism abnormalities have been intensively investigated in patients with HF. AIM: To investigate whether coexistence of impaired glucose tolerance (IGT) may decrease exercise tolerance and influence ventilatory response to exercise in patients with systolic HF. METHODS: Maximal cardiopulmonary exercise test with evaluation of peak VO2 and VE/VCO2 slope and oral glucose tolerance test were performed in 64 clinically stable patients with HF and LVEF <45%. RESULTS: Impaired glucose tolerance was diagnosed in 26 (41%) patients and normal glucose tolerance (NGT) in 38 (59%) patients. There were no significant differences in baseline clinical characteristics or LVEF between groups. There were significant differences in peak VO2 between IGT and NGT (15.4+/-4.1 vs. 18.7+/-4.2 ml/kg/min respectively; p=0.003) and VE/VCO2 slope (35.7+/-7.3 vs. 31.8+/-5.7 respectively; p=0.02). The IGT was independently related to peak VO2 and VE/VCO2 slope in multivariate regression analysis. CONCLUSION: The IGT is associated with worse exercise capacity and ventilatory response to exercise in patients with HF.     

Atriobiventricular pacing improves exercise capacity in patients with heart failure and intraventricular conduction delay

OBJECTIVES: We sought to assess the efficacy of biventricular pacing with respect to both peak and submaximal measures of exercise in patients with New York Heart Association class III heart failure (HF) and intraventricular conduction delay in a randomized, blinded study. BACKGROUND: Submaximal and maximal changes in exercise capacity need evaluating in this patient population with this novel therapy. METHODS: Graded exercise and 6-min walk tests were performed in patients randomized to three months each of active (atrio-biventricular) and inactive pacing. Minute ventilation (VE), oxygen uptake (VO(2)), ventilated carbon dioxide (VCO(2)) and heart rate were measured in patients achieving a respiratory quotient >1 (n = 30). Oxygen pulse, anaerobic threshold (AT) and ventilatory efficiency (VE/VCO(2)) were calculated. RESULTS: Active biventricular pacing increased peak VO(2) (15.8 +/- 4.3 vs. 14.4 +/- 4.6 ml/kg/min, p = 0.02), exercise time (501 +/- 223 s vs. 437 +/- 233 s, p < 0.001) and oxygen pulse (9.3 +/- 2.8 vs. 8.1 +/- 3.1 ml/beat, p < 0.01) compared with inactive pacing. The submaximal measures of exercise capacity significantly increased with active pacing: AT (11.2 +/- 4.1 ml/kg/min vs. 9.5 +/- 2.3 ml/kg/min, p = 0.02) and 6-min walk (414 +/- 94 m vs. 359 +/- 94 m, p = 0.001). Minute ventilation/ventilated carbon dioxide improved (32 +/- 9 vs. 36 +/- 11, p = 0.03) with normalization of the VE/VCO(2) slope in 59% of patients (chi-square test, p = 0.002) with active pacing. CONCLUSIONS: Biventricular pacing may improve maximal and submaximal exercise capacity in patients with advanced HF and intraventricular conduction delay.     

