Effect of step duration during incremental exercise on breathing pattern and mouth occlusion pressure

We compared the effects of two step durations on breathing pattern, mouth occlusion pressure and "effective" impedance of the respiratory system during incremental exercise. Nine normal subjects (mean age: 27.8+/-1.21 years) performed two incremental exercise tests in randomized order: one test with step increments every 1 min 30s and the other, every 4 min. After a warm-up at 25 W for the 1 min 30 s test, the power was increased by 50 W from 50 W to exhaustion. During the last minute at each power, we measured ventilation (VE), tidal volume (VT), breathing frequency (fR), inspiratory and expiratory time (TI and TE), total time of the respiratory cycle (TTOT), TI/TTOT, mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1), "effective" impedance of the respiratory system (P0.1/(VT/ TI)) and venous blood lactate concentration ([La]). Our result showed that at maximal exercise the power was significantly higher (p < 0.01) and [La] lower (p < 0.01) in the 1 min 30 s test. At 100, 150 and 200 W, the 4 min test showed significantly higher oxygen uptake (VO2), carbon dioxide output (VCO2), VE, P0.1, fR, VT/TI and HR (p <0.001) and significantly lower TI, TE and TTOT (p<0.01). [La] was significantly higher at 150 W (p<0.05) and 200 W (p<0.001). At the same VCO2, P0.1 was not significantly different between the two tests, whereas VE showed a tendency to be higher (p = 0.08) and P0.1/(VT/TI) was significantly lower during the 4 min test. In conclusion, this study allowed us to quantify the difference in inspiratory neuromuscular output and ventilatory response between 1 min 30s and 4 min tests and showed that different step durations alter the relationship between inspiratory neuromuscular output and mean inspiratory flow.     

Assessment of ventilatory neuromuscular drive in patients with obstructive sleep apnea

The presence of abnormalities of the respiratory center in obstructive sleep apnea (OSA) patients and their correlation with polysomnographic data are still a matter of controversy. Moderately obese, sleep-deprived OSA patients presenting daytime hypersomnolence, with normocapnia and no clinical or spirometric evidence of pulmonary disease, were selected. We assessed the ventilatory control and correlated it with polysomnographic data. Ventilatory neuromuscular drive was evaluated in these patients by measuring the ventilatory response (VE), the inspiratory occlusion pressure (P.1) and the ventilatory pattern (VT/TI, TI/TTOT) at rest and during submaximal exercise, breathing room air. These analyses were also performed after inhalation of a hypercapnic mixture of CO2 (delta P.1/delta PETCO2, delta VE/delta PETCO2). Average rest and exercise ventilatory response (VE: 12.2 and 32.6 l/min, respectively), inspiratory occlusion pressure (P.1: 1.5 and 4.7 cmH2O, respectively), and ventilatory pattern (VT/TI: 0.42 and 1.09 l/s; TI/TTOT: 0.47 and 0.46 l/s, respectively) were within the normal range. In response to hypercapnia, the values of ventilatory response (delta VE/delta PETCO2: 1.51 l min-1 mmHg-1) and inspiratory occlusion pressure (delta P.1/delta PETCO2: 0.22 cmH2O) were normal or slightly reduced in the normocapnic OSA patients. No association or correlation between ventilatory neuromuscular drive and ventilatory pattern, hypersomnolence score and polysomnographic data was found; however a significant positive correlation was observed between P.1 and weight. Our results indicate the existence of a group of normocapnic OSA patients who have a normal awake neuromuscular ventilatory drive at rest or during exercise that is partially influenced by obesity.     

