The estimation of maximal breathing capacity by means of chest fluoroscopy and inspiratory roentgenograms.
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Monitoring of respiratory function in the intensive care unit uses different techniques in spontaneously breathing patients and during mechanical ventilation. The simplest and most efficient means are clinical observation, non-invasive monitoring of respiratory movements and frequent blood gas analysis. The respiratory force and reserves can be assessed by measuring tidal volume, vital capacity and maximal inspiratory force (in cm H2O or mm Hg), and these values are helpful in deciding on ventilatory assistance or extubation. During mechanical ventilation the function of the respirator must be monitored by appropriate sensors and alarms. In addition, the measurement of functional residual capacity, compliance and distribution of ventilation, as well as changes therein with the application of positive end-expiratory pressure (PEEP), can contribute to evaluate of appropriate therapy and prognosis of pulmonary failure.
We analyze the effect of inspiratory muscle training (IMT) in patients with chronic obstructive pulmonary disease (COPD), with special emphasis on its effects on inspiratory muscle function and clinical outcomes. We reviewed only randomized, controlled studies that have either controlled both the load and the breathing pattern when using resistive training or have employed a threshold trainer in which the load is independent of the pattern of breathing, since methodological aspects may explain inconsistent results in the literature. In these circumstances, most of the studies demonstrated positive effects on inspiratory muscle function. Clinical effects were seldom evaluated; limited available data showed a reduction in dyspnea that was related to an increase in maximal inspiratory pressures (PIMax). When exercise capacity was evaluated through the distance the patients were able to walk in 6 or 12 minutes, most studies demonstrated a significant increase. Other reported positive effects were improvement in nocturnal SaO2, inspiratory muscle power output and maximal inspiratory flow rate. Based in this review, a recommended training regime appears to be an intermediate load (30-40% PIMax) using a threshold device for 30 minutes daily for at least 5 weeks. Although in the literature the criteria for selecting patients are not always well defined, we consider IMT as a helpful procedure for pulmonar rehabilitation in those patients with a moderately severe inspiratory muscle dysfunction presenting dyspnea during daily living activities despite optimal therapy.
Several types of filtering (air-purifying) devices, air-line (supplied-air) apparatus, and self-contained breathing apparatus are used at work. The most important parameters of the respiratory protective devices that affect physical work capacity are additional inspiratory and expiratory breathing resistance, dead space, and weight. The main physiological effects of the respirators are alterations in breathing pattern, hypoventilation, retention of carbon dioxide, and increase in the work of breathing. The undesirable effects are accentuated during heavy physical work, maximal physical work capacity thereby being reduced.
The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2-3 min at a constant level (range of increase 160-1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35-50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.
UNLABELLED: In patients with poliomyelitis, respiratory failure requiring ventilatory support may occur during the acute illness. Some patients continue to require long-term nocturnal ventilatory support; others are weaned but subsequently require support because of a late deterioration in ventilatory function. OBJECTIVES: To assess the sensitivity of sniff nasal inspiratory pressure (SNIP) to post-poliomyelitis respiratory muscle weakness and to assess the relationship between the respiratory muscle strength and the need for ventilatory support in patients with previous poliomyelitis (post-polio patients). METHODS: Respiratory muscle strength was measured in 50 post-polio patients. Tests included forced vital capacity (FVC), maximum inspiratory and expiratory pressures (MIP and MEP), and SNIP. RESULTS: Twenty-one patients used non-invasive nocturnal ventilatory support (NIV group) compared to 29 on no support (non-NIV group). The percentage predicted FVC was significantly lower in the NIV group compared to the non-NIV group (P=0.01). Similarly, the percentage predicted MIP was significantly lower in NIV group (P=0.007). Low SNIP values (both absolute value and percentage predicted) were associated with the need for ventilatory support (P<0.001). Of the patients requiring no support, those who had been ventilated during the acute episode of poliomyelitis had a significantly lower SNIP than those who had never been ventilated (P=0.04). CONCLUSIONS: Post-polio patients who are currently on nocturnal ventilation have significantly lower FVC, MIP and SNIP compared to currently non-ventilated patients. Non-ventilated patients who were ventilated during the acute episode of poliomyelitis have significantly weaker respiratory muscle strength than patients who were never ventilated. This study indicates that SNIP is more sensitive to post-polio respiratory muscle weakness than other non-invasive tests. Thus measurement of SNIP is a valuable tool for monitoring the progression of respiratory muscle weakness due to previous poliomyelitis and this can be applied to other neuromuscular disorders.
