Search PubMed⌕ Search

Biomedical subjects

K Wasserman

Publications and source records attributed to K Wasserman.

At least 181 records · Page 10Linked to original sources
PubMed1982

The value of exercise in testing beta blockade and airway reactivity in asthmatic patients.

On separate days, in double-blind fashion, 23 subjects with mild or moderate asthma were injected intravenously with a placebo or 0.4 mg pindolol. Plethysmographic and spirometric measurements were performed before and after injection and repeatedly after exhausting incremental bicycle ergometer exercise. The mean reduction in maximal exercise heart rate of 26 bpm after pindolol compared to placebo confirmed significant cardiovascular beta blockade. Baseline 1-second vital capacity (FEV1) values and other flow rates were similar in both trials. There were similar reductions in FEV1 (median of 1% to 2% and mean of 3% to 5%) and other flow rates immediately after injection of placebo or pindolol. Exercise-induced bronchospasm (EIB) occurred in 34 of 46 trials and tended to be more severe in subjects with more baseline airway obstruction. Minimal EIB (FEV1 to 80% to 90% of baseline values) developed in eight after taking placebo and in seven after taking pindolol; mild EIB (FEV1 to 60% to 79% of baseline) developed in the five after placebo and six after pindolol and moderate EIB (FEV1 to 40% to 59% of baseline) developed in three after placebo and five after pindolol. In five subjects, FEV1 was reduced to a greater extent after placebo than after pindolol (median of 6%), whereas in 13 subjects, FEV1 was reduced to a greater extent after pindolol than after placebo (median of 10%). These small differences in FEV1 between placebo and pindolol were significant by the t test after exercise but not before exercise. Thus, exercise appears to increase the sensitivity in evaluating airway reactivity in asthmatic patients and also tests the effectiveness of cardiovascular beta blockade.

Adolescent↗
PubMed1982

Pathogenesis of dialysis-induced hypoxemia.

Patients undergoing hemodialysis with acetate-containing dialysis solutions develop hypoxemia. To determine the cause of the hypoxemia, we studied and compared the ventilatory, gas-exchange and blood-gas responses in chronic renal failure patients undergoing hemodialysis with acetate and bicarbonate dialysis solutions. Seven stable chronic dialysis patients were dialyzed against acetate and bicarbonate solutions in a random order. Dialysis was carried out using a 1.5 m2 hollow fiber dialyzer at a blood flow rate of 200 ml/min and a dialysate flow rate of 500 ml/min. During acetate dialysis, PaO2 fell within 15 minutes from a mean control predialysis concentration of 84 = 6 (SEM) mmHg to a mean of 70 +/- 7.5 mmHg (P less than 0.05), and remained low throughout the study. PaO2 did not change significantly during bicarbonate dialysis. Total ventilation fell from a predialysis level of 7.2 +/- 0.7 L/min to 5.7 +/- 0.6 L/min within 15 minutes (P less than 0.05). PaCO2 was not significantly changed from predialysis levels with either acetate or bicarbonate dialysis. Measurement of blood concentration of CO2 and bicarbonate across the dialyzer indicated that the total CO2 loss (as CO2 and bicarbonate) through the dialyzer was 3 millimoles per minute or the equivalent of approximately 60 ml of CO2 per minute, i.e., about one third of the patient's metabolic production of CO2.

Acetates↗
PubMed1982

Cardiac output increase and gas exchange at start of exercise.

To determine the rapidity of increased gas exchange resulting from increased cardiac output (Q) following exercise onset, subjects performed multiple rest-exercise transitions on a cycle ergometer: the early dynamics of pulmonary gas exchange were measured during 1) rhythmic breathing with ventilation kept constant at the resting level (controlled ventilation) and 2) prolonged constant airflow exhalation. With controlled ventilation, PACO2 increased and PAO2 decreased, typically beginning in the first exercise breath. After 15 s, PACO2 had increased and PAO2 decreased by 4.5-6.2 and 8.7-12.1 Torr, respectively, graded within these narrow ranges as functions of work rate (0-100 W). Exercise starting during a prolonged exhalation caused the slopes of the alveolar phases for O2 and CO2 to increase immediately or within 2-5 s following exercise onset. Work rate had little effect on the delay or the change of alveolar gas tension slope during the subsequent 10-15 s. Thus, increased gas exchange due to increasing Q occurred very rapidly following exercise onset so that it would coincide with the first or second breath of exercise in free-breathing subjects.

Adult↗
PubMed1982

Ventilatory control during experimental maldistribution of VA/Q in the dog.

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5-2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5-2.0 min) of acute maldistribution of VA/Q.

