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At least 19 recordsLinked to original sources
PubMed2003

Determination of maximal voluntary ventilation in children with cystic fibrosis.

Maximal voluntary ventilation (MVV) may be determined directly by the sprint method or calculated from pulmonary function data, using the functions MVV = forced expired volume in 1 sec (FEV(1)) x 35 or MVV = FEV(1) x 40. The purpose of this paper was to test the validity of the equation over a wide range of lung function in children. Cystic fibrosis (CF), a chronic lung disease where children typically have a wide range of pulmonary function, was chosen as the study requirement. Spirometric data from 332 children with CF who underwent pulmonary function testing between 1987-2000 were stratified according to disease severity, and box-plots comparing the ratio of MVV to FEV(1) for each category were generated. As results indicated that the equation underestimates true MVV proportionally to the degree of airflow limitation, a new function to predict MVV for this population was derived and tested. The new equation was derived using data from patients who were tested on odd-numbered days (group A). The validity of the new equation was then tested on the patients tested on even-numbered days (group B). To test its validity, the results were compared to the "gold standard" sprint values using a Bland and Altman plot. MVV was expressed as a function of FEV(1) and predicted FEV(1): MVV = 27.7(FEV(1)) + 8.8(PredFEV(1)) (R(2) = 0.98, P < 0.05). In this way, the accuracy of the new equation was confirmed. Whenever possible, we recommend MVV be determined by the sprint method in accordance with ATS guidelines. If this is not feasible, we recommend considering the new prediction equation.

Adolescent↗
PubMed1993

Prediction equations for maximal voluntary ventilation in non-smoking normal subjects in Madras.

Maximal voluntary ventilation (MVV) was measured in 256 healthy non-smoking adults (132 males, 124 females) aged 15-63 years living in Madras. The mean MVV (+/- SD) in males was 126.7 +/- 31.9 and in females 77.7 +/- 16.4. Regression equations were derived for men and women for predicting maximal voluntary ventilation for adults in South India. MVV in South Indians were similar to those reported for other Indian subjects, but lower than those reported for caucasians.

Adolescent↗
PubMed2003

Spirometric evaluation of lung function (maximal voluntary ventilation) in welding workers.

OBJECTIVE: The present study was designed to study the effects of welding fumes on maximal voluntary ventilation (MVV) and to determine its severity in relation to duration of exposure. Additional objective was to reduce the potential health risks of welding workers by providing them with information concerning the hazards of welding fumes. METHODS: This study was conducted in the Department of Physiology, Basic Medical Sciences Institute, Jinnah Post Graduate Medical Centre, Karachi, Pakistan in 1999. In this study, the MVV was studied in 50 male control subjects and 50 male arc welding workers and all participants were non-smokers with an age range of 20-60 years. The subjects were matched for age, height, weight and socio-economic status. Maximal voluntary ventilation test was performed by using an electronic spirometer and results were compared by a paired t-test. RESULTS: Welding workers showed a significant reduction in MVV relative to controls. CONCLUSION: We conclude that MVV in welding workers is significantly decreased as compared to their matched controls. Stratification of results by years of welding shows a dose-response effect of years of welding on lung function.

Adult↗
PubMed1983

Influence of exercise on maximal voluntary ventilation and forced expiratory flow at depth.

Four to six subjects performed maximal voluntary ventilation (MVV) and forced expirations during rest, exercise (50, 125, and 200 W), and inhalation of air and CO2 and air at rest while submerged at pressures of 1.45, 2.82, 4.64, and 6.76 atm. Maximal expiratory flow (at 40% of vital capacity) and MVV at rest decreased as exponential functions of gas density, but the decrease was less than in some earlier studies. Independent of pressure, MVV increased by about 10%-17% at the heavier work loads and expiratory flow increased by 27%-48%; the increase in expiratory flow disappeared within 2 min after exercise. Exercise increased end-tidal CO2 tension by up to 9 mmHg. Carbon dioxide inhalation increasing the end-tidal level by up to about 25 mmHg during rest had no effect on MVV and a slight to moderate effect on flow, increasing it by a maximum of 21% at 4.64 atm. The enhancing effect of exercise on MVV and expiratory flow at depth apparently was mainly due to modified autonomic nervous activity reducing pulmonary flow resistance, CO2 accumulation playing an uncertain role, and passive distension of airways playing no role.

