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Comparison of two methods of postoperative pulmonary care.

A new apparatus for postoperative pulmonary care was compared to one in common use. Vital capacity, a common clinical indicator of pulmonary status in the postoperative patient, was used as an index of improvement or deterioration. In patients using the device with increased dead space and expiratory pressure, there was a significantly greater increase in vital capacity than in those of the group who used blow bottles. Since increased vital capacity is indicative of improved pulmonary function, it is suggested that the use of the dead space-expiratory pressure device should result in a decreased incidence of postoperative pulmonary complications.

Humans↗

Respiratory effects of live influenza virus vaccine: healthy older subjects and patients with chronic respiratory disease.

Twenty-one healthy, middle-aged volunteers and 8 patients with chronic lung disease were given live, attenuated influenza virus vaccine by nasal spray. Forced vital capacity, 1-sec forced expiratory volume, ratio of 1-sec forced expiratory volume to forced vital capacity, residual volume, ratio of airway conductance to lung volume, maximal expiratory flows after exhalation of 50 and of 75 per cent of the forced vital capacity, closing volume, slope of Phase III, volume of isoflow, single-breath diffusing capacity for CO, and arterial blood gases were measured before and 3, 7, 10, and 21 days after exposure. Vaccination was well tolerated by the healthy volunteers without change in pulmonary function. In contrast, the patients tended to develop increased respiratory symptoms and had a slight decrease in mean forced expiratory volume in 1 sec 3 weeks after vaccination.

Administration, Intranasal↗

Pattern of lung volumes in patients with sighing breathing.

BACKGROUND: Sighing breathing is observed in subjects suffering from anxiety with no apparent organic disease. METHODS: Lung volumes and expiratory flow rates were measured in 12 patients with a sighing pattern of breathing and in 10 normal subjects matched for age, gender, and anthropometric data. In both groups the measurements were made by spirographic and plethysmographic techniques. In normal subjects functional residual capacity (FRC) and residual volume (RV) were measured during normal breathing and again during simulated sighing breathing to exclude technical artifacts resulting from hyperventilation during measurement by the helium closed circuit method. RESULTS: Patients with a sighing pattern of breathing had a normal total lung capacity (TLC) but significantly different partitioning of lung compartments compared with normal subjects. The vital capacity (VC) was lower when measured by both spirographic and plethysmographic methods and RV was higher. The forced expiratory volume in one second (FEV1) was also lower in patients with sighing breathing. The FEV1/VC and the maximal expiratory flow rates at 50% and at 25% of the forced vital capacity (V50 and V25) were normal and similar in both groups. In normal subjects there were no differences in RV when measured during quiet or simulated sighing breathing. CONCLUSIONS: Subjects with sighing breathing have a normal TLC with a higher RV and lower VC than normal subjects. There was no obvious physiological or anatomical explanation for this pattern.

Adult↗

Physiological characterization of variability in response to lung volume reduction surgery.

This paper examines potential physiological mechanisms responsible for improvement after lung volume reduction surgery (LVRS). In 25 patients (63 +/- 9 yr; 11 men, 14 women), spirometry [forced expiratory volume in 1 s (FEV(1)) and forced vital capacity (FVC)], lung volumes [residual volume (RV) and total lung capacity (TLC)], small airway resistance, recoil pressures, and respiratory muscle contractility (RMC) were measured before and 4-6 mo after LVRS. Data were interpreted to assess how changes in each component of lung mechanics affect overall function. Among responders (DeltaFEV(1) > or = 12%; 150 ml), improvement was primarily due to an increase in FVC, not to FEV(1)-to-FVC ratio. Among nonresponders, FEV(1), FVC, and RV/TLC did not change after surgery, although recoil pressure increased in both groups. Both groups experienced a reduction in RMC after LVRS. In conclusion, LVRS improves function in emphysema by resizing the lung relative to the chest wall by reducing RV. LVRS does not change airway resistance but decreases RMC, which attenuates the potential benefits of LVRS that are generated by reducing RV/TLC. Among nonresponders, recoil pressure increased out of proportion to reduced volume, such that no increase in vital capacity or improvement in FEV(1) occurred.

Adult↗

Lung volumes in scoliosis before and after correction by the Harrington instrumentation method.

