Breath Hold Time Snorers - Buteyko Clinic
Breath-holding Time in Normal Subjects,Snorers, and Sleep Apnea PatientsVarsha Taskar, Nigel Clayton, Mark Atkins, Zubair Shaheen, PatriciaStone and Ashley WoodcockChest 1995;107;959-962DOI 10.1378/chest.107.4.959The online version of this article, along with updatedinformation and services can be found online on the WorldWide Web 7/4/959CHEST is the official journal of the American College of ChestPhysicians. It has been published monthly since 1935. Copyright2007 by the American College of Chest Physicians, 3300 DundeeRoad, Northbrook IL 60062. All rights reserved. No part of thisarticle or PDF may be reproduced or distributed without the priorwritten permission of the copyright html). ISSN:0012-3692.Downloaded from chestjournal.org on August 18, 2008Copyright 1995 by American College of Chest Physicians
Breath-holding Time in Normal Subjects,Snorers, and Sleep Apnea Patients*Varsha Taskar, MD; Nigel Clayton, HNC; Mark Atkins, HNC, BSc;Zubair Shaheen, MD; Patricia Stone, MB, ChB;Ashley Woodcock, MD, FCCPBackground: The onset of irregular inspiratory muscleactivity has been observed toward the breakpoint of thebreath-holding maneuver. We wondered if this wassimilar to the increased respiratory effort with paradoxical breathing seen during the resolution of an apnea inobstructive sleep apnea syndrome (OSAS).Study objective: To compare the breakpoint of breathholding in normal subjects, OSAS patients, and snorers.Methods: Thirty normal subjects, 30 patients withOSAS, and 16 snorers performed serial breath-holdingmaneuvers at functional residual capacity (FRC) understandardized pretest conditions using the rebreathingmethod of Read.Results: Intergroup comparisons were carried out byanalysis of variance with post hoc Tukey's Highest Significant Difference tests. Basal end-tidal carbon dioxide(EtCO2) was significantly higher in OSAS than in normalsubjects and snorers. Basal breath-holding time (BHT)was shorter in OSAS as compared with that in normalsubjects and snorers (p 0.05). The maximal EtCO2 levelattained was higher in OSAS as compared with normalsubjects (p 0.05) and snorers (p 0.052). The maximalBreath-holding time (BHT) has been used in respiratory physiology as a measure of ventilatoryresponse.1-3 The unpleasant bursting sensation in thelower chest and abdomen and the onset of irregularinspiratory muscle activity have been well documented at the breakpoint of the breath-holding maneuver.4 Increased respiratory effort with mechanical uncoupling between diaphragmatic contractionand rib cage motion (paradoxical breathing) has beenobserved during sleep.5 We have observed paradoxdeveloping toward the end of apneic episodes in obstructive sleep apnea syndrome (OSAS) in a similarmanner to that occurring at the end of a voluntarybreath-holding period.6 In the present study, we havemeasured BHT in normal subjects, OSAS patients,and snorers as the preliminary step toward understanding the different thresholds of arousal in thesethree groups.*From the Department of Respiratory Physiology, North WestLung Centre, Wythenshawe Hospital, Manchester, England.Manuscript received March 15, 1994; revision accepted August 9.BHT in OSAS was shorter than in normal subjects(p 0.05) but not in snorers. The slope of BHT/EtCO2differed significantly in OSAS compared with normalsubjects and snorers (p 0.05). No significant correlationwas found between slope BHT/EtCO2 and age or bodymass index using mutliple regression analysis. The FRCof OSAS patients and snorers were similar (p 0.792).Conclusion: We conclude that BHT and slope of BHT/EtCO2 are different in OSAS subjects as opposed to thosein normal subjects and snorers. (Chest 1995; 107:959-62)BHT breath-holding time; BMI body niass index;CPAP constant positive airway pressure; EtCO2 endtidal C02; FRC functional residual capacity;OSAS obstructive sleep apnea syndromeKey words: breath holding; respiratory paradox; sleepapnea;MATERIALSANDMETHODSClinical