Breathing patterns in infants and children under halothane anesthesia: effect of dose and CO2

We studied the amplitude, timing, and shape of the airflow waveform at the mouth of spontaneously breathing children under two sets of conditions: 1) in 30 children aged 9 wk-4.5 yr at 2, 1, and 0% inspired halothane concentration and 2) in 22 children aged 5 mo-7 yr during hyperoxic CO2 rebreathing while recovering from anesthesia. Compared with control values, the relative changes in breath parameters at 1 and 2% halothane were, respectively, as follows: total cycle time -19 and -31%, tidal volume (VT) -30 and -44%, minute ventilation -11 and -17%, and VT/inspiratory time (TI) -16 and -20%. Parameters of timing and breath shape did not change except for the significant but small increase in TI/total cycle time (by 6 and 8%, respectively). With CO2 rebreathing, parameters reflecting inspiratory drive increased significantly in all patients as shown by the slopes of the regressions of these parameters against end-tidal PCO2. Mean slopes expressed in %control value per millimeter of mercury CO2 were 12.1 for minute ventilation, 8.3 for VT, and 10.67 for VT/TI. Parameters reflecting the timing and breath shape remained essentially unchanged. Our results suggest that, in children under halothane anesthesia, the amplitude, timing, and shape of the breathing pattern are controlled independently. In particular, the amplitude and timing of the breath may vary widely without any significant change in the shape.     

Clincal, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis

To examine the effect of elastic loading on variational activity of breathing, we studied 11 healthy subjects breathing at rest and with inspiratory elastic loads of 9 and 18 cm H2O/L, applied randomly for 1 h each. Compared with rest, a load of 18 cm H2O/L decreased gross variability, quantitated as standard deviation, of tidal volume (VT) and expiratory time (TE) (p < 0.01 in both instances) but increased that of inspiratory time (TI) (p < 0.03). The autocorrelation coefficients at a lag of 1 breath for each breath component were not altered by elastic loading, although the number of breath lags with significant serial correlations for TE tended to increase with a load of 18 cm H2O/L (p = 0.08). A load of 18 cm H2O/L decreased only the fraction of variational activity of VT and TE due to uncorrelated, random behavior (white noise), while it increased that fraction for TI (p < 0.05 in each instance); the correlated and oscillatory fractions did not change. Uncorrelated random behavior constituted > 87% of the variance of each breath component, correlated behavior represented 3 to 11%, and oscillatory behavior represented < 1.5% during both rest and loaded breathing. Elastic loading changed the gross variability of each primary breath component by altering the random fraction of variational activity; it had no significant effect on the structured, correlated fraction. We speculate that the observed changes in variational activity may reflect an attempt by the controller to compensate for the increased load while simultaneously minimizing load-induced dyspnea.     

Immediate response to inspiratory resistive loading in anesthetized patients with kyphoscoliosis: spirometric and neural effects

In kyphoscoliosis (KS), lung volumes are reduced, respiratory elastance and resistance are increased, and breathing pattern is rapid and shallow, attributes that may contribute to defense of tidal volume (VT) in the face of inspiratory resistive loading. The control of ventilation of 12 anesthetized patients about to undergo corrective spinal surgery was compared to that of 11 anesthetized patients free of cardiothoracic disease during quiet breathing and the first breath through one of three linear resistors. Mean forced vital capacity (FVC) of the KS group was 48% that of the controls (C). Passive elastance (Ers) and active elastance and resistance (E'rs and R'rs, respectively) were computed according to previously described techniques (Behrakis PK, Higgs BD, Baydur A, Zin WA, Milic-Emili J (1983) Active inspiratory impedance in halothane-anesthetized humans. J Appl Physiol 54: 1477-1481). Baseline tidal volume VT, inspiratory duration Tl, expiratory duration TE, duration of total breathing cycle TT, and inspiratory duty cycle TI/TT were significantly reduced, while VE was slightly decreased in the KS. Ers, E'rs, and R'rs, were, respectively, 72, 69, and 89% greater in the KS. Driving pressure (Pmus) was derived from the equation of motion, using active values of respiratory elastance. With resistive loading, there was greater prolongation of TI in the C, while percent reduction in VT and minute ventilation VE was less in KS. Compensation in both groups was achieved through three changes in the Pmus waveform. (1) Peak amplitude increased. (2) The duration of the rising phase increased. (3) The rising Pmus curve became more concave to the time axis. These changes were most marked with application of the highest resistance in both groups. Peak driving pressure and mean rate of rise of Pmus were greater in the KS. Increased intrinsic impedance, Pmus, and differences in changes in neural timing in anesthetized kyphoscoliotics contribute to modestly greater VT defense, compared to that of anesthetized subjects free of cardiorespiratory disease.     