BACKGROUND AND PURPOSE: Previous investigations have demonstrated that a regimen of high-intensity inspiratory muscle training (IMT) resulted in changes in ventilatory function and exercise capacity in patients with chronic lung disease, although the effect of high-intensity IMT in subjects who are healthy is yet to be determined. The purpose of this study, therefore, was to examine whether high-intensity IMT resulted in changes in ventilatory function and exercise capacity in subjects who were healthy. SUBJECTS: Twenty subjects were randomly assigned to 2 groups. METHODS: The training group completed an 8-week program of IMT set at 80% of maximal effort. The control group did not participate in any form of training. Baseline and posttraining measures of body composition, pulmonary function, inspiratory muscle function (including maximal and sustained maximal inspiratory pressures [MIP and SMIP]), relaxed and contracted diaphragm thickness and thickening ratio (Tdi.rel, Tdi.cont, and TR), and exercise capacity were determined. RESULTS: The training group demonstrated significant increases in MIP, SMIP, Tdi.cont, TR, VC, total lung capacity, and exercise capacity compared with the control group, which demonstrated no change from baseline measurements at 8 weeks. DISCUSSION AND CONCLUSION: The findings of this study suggest that high-intensity IMT results in increased contracted diaphragm thickness and increased lung volumes and exercise capacity in people who are healthy.
In this study we examined the effects of hibernation on several aspects of pulmonary mechanics in golden mantled ground squirrels. Measurements were made on anesthetized animals that were active in late fall (FA, n = 7), maintained at 23 degrees C and normal photoperiod in mid-winter (WA, n = 0) and hibernating at 5 degrees C in mid-winter (H, n = 8). Compared with FA animals, WA animals showed an increase in inspiratory reserve volume (IRV) and in inspiratory, vital and total lung capacities (IC, VC, and TLC). Hibernating animals exhibited further increases in IRV, IC, VC and TLC, an elevated residual volume, and virtual elimination of the expiratory reserve volume. There was also a decrease in specific lung compliance and a sharp knee in the lower portion of the quasi-static volume-pressure curve. There was a significant increase in the elastic work required to ventilate the hibernating animals compared with FA animals. The data suggest that, despite an increase in compliance at TLC, there is decreased compliance at low volumes, gas trapping at functional residual capacity, and an increase in the work required to breathe in hibernating animals.
The aim of this study was to test the hypothesis that carbon monoxide diffusing capacity (DCO) is elevated in asthmatic patients with minimal airflow limitation and/or hyperinflation; the latter factors should reduce the possibility of technical errors in the measurement of DCO. In ten asthmatic and ten healthy subjects, DCO and its components, membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Qc) were measured by the single-breath method. Values were normalized for alveolar volume (VA). The mean DCO/VA was higher in the asthma groups as was the Qc/VA. The Dm/Qc was also higher in the asthma group. In the asthmatic but not the healthy subjects, both DCO/VA and Qc/VA were negatively correlated with the forced expiratory flow at 50 percent of vital capacity and peak inspiratory flow rate. Thus, DCO/VA may be increased in asthmatic patients with only mild airflow limitation; this may be due to an elevated capillary blood volume.
We investigated the relationship between minute ventilation (VE) and net respiratory muscle pressure (Pmus) throughout the breathing cycle [Total Pmus = mean Pmus, I (inspiratory) + mean Pmus, E (expiratory)] in six normal subjects performing constant-work heavy exercise (CWHE, at approximately 80% maximum) to exhaustion on a cycle ergometer. Pmus was calculated as the sum of chest wall pressure (elastic + resistive) and pleural pressure, and all mean Pmus variables were averaged over the total breath duration. Pmus, I was also expressed as a fraction of volume-matched, flow-corrected dynamic capacity of the inspiratory muscles (P(cap, I)). VE increased significantly from 3 min to the end of CWHE and was the result of a significantly linear increase in Total Pmus (Delta = 43 +/- 9% from 3 min to end exercise, P < 0.005) in all subjects (r = 0. 81-0.99). Although mean Pmus, I during inspiratory flow increased significantly (Delta = 35 +/- 10%), postinspiratory Pmus, I fell (Delta = -54 +/- 10%) and postexpiratory expiratory activity was negligible or absent throughout CWHE. There was a greater increase in mean Pmus, E (Delta = 168 +/- 48%), which served to increase VE throughout CWHE. In five of six subjects, there were significant linear relationships between VE and mean Pmus, I (r = 0.50-0.97) and mean Pmus, E (r = 0.82-0.93) during CWHE. The subjects generated a wide range of Pmus, I/P(cap, I) values (25-80%), and mean Pmus, I/P(cap, I) increased significantly (Delta = 42 +/- 16%) and in a linear fashion (r = 0.69-0.99) with VE throughout CWHE. The progressive increase in VE during CWHE is due to 1) a linear increase in Total Pmus, 2) a linear increase in inspiratory muscle load, and 3) a progressive fall in postinspiratory inspiratory activity. We conclude that the relationship between respiratory muscle pressure and VE during exercise is linear and not curvilinear.
