Evaluation of pulmonary function and bicycle ergometry tests in patients with Behçet’s disease

Behçet’s disease (BD) has well-defined pulmonary complications, but cardiopulmonary exercise testing and the strength of the respiratory muscles have not been studied in detail. We aimed to investigate the pulmonary functions tests, inspiratory and expiratory muscle strength and endurance, cardiopulmonary exercise test response, and the relationship of these parameters in patients with BD. Forty BD patients and 20 healthy control subjects were recruited for this study. Mean age was 32.95?±?7.66 years for the BD group and 33.85?±?6.63 years for the control group with no statistically significant difference. The ratios of slight obstructive ventilatory impairment were 32.5% for the BD group. When the values of pulmonary function tests were compared, no statistically significant difference was found in FEV₁/FVC (Forced expiratory volume during the first second/forced vital capacity), or maximal midexpiratory flow rate (all in percent) values between patient and control groups. Maximal inspiratory and expiratory pressures, peak expiratory flow rate (in percent) and maximal voluntary ventilation (in percent) values were significantly lower than those of the control group. Body’s consumption of peak oxygen (VO_2peak), oxygen consumption (milliliters per kilogram per minute), anaerobic threshold (AT), maximum exercise ventilation (VE_max), work load values, and exercise test time in the bicycle exercise test were significantly higher in control groups than in patients with BD. The values of heart rate reserve, breathing reserve, and VE/VCO₂ at the AT of BD patients were within normal limits We conclude that respiratory and aerobic exercise may be recommended to improve respiratory muscle strength and endurance as well as the aerobic capacity and maximal ventilatory capacity in patients with BD.     

Respiratory muscle deoxygenation during exercise in patients with heart failure demonstrated with near-infrared spectroscopy

Exertional dyspnea in patients with heart failure may be due, in part, to respiratory muscle underperfusion. Near-infrared spectroscopy is a new technique that permits noninvasive assessment of skeletal muscle oxygenation by monitoring changes in near-infrared light absorption. With use of near-infrared spectroscopy, serratus anterior muscle oxygenation during maximal bicycle exercise was compared in 10 patients with heart failure (ejection fraction 16 +/- 5%) and 7 age-matched normal subjects. Oxygen consumption (VO2), minute ventilation (VE) and arterial saturation were also measured. Changes in difference in absorption between 760 and 800 nm, expressed in arbitrary units, were used to detect muscle deoxygenation. Minimal change in this difference in absorption occurred in normal subjects during exercise, whereas patients with heart failure exhibited progressive changes throughout exercise consistent with respiratory muscle deoxygenation (peak exercise: normal 3 +/- 6, heart failure 12 +/- 4 near-infrared arbitrary units, p less than 0.001). At comparable work loads patients with heart failure had significantly greater minute ventilation and respiratory rate but similar tidal volume when contrasted with normal subjects. However, at peak exercise normal subjects achieved significantly greater minute ventilation and tidal volume with a comparable respiratory rate. No significant arterial desaturation occurred during exercise in either group. These findings indicate that respiratory muscle deoxygenation occurs in patients with heart failure during exercise. This deoxygenation may contribute to the exertional dyspnea experienced by such patients.     

Exercise intolerance in patients with chronic left heart failure: Relation to oxygen transport and ventilatory abnormalities

Circulatory, metabolic, and ventilatory responses to maximal and submaximal symptom-limited exercise were studied in 13 patients with chronic stable heart failure. Maximal exercise was sustained 6.5 ± 0.6 minutes (mean ± standard error of the mean) and increased minute oxygen consumption (VO₂) to 940 ± 65 ml/min, whereas submaximal exercise was sustained for 15.4 ± 2.3 minutes and increased VO₂ to 825 ± 49 ml/min (both p < 0.01 compared with maximal exercise). Both exercise protocols were terminated because of fatigue and both were associated with reduced cardiac output relative to VO₂, marked systemic oxygen extraction (80 ± 2% maximal versus 78 ± 2% submaximal) and similarly elevated blood lactate concentrations (37 ± 4 mg/dl maximal versus 36 ± 4 mg/dl submaximal), suggesting inadequate oxygen delivery to working muscle. Minute ventilation during both types of exercise was also more than twice normal relative to carbon dioxide production. However, during submaximal exercise, dyspnea was noted in only 3 patients despite these ventilatory abnormalities. During maximal exercise, dyspnea was noted in 11 patients but did not force termination of exercise or preclude achievement of marked systemic oxygen extraction and lactate production. These data suggest that patients with chronic stable cardiac failure are limited during both maximal and submaximal exercise primarily by inadequate oxygen transport to working muscle.     