Gas exchange during maximal upper extremity exercise

STUDY OBJECTIVE: to characterize gas exchange and cardiopulmonary performance during maximal progressive arm crank exercise. DESIGN: Cardiopulmonary variables were measured and arterial blood gases were determined in blood samples obtained from an indwelling radial arterial catheter during arm crank exercise (34 watts/min). Arm crank exercise was compared to maximal leg exercise performed by a different but comparable group of subjects from a previous study. PARTICIPANTS: 19 healthy young (mean +/- SEM: 20 +/- 1 yr) black males. RESULTS: Peak arm crank exercise resulted in lower values compared to peak leg exercise for: power (129 +/- 2 vs 253 +/- 10 W), VO2 (2.17 +/- 0.04 vs 3.26 +/- 0.14 L/min); VCO2 (2.9 +/- 0.11 vs 4.32 +/- 0.17 L/min); HR (168 +/- 3 vs 189 +/- 3 beats/min); AT (1.15 +/- 0.05 vs 1.83 +/- 0.07 L/min); and VE (101 +/- 2 vs 144 +/- 8 L/min), respectively. Arm crank exercise (baseline vs peak) elicited an impressive improvement in PaO2 (85 +/- 1 to 97 +/- 1 mm Hg), no change in SaO2 (96 +/- 0.2 to 96 +/- 0.2 percent), no significant increase in P(A-a)O2 (3 +/- 0.7 to 5 +/- 0.9 mm Hg) and an appropriate trending decrease in VD/VT (0.22 +/- 0.01 to 0.17 +/- 0.01). Peak arm crank values were significantly different from peak cycle exercise for PaO2 (82 +/- 2.2 mm Hg), SaO2 (93 +/- 0.4 percent), P(A-a)O2 (21 +/- 1.9 mm Hg) and VD/VT (0.08 +/- 0.01). At comparable levels of VO2 for arm crank and cycle exercise (2.17 +/- 0.04 vs 2.26 +/- 0.08 L/min), significant differences were observed for PaO2 (97 +/- 1.4 vs 81 +/- 1.9 mm Hg); SaO2 (96 +/- 0.2 vs 94 +/- 0.4 percent); P(A-a)O2 (5 +/- 0.9 vs 14 +/- 1.5 mm Hg); and VD/VT (0.17 +/- 0.01 vs 0.08 +/- 0.01), respectively. CONCLUSIONS: Maximal arm crank exercise represents a submaximal cardiopulmonary stress compared to maximal leg exercise. The differences in gas exchange observed at peak exercise between arm crank and leg exercise for the most part reflect the lower VO2 achieved. However, the persistence of these gas exchange differences even at a comparable level of VO2 suggests that factors other than VO2 may be operative. These factors may include differences in alveolar ventilation, CO2 production, ventilation-perfusion inequality, diffusion, and control of breathing.     

Cardiopulmonary exercise testing in children with heart failure secondary to idiopathic dilated cardiomyopathy

STUDY OBJECTIVE: To determine and compare the cardiopulmonary responses of healthy children and children with heart failure due to idiopathic dilated cardiomyopathy (IC) to progressive treadmill exercise testing. SETTING: University teaching hospital specializing in cardiology. PATIENTS OR PARTICIPANTS: Twenty-six children with stable, chronic heart failure (left ventricular ejection fraction < 45%) caused by IC (IC group) and 12 healthy children (control group). INTERVENTIONS: After 12-lead resting ECG, all children underwent progressive treadmill exercise testing using a modified Naughton protocol. Tests were performed in a controlled-temperature exercise facility, at least 2 h after a light meal. MEASUREMENTS AND RESULTS: Cardiopulmonary parameters were assessed at rest, at anaerobic threshold (AT), and at peak exercise. At rest, the tidal volume (VT) and O(2) consumption (VO(2)) for heart rate (O(2) pulse) were lower, while the heart rate, respiratory rate, and ventilatory equivalent for O(2) (minute ventilation [VE]/VO(2)) were higher in the IC group compared with the control group. At AT, the systolic BP, O(2) pulse, VT, exercise duration, VO(2), CO(2) production (VCO(2)), and VE were lower, while the VE/VO(2) and ventilatory equivalent for CO(2) (E/CO(2)) were higher in the IC group (p < 0.05). At peak exercise, the IC group had a significantly lower systolic BP, O(2) pulse, VE, VT, exercise duration, VO(2), and VCO(2), but higher VE/VO(2) and VE/VCO(2) than the control group (p < 0.05). The VE/VCO(2) slope was significantly higher for the IC group. No correlation existed between variables evaluated at rest vs during exercise. CONCLUSIONS: Gas exchange analysis performed during exercise successfully differentiated children with heart failure from healthy children.     

