Ventilatory and respiratory muscle responses to hypercapnia in patients with paraplegia

To evaluate ventilatory and respiratory muscle responses to hypercapnia in patients with paraplegia with paralysis of abdominal muscles, we studied seven patients with complete transection of the midthoracic cord (Th6-Th7) and six normal subjects. Minute ventilation (V E) and mean inspiratory flow responses to hypercapnia were similar in normal subjects and patients with paraplegia, but in the latter, at any given level of end-tidal CO(2) partial pressure (PET(CO(2))), tidal volume (VT) was reduced and frequency was increased. In normal subjects during hypercapnia, end-expiratory transpulmonary pressure (PL) and abdominal volume at end expiration decreased markedly, whereas end-expiratory volume of the rib cage (Vrc,E) remained constant, suggesting progressive recruitment of abdominal muscles. In patients with paraplegia compared to normal subjects the decrease in end-expiratory PL was reduced, and it was associated with a decrease in Vrc,E, suggesting recruitment of rib cage expiratory muscles. For a PET(CO(2)) of 70 mm Hg the estimated expiratory muscle contribution to VT was 10.3 and 28.4% (p < 0.02) in patients with paraplegia and normal subjects, respectively. We conclude that the V E-CO(2) relationship is preserved in patients with paraplegia with the development of a rapid and shallow pattern of breathing. This suggests that expiratory muscle paralysis elicits adaptation of the ventilatory control system similar to that observed in patients with generalized respiratory muscle weakness.     

Procainamide for dyspnea in myotonic dystrophy

We report the case of a patient with myotonic dystrophy who developed tachypnea and severe dyspnea without respiratory failure. Myotonia of inspiratory muscles was diagnosed on the grounds of marked prolongation of transdiaphragmatic pressure (Pdi) decay during sniffs. In view of the recognized sensory role of inspiratory muscles in dyspnea, it was hypothesized that antimyotonic therapy might relieve dyspnea in this patient. Procainamide therapy induced a decrease in half relaxation time of Pdi during sniffs and yielded a striking clinical improvement with cessation of tachypnea and dyspnea. Later, this beneficial effect was maintained by tocainide after procainamide was stopped because of a lupus syndrome. We conclude that myotonia of respiratory muscles can cause severe dyspnea that can be improved by antimyotonic therapy.     

Respiratory muscle dysfunction secondary to chronic tracheostomy tube placement

In patients requiring periodic mechanical ventilation, a deflated, fenestrated tracheostomy tube may impair respiratory muscle performance during spontaneous breathing. We describe a patient with severe chronic airflow obstruction (CAO) whose respiratory muscle performance and exercise duration improved after tracheostomy tube removal. Duty cycle, Pdi/Pdi max, and the tension time index were all lower during exercise after tracheostomy tube removal. We conclude that a deflated and fenestrated tracheostomy tube significantly increases airways resistance and can further limit ventilatory muscle performance in patients with airflow obstruction. Patients requiring intermittent ventilatory support may benefit from permanent tracheostomy fistulas that allow for intermittent self cannulation. This would avoid loading of the respiratory muscles when breathing spontaneously.     