Relation between chemosensitivity and the ventilatory response to exercise in chronic heart failure

Objectives. This study sought to establish the chemosensitivity of patients with chronic heart failure.Background. The ventilatory response to exercise is often increased in patients with chronic heart failure, as characterized by the steeper regression slope relating minute ventilation to carbon dioxide output. We hypothesized that the sensitivity of chemoreceptors may be reset and may in part mediate the exercise hyperpnea seen in this condition.Methods. Hypoxic and peripheral hypercapnic chemosensitivity were studied in 38 patients with chronic heart failure (35 men, 3 women; mean [±SE] age 60.2 ± 1.3 years; radionuclide left ventricular ejection fraction 25.7 ± 2.3%) and 15 healthy control subjects (11 mean, 4 women; mean age 54.9 ± 3.0 years) using transient inhalations of pure nitrogen and single breaths of 13% carbon dioxide, respectively. The change in chemosensitivity during mild exercise (25 W) was assessed in the first 15 patients and all control subjects. Central hypercapnic chemosensitivity was also characterized in 25 patients and 10 control subjects by the rebreathing of 7% carbon dioxide in 93% oxygen. Cardiopulmonary exercise testing was performed in all subjects.Results. Maximal oxygen consumption was 16.6 ± 0.9 versus 29.7 ± 2.2 ml/kg per min (p < 0.0001), and the ventilation-carbon dioxide output regression slope was 37.2 ± 1.5 versus 26.5 ± 1.4 (p < 0.0001) in patients and control subjects, respectively. Hypoxic and central hypercapnic chemosensitivity were enhanced in patients (0.707 ± 0.076 vs. 0.293 ± 0.056 liters/min per % arterial oxygen saturation [Sao₂], p = 0.0001 and 3.15 ± 0.41 vs. 2.02 ± 0.25 liters/min per mm Hg, p = 0.025, respectively) and correlated significantly with the ventilatory response to exercise. Hypoxic chemosensitivity was augmented during exercise in patients and in control subjects but remained higher in the former (1.530 ± 0.27 vs. 0.685 ± 0.12 liters/min per %Sao₂, p = 0.01). The peripheral hypercapnic chemosensitivity of patients at rest and during exercise was similar to that in control subjects, consistent with its lesser contribution to overall carbon dioxide chemosensitivity.Conclusions. Enhanced hypoxic and central hypercapnic chemosensitivity may play a role in mediating the increased ventilatory response to exercise in chronic heart failure.     

Tests of respiratory muscle function

Respiratory muscle strength and endurance should be assessed when dyspnea, respiratory failure, or poor performance on routine pulmonary function tests are unexplained. Respiratory muscle strength can be measured non-invasively from maximal mouth pressures, but measurement of transdiaphragmatic pressure refines the assessment. The maximal voluntary ventilation test is the only simple index of ventilatory or respiratory muscle endurance. Other tests for endurance and fatigue are more difficult, but some newer techniques may be applicable to the clinical laboratory. Some patients who exhibit tachypnea, marked use of neck inspiratory muscles, and chest-abdomen asynchrony may be developing respiratory muscle fatigue.     