DataWe studied 30 normal subjects, 30 patients with OSAS (meanapnea index, 46.3; SD, 8.3), and 16 snorers (apnea index 5) fromthe Sleep Clinic at Wythenshawe Hospital, North West LungCenter, United Kingdom. Normal subjects were recruited fromthe staff members after ruling out respiratory symptoms on oralquestioning. All snorers and patients with OSA had overnightpolysomnography. All OSAS patients were established on constantpositive airway pressure (CPAP) for a median time of 11 months(range, 1 to 38 months) and had normal daytime blood gas values at the time of the study. The CPAP was used for a median of5.25 h per night (range, 2 to 7 h per night). With this, the OSASpatients had a median arousal index of 10 arousals per hour(range, 3 to 28 arousals per hour). All subjects underwent serialbreath-hold measurements at functional residual capacity (FRC)with steadily increasing concentrations of end tidal CO2 (EtCO2),with the rebreathing method of Read.78 This method waspreferred since the rate of rise of PaCO2 is steady and predictableafter the first 20 s of rebreathing, with the PaCO2 remaining independent of lung volume. All measurements were made at thesame time of the day.Respiratory DataThe rebreathing circuit was set up as in Figure 1. Respiratorymovements and flow at the airway opening were monitored usCHEST / 107 / 4 / APRIL, 1995Downloaded from chestjournal.org on August 18, 2008Copyright 1995 by American College of Chest Physicians959
FIGURE 1. The rebreathing circuit andmonitors used to determine serial BHTs.ing chest and abdomen surface monitors (DENSA pneumographDMS-100, DENSA Ltd, United Kingdom) and a pneumotachograph (Fleisch, Erich Jaeger, Germany), respectively. These weredocumented on a multichannel recorder (Model No RS 3600,Gould Medical Ltd, Coventry, United Kingdom). The EtCO2 wasrecorded with a capnograph (Multicap CNO-103, Datex Instrumentation Corp, Finland). After priming the system with 100%oxygen and calibrating the capnograph, surface apnea monitors,and the pneumotachograph, the patients were connected to thecircuit with the nose clip in place. The procedure was explained,and the patients were allowed a settling period of 30 s. The EtCO2 recorded at this instant was termed as the basal EtCO2. Achange in the EtCO2 of 1% corresponded to 7.6 mm Hg startingfrom a pretest level of 0% (.0 mm of Hg. The basal breathholding maneuver was then performed by giving all patients theidentical instruction: "Hold your breath at the end of a normalbreath and keep holding it for as long as you can." At the end ofthe breath-holding maneuver, the patients remained connected tothe circuit and continued to rebreathe. The breath-holding maneuvers were repeated at each 1% increase in EtCO2 up to themaximal tolerated level or 10% if this was achieved. Tolerancewas defined as the maximal discomfort in the form of suffocation,bursting headache, or lightheadedness experienced by the patientand necessitating disconnection from the rebreathing circuit. TheEtCO2 concentration prior to termination of the test was considered the "maximal EtCO2- and the corresponding BHT was recorded as the "maximal BHT." One trial run was discarded, andthe second set of readings was considered. The BHT was calculated as the period of zero flow recorded on the moving paperrecorder. Throughout the test, the inspired oxygen in thebreathing circuit was kept greater than 60% to avoid hypoxia.Breath holding with swallowing interference as well as breathholding in which chest and abdominal movements were recordedthroughout were discarded.Each subject had at least three values of BHT at successive EtCO2 concentrations which were plotted, and the individual slopeof BHT/EtCO2 was derived for each patient.Statistical AnalysisThe values are expressed as mean SD. Intergroup comparisons of basal and maximal EtCO2 and BHT and the slope of theirrelationship were carried out using simple factorial analysis ofvariance with post