Ventilatory and metabolic effects of glucose infusions

It has been demonstrated that total parenteral nutrition (TPN) results in increased O2 consumption (VO2), CO2 production (VCO2) and minute ventilation (VE). TPN consists of a mixture of glucose and amino acids. The individual role of each of these nutrients in mediating these changes has not been well established. To examine the effects of the individual nutrients, continuous infusions of glucose in hypo- and hypercaloric amounts were given to four normal volunteer subjects and four acutely ill patients for a six-day period, with three days on each dietary intake. After each three-day period, gas exchange, VO2, VCO2, and ventilatory variables (VE), tidal volume (VT), frequency (f), mean inspiratory flow (VT/TI), inspiratory time (TI) and expiratory time (TE) were measured. With the high carbohydrate diet, CO2 production increased 18 percent (p greater than .05) and 7 percent (p greater than .05) in the normal subjects and the patients, respectively. VO2 did not change, while the RQ rose. VE rose in parallel with VCO2, with no significant change in ventilatory sensitivity to CO2. In light of previous observations, these results suggest that during administration of TPN, the protein component plays a major role in the observed ventilatory changes: a) by bringing about a rise in VO2, which acts to magnify the effect of an increased RQ on VCO2, and b) by increasing ventilatory sensitivity to CO2.     

Combining peak oxygen consumption and ventilatory efficiency in the prognostic assessment of patients with heart failure

Exercise ventilatory efficiency (VE/VCO2 slope) and peak oxygen consumption (VO2) are strong mortality predictors in patients with heart failure and we combined these 2 variables' beta coefficients from Cox regression to investigate a new prognostic index. Average follow-up was 3.8+/-1.8 years for 355 patients (72% male, 51+/-10 years). The beta coefficients from peak VO2 (17.3+/-5.0 ml x kg(-1) x min(-1)) and VE/VCO2 slope (37.0+/-9.0) constructed an exercise index defined as one half the peak VO2 subtracted from one fifth of the VE/VCO2 slope. The mean index was -1.14+/-3.79 and a more positive index was always associated with a higher probability of death. Patients with extremely poor prognoses were identified equally well by the index and by individual thresholds for peak VO2 (<14 ml x kg(-1) x min(-1)) and of VE/VCO2 slope (>40). In conclusion, the index did not add additional prognostic information in this cohort but it did display the prognostic superiority of VE/VCO2 slope.     

Pulmonary gas exchange and exercise capacity in patients with systemic lupus erythematosus

OBJECTIVE: Exercise tolerance is often reduced in patients with systemic lupus erythematosus (SLE). Mechanisms have been proposed but the underlying causes have not yet been elucidated. The study of pulmonary gas exchange during exercise may be helpful in revealing circulatory, ventilatory, and metabolic abnormalities. We hypothesized that in SLE, exercise aerobic capacity would be reduced due to chronic inactivity and poor muscle energetics. METHODS: Thirteen women with SLE and low disease activity were studied; 5 age matched subjects served as controls. Clinical examination, chest radiography, electrocardiogram, and pulmonary function test were all normal. Subjects underwent 1 min incremental cycle ergometer exercise to exhaustion. Oxygen uptake (VO2), CO2 output (VCO2), minute ventilation (VE), heart rate (HR), and arterial O2 saturation were monitored. Anaerobic threshold (AT), VO2/HR, deltaVO2/deltaWatt, respiratory rate (RR), Ti/Ttot, VE/VCO2, and breathing reserve (BR) were computed. RESULTS: At rest, patients exhibited high VE, respiratory alkalosis, and a wide alveolar-arterial O2 gradient [(A - a)O2] during 50% O2 breathing. Other indexes of respiratory function were within the normal range. In the 6 patients with SLE where pulmonary artery systolic pressure at Doppler echocardiography was measurable, mean level was in the upper limits of normal. During exercise, maximal aerobic capacity was reduced in all patients (VO2 peak, 1098+/-74 vs. 2150+/-160 ml/min, p<0.01; AT, 36 +/-3 vs. 48+/-3% predicted VO2 max, p<0.05). Ventilation adjusted for the metabolic demand (VE/VCO2 at AT) was increased (31+/-1 vs. 24+/-1; p<0.05). A normal breathing pattern was observed during all tests. No patient stopped exercising because of ventilatory limitation (i.e., they had normal breathing reserve). CONCLUSION: Reduced muscle aerobic capacity is common in SLE and is most likely because of peripheral muscle deconditioning. Increased ventilatory demand, secondary to diffuse interstitial lung disease, is not a significant contributor to the reduction in exercise tolerance.     