Anesthesia, General↗
PubMed1982

Effect of acid-base status on the kinetics of the ventilatory response to moderate exercise.

To determine the influence of altered carotid body drive on exercise ventilatory kinetics, five subjects performed four repetitions of constant-load cycle ergometer exercise during air and O2 breathing under each of the following conditions: 1) metabolic acidosis, (NH4Cl, 0.3 g . kg-1 . day-1); 2) metabolic alkalosis (NaHCO3, 0.7 g . kg-1 . day-1); and 3) control (CaCO3, 0.1 g . kg-1 . day-1). Ventilatory and gas exchange variables were computed, breath-by-breath, and the time constant of the ventilatory response in each condition was determined by a least-squares technique. While breathing air, metabolic acidosis caused the magnitude of the ventilatory response to increase and the time constant of the ventilatory kinetics to decrease. With metabolic alkalosis the increase in ventilation caused by exercise tended to be smaller and time constant larger although these changes were not statistically significant. Hyperoxia slowed the ventilatory response in the three acid-base conditions to a similar value. Thus hyperoxia slowed the ventilatory kinetics to a greater degree during acidosis than during control or alkalosis. We conclude that ventilatory dynamics during moderate exercise can be appreciably influenced by the acid-base status with acidosis significantly speeding the response dynamics. And, as these effects are abolished by hyperoxia, they appear to be mediated via the carotid bodies, in the human.

Acid-Base Equilibrium↗
PubMed1982

Parameters of ventilatory and gas exchange dynamics during exercise.

To determine the precise nonsteady-state characteristics of ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) during moderate-intensity exercise, six subjects each underwent eight repetitions of 100-W constant-load cycling. The tests were preceded either by rest or unloaded cycling ("0" W). An early component of VE, VO2, and VCO2 responses, which was obscured on any single test by the breath-to-breath fluctuations, became apparent when the several repetitions were averaged. These early responses were abrupt when the work was instituted from rest but were much slower and smaller from the 0-W base line and corresponded to the phase of cardiodynamic gas exchange. Some 20 s after the onset of the work a further monoexponential increase to steady state occurred in all three variables, the time constants of which did not differ between the two types of test. Consequently, the exponential behavior of VE, VO2, and VCO2 in response to moderate exercise is best described by a model that incorporates only the second phase of the response.

Adult↗
PubMed1982

Cardiac output as a controller of ventilation through changes in right ventricular load.

Ventilatory responses to changes in right ventricular (RV) load were studied in spontaneous breathing anesthetized dogs. Moving average RV pressure leads to (PRV) was used as an index of the RV strain. RV load was changed in two ways: 1) cardiac output (Q) was increased by infusion of isoproterenol (0.7-1.2 micrograms/min) and reduced by infusion of vasopressin (0.3-0.5 U/min); and 2) RV pressure was increased independently on Q by partial balloon obstruction of the RV outflow. When Q was changed by drug infusion there was a linear correlation between leads to PRV and Q (avg r = 0.04). Well-correlated linear relationships were found between expired minute ventilation (VE) and leads to PRV (avg r greater than 0.03), the slopes and intercepts of which were not significantly different whether leads to PRV was changed by altering Q, partial obstruction of RV outflow, or combining both procedures. Bilateral vagotomy did not alter the VE/leads to PRV slope resulting from RV balloon inflations. It is suggested that the RV strain may act as a controller of ventilation and provide a link between Q and VE.

Animals↗
PubMed1982

Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction.

The influence of chronic obstructive pulmonary disease (COPD) on exercise ventilatory and gas exchange kinetics was assessed in nine patients with stable airway obstruction (forced expired volume at 1 s = 1.1 +/- 0.33 liters) and compared with that in six normal men. Minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2) were determined breath-by-breath at rest and after the onset of constant-load subanaerobic threshold exercise. The initial increase in VE, VCO2, and VO2 from rest (phase I), the subsequent slow exponential rise (phase II), and the steady-state (phase III) responses were analyzed. The COPD group had a significantly smaller phase I increase in VE (3.4 +/- 0.89 vs. 6.8 +/- 1.05 liters/min), VCO2 (0.10 +/- 0.03 vs. 0.22 +/- 0.03 liters/min), VO2 (0.10 +/- 0.03 vs. 0.24 +/- 0.04 liters/min), heart rate (HR) (6 +/- 0.9 vs. 16 +/- 1.4 beats/min), and O2 pulse (0.93 +/- 0.21 vs. 2.2 +/- 0.45 ml/beat) than the controls. Phase I increase in VE was significantly correlated with phase I increase in VO2 (r = 0.88) and HR (r = 0.78) in the COPD group. Most patients also had markedly slower phase II kinetics, i.e., longer time constants (tau) for VE (87 +/- 7 vs. 65 +/- 2 s), VCO2 (79 +/- 6 vs. 63 +/- 3 s), and VO2 (56 +/- 5 vs. 39 +/- 2 s) and longer half times for HR (68 +/- 9 vs. 32 +/- 2 s) and O2 pulse (42 +/- 3 vs. 31 +/- 2 s) compared with controls. However, tau VO2/tau VE and tau VCO2/tau VE were similar in both groups. The significant correlations of the phase I VE increase with HR and VO2 are consistent with the concept that the immediate exercise hyperpnea has a cardiodynamic basis. The slow ventilatory kinetics during phase II in the COPD group appeared to be more closely related to a slowed cardiovascular response rather than to any index of respiratory function. O2 breathing did not affect the phase I increase in VE but did slow phase II kinetics in most subjects. This confirms that the role attributed to the carotid bodies in ventilatory control during exercise in normal subjects also operates in patients with COPD.