慢性阻塞性肺疾病急性发作期患者对比例辅助通气的生理反应

目的　探讨比例辅助通气 (PAV)不同辅助水平对慢性阻塞性肺疾病 (COPD)急性发作期患者生理反应的影响。方法　 9例COPD急性发作期患者接受三个不同比例辅助水平的PAV通气 ,观察患者吸气肌肉用力情况和呼吸方式的变化。结果　 (1)与自主呼吸 (SB)相比 ,PAV各辅助水平时的潮气量 (VT)、分钟通气量 (V·E)和呼吸频率 (RR)均稍增高 (P >0 0 5 )。各比例辅助水平之间的VT、V·E 和RR比较差异无显著性 (P >0 0 5 )。 (2 )与SB相比 ,各比例辅助水平时的跨膈压 (Pdi)、压力时间乘积 (PTP)和患者呼吸做功均明显减少 (P >0 0 1) ,Pdi、PTP和患者呼吸做功分别平均减少 8 36cmH2 O、11 4 9cmH2 O·s-1·L-1和 0 5 3J/L。随比例辅助水平的升高 ,Pdi、PTP和患者呼吸功无明显变化(P >0 0 5 )。 (3)PAV可减轻患者呼吸困难 (P <0 0 5 )。结论　本试验证实了无创PAV在COPD急性发作期患者中应用的可行性。患者感觉最舒适的PAV辅助比例水平是 (5 7± 11) %。根据患者感觉舒适情况而设定比例辅助水平的无创PAV可减轻患者的呼吸肌肉负担 ,最舒适水平时呼吸功减少5 7% ,Pdi减少 72 % ,PTP减少 6 5 % ;并改善患者的呼吸方式和呼吸困难     

Respiratory muscle fatigue limiting physical exercise?

Inspiratory muscle fatigue has been documented during loaded breathing or acute respiratory failure, but its role in exercise limitation is still undetermined. Electromyographic (EMG) signs of diaphragmatic fatigue develop in normal subjects hyperventilating above 70% of maximal voluntary ventilation (MVV), a ventilatory level commonly attained at peak exercise. EMG signs of diaphragmatic fatigue also occur during high power cycling exercise in normal subjects and chronic obstructive pulmonary disease (COPD) patients. However, a loss of respiratory muscle strength has rarely been documented following strenuous physical exercise with techniques independent of the subjects' collaboration. Prior inspiratory muscle fatigue decreases exercise tolerance in normal subjects but its effect is largely unknown in COPD patients. Respiratory muscle rest by negative pressure ventilation was reported to improve exercise tolerance in COPD, but this beneficial effect was not confirmed by controlled studies. The effect of inspiratory muscle training on exercise tolerance is still undefined by existing data, in part because of differences in methods and selection criteria between studies. Although respiratory muscle fatigue may occur during exercise, it is not clearly established whether interventions directed at respiratory muscles may improve exercise tolerance in COPD.     

Ventilatory muscle support in respiratory failure with nasal positive pressure ventilation

Long-term intermittent mechanical ventilation results in improvements in ventilatory performance and clinical status between ventilation sessions in patients with chronic respiratory failure. The application of intermittent positive pressure ventilation through a nasal mask (NPPV) is a simple, noninvasive method for the provision of chronic intermittent ventilatory support. We investigated the effects of NPPV on inspiratory muscle activity in three normal subjects and nine patients with acute or chronic ventilatory failure due to restrictive (four subjects) or obstructive (five subjects) respiratory disorders. NPPV resulted in reductions of phasic diaphragm electromyogram amplitude to 6.7 +/- 0.7 percent (mean +/- SEM) of values obtained during spontaneous breathing in the normal subjects, 6.4 +/- 3.2 percent in the restrictive group, and 8.3 +/- 5.1 percent in the obstructive group. Simultaneous decreases in activity of accessory respiratory muscles were observed. The reductions in inspiratory muscle activity were confirmed by the finding of positive intrathoracic pressure swings on inspiration in all subjects. With NPPV, oxygen saturation and PCO2 remained stable or improved as compared with values obtained during spontaneous breathing. These results indicate that NPPV can noninvasively provide ventilatory support while reducing inspiratory muscle energy expenditure in acute and chronic respiratory failure of diverse etiology. Long-term assisted ventilation with NPPV may be useful in improving ventilatory performance by resting the inspiratory muscles.     