Response in oxygen uptake and ventilation during stair climbing in patients with chronic heart failure

To examine the level of muscular work and ventilatory response to stair climbing (mobile Stairmaster staircase, 1 step/2.5 s), respiratory gas exchange, ventilation, heart rate and arterial pressure were monitored in patients with chronic heart failure and their response compared with that of normal individuals. Aerobic capacity (maximal oxygen uptake) and anaerobic threshold during treadmill exercise were also determined and used to ascertain the metabolic cost of stair climbing. No differences were observed in the response of mean arterial blood pressure between the 12 patients and 10 normal subjects during exercise or recovery. However, the heart rate and oxygen consumption obtained during exercise were significantly lower in the patients with chronic heart failure than in the normal subjects (p less than 0.05). All patients with a maximal oxygen uptake less than 20 ml/min/kg during treadmill exercise had an oxygen uptake during stair climbing that exceeded their anaerobic threshold and, consequently, they attained a significantly (p less than 0.01) higher level of ventilation during exercise and recovery. This was not the case for those patients with greater aerobic capacity. Therefore, it is concluded that stair climbing for the 12 patients with heart failure and moderate to moderately severe impairment in aerobic capacity represents strenuous anaerobic exercise. The resultant excess ventilation may explain the limiting sensation of dyspnea that is frequently experienced by these patients during and after stair climbing.     

Exercise performance improves in patients with COPD due to respiratory muscle endurance training

BACKGROUND: Impaired exercise tolerance is frequently observed in patients with COPD. Respiratory muscle endurance training (RMET) by means of normocapnic hyperpnea can be used to improve respiratory muscle function and probably exercise capacity. RMET is not applied on a large scale because complicated equipment is needed to maintain carbon dioxide homeostasis during hyperpnea, which can also be done by enlarging the dead space of the ventilatory system by breathing through a tube. Therefore, tube breathing might be a new, inexpensive method for home-based RMET. The aim of this study was to assess whether home-based RMET by means of tube breathing improves endurance exercise performance in patients with COPD. METHODS: We randomized 36 patients with moderate-to-severe COPD to RMET by paced tube breathing (n = 18) or sham training (control, n = 18). Both groups trained twice daily for 15 min, 7 days per week, for 5 weeks. RESULTS: Patients receiving RMET showed significant improvements in endurance exercise capacity (constant-load exercise on cycle ergometry; 18 min vs 28 min, p < 0.001), in perception of dyspnea (Borg score; 8.4 vs 5.4, p < 0.001), and respiratory muscle endurance capacity (sustainable inspiratory pressure; 25 cm H(2)O vs 31 cm H(2)O, p = 0.005). Quality of life (chronic respiratory disease questionnaire) also improved (78.7 to 86.6, p = 0.001). The control group showed no significant changes. CONCLUSION: Home-based RMET by means of tube breathing leads to a significant improvement of endurance exercise capacity, a reduction in perception of dyspnea, and an improvement in quality of life in patients with moderate-to-severe COPD.     

Short-term effect of nasal intermittent positive-pressure ventilation in patients with restrictive thoracic disease

BACKGROUND: The use of nasal intermittent positive pressure ventilation (NIPPV) would be expected to ameliorate dyspnea, ventilatory capacity and exercise tolerance durability in individuals with hypercapnic respiratory failure secondary to restrictive thoracic disease. OBJECTIVES: The purpose of this study was to determine the short-term effect of NIPPV on respiratory muscle endurance, exercise capacity and respiratory functions in patients with chronic respiratory failure due to restrictive thoracic disease. METHODS: Twelve patients with chronic ventilatory failure due to restrictive thoracic disease underwent nasal bilevel positive airway pressure (BiPAP) ventilation for 2 h a day during 15 consecutive days. The effects were assessed by spirometry, arterial blood gas analysis, 6-min walking test, sensation of dyspnea according to the American Thoracic Society dyspnea scoring scales (ATS) and surface electromyogram of the diaphragm (EMGdi) before and after the study (on day 15). RESULTS: Nasal BiPAP reduced the ATS dyspnea score from 2.5 +/- 0.9 to 1.6 +/- 0.4 (p < 0.01). Distances walked in 6 min increased from 320.66 +/- 93.56 to 382.41 +/- 121.20 m (p < 0.05). Comparison of baseline with levels after nasal BiPAP ventilation showed a statistically significant improvement in PaCO(2) (p < 0.05). Forced vital capacity increased from 35 to 50% of the predicted value (p < 0.01). There were no statistically significant reductions in the amplitude of EMGdi after the therapy. CONCLUSION: These results indicate that NIPPV delivered via nasal BiPAP improves respiratory functions, exercise capacity, and reduces dyspnea in the short term in patients with chronic respiratory failure due to restrictive thoracic disease. Whether such short-term improvements can be sustained merits further study.     