Effect of hyperoxia on gas exchange and lactate kinetics following exercise onset in nonhypoxemic COPD patients

STUDY OBJECTIVES: The slow oxygen uptake (VO(2)) kinetics observed in COPD patients is a manifestation of skeletal muscle dysfunction of multifactorial origin. We determined whether oxygen supplementation during exercise makes the dynamic VO(2) response faster and reduces transient lactate increase. DESIGN: Ten patients with severe COPD (ie, mean [+/- SD] FEV(1), 31 +/- 10% predicted) and 7 healthy subjects of similar age performed four repetitions of the transition between rest and 10 min of moderate-intensity, constant-work rate exercise while breathing air or 40% oxygen in random order. Minute ventilation (VE), gas exchange, and heart rate (HR) were recorded breath-by-breath, and arterialized venous pH, PCO(2), and lactate levels were measured serially. RESULTS: Compared to healthy subjects, the time constants (tau) for VO(2), HR, carbon dioxide output (VCO(2)), and VE kinetic responses were significantly slower in COPD patients than in healthy subjects (70 +/- 8 vs 44 +/- 3 s, 98 +/- 14 vs 44 +/- 8 s, 86 +/- 8 vs 61 +/- 4 s, and 81 +/- 7 vs 62 +/- 4 s, respectively; p < 0.05). Hyperoxia decreased end-exercise E in the COPD group but not the healthy group. Hyperoxia did not increase the speed of VO(2) kinetics but significantly slowed VCO(2) and E response dynamics in both groups. Only small increases in lactate occurred with exercise, and this increase did not correlate with the tau for VO(2). CONCLUSION: In nonhypoxemic COPD patients performing moderate exercise, the lower ventilatory requirement induced by oxygen supplementation is not related to improved muscle function but likely stems from direct chemoreceptor inhibition.     

Ventilatory response of moderately obese women to submaximal exercise

To investigate the effect of moderate obesity on ventilatory responses to graded exercise, we compared the ventilatory responses of ten moderately obese (35 +/- 5 percent body fat) and nine leaner women (22 +/- 2 percent body fat) during walking on a treadmill with incremental increases in percent grade. Speed remained constant at 3.0 mph. In the obese women, VO2 in l/min and ml/FFW/min, fb (b/min), VE (l/min), and HR were significantly greater (P less than 0.05) at all four absolute workloads. At 10.0 and 12.5 percent grade, VO2 (ml/kg/min) was smaller and VE/VO2 was greater in the obese women. The difference in VE/VO2 suggests a lower ventilatory threshold for the obese women. Percent VO2 max and R (VCO2/VO2) were significantly different at 12.5 percent grade only. When VO2 was divided by HR (oxygen pulse), the two groups were not significantly different at any of the four workloads tested. The groups were compared further at workloads representing approximately 55, 65, 75, and 85 percent of VO2 max. HR was not significantly different at any of the four relative exercise intensities. VE was significantly greater in the obese at 85 percent of maximum only (P less than 0.05) and fb was significantly greater at 55, 75, and 85 percent of maximum. Whereas cardiorespiratory responses of moderately obese women are increased at absolute workloads when compared to that of leaner women, HR is similar at comparable intensities of exercise. VE is also similar at comparable intensities of exercise below ventilatory threshold but fb is greater. The effect of the higher fb on exercise tolerance is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventilatory response to exercise after intracardiac repair of tetralogy of Fallot

Previous radionuclide studies have shown residual maldistribution of lung perfusion after intracardiac repair of Tetralogy of Fallot (TF). Maldistribution of perfusion may also be detectable by measurements of gas exchange during exercise. Thus, we used exercise to test for maldistribution of perfusion in 13 children (8 to 18 yr of age) who were clinically well (New York Heart Association Class 1) 7 to 14 yr after repair of TF. Sixteen children, matched to the study group by age, size, and sex, served as control subjects. Peak oxygen consumption during progressive exercise on a cycle ergometer was 28.7 +/- 6.6 (SD) ml/kg/min for the study group compared with 35.7 +/- 6.9 for the control subjects (p less than 0.05). During steady-state exercise at a VCO2 of 0.6 L/min, ventilation (VE) and the ventilatory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2) were high (VE/VCO2 = 35.9 +/- 4.4 versus 32.0 +/- 3.5, p less than 0.05), whereas mixed expired and end-tidal CO2 concentrations were low (PETCO2 = 34.0 +/- 2.4 versus 39.2 +/- 3.0 mm Hg, p less than 0.001). Indices of pulmonary function were normal; FVC values were 96 +/- 17% and FEV, values were 96 +/- 16% of predicted values. Therefore, children who are clinically well may exhibit gas exchange abnormalities compatible with mild maldistribution of lung perfusion 7 to 14 yr after repair of TF.     