Proportional assist ventilation

Partial ventilatory support techniques are intended for patients who are unable to maintain a normal alveolar ventilation, despite normal central control for respiration. Proportional assist ventilation (PAV) is a novel mode of partial ventilatory support in which the ventilator generates an instantaneous inspiratory pressure in proportion to the instantaneous effort of the patient. In theory, PAV should normalize the neuro-ventilatory coupling by making the ventilator an extension of patient's respiratory muscles, while leaving to the patient the entire control of all aspects of breathing. PAV, however, shares a common problem with the conventional partial ventilatory support modes. In mechanically ventilated patients, the respiratory system impedance may change over time. These changes may impair the good matching between ventilator output and patient's ventilatory demand and lead to patient-ventilator asynchrony. To take full advantage of PAV, the authors believe that PAV should continuously and automatically adapt to the respiratory system passive mechanics, assessed by continuous noninvasive measurement of total elastance and resistance.     

Ventilatory muscle loads and the frequency-tidal volume pattern during inspiratory pressure-assisted (pressure-supported) ventilation

Pressure support ventilation (PSV) is a new form of mechanical ventilatory support that assists a patient's spontaneous ventilatory effort with a clinician-selected amount of inspiratory pressure. In order to assess the muscle unloading effect and the ventilatory pattern response to increasing levels of this inspiratory pressure assist, we first utilized a computer respiratory system model with variable alveolar ventilation demands and impedances. From this model, we calculated ventilatory muscle loads (expressed either as the work/min or as the pressure time index) during simulated, unassisted breathing and during simulated breathing with levels of inspiratory pressure assist up to that which resulted in a VT of 800 ml and no work being performed by the muscles (defined as PSVmax for the model conditions being studied). The optimal ventilatory pattern (i.e., frequency-tidal volume) under each ventilation and impedance condition was defined as that which resulted in minimal muscle load. Under these model conditions, we found that PSVmax ranged from 5 to 41 cm H2O and that as the level of inspiratory pressure assist was increased from zero to PSVmax, there was a biphasic response of both the ventilatory muscle loading and the ventilatory pattern. Specifically, at low levels of inspiratory pressure assist, the model predicted that the applied pressure would only partially unload the ventilatory muscles. Continued muscle energy expenditure would thus still be required, whereas the ventilatory pattern would change little. Conversely, at higher levels of inspiratory pressure assist, the model predicted that the applied pressure would be sufficient to completely unload the ventilatory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and physiologic evaluation of respiratory muscle function

The ventilatory muscles are of primary importance in the maintenance of ventilation. This rather complex system of muscles centers around the diaphragm. As diaphragmatic function becomes compromised with the progression of different lung diseases, the participation of other muscles becomes necessary. This is clinically manifested by the recruitment of many of these muscles even during quiet breathing. The use of simple questions during a medical history, determination of the respiratory rate, assessment of the pattern of breathing, and observation of thoracoabdominal movements are helpful in the initial evaluation. Measurement of the FVC, lung volumes, and tidal breathing help direct attention to more specific investigation of the ventilatory muscles. Decreased respiratory muscle strength can be confirmed by measurement of PImax and PEmax. Decreased respiratory muscle endurance can be readily ascertained by measuring the MVV. Use of these simple techniques, available in most laboratories, is appropriate for initial evaluation and establishing a diagnosis. The additional measurements of esophageal and gastric pressures have added a new dimension to the study of the diaphragm; these techniques, however, remain a research tool.     

Respiratory muscle function and hypoxic ventilatory control in patients with type I diabetes.