The effect of specific inspiratory muscle training on the sensation of dyspnea and exercise tolerance in patients with congestive heart failure.

BACKGROUND: It has been previously shown that the inspiratory muscles of patients with congestive heart failure (CHF) are weaker than those of normal persons. This weakness may contribute to the dyspnea and limit exercise capacity in these patients. The respiratory muscles can be trained for both strength and endurance. HYPOTHESIS: The present study was designed to evaluate the effect of specific inspiratory muscle training (SIMT) on inspiratory muscle performance, lung function, dyspnea, and exercise capacity in patients with moderate heart failure. METHODS: Twenty patients with CHF (NYHA functional class II-III) were recruited for the study. The subjects were randomized into two groups: 10 patients were included in the study group and received SIMT and 10 patients were assigned to the control group and received sham training. Subjects in both groups trained daily, 6 times/week, for one-half h, for 3 months. The subjects started breathing at a resistance equal to 15% of their PImax for 1 week and the resistance was then increased incrementally to 60%. Spirometry, inspiratory muscle strength (assessed by measuring the PImax at residual volume), and endurance (expressed by the relationship between PmPeak and PImax), the 12-min walk test, and peak VO2 were performed before the beginning and at the end of the training period. RESULTS: All patients in the training group showed an increase in the inspiratory muscle strength [mean (+/- standard error of the mean) PImax increased from 46.5 +/- 4.7 to 63.6 +/- 4.0 cm H2O, p < 0.005], and endurance (mean PmPeak/PImax from 47.8 +/- 3.6 to 67.7 +/- 1.7%, p < 0.05), while they remained unchanged in the control group. This was associated in the training group with a small but significant increase in forced vital capacity, a significant increase in the distance walked (458 +/- 29 to 562 +/- 32 m, p < 0.01), and an improvement in the dyspnea index score. No statistically significant change in the mean peak VO2 was noted in either group. CONCLUSIONS: Specific inspiratory muscle training resulted in increased inspiratory muscle strength and endurance. This increase was associated with decreased dyspnea, increase in submaximal exercise capacity, and no change in maximal exercise capacity. This training may probe to be a complementary therapy in patients with congestive heart failure.     

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.     

Inspiratory muscle weakness in diastolic dysfunction

OBJECTIVES: To test the hypothesis that patients with well-documented diastolic dysfunction (DD) in the setting of normal systolic function will have inspiratory muscle weakness when compared to normal control subjects, and will experience dyspnea and tachypnea during exercise. BACKGROUND: Respiratory muscle weakness has been described in patients with (systolic) congestive heart failure; however, whether or not patients with DD may present with the findings of congestive heart failure is not known. METHODS: We selected for study 14 patients with DD previously referred for cardiopulmonary evaluation whose diagnosis had been confirmed by data obtained at cardiac catheterization. Seven control subjects matched for age, sex, and weight were recruited from the hospital community. Subjects performed both basic pulmonary function tests and tests of muscle strength: handgrip strength (Hgr), and maximal subatmospheric static inspiratory muscle pressure (Pimax). Subjects then performed a graded exercise test on a bicycle ergometer. Minute ventilation, oxygen consumption, carbon dioxide production, and heart rate were monitored continuously. Echocardiography was performed three times: before exercise, at a selected submaximal exercise level (20% of a predicted maximal workload), and at maximal exercise. Subjects rated their degree of dyspnea using the Borg scale at the same three time intervals. RESULTS: Pimax was - 102 +/- 17 cm H(2)O in control subjects, and - 77 +/- 19 cm H(2)O in patients with DD (p = 0.013) [mean +/- SD]. Hgr was similar between the groups. At the selected submaximal exercise level, patients with DD rated dyspnea to be 2.6 +/- 2.2 Borg scale units (control subjects, 0.5 +/- 0.8 Borg scale units). Hey plots described a rapid, shallow breathing pattern in patients with DD during exercise. Patients with DD and control subjects achieved similar maximal work loads. CONCLUSION: Patients with DD have diminished Pimax, adopt a rapid, shallow breathing pattern during exercise, and experience dyspnea at low work loads when compared to matched control subjects.     

