The pattern of breathing during hypoxic exercise

Breathing pattern was studied in six subjects in normoxia (FIO2 = 0.21) and hypoxia (FIO2 = 0.12) at rest and during incremental work-rate exercise. Ventilation (V) as well as mean inspiratory flow (VT/TI) increased with exercise intensity and were augmented in the hypoxic environment, whereas the ratio between inspiratory (TI) and total (Ttot) breath durations increased with exercise intensity but was unaffected by hypoxia. The relationship of tidal volume (VT) and inspiratory time duration (TI) showed linear, coinciding ranges for the normoxic and hypoxic conditions up to VT/TI values of about 2.5 1.s-1. At higher VT/TI values TI continued to decrease, whereas VT tended to level off, an effect which was more evident in the hypoxic condition. The results suggest that the hypoxic augmentation of exercise hyperpnea is primarily brought about by an enhancement of central inspiratory drive, the timing component being largely unaffected by the hypoxic environment, and that at low to moderate levels of exercise hyperpnea inspiratory off-switch mechanisms are essentially unaffected by moderate hypoxia.     

Regional ventilation during spontaneous breathing and mechanical ventilation in dogs

We evaluated the effects of the different patterns of chest wall deformation that occur with different body positions and modes of breathing on regional lung deformation and ventilation. Using the parenchymal marker technique, we determined regional lung behavior during mechanical ventilation and spontaneous breathing in five anesthetized recumbent dogs. Regional lung behavior was related to the patterns of diaphragm motion estimated from X-ray projection images obtained at functional residual capacity (FRC) and end inspiration. Our results indicate that 1) in the prone and supine positions, FRC was larger during mechanical ventilation than during spontaneous breathing; 2) there were significant differences in the patterns of diaphragm motion and regional ventilation between mechanical ventilation and spontaneous breathing in both body positions; 3) in the supine position only, there was a vertical gradient in lung volume at FRC; 4) in both positions and for both modes of breathing, regional ventilation was nonlinearly related to changes in lobar and overall lung volumes; and 5) different patterns of diaphragm motion caused different sliding motions and differential rotations of upper and lower lobes. Our results are inconsistent with the classic model of regional ventilation, and we conclude that the distribution of ventilation is determined by a complex interaction of lung and chest wall shapes and by the motion of the lobes relative to each other, all of which help to minimize distortion of the lung parenchyma.     

Genetic control of differential baseline breathing pattern

Tankersley, Clarke G., Robert S. Fitzgerald, Roy C. Levitt,Wayne A. Mitzner, Susan L. Ewart, and Steven R. Kleeberger. Genetic control of differential baseline breathing pattern. J. Appl. Physiol. 82(3): 874-881, 1997.The purpose of the present study was to determine the geneticcontrol of baseline breathing pattern by examining the mode ofinheritance between two inbred murine strains with differentialbreathing characteristics. Specifically, the rapid, shallow phenotypeof the C57BL/6J (B6) strain is consistently distinct from theslow, deep phenotype of the C3H/HeJ (C3) strain. The responsedistributions of segregant and nonsegregant progeny were compared withthe two progenitor strains to determine the mode of inheritance foreach ventilatory characteristic. The BXH recombinant inbred (RI)strains derived from the B6 and C3 progenitors were examined toestablish strain distribution patterns for each ventilatory trait. Toestablish the mode of inheritance, baseline breathing frequency (f),tidal volume, and inspiratory time(TI) were measured five timesin each of 178 mature male animals from the two progenitor strains andtheir progeny by using whole body plethysmography. With respect to fand TI, the two progenitor strains were consistently distinct, and segregation analyses of theinheritance pattern suggest that the most parsimonious genetic modelfor response distributions of f andTI is a two-loci model. Insimilar experiments conducted on 82 mature male animals from 12 BXH RIstrains, each parental phenotype was represented by one or more of theRI strains. Intermediate phenotypes emerged to confirm the likelihoodthat parental strain differences in f andTI were determined by more thanone locus. Taken together, these studies suggest that the phenotypicdifference in baseline respiratory timing between male B6 and C3 miceis best explained by a genetic model that considers at least two locias major determinants.