Adult↗
PubMed1982

The influence of airway obstruction and respiratory muscle strength on maximal voluntary ventilation in lung disease.

To assess the effects of airway conductance (Gaw) and respiratory muscle strength (RMS) on maximal voluntary ventilation (MVV), we studied 8 normal subjects (N), 8 patients with interstitial lung disease (ILD), and 16 with chronic airflow limitation (CAL). In the patients with ILD, RMS explains 83% of the variance in MVV (p less than 0.005), but Gaw explains none. In the patients with CAL, Gaw and RMS explain, respectively, 65 and 34% of the variance in MVV (p less than 0.02). Considering Gaw and RMS together increases the explained variance to 77% (p less than 0.005). In groups CAL and N combined, Gaw and RMS explain 86% of the variance in MVV, with 71% explained by Gaw and 34% by RMS, which the other variable alone failed to explain (p less than 0.005). When the data are normalized for age, sex, height, and lung volume, the influence of %RMS on %MVV is halved, but remains significant (p less than 0.05). We conclude that RMS is a primary determinant of MVV in patients with ILD, and an important determinant in patients with CAL.

Adult↗
PubMed1982

Respiratory muscle strength and maximal voluntary ventilation in undernourished patients.

To assess the effect of chronic debilitation on respiratory muscle function, we studied 16 poorly nourished (PN) patients without pulmonary disease, and 16 well-nourished (WN) subjects matched for age and sex. Body weight, vital capacity (VC), maximal voluntary ventilation (MVV), and maximal static inspiratory and expiratory pressures (PImax and PEmax) were measured and expressed as percent predicted. Respiratory muscle strength (RMS) was calculated as (% PImax + % PEmax)2. Body weight was 71% predicted in the PN group and 104% in the WN group. The RMS, MVV, and VC were 37%, 41%, and 63%, respectively, of the values in the WN group (p less than 0.001). The 60% reduction in RMS was shared almost equally among inspiratory and expiratory muscles, and PEmax was linearly related to body weight. Because malnutrition reduces both respiratory muscle strength and MVV, it may well impair respiratory muscle capacity to handle increased ventilatory loads in thoracopulmonary disease.

Adolescent↗
PubMed2004

Prediction of the maximal voluntary ventilation in healthy adult Chinese subjects.

OBJECTIVES: The aim of the present study was to investigate the relationship between the FEV(1) and maximal voluntary ventilation (MVV) in healthy adult Chinese subjects, and to determine the validity of existing prediction equations of MVV for use in the Chinese population. METHODOLOGY: Ninety-five healthy subjects (48 male and 47 female) stratified into five age groups (from 20 to 70 years) for both sexes were recruited from the general population. The FEV(1) and MVV of these subjects were measured with a clinical spirometer. The MVV was determined using the closed-circuit technique. The MVV was assessed for 12 s and values were calculated to obtain L/min. Multiple regression analysis was used to develop equations to predict MVV with age, height, FEV(1) as well as with FEV(1) alone as predictor variables. One-sample t-tests were used to compare the actual values of MVV for the subjects with their predicted values using equations from previous studies of MVV in healthy subjects. RESULTS: Using FEV(1) only, the following predictive equation was obtained: MVV = FEV(1) x 45.12 - 15.85 (adjusted r(2) = 0.792). Predicted MVV values using previously cited equations, including MVV = FEV(1) x 35 or 40, were all significantly different from the actual MVV values of these subjects. CONCLUSIONS: The relationship between MVV and FEV(1) among healthy adult Chinese subjects is described. Previously cited equations describing the relationship between FEV(1) and MVV cannot be applied to healthy adult Chinese subjects.

Adult↗
PubMed1988

Supine position and sleep loss each reduce prolonged maximal voluntary ventilation.

