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Assessment of ventilatory function in patients with neuromuscular disease.

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗

Ventilatory and mouth occlusion pressure responses to hypercapnia in chronic tetraplegia.

OBJECTIVE: To compare the ventilatory response to hypercapnia and the mouth occlusion pressure measured at 0.1 second following inspiration (P0.1) in hypercapnia between chronic tetraplegic and normal subjects. DESIGN: A case-control study with an uneven sample size for the study of clinical disorders. SETTING: Patients were recruited from the outpatient clinic of a rehabilitation department. PARTICIPANTS: Seven normal men and 9 men with tetraplegia who had cervical cord injuries (C5-C8), with a mean injury duration of 9.7 yrs. INTERVENTIONS: Pulmonary function tests were performed during resting, whereas minute ventilation (VE) and P0.1 were measured during CO2 rebreathing. RESULTS: The maximal voluntary ventilation (MVV), vital capacity (VC), and maximal respiratory muscle strength in the tetraplegic subjects were significantly less than in the normal subjects. Both the ventilatory and P0.1 responses to hypercapnia were significantly reduced in tetraplegic as compared with normal subjects, but the reductions were eliminated by normalizing with maximal ventilatory performance (MVV or VC) and maximal inspiratory muscle strength (PImax), respectively. CONCLUSIONS: Chronic tetraplegic persons have diminished ventilatory and P0.1 responses to hypercapnia. Respiratory muscle weakness may be a primary factor contributing to the diminished ventilatory response observed in these patients.

Adult↗

Sustained maximal ventilation after endurance exercise in athletes.

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.

Adolescent↗

Normal values and ranges for ventilation and breathing pattern at maximal exercise.

Assessment of the breathing pattern at maximal exercise in patients is limited because the range of ventilatory responses (minute ventilation; tidal volume; respiratory rate) at maximal exercise in normal humans is unknown. We studied 231 normal subjects (120 women; 111 men) equally distributed according to age from 20 to 80 years. Each subject performed a progressive incremental cycle ergometer exercise test to their symptom-limited maximum. Mean ventilation at the end of exercise (Vemax) was significantly higher in men (mean +/- SD, 97 +/- 25 L/min) than in women (69 +/- 22 L/min) (p less than 0.001). Minute ventilation at the end of exercise as a fraction of predicted maximal voluntary ventilation (Vemax/MVV) for all subjects was 0.61 +/- 0.14 (range, 0.28 to 1.02). There was no difference in Vemax/MVV between men (0.62 +/- 0.14) and women (0.59 +/- 0.14). Tidal volume at the end of exercise (Vtmax) was higher in men (2.70 +/- 0.48 L) than in women (1.92 +/- 0.41 L) (p less than 0.001). Any differences in Vtmax between men and women disappeared when Vtmax was corrected for baseline FVC. Respiratory rate at the end of exercise (RRmax) was 36.1 +/- 9.2 breaths per minute for all subjects. There was no difference in RRmax between men and women. The Vemax correlated best with carbon dioxide output at the end of exercise (r = 0.91; p less than 0.001) and with maximal oxygen uptake (r = 0.90; p less than 0.001) for all subjects. This study of a large group of subjects has demonstrated the wide range of possible breathing patterns which are adopted during exercise and has provided a wide range of "normal" responses which must be taken into consideration when maximal ventilatory data from exercise tests are analyzed.

Adult↗

Maximal ventilation after exhausting exercise.

It remains unclear whether the hyperpnea of exercise severely stresses the ventilatory musculature. We hypothesized that the ability to ventilate maximally is decreased during and immediately following exhausting exercise. Subjects performed isocapnic maximal voluntary ventilations (60-s MVV) before, during the final minute, and after exhausting treadmill exercise lasting either 3-10 min or 60 min. Severe exercise lasting 3-10 min failed to change the 60-s MVV. In contrast, during the final minute and 5 and 10 min after 60 min of exhausting exercise, eight non-runners showed significantly lower (P less than 0.01) 60-s MVV values in comparison to control values. Eight runners had a lower (P less than 0.05) 60-s MVV 10 min post-exercise as compared with control and exercise values. Our data suggest that the capacity to ventilate maximally declines only in long-term exhausting exercise and that this decrement in most pronounced in non-runners.

Adult↗

Pulmonary mechanisms and work of breathing at maximal ventilation and raised air pressure.

