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

Background: Airway function, as assessed by standard spirometry, and the intensity of dyspnea reported by asthmatic patients correlate poorly. Objective: This study tests the following two hypotheses: (1) that measures of the tendency of a patient to somatize will reduce the variation in the report of dyspnea not explained by airway function; and (2) that plethysmography is a better tool with which to estimate the degree of dyspnea associated with asthma. Design: A prospective laboratory study carried out over one study session. Participants: Forty asthmatic subjects who had withheld bronchodilator (BD) therapy overnight. Interventions: We performed spirometry, plethysmography, and an assessment of dyspnea (ie, modified Borg scale) on all subjects before and after they received BD therapy. Standard questionnaires pertaining to psychological state and trait were administered as well. Results: The change in specific airway conductance with BD therapy correlated with a decline in the Borg score (r 5 0.47; p 5 0.007). By contrast, neither spirographic measures nor measures of static lung volumes correlated. Correlation with the Borg scale score was not improved by adding indexes of either somatization or psychological state or trait. Conclusion: The relief of dyspnea reported by patients with mild asthma after BD therapy is related to dilatation of the central airways. (CHEST 2001; 120:409 ‐ 415)

Purpose : The aim of this study was to assess the utility of clinical assessment of respiratory muscle weakness in MS. Patients and methods : We studied 40 MS patients who performed pulmonary function tests using standard procedures and measures of respiratory muscle strength. Descriptive clinical indices included a history of detailed neurologic findings, including upper and lower extremity weakness, cerebellar signs, and evidence of cerebral lesions and other clinical signs including dependence in activities of daily living, shortness of breath, weak voice, dysarthria and dysphagia. We devised an index comprised of four clinical signs: the patient's report of difficulty in clearing pulmonary secretions and his report of a weakened cough, the examiner's observation of the patient's cough, and ability to count on a single exhalation. Results : Mean values of TLC (95 percent ±14) VC (91 percent ±19), and RV (106 percent ±34) were normal. By contrast, MVV (68 percent ±20), PImax (74 percent ±27) and PEmax (51 percent ±22) were decreased. Stepwise multiple regression indicated that the best single predictor of expiratory muscle weakness was the index score; the combination of index score, upper extremity weakness, and maximal voluntary ventilation accounted for 60 percent of the variance in PEmax. Conclusion : We conclude that clinical assessment is a better predictor of respiratory muscle weakness than spirometry and that a systematic clinical assessment supplemented by respiratory muscle assessment and MVV can uncover subtle respiratory muscle weakness in patients with MS.

It has been shown that patients with COPD require as long as 20 min for equilibration of oxygen tension to occur after changing the fraction of inspired oxygen (FIO2). To date, there have been no studies to determine the equilibration time for the PaO2 in mechanically ventilated patients with diffuse pneumonia. We studied seven patients (five males, two females) with radiographic evidence of diffuse pneumonia. All patients required mechanical ventilation. After introducing a change in FIO2, arterial blood gas values were measured at 5-min intervals for 30 min. Four patients achieved maximal change in PaO2 after 5 min, while four patients required 10 min. These results are similar to those found in patients with left ventricular failure who experience equilibration rapidly; however, patients with COPD experience it at a much slower pace. These observations have clinical importance when managing unstable patients where time is a critical element.

Objective To assess the reliability of maximal inspiratory pressure (P i max) and maximal expiratory pressure (P e max) in subjects with multiple sclerosis (MS) and healthy control subjects by identifying the number of testing sessions and the number of measurements needed in a single testing session to obtain consistent, reproducible results. Design A descriptive, comparative design with repeated measures was used. Setting Four sets of 10 P i max and 10 P e max measurements were obtained over a 4-week period from MS subjects in their homes. The same measurements were obtained from healthy control subjects in a private setting. Subjects Seventy-two MS patients and 61 healthy control subjects participated in the study. Measurement P i max and P e max values were obtained by using previously published methods. Results Mean P e max and P i max values for MS patients differed over the first three of the four testing sessions. By contrast, mean P e max and P i max values for healthy control subjects differed only when the first session values were compared with values from the last three sessions. For MS patients, P e max and P i max increased between the first and 10th trial during the first testing session, but not during the subsequent three sessions. Conclusions The results of this study suggest that several practice sessions should be provided in order to obtain reliable P e max and P i max values in persons with MS. At least one practice session should be provided for healthy control subjects before identifying a baseline.