Because of the prevalence of supine posture and sleep deprivation in both health and disease, we wondered how each of them influences prolonged maximal voluntary ventilation (MVV). Accordingly, we compared 12-second, 1-min, and 10-min isocapnic MVV supine with that measured in the upright posture in 8 healthy subjects. MVV decreased 6-10% supine, independent of test duration (p less than 0.01). Although end-expiratory lung volume was 0.47 liter lower during supine resting breathing (p less than 0.001), end-expiratory lung volumes during short-term MVV maneuvers were identical. To investigate any additional effect on MVV due to sleep loss, 12 healthy subjects performed 12-second, 1-min, and 30-min isocapnic MVV maneuvers in the supine position, either after normal sleep or after a 24-hour sleepless period. Sleep deprivation reduced MVV by 7-14%, again independent of test duration (p less than 0.05). Sleep loss also reduced the ventilation chosen to represent a submaximal (75%) breathing effect (p = 0.05), and it increased subjective ratings of fatigue and confusion (p less than 0.01). We conclude that supination and sleep deprivation together decrease both short- and long-term MVV by nearly 20%, with impairment of supination not caused by lung volume changes, and with the sleep loss effect occurring in tandem with a rise in the subjective assessment of breathing effort.

Adult↗
PubMed2003

Maximal voluntary ventilation in myasthenia gravis.

Assessment of respiratory muscle weakness is important at all stages of myasthenia gravis. The maximal voluntary ventilation (MVV) is an objective dynamic method for measuring the working capacity of respiratory muscles. The clinical value of this method was studied in 24 newly diagnosed patients with myasthenia gravis, classified according to Osserman criteria (grades I, IIa, and IIb). The MVV values were normal in group I, whereas a characteristic "myasthenic pattern" of decremental respiratory volumes was demonstrated during MVV in group IIa and IIb patients, with or without dyspnea. Despite some limitations and lack of specificity, MVV may be a valuable tool in the assessment of respiratory dysfunction in patients with myasthenia gravis. Muscle Nerve, 27: 715-719, 2003

Adrenal Cortex Hormones↗
PubMedDate not supplied

The effects of a 9-week program of aerobic and upper body exercise on the maximal voluntary ventilation of chronic obstructive pulmonary disease patients.

PURPOSE: The purpose of this study was to evaluate the effects of a 9-week exercise program that emphasized aerobic and upper body strength on the maximal voluntary ventilation (MVV) of patients with chronic obstructive pulmonary disease (COPD). An experimental and control group totaling 40 patients with a diagnosis of COPD was studied. METHODS: Experimental group subjects were given a pre- and post-MVV breathing test, a Patient's Attitude Toward Health (PATH) questionnaire, a knowledge of disease questionnaire and a 6-minute walk test. Pre- and post-MVV breathing tests were performed on the control group. Dependent t-test and analysis of covariance were utilized to evaluate the results. RESULTS: Significant differences were found between the pre-test and post-test within the experimental group on MVV results, program attitudes toward health (PATH scores), knowledge level about their disease state after the rehabilitation program, and 6-minute walk distance. There were no significant differences found in the MVV results between the pre-test and post-test for the control group. There was a significant difference when comparing the control group MVV results to the MVV results of the exercise group. CONCLUSIONS: These findings indicate that pulmonary rehabilitation programs can help patients realize improved lung function, improved emotional states, increased knowledge about their disease states, and an increased cardiovascular fitness level. The results of this study suggest a regimen that can improve the quality of life for patients with chronic lung disease.

Aged↗
PubMed1999

Effect of hypercapnia on maximal voluntary ventilation and diaphragm fatigue in normal humans.

Relatively little is known about the combined effects of hypercapnia and fatigue on the human diaphragm. We examined the effects of acute hypercapnia and fatigue in seven subjects by measuring changes in transdiaphragmatic pressure (Pdi) elicited by cervical magnetic stimulation after 2 min maximal voluntary ventilation (MVV) while breathing air and also with the inspired PCO(2) increased to 8% for 12 min before and during the MVV. Diaphragm strength was assessed before and at 0, 20, 40, 60, and 90 min after the MVV in both studies with the subjects breathing air. There was no difference in the level of ventilation for each run. Mean (+/- SD) twitch Pdi (TwPdi) fell significantly (p < 0.01) at 20 min after the control and hypercapnic MVV; (30.4 [7.8] to 27.0 [8.1] cm H(2)O control and 30.3 [4.1] to 27.3 [5.0] cm H(2)O CO(2)) and remained significantly (p < 0.01) below baseline. The changes in TwPdi at 20 to 90 min were not significantly different between the control and CO(2) runs. The decrease in TwPdi at 0 min after MVV, however, was greater (15%) in the hypercapnic run than in the control run (8.1%) (p < 0.05) when compared with baseline valves. Hypercapnia does not intensify long lasting fatigue but may reduce diaphragm contractility immediately after MVV.