Pulmonary ventilation (V) and the interrelationships of airflow, transpulmonary pressure, and lung volume during inspiration and expiration were studied in eight healthy subjects who performed maximal exercise (MEx; 140% VO2 max), 15-s maximal voluntary ventilation (MVV), and forced inspiratory and expiratory vital capacity (FVC) maneuvers at 1, 3, and 6 ATA. Maximal exercise ventilation and MVV amounted to 149 +/- 7 (mean +/- SE) and 193 +/- 9 l . min-1, respectively, at 1 ATA and were both reduced by approximately 37% at 3 ATA and by 50% at 6 ATA. Expiratory peak flows during MEx and MVV were equal to the maximal flows obtained during FVC at comparable lung volumes, whereas inspiratory peak flows during MEx were 20% less than the FVC flows. Despite a sixfold increase in gas density, the rate of mechanical work of breathing decreased when the pressure was raised to 6 ATA, during MEx from 8 +/- 1 to 6 +/- 1 W, and during MVV from 28 +/- 5 to 18 +/- 3 W. With increasing gas density there was a shift of lung volumes in the inspiratory direction with consequent reductions of inspiratory-to-expiratory flow ratios. We conclude that depletion of energy stores in the inspiratory muscles contributed to limiting V during MEx at raised air pressure.

Adult↗

Airway occlusion pressure (P0.1)-a useful predictor for the weaning outcome in patients with acute respiratory failure-.

Twenty-five patients who required mechanical ventilatory support (MVS) after major surgery or severe burns were studied to determine whether airway occlusion pressure (P(0.1)) is a clinically useful indicator to predict the success or failure of the weaning trial. A total of 33 weaning trials were attempted on these patients. Of the 33 trials, 24 were followed by successful weaning and 9 by failure. Although the success group, when compared with the failure group, had a lower respiratory rate ( P << 0.001), a lower minute ventilation ( P << 0.001), a higher maximal voluntary ventilation to minute ventilation ratio ( P << 0.01) and a higher forced vital capacity ( P << 0.05), no threshold values separated the success from the failure group. The alveolar-arterial P(O)(2) gradient, with an F i(O)(2) of 1.0, in weaning success and failure showed no statistical difference. In contrast, all patients in the success group had a P(0.1) of less than 3.5 cmH(2)O and those in the failure group had a P(0.1) of greater than 3.5 cmH(2)O ( P << 0.001). We conclude that P(0.1) is a clinically superior indicator for discontinuing MVS in patients with acute respiratory failure.

Journal Article↗

Effect of intravenous fructose 1,6-diphosphate administration in malnourished chronic obstructive pulmonary disease patients with chronic respiratory failure.

BACKGROUND: Weight loss and skeletal muscle wasting are common in patients with chronic obstructive pulmonary disease (COPD) and can influence the course and the prognosis of COPD. Hypophosphatemia is a pathologic status often characterized by muscle weakness and is a frequent laboratory finding in these patients. OBJECTIVE: The aim of the present study was to evaluate the effect of an organic phosphate (fructose 1,6-diphosphate, FDP) administration on respiratory performance in 45 malnourished COPD patients in stable clinical conditions. METHODS: Physiologic evaluation including spirometry, maximal voluntary ventilation (MMV), elevated arm test, maximal mouth pressures (PImax and PEmax), respiratory response to CO(2), oxygen (PaO(2)) and carbon dioxide (PaCO(2)) arterial tension, a visual analogic scale (VAS) to measure dyspnea, and complete blood tests were done at the beginning and again at the end of the study. RESULTS: After FDP administration, there was a significant increase in PImax (43.0 +/- 18.3 cm H(2)O before treatment vs. 49.8 +/- 14.9 cm H(2)O after treatment; p < 0.005). This did not occur in the placebo group (40.3 +/- 17.4 cm H(2)O before treatment vs. 42.6 +/- 20.1 cm H(2)O after treatment, nonsignificant). There was also a trend of VAS to decrease and of MVV to increase. CONCLUSIONS: These results show that FDP administration may be useful in the management of malnourished COPD patients, especially in increasing their respiratory muscle strength.

Aged↗

Long-term nasal intermittent positive pressure ventilation in advanced Duchenne's muscular dystrophy.