Social-emotional characteristics of preschool-aged children referred for Child Find screening and assessment: a comparative study

In order to determine changes in breathing patterns brought about by resistive loading, ventilation was recorded in 11 healthy subjects with four linear resistances (3.57, 5.75, 8.76 and 13.13 cmH2O L(-1) sec) added in a random order throughout the entire breath. At steady state, a breath-by-breath analysis of airflow was used to quantify the pattern of breathing in terms of respiratory variables: TI, TE, Tt, VT, VT/TI, TI/Tt, and by taking TI, TE, VT all together (TRIAD) and also the shape of the entire airflow profile quantified by harmonic analysis (ASTER). Group analysis using ANOVA showed significant changes in all variables. There were increasing changes with increasing loads in all variables, the smallest changes being in TI/Tt. Within to between-individual comparisons between two loads showed that only TI/Tt and the ASTER were more similar within than between-individuals for all comparisons. It was concluded that at steady state mechanisms of load compensation come into play inducing changes in the pattern of breathing proportional to the loads while maintaining some of the individual characteristics.     

Effect of sleep on changes in breathing pattern accompanying sigh breaths

We studied the effect of sleep on the characteristics of sigh breaths and the associated changes in breathing pattern in breaths following spontaneous sighs in 4 unrestrained dogs with an intact upper airway. The sigh breath was characterized by its large tidal volume (VT), long TI and TE in comparison with the control breath. The volume of the sigh breath was larger in awake sighs than in those recorded during non-REM (NREM) and REM sleep. The strength of Hering-Breuer reflex as determined by duration of the post-sigh apnea was similar in NREM and REM sleep. Sighs occurring during wakefulness, NREM and REM sleep were associated with augmented activity of the parasternal muscles during inspiration, and a persistent tonic abdominal muscle activity during the expiratory period. Breathing pattern in the post-sigh period was characterized by a smaller VT and longer TE in the first post-sigh breath in all sleep states (compared with the control breath), but the pattern returned to control level within the second or third post-sigh breath in both NREM and REM sleep. Sighs did not precipitate periodic breathing or other forms of abnormal breathing patterns in either wakefulness or sleep. We conclude that the respiratory control mechanisms stabilizing breathing after a sigh in the awake dog are intact in NREM and REM sleep.     

Non-invasive assessment of inspiratory muscle performance during exercise in patients with chronic heart failure