Carbon Dioxide↗
PubMed1982

Comparison of physiologic dead space/tidal volume ratio and alveolar-arterial PO2 difference during incremental and constant work exercise.

We prefer 1-min incremental exercise testing on a cycle ergometer rather than constant work studies because of its speed, repeatability, and ease of identification of the anaerobic threshold. Although values such as VO2 and anaerobic threshold from both types of studies are reported to be comparable, we questioned whether VD/VT and AaPO2, which depend on simultaneous arterial blood and mixed expired gas sampling, would also be reliable during incremental testing. In 23 patients we did both a constant work test at below the anaerobic threshold and a 1-min incremental test. At matched VO2 we found no difference between VD/VT and AaPO2 despite anticipated differences in VE, VCO2, and R because of differences in their rates of increase. We conclude that VD/VT and AaPO2, determined during 1-min incremental exercise tests, are equivalent to those from constant work tests and that a separate constant work study is not needed for these measurements if determined below the anaerobic threshold.

Adult↗
PubMed1982

Treatment of mixed-dust pneumoconiosis with whole lung lavage.

A patient with silicosis and progressive dyspnea on exertion is described in whom open lung biopsy revealed active chronic inflammation with many macrophages filling alveolar spaces. Because of the extensive involvement by the disease of small air spaces, bilateral whole lung lavage was performed. The lung lavage effluent was striking in its blackish brown color. It was composed predominantly of macrophages containing silica, silicates, and graphite. Particles in the tissue and lavage were analyzed using scanning electron microscopy and energy dispersive X-ray analysis. The dry weight of the material removed was approximately 25 g, of which an estimated 135 mg was silica. The procedure resulted in immediate symptomatic improvement in the patient. Although his pulmonary function did not change significantly, it is hoped that removal of this material will improve his long-term prognosis.

Biopsy↗
PubMed1982

Effect of ramp slope on determination of aerobic parameters from the ramp exercise test.

The effect of ramp slope on determination of aerobic parameters from the ramp exercise test. Med. Sci. Sports Exercise, Vol. 14, No. 5, pp. 339-343, 1982. We have previously demonstrated that the four parameters of aerobic function (maximal oxygen uptake (muVO2), VO2 at the anaerobic threshold (theta an), the time constant for VO2 kinetics (tau VO2), and work efficiency (eta)) may all be determined reliably from a single test in which the work rate increases continuously at a constant rate, i.e., ramp. That study, however, utilized a single ramp slope of 50 W X min-1, which may not be appropriate for subjects with very low or very high work tolerances. We therefore studied the effect of different ramp slopes on the determination of these parameters. Ramp slopes of 20, 30, 50, and 100 W X min-1 were generated on a cycle ergometer, and each was assigned randomly to 14 healthy subjects. Ventilatory and gas exchange variables were measured breath-by-breath utilizing on-line digital computation. Ramp slopes of 20, 30, and 50 W X min-1 yielded the same values for each aerobic parameter. The 100 W X min-1 ramp yielded muVO2 and eta an values that were the same as those found for the other ramp slopes, but tau VO2 and eta could not be discerned validly from this ramp slope. We conclude that valid assessment of the four parameters of aerobic function is possible with ramp slopes between 20 and 50 W X min-1; no further information on the parameters is to be gained by prolonging the tests with ramps slower than 20 W X min-1.

Adult↗
PubMed1981

Exercise performance in chronic obstructive pulmonary diseases.