The aim of our study was to evaluate the long-term effect of nasal ventilation in patients with advanced Duchenne's muscular dystrophy (DMD). To this end, we compared the clinical and pulmonary function course of five subjects affected with chronic ventilatory failure due to DMD and treated with nasal intermittent positive pressure ventilation (NIPPV) with that of an unventilated comparison group; the latter consisted of another five patients with DMD, with a similar degree of clinical and respiratory functional impairment, who refused long-term mechanical ventilation. The duration of the follow-up was 24 months. At the conclusion of the trial, all patients treated with NIPPV were still alive; in contrast, four of five patients who underwent simple conservative treatment had already died (mean survival, 9.7 +/- 5.8 months). After 6 months of follow-up, mean loss of FVC and maximal voluntary ventilation was considerably higher in nonventilated subjects (respectively: -0.23 L vs +0.03 L and -5 L/min vs -1.5 L/min). These are the first comparative results confirming that long-term NIPPV helps to stabilize pulmonary function and to prolong the expectancy of life of patients with DMD.

Adolescent↗

Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors.

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.

Adolescent↗

Factors associated with improvement in breathing capacity during exercise in patients with chronic obstructive pulmonary disease.

OBJECTIVES: The aim of this study was to explore the relationship between resting pulmonary function indices and the ratio of minute ventilation at peak exercise to the maximal voluntary ventilation (VEmax/MVV) and to determine whether an improvement in breathing capacity during exercise (i.e. VEmax/MVV > 1) is associated with greater exercise capacity in patients with COPD. METHODOLOGY: The results of pulmonary function tests and incremental, symptom-limited cardiopulmonary exercise testing in 84 patients with predominantly moderate to severe COPD were reviewed. Multiple linear regression analysis was applied to determine the relationship of VEmax/MVV with selected independent variables at rest. Multiple logistic regression was used to determine significant predictors of VEmax/MVV </= or > 1. RESULTS: FEV1/FVC and inspiratory capacity (IC) were the only variables among resting pulmonary function indices that were significant independent determinants of VEmax/MVV and the stepwise analysis generated the following equation: VEmax/MVV = (-1.05E-02 x FEV1/FVC) + (0.15 x IC) + 1.28; r= 0.701, P < 0.001. Using multiple logistic regression with VEmax/MVV </= or > 1 as a dependent categorical variable, FEV1/FVC was the only significant predictor among resting pulmonary indices of a VEmax/MVV ratio of > 1 (Odds ratio 0.93, 95%CI 0.89, 0.97). There was a significant association between VEmax/MVV and peak oxygen uptake (VO2max) after adjusting for FEV1 (r = 0.66, P < 0.001). If the categorical variable of VEmax/MVV (</= or > 1) was used instead of a continuous variable, a significant association with VO2max remained after adjusting for FEV1 (r = 0.60, P < 0.001). CONCLUSIONS: Among resting pulmonary function indices, the FEV1/FVC ratio is the best determinant of an improvement in breathing capacity during exercise in COPD patients. After adjusting for FEV1, an improvement in breathing capacity during exercise is associated with significantly higher exercise capacity.

Aged↗

Hypothyroidism presenting with respiratory muscle weakness.

A 58-yr-old woman presented with recurrent chest infections, breathlessness, and orthopnea. She complained of nonspecific tiredness and aching limbs. A chest radiograph showed an elevated right hemidiaphragm. Thyroid function tests showed her to be severely hypothyroid (T4 = 23 nmol/L; TSH greater than 50 mU/L). Measurement of maximal respiratory mouth pressures (expiratory: 50 cm H2O, normal, 94 +/- 33; inspiratory: 15 cm H2O, normal, 71 +/- 27) suggested global respiratory muscle weakness. Severe bilateral diaphragm weakness was demonstrated by a greatly reduced maximal transdiaphragmatic pressure (Pdi) (Pdi Pimax = 0, normal, 65 +/- 31 cm H2O; sniff Pdi = 25 cm H2O, normal, 121 +/- 25). No Pdi was detectable on stimulation of the right phrenic nerve, whereas, on the left, it was 11 cm H2O (normal 7 to 15 cm H2O). Phrenic nerve conduction time was prolonged to both sides (right, 12 ms, left, 10 ms; normal, less than 9.5 ms). The relaxation rate of Pdi after a maximal sniff and after bilateral phrenic nerve stimulation was abnormally slow (7.4%/10 ms, 6.3%/10 ms, respectively). Three months after starting treatment with thyroxine she had become euthyroid, and phrenic nerve conduction times and Pdi relaxation rates had returned to normal. Maximal respiratory pressures, vital capacity, and maximal voluntary ventilation improved progressively on treatment, although maximal respiratory pressures still had not reached the normal range after six months. We conclude that hypothyroidism may present with breathlessness due to respiratory muscle weakness and/or phrenic nerve neuropathy and is reversible with treatment.