AIMS: The aim of this study was to assess inspiratory performance at rest and during exercise in patients with chronic heart failure in comparison with healthy controls using a non-invasive index: the tension-time index of inspiratory muscles (TTMUS). METHODS: We studied 13 patients with chronic heart failure (57 +/- 7 years) and 10 control subjects (58 +/- 6 years) at rest and during an incremental maximal exercise test. Measurements included breathing pattern (inspiratory time, total time of respiratory cycle, minute ventilation, tidal volume and respiratory frequency), mouth occlusion pressure and mean inspiratory pressure (calculated as follows: 5 x mouth occlusion pressure x inspiratory time). The maximal inspiratory pressure was measured at rest. TTMUS was calculated from the equation: TTMUS = PI/PIMAX x TI/TTOT, where PI/PIMAX is the ratio of mean inspiratory pressure to maximal inspiratory pressure and TI/TTOT is the ratio of mean inspiratory time to total time of the respiratory cycle. RESULTS: At rest, the results in patients showed non-significantly higher mouth occlusion pressure, lower maximal inspiratory pressure (P < 0.001), and a higher ratio of mean inspiratory pressure to maximal inspiratory pressure (P < 0.01). There was no difference in the breathing pattern. TTMUS was thus significantly higher in the patients with chronic heart failure (P < 0.001). At maximal exercise (77 +/- 16 W for patients with chronic heart failure vs 142 +/- 27 W for controls, P < 0.001), the ratio of mean inspiratory time to total time of respiratory cycle, the mouth occlusion pressure and the ratio of mean inspiratory pressure to maximal inspiratory pressure were not different. TTMUS was thus comparable in the two groups. During exercise, at comparable workloads (20, 40 and 60 W), the patients showed higher mouth occlusion pressure (P < 0.01) and a higher ratio of mean inspiratory pressure to maximal inspiratory pressure (P < 0.001), whereas the ratio of mean inspiratory time to total time of the respiratory cycle was similar. TTMUS was thus higher in the patients at each workload (P < 0.05). CONCLUSION: This study shows that the determination of TTMUS at rest and during exercise allows the observation of alterations in inspiratory muscle performance as a result of both reduced inspiratory strength, as measured by the maximal inspiratory pressure, and increased ventilatory drive, as reflected by the mouth occlusion pressure in patients with chronic heart failure. The non-invasiveness of this new index is an additional argument for its use in a clinical setting.     

Effectiveness of controlled and spontaneous modes in nasal two-level positive pressure ventilation in awake and asleep normal subjects

STUDY OBJECTIVES: The purpose of the present study was to compare in awake and asleep healthy subjects, under nasal intermittent positive pressure ventilation (nIPPV) with a two-level intermittent positive pressure device (two-level nIPPV), the efficacy of the controlled and spontaneous modes, and of different ventilator settings in increasing effective minute ventilation (VE). PARTICIPANTS: Eight healthy subjects were studied. SETTING: In the controlled mode, inspiratory positive airway pressure (IPAP) was kept at 15 cm H2O, expiratory positive airway pressure (EPAP) at 4 cm H2O, and the inspiratory/expiratory (I/E) time ratio at 1. The respirator frequencies were 17 and 25/min. In the spontaneous mode experiment, IPAP was started at 10 cm H2O and progressively increased to 15 and 20 cm H2O; EPAP was kept at 4 cm H2O. MEASUREMENTS AND RESULTS: We measured breath by breath the effective tidal volume (VT with respiratory inductive plethysmography), actual respiratory frequency (f), and effective VE. Using the controlled mode, effective VE was significantly higher on nIPPV than during spontaneous unassisted breathing, except in stage 2 nonrapid eye movement sleep at 17/min of frequency; increases in f from 17 to 25/min led to a significant decrease in VT reaching the lungs, during wakefulness and sleep; effective VE was higher at 25 than at 17/min of frequency only during sleep; periodic breathing was scarce and apneas were never observed. Using the spontaneous mode, with respect to awake spontaneous unassisted breathing, two-level nIPPV at 10 and 15 cm H2O of IPAP did not result in any significant increase in effective VE either in wakefulness or in sleep; only IPAP levels of 20 cm H2O resulted in a significant increase in effective VE; during sleep, effective VE was significantly lower than during wakefulness; respiratory rhythm instability (ie, periodic breathing and central apneas) were exceedingly common, and in some subjects extremely frequent, leading to surprisingly large falls in arterial oxygen saturation. CONCLUSIONS: It appears that two-level nIPPV should be used in the controlled mode rather than in the spontaneous mode, since it seems easier to increase effective VE with a lower IPAP at a high frequency than at a high pressure using the spontaneous mode. We suggest that the initial respirator settings in the controlled mode should be an f around 20/min, an I/E ratio of 1, 15 cm H2O of IPAP, and EPAP as low as possible.     