Amrinone and exercise performance in patients with chronic heart failure

Whether cardiotonic agents can improve the ability of patients with chronic heart failure to exercise remains unknown. Accordingly, the circulatory and respiratory response of 11 patients with severe heart failure refractory to digitalis, diuretic drugs and vasodilators was assessed during upright treadmill exercise before, within 24 hours and after 4 weeks of therapy with amrinone. The purpose of this study was to determine the ability of amrinone therapy to improve exercise hemodynamics, effort tolerance and aerobic capacity of these patients. Acute intravenous administration of amrinone (1.8 ± 0.1 mg/kg body weight) produced the following changes (mean values ± standard error of the mean) in hemodynamic variables during supine rest; increased cardiac index (from 2.04 ± 0.39 to 2.99 ± 0.38 liters/min per m²; p <0.01) and reduced pulmonary wedge pressure (from 24 ± 6 to 14 ± 6 mm Hg; p <0.01) without altering heart rate or mean arterial pressure. Within 24 hours after administration of amrinone, wedge pressure decreased at the onset of (from 25 ± 7 to 14 ± 7 mm Hg) and throughout exercise (p <0.01), whereas the exercise response of cardiac output, arteriovenous oxygen difference, heart rate, pulmonary and systemic vascular resistances, maximal oxygen uptake and the pattern of ventilation remained similar to control values. However, after 4 weeks of amrinone therapy, exercise and aerobic capacities were increased 44 and 48 percent (p <0.03), respectively, whereas the ventilatory response was unchanged. Thus, amrinone is a potent cardiotonic agent that acutely improves the function of the failing heart at rest and during exercise; the maximal aerobic capacity was increased after 4 weeks of therapy. Amrinone therefore appears to hold promise for the management of patients with chronic heart failure.     

Respiratory muscle endurance training in chronic obstructive pulmonary disease: impact on exercise capacity, dyspnea, and quality of life

Inspiratory muscle training may have beneficial effects in certain patients with chronic obstructive pulmonary disease (COPD). Because of the lack of a home training device, normocapnic hyperpnea has rarely been used as a training mode for patients with COPD, and is generally considered unsuitable to large-scale application. To study the effects of hyperpnea training, we randomized 30 patients with COPD and ventilatory limitation to respiratory muscle training (RMT; n = 15) with a new portable device or to breathing exercises with an incentive spirometer (controls; n = 15). Both groups trained twice daily for 15 min for 5 d per week for 8 wk. Training-induced changes were significantly greater in the RMT than in the control group for the following variables: respiratory muscle endurance measured through sustained ventilation (+825 +/- 170 s [mean +/- SEM] versus -27 +/- 61 s, p < 0.001), inspiratory muscle endurance measured through incremental inspiratory threshold loading (+58 +/- 10 g versus +21.7 +/- 9.5 g, p = 0.016), maximal expiratory pressure (+20 +/- 7 cm H(2)O versus -6 +/- 6 cm H(2)O, p = 0.009), 6-min walking distance (+58 +/- 11 m versus +11 +/- 11 m, p = 0.002), V O(2peak) (+2.5 +/- 0.6 ml/kg/min versus -0.3 +/- 0.9 ml/kg/min, p = 0.015), and the SF-12 physical component score (+9.9 +/- 2.7 versus +1.8 +/- 2.4, p = 0.03). Changes in dyspnea, maximal inspiratory pressure, treadmill endurance, and the SF-12 mental component score did not differ significantly between the RMT and control groups. In conclusion, home-based respiratory muscle endurance training with the new device used in this study is feasible and has beneficial effects in subjects with COPD and ventilatory limitation.     