To evaluate the bioavailability of a new theophylline preparation suitable for once-a-day (od) oral administration, we performed a nonrandomized crossover study in which the absorption of the OD and a standard twice-a-day (bid) preparation were compared. Eight stable asthmatic patients, after having achieved steady-state, received an average of 975 mg of OD preparation at 8 pm. The protocol was later repeated with the same subjects receiving 487.5 mg of the bid preparation at 8 pm and again at 8 am using the same total dose. The maximal mean serum concentrations were 15.5±1.6 (SEM) µg/ml for the od preparation on the 8th hour and 12.7±2.2 for the bid regimen. The trough level was 7.4±1.2 µg/ml for the od regimen and 10.6±1.6 for the bid regimen. With either regimen, therapeutic theophylline levels could be observed throughout the 24-hour study period. Anhydrous theophylline may be administered as a single daily dose agent.

We compared tidal volume (VT) measured from the integrated airflow signal of a pneumotachygraph (PNTG) in ten patients, seated comfortably, with airway obstruction to VT, recorded simultaneously, by three chest-wall volume-displacement methods: two-channel magnetometer, isovolume calibration (mag-isov); respiratory inductance plethysmograph, isovolume calibration (rip-isov); and, inductance plethysmograph, least squares calibration (rip-l sq). There was no difference between VT, measured without PNTG, with each of the methods. When mouthpiece, noseclips, PNTG, and finally, dead space were included in a breathing circuit, VT increased to approximately one and one-half times that measured without the mouthpiece. Inspiratory volumes were measured with similar error by each method (mag-isov, 8.61 +/- 5.73 percent SD; rip-isov, 9.30 +/- 6.12 percent SD; rip-l sq, 8.43 +/- 6.27 percent SD). We conclude that in airway obstruction patients seated in a constant position, over the range of inspiratory volumes studied, error associated with chest wall volume-displacement methods is no greater than in normal subjects.

To investigate the mechanism for hyperventilation in two common but dissimilar conditions, asthma (A) and lobar pneumonia (P), we examined the ventilatory pattern in 17 A and six P subjects. When acutely ill, hyperventilation (PaCO2) was similar in the two groups. Minute ventilation (VE) however, was slightly greater in group A than in P. In A patients, measurements of occlusion pressure (dP/dT) and inspiratory flow rate (VT/ti) during quiet breathing showed enhancement of respiratory center output. By contrast, in P patients, dP/dT and VT/ti were not elevated. Tidal volume (VT) was 0.59 +/- 0.19 L in A; 0.45 +/- 0.09 in P. Respiratory rate was increased in both groups. With supplementary oxygen therapy, neither VE nor PaCO2 changed in either group. The mechanism for the increased ventilatory drive in group A is unclear. Most likely, reflexes initiated by either bronchospasm or by the sudden increase of end-expiratory lung volume (EELV), not operative in P, account for the increased respiratory center output seen in A. To examine the latter possibility, we studied the ventilatory pattern at both normal and increased EELV in six nonasthmatic subjects. Both dP/dT and VT/ti were increased in all subjects after elevation of EELV. Thus, changes in EELV may be important for the regulation of ventilation during bronchospasm.

Increased (more positive) end-expiratory and decreased (more negative) end-inspiratory values for intrapleural pressure (Ppl) invariably accompany acute bronchoconstriction. We hypothesize that both the increase in vital capacity (VC) and the decrease in residual volume (RV) observed after dilation of the central airways in patients with reversible obstruction of the airways result, in part, from a restoration of normal Ppl during unforced exhalation. To test this hypothesis, we examined the end-expiratory Ppl during breathing at rest in ten emphysematous and eight asthmatic subjects before and after inhalation of isoproterenol. The VC increased by 0.38 L after therapy, and the specific airway resistance and the RV decreased by 6.8 cm H 2 sec and 0.63 L, respectively. Total lung capacity was unchanged. The response of the VC to administration of isoproterenol is an important sequel to dilation of the large airways. Bronchioles close at a critical Ppl during exhalation. Because Ppl normalizes with administration of isoproterenol, this closure may be delayed to a lower pulmonary volume even if improvement in the function of peripheral airways does not occur.

Augmentation of inspiratory muscle strength (Pimax) represents an adaptive response to airway obstruction. We explore the possibility that respiratory muscle weakness may herald hospital admission during acute bronchospasm. The Pimax measured 81 +/- 25 percent of a predicted value in 20 patients with acute bronchospasm (forced expiratory volume in one second, 36 +/- 17 percent predicted). Pimax was related to both hyperinflation (functional residual capacity, as percent predicted) and body weight (subjects were 122 +/- 29 percent ideal body weight), but not to the degree of airway obstruction per se. Furthermore, measurements of axial (craniocaudal) motion of the rib cage and asynchrony of rib cage and abdominal motions during tidal breathing did not correlate with either the degree of air flow obstruction or Pimax. We conclude that little if any respiratory muscle weakness occurs with bronchospasm. Furthermore, Pimax does not correlate with the degree of airway obstruction and does not explain abnormalities of rib cage and abdominal motion associated with asthma.