A volume-dependent apneic threshold during NREM sleep in the dog

We determined the causes of central apnea that commonly follow the hyperpnea resulting from brief airway occlusion during non-rapid-eye-movement (NREM) sleep. Ventilation and end-tidal gases were measured before, during, and after 214 trials of 15-20 s of tracheal occlusion in three dogs during NREM sleep. Airway occlusion was accompanied by progressive increases in inspiratory effort and was followed by transient one- to four-breath hyperapneas, with subsequent central apnea [3-15 times eupneic control expiratory duration (TE)] in 62% of occlusion trials. Significant TE prolongation after hyperventilation did not occur until tidal volume (VT) was three times greater than control; i.e., there was a volume-dependent apneic threshold. Transient electroencephalogram arousal at the end of the occlusion often augmented VT, thereby contributing to the subsequent central apnea; however, arousal was not required for the apnea to occur. Significant transient hypocapnia (up to -12 Torr arterial PCO2) commonly occurred after release of airway occlusion but was not closely correlated with the length of central apnea. During vagal blockade, after release of airway occlusion, significant transient hyperventilation occurred but at VT < 40% greater than control, and TE prolongation was markedly reduced. In summary, after release of airway occlusion in NREM sleep, 1) VT greater than three times eupnea was necessary to cause central apnea, 2) transient arousal at the termination of airway occlusion caused longer apneas by augmenting VT, and 3) transient hypocapnia per se made a significant but minor contribution to the postocclusion central apnea.     

Effects of body temperature on ventilatory response to hypoxia and breathing pattern in man

The ventilatory response to hypoxia (PAO2 55 and 45 Torr) at each of four levels of PACO2 was studied in five healthy subjects before and after a rise in rectal temperature of 1.4 degrees C had been induced by means of a heated flying suit. At a given level of chemical drive both ventilation and mean inspiratory flow increased after heating, frequency relatively more than tidal volume. In isoventilation comparisons mean inspiratory flow was identical in normo- and hyperthermia, whereas the durations of inspiration (TI) and expiration (TE) were proportionately shortened. It is suggested that a rise in temperature shortens TI by affecting a central "clock" and that TE changes are secondary to changes in end-inspiratory volume. The euoxic CO2 response in hyperthermia was suggestive of multiplication between CO2 and temperature. Hypoxic sensitivity was significantly increased, indicating a temperature effect on the arterial chemoreceptors. The breathing pattern was in either temperature condition identical in euoxia and in hypoxia.     

Changes in maximal exercise ventilation and breathing pattern in boys during growth: a mixed cross-sectional longitudinal study

The aim of this mixed cross-sectional longitudinal study covering a total age range of 11-17 years, i.e. the entire pubertal growth period, was (1) to specify the changes in maximal breathing pattern during incremental exercise; (2) to determine what parts of the changes are due to anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength; and (3) to determine if the role of these variables is identical before, during and after pubertal growth spurt. This study was conducted in 44 untrained schoolboys separated into three groups, with an initial age of 11.2 +/- 0.2 years for group A, 12.9 +/- 0.25 years for group B, and 14.9 +/- 0.26 years for group C. These children were subsequently followed for 3 years, during the same time period each year. The maximal inspiratory and expiratory pressures (PI max and PE max) were used as an index of the respiratory muscle strength. During an incremental exercise test, maximal ventilation (VE max), tidal volume (VT max), breathing frequency (fmax), inspiratory and expiratory times (tI max and tE max) and mean inspiratory flow (VT/tI max) were measured at maximal oxygen uptake (VO2max). Our study showed that there was a marked increase with age in VE max, VT max, and VT/tI max, and no significant changes in fmax, tI max and tE max. PI max and PE max showed a general trend towards an increase between 11 and 17 years. The study of the linear correlations between maximal breathing pattern and the anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength showed that, in the three groups of children, (1) lean body mass was the major determinant of VE max, VT max and VT/tI max and the relationships were significantly different before, during and after the pubertal growth spurt; (2) physical fitness was the main determinant of tI max, tE max and fmax before and after the pubertal growth spurt; and (3) maximal respiratory strength did not play a significant role. In conclusion, this mixed cross-sectional longitudinal study showed, at maximal exercise, a significant increase in VE max during growth due only to a significant increase in VT max and VT/tI max, and that the relationships of anthropometric characteristics and physical fitness with maximal breathing pattern change during growth.     