Studies of static lung volumes were performed before and after surgery in 92 scoliotic patients, aged 10 to 25 years. The majority of the patients had idiopathic dorsal curves. Vital capacity, total lung capacity, functional residual capacity and residual volume were measured at least 18 months after surgery. A significant increase was observed in all static volumes, averaging 10 per cent; the pre- and postoperative values were expressed in per cent of predicted normal values according to age and height. Correction of body height was taken into consideration in the prediction of normal values. Patients with the more advanced scoliosis had the greatest improvement in lung volumes. The patients were treated postoperatively with a Milwaukee brace for an average of 15 months. The use of this brace, which allows for chest expansions, might account for the improved lung function compared to previous series where plaster body jackets were used. Thus the correction of idiopathic scoliosis by the standard posterior fusion with Harrinton instrumentation together with our postoperative routine provides a lasting reduction of the spinal deformity, prevents progression of respiratory impairment and, in fact, increases the lung volumes, vital capacity, total lung capacity and functional residual capacity by an average of 10 per cent.

Adolescent↗

Regional diffusing capacity in normal lungs during a slow exhalation.

From an analysis of carbon monoxide uptake and xenon-133 distribution after two bolus inhalations of these gases, we calculated regional diffusing capacity in the upper and lower volume halves of the lungs during the middle 60% of an exhaled vital capacity in five seated normal subjects. We found that the regional diffusing capacity of the upper half of the lungs was 11.6 +/- 4.2 (mean +/- SD) ml.min-1.Torr-1 and that the regional diffusing capacity of the lower half of the lungs was 24.4 +/- 2.4 ml.min-1.Torr-1 after 25% of the vital capacity had been exhaled. These values remained relatively constant as lung volume decreased from 25 to 75% of the exhaled vital capacity. Diffusing capacity in the upper half of the lungs ranged from 9.4 to 12.4 ml.min-1.Torr-1 during exhalation, and in the lower half of the lungs from 21.0 to 28.6 ml.min-1.Torr-1 during exhalation. These results suggest that total lung diffusing capacity remains relatively constant over this midrange of lung volumes and that this occurs because the regional diffusing capacities in both the upper and lower halves of the lungs remain relatively constant.

Adult↗

The influence of lower respiratory illness in infancy and childhood and subsequent cigarette smoking on lung function in Sydney schoolchildren.

A prospective study of respiratory illness history and lung function of 10,898 school children in Sydney was begun in 1971. At the first visit, a history of previous asthma and of bronchitis before and after the first 2 years of life was obtained from a parental questionnaire, and maximal expiratory flow-volume curves were recorded. These lung function studies were repeated yearly between 1972 and 1974, at which time a history of respiratory illness during the previous 12 months and a personal smoking history were recorded, Two groups of children from a random selection of primary and secondary schools in Sydney were studied. Their respective mean ages were 8.9 yr (primary group) and 12.6 yr (high school group) in 1971. Mean values for the maximal flow at 50 percent of the forced vital capacity were lower in children with a history of bronchitis and/or asthma than those in the control group. This was true in both age groups in both sexes. No differences were found in the 0.5-s forced expiratory volume or forced vital capacity. The differences in maximal flow at 50 per cent of the forced vital capacity were present again in 1974. In 1974, the data from smokers were compared with those from nonsmokers; small differences were found. The results suggest that bronchitis in infancy and childhood as well as asthma may affect lung function as children grow, that the abnormality may not be detected by the forced expiratory volume, that the abnormality persists, and that it is possible that the abnormality is further affected by smoking.

Adolescent↗

Influence of passive smoking on basic anthropometric characteristics and respiratory function in young athletes.

The primary objective of this study is to investigate the maintenance difference in basic anthropometric characteristics and to outline the dynamics of respiratory function change in youngsters athletes exposed to passive smoking (PS) and athletes not exposed to passive smoking in their families (NPS). High and weight were determined as basis anthropometric characteristics. Measured parameters for respiratory function were vital capacity (VC), forced expiratory volume in the first second (FEV1), maximum expiratory flow (PEF), forced expiratory flow at 50% forced vital capacity (MEF 50) and forced expiratory flow at 25% forced vital capacity (MEF 25). Significant statistical differences in separate spirometric variable were found in three variables (FEV1, MEF50, and MEF25) for group older youngsters. Analysis of variance showed statistical differences between athletes unexposed to passive smoking (NPS) and athletes exposed to passive smoking (PS) in even four spirometric variables (VC, FEV1, MEF50 and MEF25).