STUDY OBJECTIVES: The interaction among pulmonary mechanics, respiratory muscle performance, and ventilatory control in subjects with insulin-dependent diabetes mellitus has so far received little attention. We therefore decided to assess the role of central factors and peripheral factors on the ventilatory response to a hypoxic stimulus in type I diabetic patients. SUBJECTS: Eight patients in stable condition aged 19 to 48 years old, with insulin-dependent diabetes mellitus (duration of the disease, 36 to 240 months) and no history of smoking, cardiopulmonary involvement, or autonomic neuropathy; and an age- and gender-matched control group. MEASUREMENTS: In each patient, we measured the following: pulmonary volumes; diffusing capacity of the lung for carbon monoxide (D(LCO)); time and volume components of ventilation (tidal volume [V(T)] and respiratory frequency); static compliance (Clstat) and dynamic compliance (Cldyn); swings in pleural pressure (Pes) and gastric pressure (Pg); and transdiaphragmatic pressure (Pdi), obtained by subtracting Pes from Pg. Maximal inspiratory Pes and Pdi during a maximal sniff maneuver were also measured. Swings in Pes and Pdi during V(T) as a percentage of Pes and Pdi during the maximal sniff maneuver [Pessw(%Pessn) and Pdisw(%Pdisn), respectively] were both considered as a measure of central respiratory output, and the Pessw(%Pessn)/V(T) ratio was considered as an index of neuroventilatory dissociation (NVD) of the inspiratory pump. Subjects were studied at baseline and during hypoxic rebreathing. RESULTS: Pulmonary volumes and D(LCO) were normal or slightly reduced. A lower Cldyn, higher central respiratory output, and NVD were found. During hypoxic rebreathing, patients had lower V(T), similar central respiratory output, and greater NVD per unit change in arterial oxygen saturation compared with values in control subjects. An increase in dynamic elastance, computed as 1/Cldyn, during hypoxia was found in patients, but not in normal subjects, and was directly related to concurrent changes in NVD. CONCLUSIONS: We have shown that the assessment of a normal Clstat and normal routine parameters of airway obstruction does not permit the definite exclusion of the role of peripheral airway involvement in insulin-dependent diabetes mellitus. Peripheral airway involvement is likely to influence indices of hypoxic ventilator) drive by modulating a normal central motor output into a rapid and shallow pattern of ventilatory response.     

Efficacy of positive vs negative pressure ventilation in unloading the respiratory muscles

We compared the efficacy of positive pressure ventilation (PPV) vs negative pressure ventilation (NPV) in providing ventilatory muscle rest for five normal subjects and six patients with chronic obstructive pulmonary disease (COPD). All participants underwent measurement of transdiaphragmatic pressure (Pdi), pressure time integral of the diaphragm (PTI), integrated diaphragmatic electromyogram (iEMG), minute ventilation (Ve), tidal volume (Vt), and end-tidal CO2 (etCO2) during 15 minutes of PPV and NPV. For each subject, ventilator adjustments were made to obtain Ve similar to levels measured during quiet breathing (QB). We found that the iEMG, Pdi, PTI, and average coefficient of variation of the tidal volume (CV-Vt) were consistently lower during PPV as compared with NPV (p = 0.01). The iEMG normalized for Ve and Vt was also significantly lower during PPV (p = 0.01). During PPV, subjects were mildly hyperventilated (lower etCO2 and higher Ve) compared with QB and NPV, but no significant correlation was noted between the change in etCO2 and the change in iEMG. The change in PTI was significantly correlated with the change in iEMG (p less than 0.01). We conclude that in the short term, PPV is more effective than NPV in reducing diaphragmatic activity. Positive pressure ventilation may be the preferred method of assisted ventilation in future studies of ventilatory muscle rest therapy.     

Improved efficacy of spontaneous breathing with inspiratory pressure support

During inspiratory pressure support (IPS) ventilation, first a negative airway pressure is produced by the patient to open a demand valve and then a constant positive airway pressure is maintained at a present level while the patient inhales. The aim of this study was to assess the ability of 10 cm H2O IPS to improve the efficacy of spontaneous ventilation. We studied 8 intubated patients recovering from acute respiratory failure, all were breathing spontaneously via 3 different systems: a Servo 900 C ventilator (SCV) without IPS, a Servo 900 C ventilator with 10 cm H2O IPS, and a continuous flow system (CFS). Compared with the CFS, breathing with the SVC without IPS resulted in an increased respiratory rate (RR), increased tidal Volume (VT), increased transdiaphragmatic pressure (Pdi), and no significant change in PaO2 or PaCO2. Ventilation with IPS resulted in significant improvements in VT, PaO2, and PaCO2 with a decreased RR and Pdi when compared with both the other modes of spontaneous ventilation. A significant decrease in the pressure-time index of the diaphragm (i.e., the product of the mean transdiaphragmatic pressure and the inspiratory duty cycle) occurred during IPS. In 2 patients, we recorded diaphragmatic electromyographic activity during both SVC and IPS. In both patients during IPS, an increased VT and a decreased Pdi coincided with a major reduction of electromyographic activity. We conclude that IPS at a level of 10 cm H2O markedly increases the efficacy of spontaneous breathing while reducing the activity of the inspiratory muscles.     