The upper body posture naturally adopted by long distance runners was quantified, and its effects on ventilation were assessed in 14 subjects. Maximum voluntary ventilation (MVV) and flow-volume loop maneuvers were performed in three seated positions: 1) natural running posture (RUN), with back angled forward 11 degrees, neck flexed, and head extended 35 degrees forward of the spinal column; 2) back vertical with head and neck as above (NEF); and 3) head and back vertical (VERT). MVV was significantly higher in RUN compared with both NEF and VERT, as were peak inspiratory pressure (PImax) from functional residual capacity, peak expiratory flow (PEF), and peak inspiratory flow (PIF). Expiratory flow at 50% of vital capacity was significantly higher in RUN and NEF than in VERT, consistent with reported increases in flow due to tracheal stiffening. The increased PIF and PImax in RUN indicate increased inspiratory muscle tension and/or improved transduction of tension into a more negative pleural pressure. Magnetometer tracings of rib cage dimensions demonstrated greater anteroposterior stability during maximal inspiratory efforts in RUN compared with VERT. The improved inspiratory function seen in RUN may be due to more effective diaphragmatic and/or accessory muscle function. These findings demonstrate that the position naturally adopted by long distance runners favors ventilation.
We studied 12 physically fit (VO2 max = 44 ml.kg-1.min-1) older subjects (age = 63 to 77 yr) who showed the usual age-related declines in lung function (i.e., reduced maximal expiratory flow rates, vital capacity and increased functional residual capacity, closing capacity, and residual volume). We measured the optimal transpulmonary pressures for maximal expiratory airflow and the capacity of the muscles of inspiration for developing pleural pressure (taking into account the effects of lung volume and flow rate). Within these mechanical constraints to ventilation we plotted tidal pleural pressure-volume loops for mild through maximal exercise according to a measured end-expiratory lung volume (EELV). We found EELV to decrease a mean of 0.26 +/- 0.09 L and maximal effective pleural pressures to be reached in nine subjects near EELV with only light to moderate exercise intensities, whereas peak inspiratory pressure was only 45% of the capacity for pressure generation. With progressive increases in exercise intensity, EELV increased, and pleural pressures encroached to a greater extent on the maximal effective pressures; however, they remained effective in the majority of subjects. During maximal exercise EELV was 0.13 +/- 0.10 L greater than resting values, 20% of the Vt reached maximal effective pressures, and 83% of the capacity for inspiratory pressure was achieved. Three subjects significantly surpassed their maximal effective expiratory pressures, and four subjects achieved 95 to 100% of the capacity for inspiratory pressure generation. These subjects also showed no further increase in ventilation while breathing 0.02 to 0.05 FICO2 at maximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
We looked for evidence of changes in lung elastic recoil and of inspiratory muscle fatigue at maximal exercise in seven normal subjects. Esophageal pressure, flow, and volume were measured during spontaneous breathing at increasing levels of cycle exercise to maximum. Total lung capacity (TLC) was determined at rest and immediately before exercise termination using a N2-washout technique. Maximal inspiratory pressure and inspiratory capacity were measured at 1-min intervals. The time course of instantaneous dynamic pressure of respiratory muscles (Pmus) was calculated for the spontaneous breaths immediately preceding exercise termination. TLC volume and lung elastic recoil at TLC were the same at the end of exercise as at rest. Maximum static inspiratory pressures at exercise termination were not reduced. However, mean Pmus of spontaneous breaths at end exercise exceeded 15% of maximum inspiratory pressure in five of the subjects. We conclude that lung elastic recoil is unchanged even at maximal exercise and that, while inspiratory muscles operate within a potentially fatiguing range, the high levels of ventilation observed during maximal exercise are not maintained for a sufficient time to result in mechanical fatigue.