NMDA receptors mediate peripheral chemoreceptor afferent input in the conscious rat

N-methyl-D-aspartate (NMDA) glutamate receptors mediate critical components of cardiorespiratory control in anesthetized animals. The role of NMDA receptors in the ventilatory responses to peripheral and central chemoreceptor stimulation was investigated in conscious, freely behaving rats. Minute ventilation (VE) responses to 10% O2, 5% CO2, and increasing intravenous doses of sodium cyanide were measured in intact rats before and after intravenous administration of the NMDA receptor antagonist MK-801 (3 mg/kg). After MK-801, eupcapnic tidal volume (VT) decreased while frequency increased, resulting in a modest reduction in VE. Inspiratory time (TI) decreased, whereas expiratory time remained unchanged. The VE responses to hypercapnia were qualitatively similar in control and MK-801 conditions, with slight reductions in respiratory drive (VT/TI) after MK-801. In contrast, responses to hypoxia were markedly attenuated after MK-801 and were primarily due to reduced frequency changes, whereas VT was unaffected. Sodium cyanide doses associated with significant VE increases were 5 and 50 microg/kg before and after MK-801, respectively. Thus 1-log shift to the right of individual dose-response curves occurred with MK-801. Selective carotid body denervation reduced VE during hypoxia by 70%, and residual hypoxic ventilatory responses were abolished after MK-801. These findings suggest that, in conscious rats, carotid and other peripheral chemoreceptor-mediated hypoxic ventilatory responses are critically dependent on NMDA receptor activation and that NMDA receptor mechanisms are only modestly involved during hypercapnia.     

Echocardiographic evaluation of tricuspid valve endocarditis: an M mode and two dimensional study

To investigate the reflex mechanisms of sighs (spontaneous large breaths) (VT greater than 2 X control VT) in infants, recordings of respiratory flow and tidal volume (VT) were made during sleep. The frequency of sighs was greater at 1 than at 5 days of age, while respiratory frequency and control VT did not change. Most sighs (93%) had a biphasic pattern of inspiratory flow characterized by an inspiratory duration nearly twice that of control breaths, with an abrupt change in flow rate halfway through inspiration. Interruption of ventilation (3-7 s of airway occlusion) appeared to generate a stimulus for biphasic sighs, since sighs occurred during the first breath after termination of airway occlusion more frequently after long than after brief occlusions. However, a biphasic inspiratory pattern in airway pressure was rarely observed while the airways were occluded, regardless of occlusion duration. This suggests that increase in lung volume during the initial part of the biphasic inspiration following occlusion is a stimulus for the second part. Thus the underlying reflex mechanism of sighs in human infants appears to be the same as occurs in the so-called Head's paradoxical response to lung inflation.     

Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.     

Effects of nasal continuous positive airway pressure on breathing pattern and respiratory drive in patients with obstructive sleep apnea syndrome