Respiratory muscle function during obstructive sleep apnea

Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction during sleep. Inspiratory muscles may be subjected to potentially fatiguing loads during an obstructive apnea and this may be related to the termination of obstructive apnea. We have measured transdiaphragmatic pressure (Pdi) and breathing patterns in six male patients with OSA during sleep to characterize respiratory muscle function in OSA and determine whether apnea termination is consistently related to a pressure time index of the diaphragm (PTI) associated with respiratory muscle fatigue. There was a large intersubject variability in Pdi generation during apnea. No consistent level of PTI was associated with apnea termination. During prolonged apneas, the respiratory duty cycle plateaued, which is suggestive of an inhibitory reflex possibly mediated by chest wall afferents. There were intersubject differences in both inspiratory and expiratory muscle recruitment during apnea. In the majority of patients, the diaphragm appeared to be the primary inspiratory muscle during apnea, but in some it appeared to be the intercostal/accessory muscles. The majority of patients demonstrated an increase in gastric pressure and inward abdominal movement during the expiratory phases of an apnea, consistent with abdominal muscle recruitment stimulated by increased ventilatory drive.     

Diaphragm function after pulmonary resection. Relationship to postoperative respiratory failure

We studied the lung mechanics and respiratory muscle function in 20 patients undergoing pulmonary resection. Transdiaphragmatic pressure (delta Pdi) during quiet breathing did not show any remarkable change after the operation (9.5 +/- 1.1 to 10.9 +/- 1.0 cm H2O), while the ratio of abdominal to transdiaphragmatic pressure changes (delta Pab/delta Pdi) revealed a significant difference between the preoperative and the early postoperative periods (0.32 +/- 0.06 to 0.00 +/- 0.11, p less than 0.05). The postoperative delta Pab/delta Pdi correlated significantly with the work of breathing (r = -0.60, p less than 0.01). The maximal transdiaphragmatic pressure (Pdimax) decreased significantly after operation (75.0 +/- 15.8 to 32.8 +/- 12.4 cm H2O, p less than 0.05), with no significant change in the maximal inspiratory mouth pressure (MIP) (74.2 +/- 16.8 to 39.5 +/- 11.6 cm H2O). Four of 20 patients developed respiratory failure postoperatively and required mechanical ventilation. delta Pab/delta Pdi in these patients was significantly lower than in the other patients (-0.62 +/- 0.24 versus 0.16 +/- 0.09, p less than 0.005). Our results suggested that during quiet breathing diaphragmatic function was preserved and intercostal/accessory muscles recruitment increased, but maximal strength of the diaphragm might be reduced in patients undergoing pulmonary resection.     

Respiratory response and ventilatory muscle recruitment during arm elevation in normal subjects.