Myositis associated with graft-versus-host-disease (GVHD) typically presents with proximal muscle weakness, myalgias, and a raised creatinine phosphokinase (CPK) level. We report a case of a 51 year old man who developed respiratory muscle weakness five years after an allogeneic bone marrow transplant for multiple myeloma. His symptoms included tachypnoea, abdominal paradox, and orthopnoea. Pulmonary function tests revealed diminished vital capacity and maximal inspiratory and expiratory pressures. Serum CPK levels were raised and a peripheral muscle biopsy specimen was consistent with GVHD. He improved with immunosuppressive therapy.
We studied whether bronchodilatation occurs with exercise during the late asthmatic reaction (LAR) to allergen (group 1, n = 13) or natural asthma (NA; group 2, n = 8) and whether this is sufficient to preserve maximum ventilation (VE(max)), oxygen consumption (VO(2 max)), and exercise performance (W(max)). In group 1, partial forced expiratory flow at 30% of resting forced vital capacity increased during exercise, both at control and LAR. W(max) was slightly reduced at LAR, whereas VE(max), tidal volume, breathing frequency, and VO(2 max) were preserved. Functional residual capacity and end-inspiratory lung volume were significantly larger at LAR than at control. In group 2, partial forced expiratory flow at 30% of resting forced vital capacity increased greatly with exercise during NA but did not attain control values after appropriate therapy. Compared with control, W(max) was slightly less during NA, whereas VO(2 max) and VE(max) were similar. Functional residual capacity, but not end-inspiratory lung volume at maximum load, was significantly greater than at control, whereas tidal volume decreased and breathing frequency increased. In conclusion, remarkable exercise bronchodilation occurs during either LAR or NA and allows VE(max) and VO(2 max) to be preserved with small changes in breathing pattern and a slight reduction in W(max).
Pulmonary mechanics and oxygenation were measured in 24 consecutive patients with posttraumatic flail chest requiring continuous mechanical ventilation. The mean duration of mechanical ventilation was fourteen days. Mortality was 38% for all patients, 29% if deaths from head injury are excluded. Pneumonia occurred in 4 patients (17%) and pneumothorax in 1 (4%). Vital capacity and maximal inspiratory force measurements were useful in assessing chest wall stabilization. Total lung compliance correlated negatively with fatal outcome from respiratory failure. The alveolar-arterial oxygen gradient was not useful in assessing chest wall stabilization.
In patients on continuous ambulatory peritoneal dialysis (CAPD) for more than 6 wk, we measured functional residual capacity (FRC), maximum inspiratory and transdiaphragmatic pressure, diaphragm length, and radius of curvature (roentgenographic methods) as functions of the volume of peritoneal dialysate (PD) instilled within the abdominal cavity. This allowed in vivo characterization of the human diaphragm's force-length relationship. As PD volume increased from zero to 3 L, FRC decreased from 2.41 +/- 0.29 L to 1.93 +/- 0.072 L; mean total diaphragm length index (TDLI) increased from 0.22 +/- 0.01 to 0.28 +/- 0.01, and diaphragm radius of curvature remained unchanged. Respiratory muscle strength increased as a function of dialysate volume, reaching its maximum after the infusion of 3 L PD. In contrast, normal subjects achieved maximal inspiratory muscle force at their normal FRC, with a mean TDLI of 0.26 +/- 0.01 and showed no further increase as the diaphragm lengthened. We conclude that the human diaphragm may be capable of an adaptive rightward shift in its force-length relationship when it is chronically lengthened by CAPD.
We measured pressures in 2 lung regions in 5 seated subjects with 2 esophageal balloons placed 7.2 +/- 0.6 cm (mean +/- SE) apart in the mid-thorax in order to obtain the esophageal pressure gradient (EPG). Pressure differences between the lower thoracic balloon and a balloon placed in the stomach were obtained to measure transdiaphragmatic pressure (pdi). Inspiratory maneuvers were made from functional residual capacity (FRC) at either low inspiratory flow rates (slow VI) (mean slow VI: 0.22 +/- 0.05 L/sec) or at rapid flow rates (fast VI) (2.15 +/- 0.15 L/s). At FRC the mean EPG was 0.19 +/- 0.04 cm H2O/cm. The mean EPG was consistently lower at 500 cc above FRC during fast VI (0.14 +/- 0.03 cm H2O/cm) than during slow VI (0.28 +/- 0.05 cm H2O/cm) (P less than 0.001, paired 't' test). Fast VI results in amplification of pressure in the lower as compared to the upper region wih reduction in EPG. Diaphragmatic contraction appears to influence alterations in EPG during fast VI.