Diaphragm↗

Relationship between breathlessness and hypoxic and hypercapnic ventilatory response in patients with COPD.

The purpose of this study is to examine the relationship between breathlessness and the ventilatory response to hypercapnia or hypoxia in patients with chronic obstructive pulmonary disease (COPD). Fifteen male patients (mean forced expiratory volume in one second (FEV1): 1.13 L) underwent tests to determine hyperoxic hypercapnic ventilatory response (HCVR) and isocapnic hypoxic ventilatory response (HVR) with simultaneous quantification of breathlessness by modified Borg scale. The ventilatory output was evaluated by the ratio of minute ventilation (V'E) divided by measured maximal voluntary ventilation (MVV). The magnitude of HCVR or HVR was assessed as the slope value of the V'E/MVV-end-tidal carbon dioxide pressure (PET,CO2) or arterial oxygen saturation (Sa,O2) regression line, respectively. The breathlessness during the tests was evaluated not only linearly in relation to V'E/MVV, but also at given levels of PET,CO2 or Sa,O2. The mean value of the breathlessness at two different levels of ventilation was greater during HVR than during HCVR, suggesting that hypoxia is dyspnogenic independently of ventilatory stimulation. The HCVR was inversely correlated with the breathlessness response to ventilation, while similar correlation was partly present for HVR. The HVR was positively correlated with the breathlessness at an Sa,O2 of 80%, whilst there was no such correlation between the HCVR and the breathlessness related to PET,CO2. Therefore, patients with a higher breathlessness related to increased ventilation had a lower HCVR and HVR, whilst those with a higher breathlessness with desaturation, which might include a direct influence of hypoxia, had a higher HVR. These findings suggest an interaction between ventilatory response and breathlessness during the test, which may partly include behavioural modulation of HCVR and HVR through the breathlessness in various ways, depending on the origin and nature of the sensation.

Aged↗

[Evaluation of the effect of radical parietal pleurectomy on ventilatory function of the lungs in patients treated for recurrent spontaneous pneumothorax].

Pleurectomy as a method for treatment of recurrent pneumothorax and its influence on pulmonary ventilation are analyzed. Fifty-one patients were hospitalised twice at the Thoracic Surgery Department in Szczecin. The pneumothorax was treated by a chest tube drainage at the first time, and by pleurectomy in case of recurrent incident. Each time--with both lungs expanded--VC (vital capacity), MVV (maximal voluntary ventilation) and FEV1 (forced expiratory volume) were measured, thus it was possible to compare pre- and postoperative spirometric results. There was no statistically significant deficiency of ventilation after pleurectomy. The risk of different therapeutical methods and effectiveness in the protection against recurrence of pneumothorax were discussed. The results of own observations are compared with other authors' ones.

Adolescent↗

Relationship between bronchial responsiveness to hyperventilation with cold and methacholine in asthma.

Twenty-seven subjects with asthma and normal baseline lung function were challenged with aerosols of methacholine (M) and by isocapnic hyperventilation with cold air (HV). Stimulus-effect relationships were determined for each provocational technique on separate days and were expressed as the dose required to produce a 20% fall in forced expired volume in 1 sec (FEV1) obtained by linear interpolation from log stimulus vs. response curves (PD20). Each stimulus was applied with a sufficient intensity to produce a 20% or greater fall in FEV1 in each subject. The PD20 for M correlated significantly with the PD20 for HV (p less than 0.001) when the latter was expressed in liters per minute. The correlation between cumulative M PD20 and HV PD20 expressed as a percent of maximal voluntary ventilation was significant but less strong. We conclude that the airway response to HV reflects nonspecific bronchial hyperresponsiveness and that the dose of HV is best determined as the absolute level of ventilation.

Adolescent↗

Hypercapnic ventilation response in patients with lung disease: improved accuracy by correcting for ventilation ability.

The hypercapnic ventilation response (HCVR) is positively correlated with forced expired volume in 1 s (FEV1). Therefore, subjects of small stature or patients with lung disease have low values for HCVR. However, indexing the HCVR for the subject's predicted maximal voluntary ventilation (MVV) results in a corrected HCVR (CHCVR) which is not dependent on FEV1 in normal subjects [Respiration 1993;60:197-202]. We hypothesized that the CHCVR would also be useful in assessing chemosensitivity in patients with poor lung function. To obtain the predicted MVV, we used the linear regression for FEV1 vs. measured MVV obtained from 411 patients with a wide range of FEV1 values (MVV = 31.2 x FEV1 + 11.8, r = 0.90, p < 0.001). We compared HCVR and CHCVR to the occlusion pressure response to hypercapnia (OPRH) in 34 patients with chronic obstructive pulmonary disease (COPD) and in 19 patients with low FEV1 due to small stature. All patients had been referred for assessment of possible sleep apnea. The results for the two groups of patients were similar. For the COPD patients, the HCVR had high values for sensitivity (86%) and negative predictive value (94%), but specificity, positive predictive value and accuracy were low (59, 35 and 65%, respectively). In contrast, CHCVR had high values for all the foregoing (86, 96, 100, 100 and 97%, respectively). Our results suggest that the CHCVR is useful in assessing chemosensitivity in patients who are ventilation-limited.