Despite the fact that the arms are used extensively in daily life and that some of the muscles of the shoulder girdle share both a respiratory and a positional function for the arms, surprisingly little is known about the respiratory response to unsupported upper extremity activity. To determine the respiratory consequences of simple arm elevation during tidal breathing, we measured minute ventilation (VE), tidal volume (VT), respiratory rate (f), heart rate (HR), oxygen uptake (VO2), and carbon dioxide production (VCO2) in 22 normal subjects seated with arms elevated in front of them to shoulder level (AE) for 2 min and down at the sides (AD) for the same time period. The sequence was randomized. Compared with AD, during AE there were significant increases in VO2 (336 +/- 18 vs 289 +/- 14 ml/min, p less than 0.001), VCO2 (315 +/- 23 vs 245 +/- 16 ml/min, p less than 0.001), HR (84 +/- 6 vs 73 +/- 4 beats/min, p less than 0.05), VE (11.5 +/- 0.9 vs 9.3 +/- 0.6 L/min, p less than 0.001), and VT (868 +/- 66 vs 721 +/- 48 ml, p less than 0.001). In 11 subjects, breath-by-breath metabolic and ventilatory parameters were studied with AD for 2 min, AE for 2 min, and with AD for 3 min while also recording gastric (Pg), pleural (Ppl), and transdiaphragmatic pressures (Pdi). With AE, there was a significant increase in Pg at end inspiration (PgI, 15.4 +/- 3.2 vs 11.9 +/- 2.7 cm H2O, p less than 0.01) and in Pdi (26.5 +/- 3.4 vs 21.4 +/- 2.4 cm H2O, p less than 0.01) with no change in Pg at end expiration (PgE) or in Ppl. The increases in VO2, VCO2, VE, and VT during arm elevation persisted for 2 min after arm lowering, whereas Pgi and Pdi abruptly dropped as the arms were lowered. We conclude that simple arm elevation during tidal breathing results in significant increases in metabolic and ventilatory requirements. These increased demands are associated with higher PgI and Pdi suggesting an increased diaphragmatic contribution to the generation of ventilatory pressures. The sudden drop in Pg with arm lowering indicate a change in ventilatory muscle and or torso recruitment independent of the metabolic drive and ventilatory needs. These findings may help explain the limitation that has been reported in some normal subjects and in many patients with lung disease during unsupported upper extremity activity.     

Diaphragmatic performance during recovery from acute ventilatory failure in Guillain-Barré syndrome and myasthenia gravis

Diaphragmatic muscle performance during acute ventilatory failure due to Guillain-Barré syndrome and myasthenia gravis was assessed to evaluate (1) diaphragmatic function during weaning from ventilatory support and (2) diaphragmatic tension-time integral (TTdi) during ventilatory failure. We used a multilumen nasogastric tube and a pneumotachograph to measure transdiaphragmatic pressure per breath (Pdi), maximum transdiaphragmatic pressure (Pdimax), tidal volume (VT), and inspiratory time fraction during 74 spontaneous breathing trials in nine patients. Diaphragmatic performance was poor in all patients. The Pdi, Pdimax, and VT improved significantly, but values for Pdi and Pdimax remained low even after weaning. Improvement in Pdimax was the best predictor of recovery (r = 0.48; p less than 0.001). Maximal inspiratory force correlated with Pdimax (r = 0.48; p less than 0.005), but FVC did not. The TTdi rarely exceeded the expected fatigue threshold of 0.15 in spite of the patient's inability to sustain ventilation. Although our patients demonstrated diaphragmatic weakness, TTdi did not demonstrate diaphragmatic fatigue.     

Respiratory muscle fatigue

To estimate the effect of the increase in ventilation induced by exercise on the dynamics of respiratory muscle in normal subjects and cases of respiratory diseases, we measured the changes of transdiaphragmatic pressure (Pdi), gastric pressure (Pga), tension time index of the diaphragm (TTdi) and tension time index of the abdomen (TTab). To confirm the effect of oxygen on exercise endurance, we investigated changes of parameters measured during exercise under air breathing and oxygen inhalation. In normal subjects, we found the increase in diaphragmatic activity as a gradual increase of exercise level, but TTdi always stayed in the non-fatigue zone. On the contrary, patients with COPD showed that TTdi was near fatigue threshold during quiet breathing and crossed easily into fatigue zone during exercise. There was an increase in endurance time with oxygen for COPD patients. Breathing with oxygen was associated with a smooth increase in Pdi during the inspiratory phase which indicates efficient contraction of the diaphragm. During the expiratory phase, the degree of increase in Pga was markedly reduced by oxygen inhalation.     