Slowed glycogen utilization enhances exercise endurance in patients with heart failure

OBJECTIVES: The objective of the study was to investigate the impact of alteration of glycogen stores and metabolism on exercise performance in patients with heart failure. BACKGROUND: In normal subjects, muscle glycogen depletion results in increased exertional fatigue and reduced endurance. Skeletal muscle biopsies have revealed reduced glycogen content in patients with congestive heart failure (CHF). Whether glycogen depletion contributes to reduced endurance and abnormal ventilation in these patients is unknown. METHODS: Bicycle exercise tests with measurement of respiratory gases were performed following dietary manipulations to induce glycogen depletion (60% protein, 40% fat) and slow glycogen utilization (60% carbohydrate, 30% fat, 10% protein) in 13 patients with CHF (left ventricular ejection fraction 22+/-6%; age 48+/-9 years) and 7 control subjects (age 45+/-5 years). Maximal exercise, exercise at 75% of peak workload until exhaustion and 1-min cycles of supramaximal exercise at 133% of peak were performed on three occasions over a two-week period. RESULTS: Significant changes in resting respiratory quotients (RQs) in normal (Baseline: 0.78+/-0.03; Depleted: 0.69+/-0.05) and CHF subjects (Baseline: 0.84+/-0.05; Depleted: 0.72+/-0.05) were observed (both p<0.05). Peak Vo2 (oxygen consumption) in both groups was unchanged. The ventilatory response to exercise was analyzed by correlating CO2 production (V(CO2)) to minute ventilation (VE) in each test. The slopes of these correlations were not affected in either group. With glycogen depletion, exercise endurance was reduced from 17 to 6.1 min (57+/-19%) in normal subjects versus a reduction of 9.4 to 8.1 min (11+/-19%) in patients (p<0.05). With slowed glycogen use, CHF patients increased exercise endurance from 9.4 to 16.5 min (65%) versus 17 to 20.6 min (18%) in normal subjects (p<0.05). CONCLUSIONS: Glycogen depletion minimally affects maximal exercise performance, endurance or ventilation in CHF patients, whereas slowed glycogen utilization markedly enhances exercise endurance. Therapeutic interventions that increase or slow use of glycogen stores may have clinical benefit.     

Ventilatory mechanisms of exercise intolerance in chronic heart failure.

Mechanisms that have been suggested to underlie the abnormal ventilatory response to exercise in patients with chronic congestive heart failure (CHF) include high pulmonary pressures, ventilation-perfusion mismatching, early metabolic acidosis, and abnormal respiratory control. To evaluate the role that ventilation and gas exchange play in limiting exercise capacity in patients with CHF, data from 33 patients with CHF and 34 normal subjects of similar age who underwent maximal exercise testing were analyzed. Maximal oxygen uptake was higher among normal subjects (31.7 +/- 6 ml/kg/min) than among patients with CHF (17.7 +/- 4 ml/kg/min; p less than 0.001). The ventilatory equivalent for oxygen, expressed as a percentage of maximal oxygen uptake, was 25% to 35% higher among patients with CHF compared with normal subjects throughout exercise (p less than 0.01). A steeper component effect of ventilation on maximal oxygen uptake was observed among normal subjects compared with patients with CHF, which suggests that a significant portion of ventilation in CHF is wasted. Maximal oxygen uptake was inversely related to the ratio of maximal estimated ventilatory dead space to maximal tidal volume (VD/VT) in both groups (r = -0.73, p less than 0.001). Any given oxygen uptake at high levels of exercise among patients with CHF was accompanied by a higher VD/VT, lower tidal volume, and higher respiratory rate compared with normal subjects (p less than 0.01). Relative hyperventilation in patients with CHF started at the beginning of exercise and was observed both below and above the ventilatory threshold, which suggests that the excess ventilation was not directly related to earlier than normal metabolic acidosis. Thus abnormal ventilatory mechanisms contribute to exercise intolerance in CHF, and excess ventilation is associated with both a higher physiologic dead space and an abnormal breathing pattern. The high dead space is most likely due to ventilation-perfusion mismatching in the lungs, which is related to poor cardiac output, and the abnormal breathing pattern appears to be an effort to reduce the elevated work of breathing that is caused by high pulmonary pressures and poor lung compliance.     