     

Mechanical work of breathing during maximal voluntary ventilation

With the use of the esophageal balloon technique, the workingcapacity of the respiratory muscles was assessed in four normal subjects by measuring the work per breath (W) and respiratory power() during maximal voluntary ventilationwith imposed respiratory frequencies (f) ranging from 20 to 273 cycles/min. Measurements were made in a body plethysmograph to assessthe work wasted as a result of alveolar gas compressibility(Wg'). In line with other types of human voluntary muscleactivity, W decreased with increasing f, whereas exhibited a maximum at f of ~100cycles/min. Up to this f value, Wg' was small relative to W. Withfurther increase in f, the Wg'/W ratio increased progressively,amounting to 8-22% of at f of 200 cycles/min.

     

Exercise breathing pattern during chronic altitude exposure

Breathing pattern in response to maximal exercise was examined in four subjects during a 7-day acclimatisation to a simulated altitude of 4247 m (barometric pressure, PB = 59.5 kPa). Graded exercise tests to exhaustion were performed during normoxia (day 0), and on days 2 and 7 of hypoxia, respectively. Ventilation was significantly augmented in the hypoxic environment, as were both the mean inspiratory flow (VT/TI) and inspiratory duty cycle (TI/TTOT) components of it. VI/TI was increased due to a significant increase in tidal volume (VT) and a corresponding decrease in inspiratory time duration (TI). Throughout a range of exercise ventilation, TI/TTOT was increased due to an apparently greater decrease in expiratory time duration (TE) with respect to TI. In all cases, the relation between VT and TI displayed a typical range 2 behaviour, with evidence of a range 3 occurring at very high ventilatory rates. There was essentially no difference observed in the VT-TI relation during exercise between the normoxic and hypoxic conditions. No significant changes were observed in the breathing pattern in response to exercise within the exposure period (from day 2 to day 7), although there was a discernible tendency to a higher stage 3 plateau by day 7 of altitude exposure.     

Influence of anthropometric characteristics on changes in maximal exercise ventilation and breathing pattern during growth in boys.

The aim of this study was to investigate the effect of growth on ventilation and breathing pattern during maximal exercise oxygen consumption (VO2max) and their relationships with anthropometric characteristics. Seventy six untrained schoolboys, aged 10.5-15.5 years, participated in this study. Anthropometric measurements made included body mass, height, armspan, lean body mass, and body surface area. During an incremental exercise test, maximal ventilation (VEmax), tidal volume (VTmax), breathing frequency (fmax), inspiratory and expiratory times (tImax and tEmax), total duration of respiratory cycle (tTOTmax), mean inspiratory flow (VT/tImax), and inspiration fraction (tI/tTOTmax) were measured at VO2max. A power function was calculated between anthropometric characteristics and ventilatory variables to determine the allometric constants. The results showed firstly, that VEmax, VTmax, tImax, tEmax, tTOTmax, and VT/tImax increased with age and anthropometric characteristics (P less than 0.001), fmax decreased (P less than 0.001), and tI/tTOTmax remained constant during growth; secondly that lean body mass explained the greatest percentage of variance of VEmax (62.1%), VTmax (76.8%), and VT/tImax (70.6%), while anthropometric characteristics explained a slight percentage of variance of fmax and timing; and thirdly that VEmax, VTmax, and VT/tImax normalized by lean body mass did not change significantly with age. We concluded that at VO2max there were marked changes in ventilation and breathing pattern with growth. The changes in VEmax, VTmax, and VT/tImax were strongly related to the changes in lean body mass.     

