Respiration during Sleep in Children with COPD

Respiration during Sleep in Children with COPO* C. Gaultier, M.D.;]. P. Proud, M.D.; A Clement, M.D.; A M. trsu-«. M.D.; M. Khiati, M.D.; G. Tournier; M.D.; and F. Girard, M.D. Seventeen children (mean age, nine years) with chronic obstructive pulmonary disease (COPD) were studied during sleep. Electroencephalography, electrooculography, and electromyography were all recorded. Airflow was measured by nasal and oral thermistors, and abdominal and thoracic anteroposterior diameters by magnetometers. Transcutaneous partial pressure of O 2 (tcPo2) and of CO2 (tcPco2 ) were monitored. The average total sleep time was 283 min ± 36 (1SD). Breathing pauses (BP) five seconds or longer were measured. The mean time of BP expressed as a percentage of TST was 1.3 percent±O.8 (1 SD). The BP occurred most frequently during REM sleep. Forty-six

percent of BP were obstructive (OBP). The percentage of OBP was significantly related to the degree of lung resistance during wakefulness. Periodic breathing was observed with a mean frequency of 2.2 times per night (range: 0 to 7). Episodes with paradoxic inward rib cage motion were seen one to 29 times (mean 6.6). Drops in tcPcos greater than 5 mm Hg occurred one to eight times and 67 percent were observed during REM sleep. Compared to tcPcos during W the mean maximal decrease in tcf'co, was 14 mm Hg (range 8 to 29). tcPco 2 rose with a mean maximal of 9.1 mm Hg (range 6 to 13). It was concluded that children with COPD had worsened gas exchange during sleep.

The effects of sleep on respiration in normal children have recently been documented. Breathing pauses (BP),1,2 oxygen desaturation.P" and increase in the

diaphragmatic workload" all have been found to occur especially during REM sleep. Various respiratory disorders have been shown to aggravate some or all of these sleep events. Upper airway obstruction increased the frequency of obstructive B~ 7-9 asthma.v':" and cystic fibrosis":" induced greater oxygen desaturation than in normal subjects. In the present study, we determined the frequency of B~ and the changes in blood gas levels and in abdominothoracic movements in a group of children with chronic obstructive pulmonary disease (COPD).

*From the Laboratory of Physiology and Pediatrics Department (GT), Hopital Trousseau, Paris, France. This work was supported by "le Cornite National de la Tuberculose et des Maladies respiratoires" grant 83-MR-4 and by INSERM gran t 805007. This paper has been read in part before at the "International Conference on sleep in relation to disease" Oxford, 1983, and at the American Thoracic Society, Miami, 1984. Manuscript received March 13; revision accepted July 3. Reprint requests: Prof Girard. Hopital Trousseau, 26 Au A. Netter,

75012 Paris, France

Table I-Pulmonary Function Tests Data During Wakefulness in 17 Children with COPD* Case

Sex

Agel

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Mean ±1 SD

M M F

NB NB 6mo 3 yr 2.3 yr 1.4 yr 3.9 yr 1.6 yr 6 yr 9mo I I I I I 5 yr 3 yr

F M M M M M M M F F M F M F

Age"

(yr)

Weight (kg)

Height (ern)

3 3.2 4.6 5 6.3 8.4 8.9 9.2 9.5 10.9 5.5 8 9 10.5 11.5 17.2 20.2 8.9 4.5

12 12 12 14 14 25 22 15 29 41 15 21 37 20 25 57 52 25 14

91 92 95 104 109 125 123 128 131 140 104 125 140 123 131 172 158 123 22

TGV (pred)

181 189 164 196 141 139 127 144 160 26

RL (pred) Cdyn (pred) 244 138 192 264 200 229 157 270 214 344

195 139 172 138 213 230 162 213 55

76 57 12 29 48 54

69 57 69 44 71 65

58 40 79 46 71 56 18

°

Pa02 (mm Hg)

PaC 2 (mmHg)

75 (88) 77 (91) 53 (60) 68 (77) 64 (73) 69 (75) 83 (90) 75 (82) 79 (86) 67 (72) 75 (85) 78 (85) 72 (78) 73 (78) 64 (69) 66 (69) 81 (85) 72 (79) 5 ( 9)

36 36 51 36 43 38 37 35 36 37 35 35 35 36 33 44

37 38 4

*Agel, age at the onset of the bronchial obstruction; NB, newborn period; I, infancy; age", age at the time of the sleep study; TG~ thoracic gas volume; RL, total pulmonary resistance; Cdyn, lung dynamic compliance; pred, expressed as a percentage of the predicted values for height; Pa02 , PaC02 , partial pressure of O 2 and CO 2 of the arterialized capillary blood, values in brackets for Pa0 2 are expressed as a percentage of the predicted values for age.