Adult↗

Respiratory muscle strength, lung function, and dyspnea in patients with sarcoidosis.

BACKGROUND: Sarcoidosis is a systemic granulomatous disorder that is estimated to involve the skeletal muscles in up to 50% of patients. There is little information on the relationship among respiratory muscle strength, lung volumes, and the degree of dyspnea in patients with sarcoidosis. DESIGN AND PATIENTS: Lung function and maximal respiratory muscle force generation were measured in 36 patients with sarcoidosis (24 patients with pulmonary parenchymal infiltration) and 25 control subjects free of cardiorespiratory disease. Dyspnea in the sarcoidosis patients was quantitated by a score based on an activity tolerance assessment scale (ranging from rest to climbing hills or stairs). SETTING: Outpatient clinics of two teaching hospitals. RESULTS: Mean FVC, maximal voluntary ventilation, total lung capacity (TLC), functional residual capacity, residual volume (RV), and diffusing capacity of the lung for carbon monoxide (DLCO) were all at least 16% less than corresponding control values (in all cases, p < 0.001), while maximal inspiratory mouth pressure (PImax) and maximal expiratory mouth pressure (PEmax) were 37% and 39% less, respectively, than control values (both at p < 0.0001). PImax and PEmax declined with increasing dyspnea in a more graded, steady manner than did spirometric and DLCO values. For all measurements, however, the lowest mean values were found in patients with the most severe level of dyspnea. Strong inverse relationships were observed between PEmax and PImax with dyspnea level (p < 0.0001 and p < 0.01, respectively). Both PImax and PEmax correlated best with absolute values of FVC, while only PEmax correlated with RV (absolute and percent predicted) and percent predicted values of TLC. CONCLUSIONS: Maximal respiratory pressures correlate more closely with dyspnea level than lung volumes and DLCO. Since dyspnea is the most common presentation in early to moderately advanced sarcoidosis, respiratory pressures may be a more reliable index of functional work capacity and reflection of activities of daily living than standard tests of lung function.

Adult↗

Multum in parvo: explorations with a small bag of carbon dioxide.

A collection of 12 papers published between 1957 and 1972 are revisited. The papers had a common theme of the use of rebreathing carbon dioxide and explored a variety of topics in respiratory physiology. The first study established a method for the noninvasive and indirect estimation of arterial carbon dioxide pressure that was suitable for the routine clinical monitoring of respiratory failure and whose clinical utility remains to this day, but which also provided observations that were the stimulus for the studies that followed. The rate of rise in the partial pressure of carbon dioxide (PCO(2)) during rebreathing led to an analysis of body carbon dioxide storage capacity. Knowledge of carbon dioxide storage led to a method for quantifying lactate production in exercise without the need for blood sampling. The changes in ventilation that accompanied the increase in PCO(2) provided the basis for a rapid method for measuring aspects of breathing control (Read's method), which was later modified to measure the ventilatory response to hypoxia. The physiology of breath-holding was explored through observations of the fall in breath-holding time as PCO(2) climbed. Rebreathing also allowed increases in voluntary ventilation to be achieved without the development of alkalosis, leading to studies of maximal voluntary ventilation and respiratory muscle fatigue. Equilibration of PCO(2) during rebreathing was used to measure mixed venous PCO(2) during exercise and develop an integrated approach to the physiology of exercise in health and disease; alveolar-arterial disequilibrium in PCO(2) during exercise was uncovered. Equilibration of PCO(2), as well as PO(2), during rebreathing of carbon dioxide and nitrogen gas mixtures showed different time courses of venous gases at the onset of exercise. Starting with the rebreathing of carbon dioxide in oxygen mixtures in a small rubber bag, an astonishing range of topics in respiratory physiology was explored, with observations that remain valid, but in some respects unresolved, to the present day.

Carbon Dioxide↗