Differential contribution of dead space ventilation and low arterial pCO2 to exercise hyperpnea in patients with chronic heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

In chronic heart failure (CHF), the abnormally large ventilatory response to exercise (VE/VCO(2) slope) has 2 conceptual elements: the requirement of restraining arterial partial pressure of carbon dioxide (pCO(2)) from increasing (because of an increased ratio between increased physiologic dead space and tidal volume [VD/VT]) and the depression of arterial pCO(2) by further increased ventilation, which necessarily implies an important non-carbon dioxide stimulus to ventilation. We aimed to assess the contribution of these 2 factors in determining the elevated VE/VCO(2) slope in CHF. Thirty patients with CHF underwent cardiopulmonary exercise testing (age 65 +/- 11 years, left ventricular ejection fraction 34 +/- 15%, peak oxygen uptake 15.2 +/- 4 ml/kg/min, VE/VCO(2) slope 36.4). At rest and during exercise, arterial pCO(2) was measured and VD was calculated and separated into serial and alveolar components. VD/VT decreased from 0.57 at rest to 0.44 at peak exercise (p <0.01). VE/VCO(2) slope was correlated with peak exercise VD/VT (r = 0.67), the serial VD/VT ratio (r = 0.64), and alveolar VD/VT ratio (r = 0.51) at peak exercise (all p <0.01). VE/VCO(2) slope was also correlated with arterial pCO(2) (r = -0.75, p <0.001). Despite this, arterial pCO(2) was not related to peak oxygen uptake (r = 0.2) or to arterial lactate (r = -0.25) and only weakly to New York Heart Association functional class (F = 3.7). First, the increased VE/VCO(2) slope was caused by both the high VD/VT ratio and by other mechanisms, as shown by low arterial pCO(2) during exercise. Second, this latter component (depression of arterial pCO(2)) was not related to conventional measures of heart failure severity.     

Prognostic value of serum levels of tumor necrosis factor-alpha in patients with heart failure

INTRODUCTION AND OBJECTIVE: Tumor necrosis factor-alpha is an inflammatory cytokine which rises in heart failure and has prognostic value in severe cases. Its value is less established in moderate cases. Our aim was to determine its prognostic value in cases from a community hospital. PATIENTS: We studied 50 patients, average age 59.5 12.3 years, with dilated cardiomyopathy (72% non-ischemic) and moderate heart failure (59% functional class II). METHODS: Patients were evaluated with an echocardiogram and cardiopulmonary treadmill stress test (Naughton), muscular strength measurements (hand dynamometer), blood tumor necrosis factor levels, and an average follow-up of 17.5 9 months (range, 1-29 months). All causes of mortality, cardiac transplantation, and readmissions for heart failure were recorded. RESULTS: Twenty-three patients experienced events. These patients were older (63 +/- 12.7 vs 55.7 +/- 11.4 years; p = 0.042), had a lower peak VO2 (13.7 +/- 3.9 vs 16 +/- 3.3 ml/kg/min; p = 0.035), and higher peak VE/VCO2 and factor levels [41.9 +/- 10.6 vs 33.2 +/- 5.7; p = 0.001 and 4.3 (3.1-7.9) vs 3.3 (2.4-4.3) pg/ml; p = 0.021, respectively]. In the Cox model, the only variable with independent prognostic value was peak VE/VCO2 [HR 1.13 (1.07-1.19); p < 0.001]. The best cutoff point was 34.5 (sensitivity, 86.4%; specificity, 58.3%; p = 0.0007). The cytokine had no independent prognostic value. CONCLUSIONS: Our patients with events were older, had a lower peak VO2, and higher peak VE/VCO2 and serum tumor necrosis factor levels. However, only peak VE/VCO2 had independent prognostic value.     