To examine the influence of continuous positive airway pressure (CPAP) therapy on respiratory center drive in patients with obstructive sleep apnea syndrome (OSAS), 20 normocapnic OSAS patients (group 0) and 20 simple snoring patients were studied. In the first night, diagnostic polysomnography (PSG) was performed. Before and after PSG monitoring, mouth occlusion pressure (P0.1), tidal volume (VT), minute ventilation (VE), respiratory rate (RR), inspiratory time (Ti), expiratory time (Te), total cycle duration (Ttot), inspiratory duty cycle (Ti/Ttot), mean inspiratory flow (VT/Ti) and effective inspiratory impedance (P0.1/VT/Ti, Ieff) were measured while they were breathing room air. In the following night the OSAS patients were treated with nasal CPAP and PSG monitoring and the above mentioned measurements were repeated. The results showed that pre-PSG values of P0.1, RR and P0.1/VT/Ti in the OSAS patients were significantly higher than those in the snoring patients, while VT, Ti, Te and Ttot values were lower. In the first night, the post-PSG P0.1 value in the OSAS patients increased markedly as compared with the pre-PSG. After overnight nasal CPAP therapy, the respiratory disorder index in the OSAS patients decreased markedly, the nadir SaO2 increased markedly, but the post-PSG P0.1 value did not increase significantly. It is concluded that, before sleep, OSAS patients exhibit a higher respiratory drive and a shallow and frequent breathing pattern as compared with simple snoring patients. After nocturnal sleep, the respiratory drive of OSAS patients increases significantly, the breathing pattern becomes more shallow and frequent. Nasal CPAP may effectively relieve the sleep apnea and hypopnea as well as the resulting hypoxemia and therefore correct the changes in breathing pattern and respiratory drive through nocturnal sleep in patients with OSAS.     

The determinants of respiratory rate during mechanical ventilation

The independent and interactive effect of feedback related to volume, CO2, inspiratory flow, and arousal state on the regulation of respiratory rate in mechanically ventilated humans is not well characterized. We examined the rate response of eight normal volunteers during both quiet wakefulness and non-rapid-eye-movement (NREM) sleep, while mechanically ventilated through a nasal mask in an assist/control mode with a machine back-up rate of 2 breaths/min. Tidal volume (VT) was set slightly above spontaneous VT and then increased by 0.2 L every 3 min up to 1.8 L or 25 ml/kg. Either an inspiratory flow of 40 L/min or an inspiratory time of 2 s (iso-T(I)) was set, with CO2 added (F(I)CO2 > 0) or F(I)CO2 = 0. Measurements were made during both quiet wakefulness and NREM sleep. We found that as VT increased, the respiratory rate decreased; the rate decline was observed during wakefulness and sleep, and under isocapnic as well as hypocapnic conditions. Increasing inspiratory flow raised the respiratory rate during wakefulness and NREM sleep. During NREM sleep, hypocapnia resulted in wasted ventilator trigger efforts. In summary, both VT and inspiratory flow settings affect the respiratory rate, and depending on state, can affect CO2 homeostasis. Ventilator settings appropriate for wakefulness may cause ventilatory instability during sleep.     

One-sample pregnancy diagnosis in elk using fecal steroid metabolites

In utero hypoxia may affect the development of the brain and result in altered respiratory responses postnatally. Using a barometric plethysmograph, we examined the effects of exposing pregnant guinea pigs to 200 ppm carbon monoxide (CO) for 10 h/d from d 23-25 of gestation until term (approximately 68 d) on the ventilatory responses of their 4-5-d-old neonates at rest, and during progressive asphyxia and steady state hypercapnia. Exposure to this concentration of CO produced significantly higher levels of carboxyhemoglobin (COHb) in maternal (8.53 +/- 0.6% versus 0.25 +/- 0.1%) and fetal blood (13.0 +/- 0.4% versus 1.6 +/- 0.1%) from CO-treated animals when compared with controls. Hematocrit was significantly higher in the CO-treated neonates (46.3 +/- 1.0% versus 41.3 +/- 0.9%) at 5-6 d of age, although no difference existed between the groups for COHb at this time. There was no difference between the groups for length of gestation, litter size, or birth weight, but CO-treated neonates were significantly smaller at 4 d of age (102.4 +/- 3.7 g) compared with controls (132.0 +/- 5.0 g). At 4-5 d of age there was no difference between the groups for either tidal volume (VT), respiratory frequency (f), or minute ventilation (VE) at rest, but during steady state hypercapnia (4 and 6% CO2) the CO-treated neonates had a significantly greater VT and VE (but not f) than did controls. During progressive asphyxia, CO-treated animals had a significantly greater VT than did controls from 1-8% CO2. There was a significant fall in f at 1 and 3% CO2 in CO-treated animals; however, this effect did not persist, resulting in a significantly increased VE from 3 to 8% CO2. The inspiratory flow rate (VT/expiratory time) was significantly increased in the CO-treated neonates during progressive asphyxia; this occurred in the absence of a difference in inspiratory time between the groups. These results indicate that prenatal exposure to CO increases CO2 sensitivity in 4-5-d-old guinea pigs. This may be due to developmental alterations in the areas of the brainstem responsible for respiratory control.     

