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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)

Objective: To evaluate the natural history of chronic fatigue syndrome (CFS) in a severely ill group of patients at three points in time. Design: Patients were enrolled from April 1992 to February 1994 and were evaluated three times. Time 1 (at enrollment): history, physical evaluation, and psychiatric evaluation; Time 2 (median = 1.6yrs after initial evaluation): postal questionnaire to assess current condition; Time 3 (median = 1.8yrs after Time 2): medical and psychiatric evaluations. Setting: The New Jersey CFS Cooperative Research Center, an ambulatory setting. Patients: Twenty-three patients fulfilled the 1988 case definition for CFS and had symptom complaints that were substantial or worse in severity. All patients were ill less than 4.5 years; and none had a DSM-III-R psychiatric disorder in the 5 years before illness onset; none had substance abuse in the 10 years before enrollment. Main Outcome Measures: Severity of CFS symptoms was assessed by self-report questionnaires, laboratory tests, and medical examination. Psychological status was assessed using the Q-D15 and the Centers for Epidemiological Study—Depression Scale. At each time of evaluation, patients were categorized as severe, slightly improved, improved, and recovered. Results: Over the 4 years of the study, 13 patients remained severely ill, 9 improved but still fulfilled the 1994 case definition for CFS, and 1 recovered. Illness duration, mode of onset, psychiatric status or depressed mood at intake, or chemical sensitivity did not predict illness outcome. One patient was diagnosed with an alternate illness, but it probably did not explain her CFS symptoms. Mood improved for those patients whose illness lessened. Conclusions: The prognosis for recovery was extremely poor for the severely ill subset of CFS patients. The majority showed no symptom improvement and only 4% of the patients recovered. Illness severity between Times 2 and 3 remained stable.

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.

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.

SUMMARY Ventilation (liters of air per minute) increases during an acute attack of asthma. Hypocapnia is the rule, although eucapnia may occur. This suggests both that respiratory center output is increased and that acidemia is not the major stimulus to augmented respiration. Mechanical receptors responding to change in end-expiratory respiratory system volume or airway dimensions, cortical stimulation to the medullary respiratory centers, and possibly hypoxemia function in concert to regulate ventilation in asthma. Newer laboratory techniques permit independent assessment of chemical and cortical components of ventilatory drive. These techniques have provided fresh insights into the effects of various therapeutic interventions upon respiration in asthma.