Hemodynamic effects of supplemental oxygen administration in congestive heart failure

Objectives. This study sought to determine the hemodynamic effects of oxygen therapy in heart failure.Background. High dose oxygen has detrimental hemodynamic effects in normal subjects, yet oxygen is a common therapy for heart failure. Whether oxygen alters hemodynamic variables in heart failure is unknown.Methods. We studied 10 patients with New York Heart Association functional class III and IV congestive heart failure who inhaled room air and 100% oxygen for 20 min. Variables measured included cardiac output, stroke volume, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance, mean arterial pressure and heart rate. Graded oxygen concentrations were also studied (room air, 24%, 40% and 100% oxygen, respectively; n = 7). In five separate patients, muscle sympathetic nerve activity and ventilation were measured during 100% oxygen.Results. The 100% oxygen reduced cardiac output (from 3.7 ± 0.3 to 3.1 ± 0.4 liters/min [mean ± SE], p < 0.01) and stroke volume (from 46 ± 4 to 38 ± 5 ml/beat per min, p < 0.01) and increased pulmonary capillary wedge pressure (from 25 ± 2 to 29 ± 3 mm Hg, p < 0.05) and systemic vascular resistance (from 1,628 ± 154 to 2,203 ± 199 dynes's/cm⁵, p < 0.01). Graded oxygen led to a progressive decline in cardiac output (one-way analysis of variance, p < 0.0001) and stroke volume (p < 0.017) and an increase in systemic vascular resistance (p < 0.005). The 100% oxygen did not alter sympathetic activity or ventilation.Conclusions. In heart failure, oxygen has a detrimental effect on cardiac output, stroke volume, pulmonary capillary wedge pressure and systemic vascular resistance. These changes are independent of sympathetic activity and ventilation.     

Improvement in exercise endurance in patients with chronic airflow limitation using continuous positive airway pressure

To cope with the increased ventilatory demands of exercise, patients with severe expiratory flow limitation adopt strategies that ultimately place greater demands on their inspiratory muscles. Increased inspiratory muscle work may contribute to dyspnea causation and exercise limitation in such patients even before their ventilatory ceiling is attained. In this setting, continuous positive airway pressure (CPAP) should, by favorably affecting inspiratory muscle function and respiratory sensation, improve exercise performance. Six patients with chronic airflow limitation (CAL) (FEV1 +/- SD = 35 +/- 12% predicted) undertook constant-load, submaximal, cycle exercise at 50% of their predetermined maximal oxygen consumption: CPAP of 4 to 5 cm H2O was delivered during one exercise session and bracketed by one or two unassisted control sessions. In four patients, CPAP-assisted (4 to 5 cm H2O) exercise was bracketed by two unassisted control exercise sessions; two remaining patients undertook CPAP-assisted exercise and one unassisted control session. CPAP resulted in a significant increase in exercise endurance time (TLIM) (by 48%: CPAP TLIM (mean +/- SE) = 8.82 +/- 1.90 min; averaged control TLIM = 5.98 +/- 1.23 min (p less than 0.01). CPAP effectively ameliorated exertional dyspnea in the majority of patients; selected dyspnea ratings (Borg scale) during control (final minute) and CPAP at isotime, at comparable levels of ventilation, were (mean +/- SD) 7.83 +/- 2.25 and 5.5 +/- 2.2, respectively (p less than 0.025). Breathing frequency fell significantly during CPAP application (at isotime) by 17% (p less than 0.02); other steady-state ventilatory variables and end-expiratory lung volumes were not significantly different during CPAP and control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oscillatory hyperventilation in severe congestive heart failure secondary to idiopathic dilated cardiomyopathy or to ischemic cardiomyopathy