188

Sleep in Children with COPO (Gaultier et al)

100

----- --------------------------------

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01

=

E E

N C)

a:=

--------~

60

ol_--'-__ o 2

--L-_ _. & . -_ _--L-_ _--'

6

AGE

YEAR

10

12

16

20

FIGURE 1. The ages of the patients are displayed on the abscissa, the partial pressure of arterialized capillary sample (PaO,J on the ordinate. The solid line represents the mean predicted value, the dotted lines indicate respectively minus 2,4, and 6 standard deviations. Longitudinal study of PeO, is shown for each child:filled squares represent PaO, at the time of the sleep studies (Table 1) and are connected by full lines to circles representing previous values of PaO,. MATERIAL AND METHODS

Seventeen children (11 boys and six girls) with COPD were tested. Their age, height, and weight are reported in Table 1. None of them was obese. Chronic bronchial obstruction had been clinically evident for at least two years in all patients. Different etiologies of COPD were found. Cases 1 and 2 had bronchopulmonary dysplasia. In cases 3 to 9, COPD was related to the sequelae of viral infection proved by increasing complement fixing antibody in cases 3 to 6 or suspected in the remaining cases on clinical grounds (cases 7 to 9)." Abnormal cilia were observed by electronic microscopy in cases 10to 15,16 while cases 16 and 17 had idiopathic bronchiectasis. The ages of onset of diseases are reported in Table 1. Follow-up blood gas determinations during wakefulness are illustrated by Figure 1. At the time of the sleep study, all the patients were in an infection-free period. None had periods of diurnal somnolence. The parents did not mention any abnormalities during their children's sleep. Awake pulmonary function tests (PIT) were performed between 9 and 12 AM during the same 24-hour period as the sleep study. Thoracic gas volume (TGV) (plethysmographic method), total pulmonary resistance (RL) and dynamic lung compliance (Cdyn) (esophageal catheter technique)" were measured. Blood gas levels were determined in arterialized capillary samples using a reliable technique previously published. 10 The children were tested in the sitting position. No premedication was used. Sleep studies were done during a single night in a sleep laboratory under the surveillance of a physician. No sedation was used. Parental consent was given. Electroencephalography, electrooculography, and chin electromyography were all simultaneously recorded during sleep. Sleep stages were scored according to published criteria." When it was not possible to score a sleep period, it was reported as undetermined (U). Nasal and oral thermistors were used to detect airflow and anteroposterior magnetometers were placed at the nipple line and just above the umbilicus to detect rib cage and abdominal motions. The occurrence of inward rib cage motion during inspiration concurrently with outward abdominal motion was called episode of paradoxic inward rib cage motion (PIRe). Breathing pauses longer than five seconds were counted. The BPs were

considered to be central when there were no discernable respiratory efforts. Periodic breathing was noted if two BPs occurred within a 20second interval. 'Transcutaneous tension of'O, (tcPo,Jwas monitored using an electrode heated to 44'C. Episodes of drop in tcPo, (DP) were counted if greater than 5 mm Hg. Transcutaneous tension of CO, was monitored with an electrode heated to 42'C. ~ The two electrodes were placed on the anterior part of the thorax. Calibration of the electrodes was verified every four hours.

Wakefulness

RESULTS

Results of PFT during wakefulness are displayed in Table 1. Patients had increased RL and decreased Cdyn." Overinflation was observed in the children in whom TGV was measured. As shown in Figure 1, 15 children had a waking Pa0 210wer than normal limits. 1. The PaC0 2 was greater than 40 mm Hg in cases 3, 5, and 16.

Sleep

On the average, patients went to sleep at 10:30 PM (range: 9 to 12 PM) and woke up at 5:00 AM (range: 3:30 to 5:50 AM). Individual values of the total sleep time (TST) and of the time of the different sleep stages expressed as a percentage ofTST are reported in Table 2. No REM sleep stage was observed in cases 4 and 10. The mean sleep time spent in REM stages was 15 percent ofTST. Snoring was noticed in cases 1, 6, 7, 12, and 15. Individual analysis ofBP is displayed in Table 2. The mean time of BP expressed as a percentage of the TST was 1.3 ± 0.8 (1 SO). The BP occurred most frequently during REM and stage 2 sleep periods; the mean time CHEST I 87 I 2 I FEBRUARY. 1985

169

Table 2-Skep Data in 17 Children with COPD* Case

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

Mean ±1 SD

TST (min)

248 210 312 340 243 347 280 300

243 270

300

275 262

300

318 275 280 283 36

1

2

3-4

U

(%)

(%)

(%)

(%)