Peak physiologic responses to arm and leg ergometry in male and female patients with airflow obstruction

STUDY OBJECTIVE: To investigate differences in work capacity for the arms and legs in patients with moderate-to-severe COPD. DESIGN: Cross-sectional investigation. PATIENTS: One hundred twenty-four patients (90 men and 34 women) aged 45 to 81 years with moderate-to-very severe COPD. FEV(1) ranged from 0.70 to 2.79 L/min (FVC, 1.73 to 5.77 L; FEV(1)/FVC, 24 to 69%). All patients were in stable condition at the time of testing and receiving a stable drug regime. MEASUREMENTS: Each patient completed a demographic and medical history questionnaire, pulmonary function studies (spirometry, lung volumes, and diffusion capacity), peak exercise ergometry with gas exchange for the arms and legs; they also rated their subjective assessment of perceived dyspnea and extremity fatigue using Borg scores during exercise. RESULTS: Patients were of comparable age, with men taller and heavier than women. Smoking history was significantly less for women (47.9 pack-years vs 66.6 pack-years for men) even though each group presented with equivalent age (p > 0.05). Women were less obstructed than men, with FEV(1)/FVC (mean +/- SD) of 46.5 +/- 10.9% vs 40.2 +/- 9.3%, respectively. Ventilatory limitation during exercise was noted for all patients studied. Peak work capacity was greater for men, and leg peak responses were greater than arm values for each gender. As airway obstruction increased, work capacity became more limited. Peak arm work achieved was 38.9 +/- 19.6 W, oxygen uptake (VO(2)) was 903.9 +/- 263.5 mL/min, and minute ventilation (VE) was 33.7 +/- 9.5 L. Peak leg work value was 62.9 +/- 24.8 W, VO(2) was 1,091.4 +/- 321.5 mL/min, and VE was 39.3 +/- 12.0 L. Hence, arm values were 62%, 83%, and 85% of the measured leg values, respectively. Dyspnea and extremity effort scores were similar for men and women, and for arms and legs. Regression analysis was used to derive prediction equations for arm work from measured leg ergometry testing. For watts of work, a three-variable model emerged explaining 66% of the variance; VO(2) yielded a four-variable model with 80% of the variance explained; and VE yielded a three-variable model explaining 72% of the variance. CONCLUSION: Arm work is reduced by 38% that of the legs, while more modest reductions are noted for VO(2) and VE, suggesting greater mechanical efficiency for leg work as compared to arm work. These data also suggest greater metabolic demand for respiratory muscles and arm ergometry. Dyspnea and extremity Borg scores were equivalent for each modality and level of airway obstruction studied, suggesting that perception plays an important role in limiting exercise, and that a threshold for termination of exercise may exist. Further, peak leg ergometry results can be used with pulmonary function indexes to predict peak arm workload in watts, VO(2), and VE. These data may be used to assist the clinician in prescribing rehabilitation or estimating arm exercise ability when arm testing is unavailable.     

Effect of continuous positive airway pressure on respiratory mechanics and pattern of breathing in induced asthma

We studied the effects of continuous positive airway pressure (CPAP) in 8 asthmatic subjects in whom bronchospasm was induced by aerosolized histamine. The CPAP (12.0 +/- 0.9 cm H2O) increased functional residual capacity by only 0.27 +/- 0.12 L, raised the minimal pleural pressure (Ppl) during inspiration from -32.3 +/- 2.6 cm H2O to -22.8 +/- 2.3 cm H2O (p less than 0.01), and decreased the swings in transdiaphragmatic pressure (Pdi) from 35.1 +/- 2.4 cm H2O to 29.6 +/- 3.7 cm H2O (p less than 0.05). Although ventilation (VE) increased, the inspiratory work per liter of VE fell significantly. More importantly, the pressure-time product for the inspiratory muscles (integral of Ppl.dl) measured over 60 s, fell from 830 +/- 111 to 573 +/- 41 cm H2O.s (p less than 0.05), whereas that for the diaphragm (integral of Pdi.dt) fell from 690 +/- 91 to 497 +/- 74 cm H2O.s (p less than 0.05). We conclude that in induced asthma, CPAP reduces the load on the inspiratory muscles, improving their efficiency and decreasing the energy cost of their action. Our results justify further investigation into the role of CPAP in the treatment of respiratory failure caused by severe bronchial asthma.