Adolescent↗

Diaphragm function after upper abdominal surgery in humans.

Patients undergoing upper abdominal surgery characteristically develop changes in lung function and are liable to develop atelectasis in the lower lobes. We studied 15 patients to assess lung function and, in particular, diaphragm function in patients undergoing cholecystectomy. Postoperatively, forced expiratory volume in one second and vital capacity decreased in all patients. The alveolar-arterial oxygen difference widened in the 10 patients in whom it was measured. Chest roentgenograms demonstrated patchy atelectasis in 9 of the 10 patients in whom films were obtained. There was a significant reduction in tidal volume with no change in minute ventilation immediately postoperatively. Diaphragm function was assessed by: changes in transdiaphragmatic pressure swings during quiet tidal breathing, the ratio of changes in gastric to esophogeal pressure swings, and the ratio of changes in abdominal to rib cage diameters. The results showed a significant decrease in changes in transdiaphragmatic pressure and the ratio of changes in gastric to esophogeal pressure swings in the postoperative period. In the 4 patients studied with magnetometers, there was a reduction in the ratio of changes in abdominal to rib cage diameters in all patients. These data indicate reduced diaphragm activity in the postoperative period, with a shift from predominantly abdominal to rib cage breathing. There was a reversal toward normal function by 24 h. This reduction in diaphragm function may be responsible for the atelectasis, reduced vital capacity, and hypoxemia in postoperative patients.

Adult↗

Cardiomegaly as a possible cause of lung dysfunction in patients with heart failure.

BACKGROUND: Our hypothesis is that an enlarged heart may compete for space with the lungs, causing a restrictive pattern that is often seen in patients with chronic heart failure. METHODS: Eighty patients with stable congestive heart failure in New York Heart Association classes II and III participated in the study. We measured cardiothoracic index (chest radiography), FEV1, vital capacity, alveolar volume, lung diffusion capacity for carbon monoxide (DLCO), and its 2 subcomponents alveolar-capillary membrane diffusion (DM), and pulmonary capillary blood volume. RESULTS: Reliable measurements were obtained in 72 of 80 participants enrolled. Cardiothoracic index averaged 57% +/- 7%. FEV1, vital capacity, alveolar volume, DLCO, and DM were inversely related to the cardiothoracic index (r = -0.514, -0.557, -0.522, -0.475, and -0.480, respectively). However, the relations of DLCO and DM with the cardiothoracic index were lost when DLCO and DM were adjusted for alveolar volume. A significant correlation (P < .01) was found between alveolar volume and vital capacity, FEV1, and DLCO (r = 0.799, 0.705, and 0.614, respectively). At multivariate analysis, cardiothoracic index, FEV1, and pulmonary capillary blood volume were independent predictors of DLCO, whereas alveolar volume, FEV1, and left ventricular ejection fraction were independent predictors of DM. CONCLUSIONS: Cardiac enlargement in chronic heart failure appears to be involved in causing restrictive lung pattern and a reduced alveolar volume that disturbs carbon monoxide diffusion.

Aged↗

Does chronic cervical myelopathy affect respiratory function?

OBJECT: Although respiratory function is often impaired by acute cervical spinal cord injury, changes in respiratory function in patients with chronic cervical myelopathy (CCM) are not well documented. The purpose of this study was to evaluate the respiratory function of patients with CCM. METHODS: Spirometric parameters were measured in 94 patients with CCM before they underwent expansive laminoplasty. These measurements were compared with those obtained in age- and sex-matched control group patients without myelopathy. The study patients were also subdivided into two groups: those with spinal compressive lesions above or below the C3-4 disc level were compared in terms of respiratory function. The vital capacity values measured in patients with CCM were significantly lower than those in the control group. In patients in whom spinal cord compression was present above C3-4, vital capacity values were lower than in patients in whom the compression level was below C3-4. The resting respiratory rate per minute was elevated in the CCM group. Peak expiratory flow rate was significantly decreased, and expiratory velocities at 50 and 25% of vital capacity were significantly increased in the CCM group. CONCLUSIONS: The results indicated that expiratory flow may be impaired or incomplete in patients with CCM. An underlying subclinical respiratory dysfunction appears to be associated with CCM.