Thirty-one subjects with chronic congestive heart failure (CHF) were separated into 3 groups according to ventilatory patterns during graded exercise: Group 1--oscillators (n = 6); group 2-intermediate oscillators (n = 14); and group 3--nonoscillators (n = 11). Group 1 patients showed cyclic fluctuations in minute ventilation (change of 30 to 40 liters/min) and arterial PO2 (change of 38.0 +/- 4.1 mm Hg) and PCO2 (change of 11 +/- 2.8 mm Hg). The nadir in arterial PO2 occurred at times when wasted ventilatory effort was maximal. The amplitude of ventilatory oscillations in group 1 patients increased in the transition from rest to light exercise and damped with heavy exercise. There was no evidence of alveolar hypoventilation at the nadirs of minute ventilation; arterial PCO2 was always 40 mm Hg or less. Substantial hyperventilation (ventilatory equivalent for CO2 twice normal) occurred with maximal minute ventilation in group 1 patients. Oscillatory hyperventilation correlated with severity of CHF. Maximal oxygen uptake was significantly lower in group 1 (11.7 +/- 1.1 ml/kg/min) than group 3 (17.9 +/- 1.8 ml/kg/min) (p less than 0.05). Oscillatory hyperventilation during exercise may accompany severe CHF and compounds the inadequate delivery of oxygen by the failing heart.     

Selective low-level leg muscle training alleviates dyspnea in patients with heart failure

OBJECTIVES: The purpose of this study was to demonstrate in patients with moderate to severe heart failure that exertional dyspnea can be alleviated by improving muscle function. BACKGROUND: Dyspnea is a frequent limiting symptom in patients with chronic heart failure (CHF). This sensation may originate from activation of receptors in the musculature rather than the lung. METHODS: To investigate whether dyspnea could be alleviated by selective changes in leg muscle function, we performed isolated lower-limb training in 17 patients with severe CHF. Eight patients learned guided imagery relaxation techniques and served as an active control group. Exercise training consisted of three months of low-level bicycle and treadmill exercise such that minute ventilation was <25 l/min. Leg calisthenics were also performed. Maximal and submaximal exercise performance, respiratory and quadriceps muscle strength and endurance and quality-of-life and dyspnea scales were measured before and after each intervention. Metabolic stress testing (VO(2)), pulmonary function tests and isokinetic strength testing were also performed. RESULTS: In the active control group, no changes in leg muscle function, pulmonary function, maximal and submaximal exercise performance or quality-of-life questionnaires were observed. In the training group, peak torque of leg flexors (pre: 39 +/- 15 ft-lb; post: 50 +/- 13 ft-lb; p < 0.002) increased and the fatigue ratio decreased, indicating improved strength and endurance of the leg muscles. Maximal inspiratory and expiratory mouth pressures and maximum voluntary ventilation were unchanged. Peak VO(2) was increased (pre:12 +/- 2.2 ml/kg/min; post: 14 +/- 2.6 ml/kg/min) as well as the duration of exercise at 70% peak VO(2) increased (pre: 11.5 +/- 3.1 min; post: 21.5 +/- 5.4 min; p < 0.003). Perceived dyspnea during the submaximal testing was decreased. Minnesota Living with Heart Failure Score, Guyatt Dyspnea Scale, and the Transitional Dyspnea Index were all improved with training (all p < 0.05). CONCLUSIONS: We concluded that improvement of limb muscle function alleviates dyspnea and improves exercise performance in patients with CHF.     

Exertional dyspnea and ventilation in hyperthyroidism.

Dyspnea is recognized to be an important feature in patients with hyperthyroidism at rest and during exercise. However, its etiology is not well-understood. Since dyspnea is thought to be related to the perception of excessive ventilatory effort, we explored the possibility that dyspnea in these patients might be related to an inappropriate ventilatory response to the increased metabolic rate. We studied 11 hyperthyroid patients and 11 age- and sex-matched controls, performing spirometry, lung volumes, mouth pressure measurements, and incremental exercise test. Central drive was estimated by measuring P0.1 and sensation of dyspnea by the Borg scale. We found that hyperthyroid patients (1) have higher ventilation than normal subjects during exercise even when corrected for VCO2 levels; (2) this increased ventilation is secondary to increased central drive which is correlated to the T3ria level (r = 0.85, p less than 0.01); (3) hyperthyroid patients are more dyspneic than controls; and (4) the increased drive can be normalized by beta-blockade. We conclude that the main ventilatory abnormality in hyperthyroid patients is an inappropriate increase in respiratory drive, possibly secondary to increased adrenergic stimulation.