Postnatal maturation of ventilation and breathing pattern in kittens: influence of sleep

Ventilation and breathing pattern were studied in kittens at 1, 2, 3, 4, and 8 wk of life during quiet wakefulness (W), quiet sleep (QS), and active sleep (AS) with the barometric method. Tidal volume (VT), respiratory frequency (f), ventilation (VE), inspiratory time (TI), expiratory time (TE), mean inspiratory flow (VT/TI), and respiratory "duty cycle" (TI/TT) were measured. VT, VE, TI, TE, and VT/TI increased; f decreased and TI/TT remained constant during postnatal development in wakefulness and in both sleep states. No significant difference was observed between AS and QS for all the ventilatory parameters except TI/TT, which was greater in QS than in AS at 2 wk. VE was larger in W than in both AS and QS at all ages. This was mainly due to a greater f, TI/TT remaining constant. VT/TI, which represents an index of the central inspiratory activity, was larger in W than in sleep, VT not being significantly different whatever the stage of consciousness. The results of this study show that in the kitten 1) unlike in the adult cat, ventilation and breathing pattern are similar in QS and in AS; 2) in sleep, the central inspiratory drive appears to be independent of the type of sleep; and 3) in wakefulness, the increase of the central inspiratory activity could be related to important excitatory inputs.     

Control of breathing during sleep assessed by proportional assist ventilation

Meza, S., E. Giannouli, and M. Younes. Control ofbreathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3-12, 1998.We used proportional assist ventilation (PAV) to evaluate thesources of respiratory drive during sleep. PAV increases the slope ofthe relation between tidal volume(VT) andrespiratory muscle pressure output (Pmus). We reasoned that ifrespiratory drive is dominated by chemical factors, progressiveincrease of PAV gain should result in only a small increase inVT because Pmus would bedownregulated substantially as a result of small decreases inPCO₂. In the presence of substantialnonchemical sources of drive [believed to be the case inrapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reductionin PCO₂ as the output related to thechemically insensitive drive source is amplified severalfold. Twelvenormal subjects underwent polysomnography while connected to a PAVventilator. Continuous positive air pressure (5.2 ± 2.0 cmH₂O) was administered tostabilize the upper airway. PAV was increased in 2-min steps from 0 to20, 40, 60, 80, and 90% of the subject's elastance and resistance.VT, respiratory rate, minuteventilation, and end-tidal CO₂pressure were measured at the different levels, and Pmus wascalculated. Observations were obtained in stage 2 sleep (n = 12), slow-wave sleep(n = 11), and REM sleep(n = 7). In all cases, Pmus wassubstantially downregulated with increase in assist so that theincrease in VT, althoughsignificant (P < 0.05), was small(0.08 liter at the highest assist). There was no difference in responsebetween REM and non-REM sleep. We conclude that respiratory driveduring sleep is dominated by chemical control and that there is nofundamental difference between REM and non-REM sleep in this regard.REM sleep appears to simply add bidirectional noise to what isbasically a chemically controlled respiratory output.

     

A review of the control of breathing during exercise

During the past 100 years many experimental investigations have been carried out in an attempt to determine the control mechanisms responsible for generating the respiratory responses observed during incremental and constant-load exercise tests. As a result of these investigations a number of different and contradictory control mechanisms have been proposed to be the sole mediators of exercise hyperpnea. However, it is now becoming evident that none of the proposed mechanisms are solely responsible for eliciting the exercise respiratory response. The present-day challenge appears to be one of synthesizing the proposed mechanisms, in order to determine the role that each mechanism has in controlling ventilation during exercise. This review, which has been divided into three primary sections, has been designed to meet this challenge. The aim of the first section is to describe the changes in respiration that occur during constant-load and incremental exercise. The second section briefly introduces the reader to traditional and contemporary control mechanisms that might be responsible for eliciting at least a portion of the exercise ventilatory response during these types of exercise. The third section describes how the traditional and contemporary control mechanisms may interact in a complex fashion to produce the changes in breathing associated with constant-load exercise, and incorporates recent experimental evidence from our laboratory.     

Brain activation during volitional control of breathing

Functional magnetic resonance imaging (fMRI) was used to demonstrate the brain activation during volitional control of breathing in nine healthy human subjects. This type of breathing was induced by acoustic stimuli dictating the respiratory frequency. During the period of dictated breathing not only the frontal and temporal lobes of the brain, but also the parietal lobes were bilaterally activated. The frontal lobe was activated bilaterally in all subjects, with frequent activation of Brodmann areas 4 and 6. In the parietal lobe, activation could mostly be demonstrated in gyrus postcentralis and the same was true for area 22 in the temporal lobe.     