Patients with chronic obstructive pulmonary diseases demonstrate exercise limitation as a consequence of both an increased ventilatory requirement and a decreased ventilatory capacity. The increased ventilatory requirement arises from the elevated wasted ventilation fraction of each breath (VD/VT) and hypoxemia secondary to ventilation-perfusion mismatching, both of which stimulate minute ventilation of increase. The reduced ventilatory capacity is primarily the result of airflow obstruction, which causes an increased work of breathing. Respiratory muscle fatigue may also play a role in reducing ventilatory capacity. The differentiation of heart failure from chronic obstructive pulmonary diseases as a cause of dyspnea can be accomplished using a variety of noninvasive and invasive techniques during exercise, including measurements of minute ventilation, the expiratory airflow pattern, ventilatory reserve (VEmax/MVV), ventilatory efficiency (VD/VT), arterial blood gases, the anaerobic threshold, heart rate, cardiac output, pulmonary hemodynamics and ventricular ejection fraction. Exercise training of patients with chronic obstructive pulmonary diseases improves exercise intolerance but appears to have little effect on pulmonary function tests, arterial blood gases and pulmonary hemodynamics. Supplemental oxygen during exercise training may be a useful adjunct for improving exercise tolerance in patients with chronic obstructive pulmonary diseases.

Dyspnea↗
PubMed1981

A test to determine parameters of aerobic function during exercise.

A short-duration cycle ergometer exercise test has been developed that allows four parameters of aerobic function to be discerned. These are the maximum O2 uptake, anaerobic threshold, work efficiency, and the time constant for O2 uptake kinetics. The test form is a ramp of 4-8 min duration to the limit of tolerance. The parameters determined from the ramp faithfully reproduced those obtained from several standard procedures. We conclude that a profile of aerobic function in man can be obtained from a single short-duration ramp test.

Adult↗
PubMed1981

Effect of CO2 set point on ventilatory response to exercise.

The ventilatory response to exercise was determined in seven normal adults during induced chronic metabolic acidosis, chronic metabolic alkalosis, and a control state. Incremental and constant-load exercise tests were performed in each condition on a cycle ergometer. Ventilation and gas exchange variables were determined breath by breath, and CO2 partial pressure (PCO2), pH, and HCO3 were determined from arterialized venous blood (Pa-VCO2). During chronic metabolic acidosis PaVCO2 was lower than control (36.3 +/- 2.1 and 43.7 +/- 2.9 Torr, respectively) and during alkalosis it was elevated to 47.1 +/- 1.3 Torr. The new PCO2 levels caused by chronic acid-base alterations were unchanged during moderate exercise. The ventilatory response (VE) to the same metabolic rate increment was therefore larger (delta VE = 20.6 +/- 2.91/min) when PCO2 was lower than the control level (delta VE = 14.5 +/- 2.01/min. VE also increased more steeply in response to incremental exercise tests when PCO2 was reduced. Thus the hyperpnea of moderate exercise reflects the level at which arterial PCO2 is regulated at rest, as well as the metabolic load (VCO2).

Acidosis↗
PubMed1981

Ventilatory responses to cardiac output changes in patients with pacemakers.

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.

Adult↗
PubMed1981

Breath-by-breath measurement of true alveolar gas exchange.

A method has been developed for on-line breath-by-breath calculation of alveolar gas exchange by correcting the gas exchange measured at the mouth for changes in lung gas stores. The corrections are applied to the total lung gas exchange, which is found by directly subtracting expired from inspired volume of each gas. Corrections are made for both breath-to-breath changes in lung volumes and changes in alveolar gas concentrations. The lung volume correction term has the effect of reducing the large error sensitivity of O2 exchange that has, in the past, resulted from direct determination by total lung gas exchange. Error each gas. Corrections are made for both breath-to-breath changes in lung volumes and changes in alveolar gas concentrations. The lung volume correction term has the effect of reducing the large error sensitivity of O2 exchange that has, in the past, resulted from direct determination by total lung gas exchange. Error each gas. Corrections are made for both breath-to-breath changes in lung volumes and changes in alveolar gas concentrations. The lung volume correction term has the effect of reducing the large error sensitivity of O2 exchange that has, in the past, resulted from direct determination by total lung gas exchange. Error sensitivity analysis shows that the effect of inaccuracies due to errors in measuring gas flow or gas concentrations are similar in magnitude to those in the open-circuit method that has traditionally been used. The algorithm for alveolar gas exchange has been implemented in a computer program for on-line respiratory analysis alongside the open-circuit calculation of gas exchange at the mouth that has been used in out laboratory. By use of several experimental studies, it is shown that there are very apparent breath-to-breath differences between the gas exchange measured by the two methods. During metabolic and respiratory transients, these differences often have significant influence on interpretation of the underlying physiology.

Breath Tests↗