Adult↗

Proteomic Profiling of Pulmonary Function and Cardiovascular Disease Risk in the Atherosclerosis Risk in Communities Study.

BACKGROUND: Pulmonary function is linked to cardiovascular disease risk; however, the underlying mechanisms remain unclear. We aimed to identify protein biomarkers associated with pulmonary function and examine their impact on incident chronic obstructive pulmonary disease, coronary heart disease, heart failure, and all-cause mortality. METHODS: Data from White and Black Americans in the Atherosclerosis Risk in Communities study (visit 2: N=11&#x2009;354, mean age=57 years; visit 5: N=3517, mean age=75 years), a prospective cohort, were analyzed. Linear regression assessed associations between protein levels and pulmonary function measures, including forced expiratory volume in 1 second and forced vital capacity. The impact of the identified proteins on incident chronic obstructive pulmonary disease, coronary heart disease, heart failure, and mortality was estimated using logistic regression and Cox proportional hazards models. Pathway enrichment and Mendelian randomization explored underlying biological functions and causal effects. RESULTS: Of 4766 proteins analyzed, 364 were cross-sectionally associated with forced expiratory volume in 1 second (and forced vital capacity (false discovery rate<0.05). Ninety-four and 270 proteins had concordant positive and negative effects, respectively. Five pathways related to pulmonary and cardiac function were enriched. Of the 364 proteins, 112 were linked to all 4 outcomes, where 86 were associated with increased risk (odds ratio/hazard ratio [OR/HR], 1.05-1.42) and 26 with reduced risk (OR/HR, 0.69-0.96). Six proteins (STAT3 [signal transducer and activator of transcription 3], MIC-1 [growth differentiation factor 15], apoA-II [apolipoprotein A-II], TPST1 [protein-tyrosine sulfotransferase 1], integrin a1b1 [integrin alpha-I: beta-1 complex], and BLC [C-X-C motif chemokine 13]) showed potential inverse causal effects on with forced expiratory volume in 1 second and forced vital capacity, and integrin a1b1 demonstrated consistent inverse associations with chronic obstructive pulmonary disease, coronary heart disease, and heart failure risks. CONCLUSIONS: Proteins associated with pulmonary function may influence CVD risk. Six proteins, including integrin a1b1, represent promising targets for future interventions.

Aged↗

Upper airflow obstruction and pulmonary function in acromegaly: relationship to disease activity.

Pulmonary function and disease activity were assessed in a large series of patients with acromegaly (19 men and 16 women). Large lungs, defined as a vital capacity greater than 120 per cent of predicted normal occurred in six of 19 males and six of 16 females. Ten of the 12 patients with elevated vital capacity had active disease (growth hormone greater than 5 mU/l during a glucose tolerance test). There was no association with duration of disease. Diffusing capacity was normal overall but DLCO greater than 120 per cent occurred in six of 14 females and one of 18 males. Significant intrathoracic airflow obstruction occurred in eight of 35 patients, six of whom were nonsmokers. Upper (extrathoracic) airflow obstruction was the most common pulmonary function abnormality. A maximal expiratory/inspiratory flow ratio greater than 1.0 at 50 per cent vital capacity occurred in 13 of 18 males and four of 16 female patients, and there was an association with disease activity (17 of 25 subjects with active disease had upper airflow obstruction compared to one of nine in remission; p = 0.01). Nocturnal hypoxaemia occurred in three of 13 patients studied: six of this group had upper airways obstruction. They were all male with elevated growth hormone levels and upper airflow obstruction. In summary, in 35 acromegalics (26 with active disease), large lungs occurred in 12 patients (34 per cent) and upper airflow obstruction in 17 patients (50 per cent). The latter may develop nocturnal hypoxaemia--this was seen in three of six patients with upper airflow obstruction. Upper airways obstruction was more common in males (13 of 18 compared to four of 16 females; p = 0.04) and its presence in males should arouse suspicion of nocturnal hypoxaemia.

Acromegaly↗

Blood pressure increase between 55 and 68 years of age is inversely related to lung function: longitudinal results from the cohort study 'Men born in 1914'.