Pulmonary gas mixing during spontaneous breathing and at high-frequency ventilation

This work is intended to estimate the contribution of either laminar or turbulent dispersion during spontaneous breathing on one hand, and at high-frequency pulmonary ventilation on the other. For that purpose, we performed a computer simulation of a mathematical model of gas transport in the human airways governed by a combination of axial convection and longitudinal dispersion. Calculations were carried out by incorporating two dispersion coefficients, proposed by Taylor and Scherer respectively, into the mathematical model. Moreover, computations were performed with five constant flow rates and two inert heavy (SF₆) and light (He) gases to enhance the effect of mixing. It is concluded that Taylor laminar dispersion cannot play a significant role in the human airways; however, it seems that convective gas mixing with disturbed dispersion - corresponding to a regime of quasi-steady state-can account for most gas transport during spontaneous respiration and high-frequency ventilation.     

Automatic detection of AutoPEEP during controlled mechanical ventilation

ABSTRACT: BACKGROUND: Dynamic hyperinflation, hereafter called AutoPEEP (auto-positive end expiratory pressure)with some slight language abuse, is a frequent deleterious phenomenon in patients undergoingmechanical ventilation. Although not readily quantifiable, AutoPEEP can be recognized onthe expiratory portion of the flow waveform. If expiratory flow does not return to zero beforethe next inspiration, AutoPEEP is present. This simple detection however requires the eye ofan expert clinician at the patient's bedside. An automatic detection of AutoPEEP should behelpful to optimize care. METHODS: In this paper, a platform for automatic detection of AutoPEEP based on the flow signalavailable on most of recent mechanical ventilators is introduced. The detection algorithms aredeveloped on the basis of robust non-parametric hypothesis testings that require no priorinformation on the signal distribution. In particular, two detectors are proposed: one is basedon SNT (Signal Norm Testing) and the other is an extension of SNT in the sequentialframework. The performance assessment was carried out on a respiratory system analog andex-vivo on various retrospectively acquired patient curves. RESULTS: The experiment results have shown that the proposed algorithm provides relevant AutoPEEPdetection on both simulated and real data. The analysis of clinical data has shown that theproposed detectors can be used to automatically detect AutoPEEP with an accuracy of 93%and a recall (sensitivity) of 90%. CONCLUSIONS: The proposed platform provides an automatic early detection of AutoPEEP. Such functionalitycan be integrated in the currently used mechanical ventilator for continuous monitoring of thepatient-ventilator interface and, therefore, alleviate the clinician task.     

Effects of temperature and hypercapnia on ventilation and breathing pattern in the lizard Uromastyx aegyptius microlepis

In most reptiles, the ventilatory response to hypercapnia consists of large increases in tidal volume (V(T)), whereas the effects on breathing frequency (f(R)) are more variable. The increased V(T) seems to arise from direct inhibition of pulmonary stretch receptors. Most reptiles also exhibit a transitory increase in ventilation upon removal of CO(2) and this post-hypercapnic hyperpnea may consist of changes in both V(T) and f(R). While it is well established that increased body temperature augments the ventilatory response to hypercapnia, the effects of temperature on the post-hypercapnic hyperpnea is less described. In the present study, we characterise the ventilatory response of the agamid lizard Uromastyx aegyptius to hypercapnia and upon the return to air at 25 and 35 degrees C. At both temperatures, hypercapnia caused large increases in V(T) and small reductions in f(R), that were most pronounced at the higher temperature. The post-hypercapnic hyperpnea, which mainly consisted of increased f(R), was numerically larger at 35 compared to 25 degrees C. However, when expressed as a proportion of the levels of ventilation reached during steady-state hypercapnia, the post-hypercapnic hyperpnea was largest at 25 degrees C. Some individuals exhibited buccal pumping where each expiratory thoracic breath was followed by numerous small forced inhalations caused by contractions of the buccal cavity. This breathing pattern was most pronounced during severe hypercapnia and particularly evident during the post-hypercapnic hyperpnea.