Respiratory muscle energetics during exercise in healthy subjects and patients with COPD

The energy expenditure required by the respiratory muscles during exercise is a function of their work rate, cost of breathing, and efficiency. During exercise, ventilatory requirements increase further exacerbating the potential imbalance between inspiratory muscle load and capacity. High level of exercise intensity in conjunction with contracting respiratory muscles is the reason for respiratory muscle fatigue in healthy subjects. Available evidence would suggest that fatigue of the diaphragm and other respiratory muscles is an important mechanism involved in redistribution of blood flow. Reflex mechanisms of sympathoexcitation are triggered in fatigued diaphragm during heavy exercise when cardiac output is not sufficient to adequately meet the high metabolic requirements of both respiratory and limb musculature. It is very likely that local changes in locomotor muscle blood flow may occur during exhaustive endurance exercise and that changes may have important effect on O2 transport to the working locomotor muscles and, therefore, on their fatigability. In a condition when the respiratory muscles receive their share of blood flow at the expense of limb locomotor muscles, minimizing mechanical work of breathing and therefore its metabolic cost allows a greater amount of cardiac output to be available to be delivered to working limb muscles. Malfunction in any of the multiple components responsible for circulatory flow and O2 delivery will limit the blood supply therefore inhibiting the supply of O2 and the energy substrate to the contracting muscles. Studies are needed to overcome these limitations.     

Supine position and sleep loss each reduce prolonged maximal voluntary ventilation

Because of the prevalence of supine posture and sleep deprivation in both health and disease, we wondered how each of them influences prolonged maximal voluntary ventilation (MVV). Accordingly, we compared 12-second, 1-min, and 10-min isocapnic MVV supine with that measured in the upright posture in 8 healthy subjects. MVV decreased 6-10% supine, independent of test duration (p less than 0.01). Although end-expiratory lung volume was 0.47 liter lower during supine resting breathing (p less than 0.001), end-expiratory lung volumes during short-term MVV maneuvers were identical. To investigate any additional effect on MVV due to sleep loss, 12 healthy subjects performed 12-second, 1-min, and 30-min isocapnic MVV maneuvers in the supine position, either after normal sleep or after a 24-hour sleepless period. Sleep deprivation reduced MVV by 7-14%, again independent of test duration (p less than 0.05). Sleep loss also reduced the ventilation chosen to represent a submaximal (75%) breathing effect (p = 0.05), and it increased subjective ratings of fatigue and confusion (p less than 0.01). We conclude that supination and sleep deprivation together decrease both short- and long-term MVV by nearly 20%, with impairment of supination not caused by lung volume changes, and with the sleep loss effect occurring in tandem with a rise in the subjective assessment of breathing effort.     

Ventilatory control in patients with hypoxemia due to obstructive lung disease.

In 20 patients with chronic hypoxemia due to chronic obstructive pulmonary disease, we measured responses to CO2 and hypoxia in terms of ventilation and P0.1, the pressure generated by the respiratory muscles during the first 0.1 s of inspiratory effort against a closed airway at functional residual capacity. These responses were compared to those of a control group of 17 patients with similar ventilatory abnormality but without hypoxemia. Hypoxemic patients demonstrated significantly less response to hypoxia than did control subjects in terms of both ventilation and P0.1 The decreased hypoxic response might be analogous to that reported in high altitude dwellers and patients with cyanotic congenital heart disease. Ventilatory responses to CO2 were depressed in hypoxemic patients, but P0.1 responses were not significantly decreased. While breathing at rest with arterial O2 saturation of 95 per cent, hypoxemic patients demonstrated the same minute ventilation as control subjects, but tidal volume was smaller, inspiratory duration was shorter, and breathing frequency was slightly higher. This breathing pattern appeared to be independent of whether or not these patients retained CO2.