Adult↗
PubMed1998

Mechanical work of breathing during maximal voluntary ventilation.

With the use of the esophageal balloon technique, the working capacity of the respiratory muscles was assessed in four normal subjects by measuring the work per breath (W) and respiratory power (W) during maximal voluntary ventilation with imposed respiratory frequencies (f) ranging from 20 to 273 cycles/min. Measurements were made in a body plethysmograph to assess the work wasted as a result of alveolar gas compressibility (Wg'). In line with other types of human voluntary muscle activity, W decreased with increasing f, whereas W exhibited a maximum at f of approximately 100 cycles/min. Up to this f value, Wg' was small relative to W. With further increase in f, the Wg'/W ratio increased progressively, amounting to 8-22% of W at f of 200 cycles/min.

Adult↗
PubMed1997

Diaphragm performance during maximal voluntary ventilation in chronic obstructive pulmonary disease.

In normal subjects 2 min of maximal voluntary hyperventilation results in failure of tension generation and low-frequency fatigue of the diaphragm. Patients with severe chronic obstructive pulmonary disease (COPD) do not develop diaphragm fatigue during exhaustive treadmill exercise despite excessive inspiratory muscle loading and we hypothesized that they might be relatively resistant to the development of diaphragm fatigue during maximal ventilation. In six patients with severe COPD (mean FEV1 0.671) we therefore loaded the diaphragm using 2 min of maximal isocapnic ventilation (MIV). Initial mean ventilation was 28.6 L/min and diaphragm pressure-time product (PTPdi) 602 cm H2O x s/min; these values were sustained throughout MIV without significant decline. Mean twitch transdiaphragmatic pressure (Tw Pdi) was 19.7 cm H2O 25 min after a control run and 20.5 cm H2O at the same time after MIV [corrected]. Compared with normal subjects previously studied in our laboratory (Hamnegard, C.-H., et al. Eur. Respir. J. 1996;9:241-247) the reduction in PTPdi was disproportionately greater than the reduction in Tw Pdi. We conclude that, unlike normal subjects, 2 min of MIV causes neither failure of diaphragm performance nor low-frequency diaphragm fatigue in patients with severe COPD. It is likely that the diaphragm makes a relatively limited contribution to the generation of maximal levels of ventilation in severe COPD.

Aged↗
PubMed1988

Discontinuation of mechanical ventilation.

The vast majority of patients who undergo mechanical ventilation are able to discontinue ventilatory assistance within a few days. Typically, patients who require only short-term mechanical ventilation do not have severe underlying lung disease, and the problem for which they require ventilatory support is most commonly rapidly reversible. In these patients on short-term ventilatory support, parameters of spontaneous ventilatory requirements and respiratory muscle strength, including minute ventilation, maximal voluntary ventilation, vital capacity, and maximal inspiratory pressure, are useful in predicting the success of discontinuation of mechanical ventilation. Ventilatory support can generally be discontinued by a variety of techniques in these patients without the need for weaning from the ventilator per se. The smaller group of patients in whom it is not possible to discontinue mechanical ventilation within less than 7 days comprises individuals who frequently have severe acute or chronic lung disease, multisystem extrapulmonary disease, or neuromuscular disease. After a period of prolonged mechanical ventilatory support, these complicated patients require a process of progressive weaning in which they gradually become able to support spontaneous ventilation. Spontaneous ventilatory parameters do not correlate well with weaning ability in patients on long-term ventilatory support. A systematic and comprehensive approach in which attention is focused on optimizing pulmonary and nonpulmonary factors that affect the weaning process provides the best chance for successful withdrawal of ventilatory support after long-term mechanical ventilation. Inadequate ventilatory drive, respiratory muscle weakness and fatigue, increased work of breathing, excessive CO2 production, and cardiac failure are potential mechanisms that may play a role in inhibiting successful weaning. Adverse factors relevant to each of these mechanisms must be addressed and corrected to whatever extent possible. Studies have not demonstrated the superiority of either classic T-piece weaning or IMV weaning methods in difficult-to-wean patients on long-term ventilatory support. Both techniques may be used successfully as long as all patient variables that may adversely affect weaning ability are corrected or optimized and close care and attention to the details of the weaning process itself are provided.(ABSTRACT TRUNCATED AT 400 WORDS)

Heart Failure↗