hoc comparison by Tukey's Highest SignificantDifference test. Univariate regression analysis was used to determine the correlation between slope of BHT/EtCO2 and body960mass index (BMI) and age. Statistical significance was consideredat a probability of less than 0.05. The analysis was carried out witha statistical software program SPSS version 5 (Statistical Packagefor Social Sciences, SPSS, Chicago, IL).RESULTSIn our group of 76 subjects, 30 had OSAS (meanapnea index, 46.3 8.3) and 16 were nonapneicsnorers. Their mean age, sex distribution, and BMIare described in Table 1. All patients had normal lungfunction tests and normal daytime blood gases at thetime of the study. The subgroups, therefore, differedonly in terms of their BMI and apnea index.As shown in Table 2, OSAS patients had a significantly higher basal EtCO2 compared with that ofnormal subjects and snorers. The basal BHT (seconds)was significantly shorter in OSAS compared withnormal subjects and snorers. The maximal EtCO2that OSAS subjects could tolerate was significantlyhigher than in normal subjects but marginally higherthan in snorers (p 0.052). The maximal BHT inOSAS subjects was significantly lower than in normalsubjects. It was also lower in OSAS subjects as compared with snorers, but the difference did not achievestatistical significance. The proportion of subjectswho tolerated an EtCO2 of more than 8% wassignificantly greater in OSAS subjects (20 of 30)compared with snorers (8 of 16) and normal subjects(9 of 30 [p 0.018, x2 test]).The slope of the relationship between BHT andEtCO2 in OSAS was signficantly different from thatin normal subjects and snorers. There was no relationship between the slope of BHT/EtCO2 and age(r 0.3), sex (r 0.1), and BMI (r 0.2) in OSAS subjects and similarly in snorers (age [r 0.3], sex [r 0.4],BMI [r 0.2]) and normal subjects (age [r 0.2], sex[r 0.2], BMI [r 0.1]). Lung function overall waswithin normal limits and in particular (FRC) valuesBreath-holding Time in Normal Subjects, Snorers, and Sleep Apnea Patients (Taskar et al)Downloaded from chestjournal.org on August 18, 2008Copyright 1995 by American College of Chest Physicians
Table 1-Characteristics of the Subjects*NormalSubjectsTotalAge, yrM to F ratioBMIApnea indexFRC, L3047.4 (10.2)126:423.8 (3.3)1.Snorers1647.0 (10.5)f13.326.6 (3.3)4.2.9 (0.58)§OSASPatients3050.3 (10.6)t28:233.9 (5.5)t46.3 (8.3)2.8 (0.83)§Table 2-Measured Variables in Normal Subjects,OSAS Patients, and Snorers*NormalsSnorers36.2 12.0 33.6 21.7Basal BHT, s6.0 0.53.8 0.6Basal EtCO2, %16.4 10.518.4 7.0Maximal BHT, s7.7 1.07.5 0.7Maximal EtCO2-12.5 4.8 -11.9 10.2Slope (BHT/EtCO2)8 of 169 of 30Subjects with EtCO2 8%OSAS20.6 11.9f6.7 1.2113.2 6.18.3 0.911-6.5 5.1}20 of 30**DISCUSSION*Values are mean SD.tProbability value less than 0.05 compared with normal subjects andsnorers.tProbability value less than 0.05 compared with normal subjects andsnorers.§Probability value less than 0.05 compared with normal subjects(p 0.052 compared with snorers).lProbability value less than 0.05 compared with normal subjects(p NS compared with snorers).¶Probability value less than 0.05 compared with normal subjects andsnorers.**The x2 test (p 0.018 compared with normal subjects and snorers).This study shows that OSAS patients have adifferent relationship between BHT and EtCO2 ascompared with normal subjects and snorers. Thebasal BHT is shorter with a higher basal EtCO2, andthe slope BHT/EtCO2 is steeper. The steeper slopecould be caused by a curvilinear relationship betweenBHT/EtCO2 combined with a shift to the right dueto the higher basal EtCO2. Respiratory drive may berelated to BMI. A previous study showed that BHTwas shorter in obese subjects compared with normalsubjects, though this was not specifically associatedwith EtCO2.9 Miyamura et all' studied the slope ofthe hypercapnic ventilatory response and found it tobe lower in subjects with a high BMI compared withthat of the normal subjects. However, in