BACKGROUND: Although age is associated with increasing blood pressure, there is a substantial heterogeneity within a certain birth cohort. Whether increase in systolic and diastolic blood pressure is related to pulmonary function is largely unknown. OBJECTIVE: To study blood pressure elevation between 55 and 68 years of age in relation to vital capacity (VC) and forced expiratory volume (FEV1.0) at 55. DESIGN: Population-based cohort study. PARTICIPANTS: A total of 375 men without antihypertensive medication at baseline. MAIN OUTCOME MEASURE: Change in systolic blood pressure (SBP) and diastolic blood pressure (DBP) over 13 years. RESULTS: Blood pressure increase between 55 and 68 years was highest among men who at 55 years had low vital capacity. Average increase in systolic blood pressure for men with vital capacity in the first, second, third and fourth quartile was 20.4, 18.7, 16.5 and 11.1 mmHg, respectively (P for trend = 0.005). Average increase in diastolic blood pressure was 10.6, 9.9, 9.0 and 6.3 mmHg, respectively (P= 0.02). The trends remained statistically significant after adjustments for baseline blood pressure, tobacco consumption, smoking cessation between 55 and 68, weight change between 55 and 68, physical activity and diabetes. Further analysis showed that the relationships could be found among men with blood pressures < or = 140/ 90 mmHg at baseline, whereas no significant association was found for men whose baseline SBP or DBP exceeded 140/90 mmHg. FEV1.0 showed similar associations with change in blood pressure. CONCLUSION: Lung function is inversely associated with future blood pressure increase. It is suggested that this association could contribute to the relationships between lung function and incidence of cardiovascular disease.

Aged↗

Impact of cigarette smoking on pulmonary function in non-allergic subjects.

BACKGROUND: Cigarette smokers have been shown to have a greater tendency to develop respiratory allergies than non-smokers. Since the early obstructive airway changes seen in respiratory allergy and smoking are similar, the early airway changes seen in populations of young smokers might be attributed to the fact that a proportion of smokers are allergic. We therefore studied the effects of smoking on non-allergic individuals. METHODS: Forced expiratory spirograms and peak expiratory flows were measured in a population of asymptomatic non-allergic male medical students, 59 smokers and 110 non-smokers. They had between 2 and 5 examinations performed serially over a period of 4 years. RESULTS: Smoking had a negative impact on pulmonary function. Analysis of covariance and multiple regression analysis using age, height gain and weight change as covariables showed that smokers, when compared to non-smokers, had a significantly greater percentage decline in the forced expiratory volume in one second expressed as a fraction of the forced vital capacity (4.01 +/- 4.6 v. 1.52 +/- 5.84), the forced expiratory flow in the middle half of the forced vital capacity (FEF25%-75%; 11.36 +/- 15.09 v. 5.3 +/- 17.58) and the ratio of the FEF25%-75% to the forced vital capacity (FEF/FVC; 14.06 +/- 14.45 v. 6.95 +/- 17.94). CONCLUSIONS: Our results suggest that young smokers, within a few years of starting to smoke, develop changes in pulmonary function indicating early peripheral airway narrowing, and that these effects worsen progressively with continued smoking.

Adult↗

Effects of passive smoking on lung growth in children.

The objective of this study was to determine the effects of passive smoking on functional lung growth in children and adolescents. It was hypothesized that passive smoking might reduce lung function growth, especially in susceptible children. The assumption was that those most susceptible would be children who started with low lung function, as it had been shown that they had slower growth of lung function, and start to decline earlier. There were 138 non-Hispanic Caucasian children and adolescents, ages 5 through 15, who had at least three satisfactory longitudinal lung function tests over a 13 year period in the Tucson epidemiological study of airway obstructive diseases. Those who started in childhood with normal function did not show any effect of passive smoking, nor did females who started with low lung function. Males starting with low lung function whose parents smoked showed definite changes. Their forced expiratory volume in 1 second (FEV1) grew even more slowly between ages 13 through 16, related primarily to continuous parental smoking. They also had higher rates of decline for FEV1 to forced vital capacity (FVC) ratio and maximum flow at 50% vital capacity to FVC ratios than either the low function group without passive smoking or the normal function groups. This was independent of any symptoms or diagnoses present in this male low function group.

Adolescent↗

Association between exposure to environmental tobacco smoke and exacerbations of asthma in children.