Electrical stimulation of the lingual musculature in obstructive sleep apnea

The influence of lingual muscle activity on airflow dynamics in the upper airway was examined in nine patients with obstructive sleep apnea. Muscles that retract the tongue (hyoglossus and styloglossus) and protrude the tongue (genioglossus) were selectively stimulated electrically during sleep with fine wire electrodes placed intramuscularly transorally. We confirmed that stimulation with 50 Hz and 40-microseconds pulse duration did not elicit changes in electroencephalographic patterns or heart rate or alter airflow after the stimulation burst had ceased. The highest stimulus intensity that did not arouse patients from sleep was then utilized to examine the effect of lingual muscle recruitment on airflow dynamics during steady-state periods of inspiratory airflow limitation. When applying a stimulus burst during single inspirations, maximal inspiratory airflow decreased by 239 +/- 177 ml/s (P < 0.05) during retractor stimulation, whereas maximal inspiratory airflow increased by 217 +/- 93 ml/s during protrusor stimulation (P < 0.001) compared with breaths immediately before and after the stimulated breath. When consecutive inspirations were stimulated repeatedly, protrusor stimulation decreased the frequency of obstructive breathing episodes in four patients breathing at 3.9 +/- 3.4 (SD) cmH2O nasal pressure. The findings suggest that stimulation of the lingual muscles can increase or decrease airflow depending on the specific muscles stimulated without arousing patients from sleep.     

Respiratory sinus arrhythmia. A phenomenon improving pulmonary gas exchange and circulatory efficiency

BACKGROUND: The primary mechanisms of respiratory sinus arrhythmia (RSA) are understood to be the modulation of cardiac vagal efferent activity by the central respiratory drive and the lung inflation reflex, and the degree of RSA increases with cardiac vagal activity. However, it is unclear whether RSA serves an active physiological role or merely reflects a passive cardiovascular response to respiratory input. We hypothesized that RSA benefits pulmonary gas exchange by matching perfusion to ventilation within each respiratory cycle. METHODS AND RESULTS: In seven anesthetized dogs, a model stimulating RSA was made. After elimination of endogenous autonomic activities, respiration-linked heartbeat fluctuations were generated by electrical stimulation of the right cervical vagus during negative pressure ventilation produced by phrenic nerve stimulation (diaphragm pacing). The vagal stimulation was performed in three conditions; phasic stimulation during expiration (artificial RSA) and during inspiration (inverse RSA) and constant stimulation (control) causing the same number of heartbeats per minute as the phasic stimulations. Although tidal volume, cardiac output, and arterial blood pressure were unchanged, artificial RSA decreased the ratio of physiological dead space to tidal volume (VD/VT) and the fraction of intrapulmonary shunt (Qap/Qt) by 10% and 51%, respectively, and increased O2 consumption by 4% compared with control. Conversely, reverse RSA increased VD/VT and Qap/Qt by 14% and 64%, respectively, and decreased O2 consumption by 14%. CONCLUSIONS: These results support our hypothesis that RSA benefits the pulmonary gas exchange and may improve the energy efficiency of pulmonary circulation by "saving heartbeats."