this study,differences in BHT seen in sleep apnea could not beattributed to obesity or to an abnormality of FRC.The determinants of a maximal voluntary breathhold are initial lung volume, prior oxygenation, andprior PaCO2.2'11 By flushing our rebreathing circuitwith 100% oxygen prior to the test, we ensured thathypoxemia or variation in rates of fall of oxygen saturation did not affect the BHT. During the test, thesubject's psychological willpower and endurance influence the duration of the breath holding. Thebreakpoint of breath holding is preceded by the onset of respiratory movements. These irregular contractions of the inspiratory muscles reduce the unpleasant sensation in the lower thorax and abdomenthat occurs progressively through a breath-holdingperiod.'2 Campbell et al'3 showed that completemuscle paralysis with curare caused prolongation ofthe BHT in the absence of the unpleasant sensationof breath holding and concluded that inspiratorymuscle activity was the final common pathwaydetermining the breakpoint. The onset of electricalactivity during a breath holding period is closely re-lated to the alveolar Pc02.'4 In this study, all patientswith OSAS had PaCO2 of less than 45 mm Hg.However in OSAS, after settling on the breathingcircuit, the basal EtCO2 was higher than normalsubjects or snorers (Table 2). In addition, OSAS patients tolerated breath holding at a higher maximalEtCO2. This may indicate a greater tolerance of inspiratory loading inevitably seen with this experimental setup, perhaps suggesting diminished ventilatory response to CO2.Another possibility for the shorter BHTs in OSASand the absence of any difference between snorersand normal subjects can be derived from the continuum hypothesis of sleep-disordered breathing.1516Accordingly, normal subjects, snorers-which wouldinclude a diverse group of symptomatic individualswith and without an increased upper airway resistance (not assessed in the present study), and OSASpatients have a progressive increase in the severity ofsymptoms associated with a reduction of BHT.All OSAS patients were already established on nasal CPAP. A previous study on the effect of nasalCPAP on daytime hypercapnic ventilatory response17showed that the slope of the ventilatory response remains essentially unchanged in the absence of daytime hypercapnia. One mechanism for the depressedventilatory response to CO2 in OSAS could be sleepfragmentation, since a night of total sleep deprivationproduces a reversible decrease in the hypercapnicventilatory response in normal human volunteers.'8However, in the present study, patients were notsleep-deprived, being already maintained on nasalCPAP and corroborated by their arousal index. Afurther study would be needed to establish whetherbreath holding is changed by institution of CPAPtherapy.*Values are expressed as mean SD.tAge similar in the three groups (p 0.16).4The BMI in OSAS was greater than the BMI in the other two groups(p o.OOl).§The FRC values in OSAS patients and snorers were comparable(p 0.792).in OSAS patients (2,834 829.5 mL) and snorers(2,920 586.5 mL) were comparable (p 0.792).Downloaded from chestjournal.org on August 18, 2008Copyright 1995 by American College of Chest PhysiciansCHEST / 107/4/ APRIL, 1995961
Recent evidence has suggested that increasedventilatory effort may be the stimulus to arousal fromsleep.19 The different threshold for perception ofbreathing discomfort from the respiratory musclesmay explain the variability in the length of apneasprior to arousal in different patients. A further studyof the breath-holding response is needed within alarge group of patients with OSAS to investigatewhether there is any link between the tolerance ofrespiratory discomfort during a breath-holding maneuver and the length of time to arousal during apnea in patients with OSAS.8 Clark TJH, Clark BG, Hughes JMB. A simple technique formeasuring changes in ventilatory response to CO2. Lancet 1966;2:368-719 Hurewitz AN, Sampson MG. Voluntary breath holding in theobese. J Appl Physiol 1987; 62:2371-7610 Miyamura M, Hachiya T, Hiruta S, et al. The influence of bodysize on the ventilatory response to hypercapnia. Japan J Physiol 1985; 35:169-7411 Hill L, Flack M. The effect of excess carbon dioxide and of wantof oxygen upon the respiration and the circulation. J Physiol1908; 37:77-11112 Campbell EJM, Freedman S, Clark TJH, et al. The effect of13REFERENCES1 Nunn JF. Chapter 2: Control of breathing: breath holding. In:Applied respiratory physiology. 