BACKGROUND: Exposure to environmental tobacco smoke, as reported by parents, has been linked to diminished pulmonary function and more frequent exacerbations of asthma in children with the disease. Further insight into this association might be gained by using urine cotinine levels to measure actual exposure. METHODS: We measured urine cotinine levels in 199 children with asthma; 145 also underwent pulmonary-function studies. A parent answered questions about each child's exposure to environmental tobacco smoke. Acute exacerbations of asthma during the preceding year were documented through blinded review of medical records. Possible confounding factors were accounted for by the use of multivariate analysis and by comparisons of serum theophylline levels in exposed and unexposed children. RESULTS: The median urine cotinine levels were 5.6 ng per milliliter in the 116 children reported not to have been exposed to tobacco smoke, 13.1 ng per milliliter in the 53 children exposed to cigarette smoking by the mother or other persons, and 55.8 ng per milliliter in the 30 children exposed to cigarette smoking by the mother and other persons. Acute exacerbations of asthma increased with exposure, whether such exposure was reported by a parent or identified on the basis of the cotinine level; the relative risks for the highest as compared with the lowest exposure category were 1.8 (95 percent confidence interval, 1.4 to 2.2) for reported exposure and 1.7 (95 percent confidence interval, 1.4 to 2.1) for exposure indicated by cotinine levels. The forced expiratory volume in one second (FEV1), the forced expiratory flow between 25 and 75 percent of vital capacity, and the ratio of FEV1 to forced vital capacity also decreased with increases in both measures of exposure. CONCLUSIONS: Measurement of urine cotinine levels provides further evidence of an association between exposure to environmental tobacco smoke and pulmonary morbidity in children with asthma. These data emphasize the need for systematic, persistent efforts to stop the exposure of children with asthma to environmental tobacco smoke.

Adolescent↗

Comparison of the bronchodilatory effects of cetirizine, albuterol, and both together versus placebo in patients with mild-to-moderate asthma.

BACKGROUND: Many potential users of the H1 antihistamine cetirizine are asthmatic and may be using inhaled albuterol. This study was conducted to assess the possible bronchodilatory effect of cetirizine in patients with mild-to-moderate asthma and to determine whether cetirizine interacts with albuterol. METHODS: In a randomized, double-blind, placebo-controlled, crossover study, the effects on pulmonary function of 5, 10, and 20 mg oral doses of cetirizine with and without inhaled albuterol (180 micrograms) were determined in 12 patients at 11 time points over 8 hours. The primary measure of efficacy was forced expiratory volume in 1 second (FEV1). RESULTS: Cetirizine with or without albuterol significantly increased FEV1, peak expiratory flow rate, and forced expiratory flow rate between 25% and 75% of vital capacity relative to baseline and placebo but did not have a significant effect on forced vital capacity. The effect of 20 mg of cetirizine on FEV1 was generally greater than that of 10 or 5 mg, but the difference was statistically significant only at the 30-minute time point (p < 0.05). All three cetirizine doses produced significantly greater increases than placebo in FEV1 and forced expiratory flow rate between 25% and 75% of vital capacity for 8 hours and in peak expiratory flow rate for 7 hours (p < 0.02). Albuterol alone had a significant effect on the four pulmonary function variables from 1 to 5 hours after baseline (p < 0.05), which is consistent with albuterol's recommended dosing frequency of every 4 to 6 hours. Albuterol alone increased FEV1 significantly more than 5 mg of cetirizine alone but not 10 mg or 20 mg of cetirizine alone at 60, 90, and 120 minutes after baseline, but all three doses of cetirizine increased FEV1 significantly more than albuterol 7 and 8 hours after baseline (p < 0.05), indicating that the bronchodilatory action of cetirizine lasts longer than that of albuterol. Cetirizine neither potentiated nor inhibited the bronchodilatory action of albuterol, but the two drugs appeared to have an additive bronchodilatory effect. None of the cetirizine treatments caused a worsening of pulmonary function, and all were well tolerated. CONCLUSIONS: Cetirizine has a significant bronchodilatory effect in patients with mild-to-moderate asthma and can be used to treat concomitant conditions (e.g., allergic rhinitis) without concern that it will interfere with the bronchodilatory effect of albuterol or cause worsening of asthma by itself.

Albuterol↗