2nd ed. London, England:Butterworth, 1977; 95-92 Godfrey S, Campbell EJM. Mechanical and chemical control ofbreath holding. Q J Exp Physiol 1969; 54:117-283 Godfrey S, Campbell EJM. The control of breath holding.Respir Physiol 1968; 5:385-4004 Fowler WS. Breakpoint of breath holding. J Appl Physiol 1954;6:539-455 Tusiewicz K, Moldofsky H, Bryan AC. Mechanics of the ribcage and diaphragm during sleep. J Appl Physiol 1977;43:600-026 Shaheen MZ, Atkins NCM, Clayton N, et al. Phase angle (PA)changes as a measure of paradoxical breathing during sleeprelated apneas/hypopnoeas in patients with sleep apnea. Thorax 1992; 47:8797 Read DJC. A clinical method for assessing the ventilatoryresponse to carbon dioxide. Aust Ann Med 1967; 16:20-32962141516171819muscular paralysis induced by tubocurarine on the durationand sensation of breath holding. Clin Sci 1967; 32:425-32Campbell EJM, Godfrey S, Clark TJH, et al. The effect ofmuscular paralysis induced by tubocurarine on the durationand sensation of breath holding during hypercapnia. Clin Sci1969; 36:323-28Agostoni E. Diaphragm activity during breath holding: factorsrelated to its onset. J Appl Physiol 1963; 18:30-6Lugaresi E, Cirighotta F, Montana P. Snoring: pathogenic,clinical, and therapeutic aspects. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine.Philadelphia: WB Saunders, 1989; 494-500Downey R, Perkin RM, MacQuarrie J. Upper airway resistancesyndrome: symptomatic but underrecognized. Sleep 1993;16:620-23Berthon-Jones M, Sullivan CE. Time course of change in ventilatory response to CO2 with long-term CPAP therapy for obstructive sleep apnoea. Am Rev Respir Dis 1987; 135:144-47Cooper KR, Phillips BA. Effect of short term sleep loss onbreathing. J Appl Physiol 1982; 53:855-58Gleeson K, Zwillich CW, White DP. The influence of increasing ventilatory effort on arousal from sleep. Am Rev Respir Dis1990; 142:295-300Breath-holding Time in Normal Subjects, Snorers, and Sleep Apnea Patients (Taskar et al)Downloaded from chestjournal.org on August 18, 2008Copyright 1995 by American College of Chest Physicians
Breath-holding Time in Normal Subjects, Snorers, and Sleep ApneaPatientsVarsha Taskar, Nigel Clayton, Mark Atkins, Zubair Shaheen, PatriciaStone and Ashley WoodcockChest 1995;107;959-962DOI 10.1378/chest.107.4.959This information is current as of August 18, 2008Updated Information& ServicesUpdated information and services, includinghigh-resolution figures, can be found at:http://chestjournal.orgPermissions & LicensingInformation about reproducing this article in parts(figures, tables) or in its entirety can be found mlReprintsInformation about ordering reprints can be shtmlEmail alerting serviceReceive free email alerts when new articles cite thisarticle sign up in the box at the top right corner of theonline article.Images in PowerPoint format Figures that appear in CHEST articles can bedownloaded for teaching purposes in PowerPointslide format. See any online article figure fordirections.Downloaded from chestjournal.org on August 18, 2008Copyright 1995 by American College of Chest Physicians
fluence the duration of the breath holding. The breakpoint of breath holding is preceded bythe on-set of respiratory movements. These irregular con-tractions of the inspiratory muscles reduce the un-pleasant sensation in the lower thorax andabdomen that occurs progressively through a breat
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