16 13 4 31 10 0 2 2 24 10 7 10 6 26 3 4 2 9 9

28 45 33 51 37

21 26 26 14 21

9 4

35 44 35

18 43

44 56

41 32 51 48

50

41 10

38

32 29 31 10 30

16 24 22

24 22

20 24 16

25

4 4 12 14 20 5 23

3 8 8 20 6 16 6 11 7

REM TBPrrST mean d (s) (%) (%)

26 12 12 0 28 15 8 14 22

16 16 10 21 0 16 10 22 15 8

1.7 2 1.1

0.4 1.7 0.8 0.9 2.5 3 1.7 1.3 0.5

1.1

0.4 1.2 0.3 1.4 1.3 0.8

max d (s)

OBP (%)

PB

PIRC

11 10 11 10 11 7 12 13 11 14 15 8 12 7 16 13 16 11.5 2.8

48 0 52

2 0 0 2 3 0 4 3 2 7 6 1 2 0 2 1 3 2.2 2.0

3 0 4 15 1 2 29 4 0 14 11 0 7 9 7 4 3 6.6 7.4

9 6.7 5.8 7 6 6 5.8 6.8 5.7 7.2 6.9 5.5 6.9 5.7 6.6 7.4 7.4 6.6 0.9

60 30

48 47 44

16 48 57

84

46 82 48 50

21 46 21

I1tcPo 2 I1tcPco2 (mm Hg) (mm Hg)

29 15 12 8

13 8 10 13 11 10 6

10

19 15 9 10 21 15 17 11 14 13 11 14.3 5.3

9 9 8 11 8 7 5 9.1 2.4

*TST is total sleep time; 1, 2, 3-4, U (undetermined), REM (rapid eye-movement) are sleep stages; %, time of the preceding sleep stages as a percentage ofTST; TBPffST, total breathing pauses time as percent ofTST; mean d, mean duration of BP in second(s); max d, mean maximal duration ofBP; OBp, obstructive BP as percent of the total number ofBP; PIRC, number of episodes of paradoxic inward rib cage motion; ~tCPo2' difference between the bedtime resting supine transcutaneous partial pressure of O 2 and the lowest tcPo2 during sleep; I1tcPco2, difference between the bedtime resting supine transcutaneous partial pressure of CO 2 and the highest tcf'co, during sleep.

of BP as a percentage of the sleep time in these two stages was respectively 2.8 percent±2.1 and 1.4 percent±1.6 (1 SO). The mean duration of BP was 6.6 s ± 0.9 (1SO) and the maximal duration 11.5s ± 2.8 (1 SO). The number of BP per hour of sleep was 4.2 ± 0.7 (1 SO), 0.7 ± 0.8 which were longer than 10s. Forty-six percent of the BP was obstructive. The percentage of OBP was signi6cantly related to the increase in total pulmonary resistance during wakefulness (r = 0.68, p
Maximal drop in tcf'o, (~tCP02) calculated by the difference between tcf'o, and the lowest tcf'o, during sleep, showed a mean of 14.3 mm Hg (range 8 to 29) (Table 2). Assuming a normal O 2 saturation curve and pH, the mean atcPo2 corresponded to the mean drop in O 2saturation equal to 4 percent, reaching 11 percent lID

•

75

50

25

100

300

FIGURE 2. The increase in total pulmonary resistance (RL) during wakefulness (Table 1)expressed as a percentage of predicted values is shown on the ordinate with the percentage of obstructive breathing pauses (OBP) on the abscissa. Increase in RL was correlated to frequency ofOBp, r=O.68, p
Sleep in Children with COPO (Gaultier et 8/)

1~--------------------

........

Imin FIGURE 3. Changes in transcutaneous partial pressure of CO. (tcPeoJ and of 0. (tcPoJ for case 14. The arrow indicates the change in sleep stages from stage 3-4 to RE M sleep. During RE M sleep, several episodes of drops in tcPo. occurred and tcPeo. was increased when compared to the preceding period of stage 3-4.

in case 1. There was no significant relationship between the maximal drop in tcl'o, during sleep and the awake Pa0 2 • The tcl'co, was successfully monitored in 14 children. The bedtime resting awake supine tcf'co, (tcPc0 2W) was related to the awake seated PaC0 2 (Table 1)(tcl'co, = 0.84 PaC0 2 + 28, r = 0.56, p<0.05). During sleep episodes of increase in tcPco2 occurred, the maximal increase in tcf'co, (atcpco 2) calculated by the difference between tcl'co.W and the highest tcf'oo, during sleep showed a mean of 9.1 (range 5 to 13) (Table 2). The highest «Pco, occurred in nine children during REM sleep and in the other cases during stage 2 sleep periods. The maximal increase in tcf'co, was observed in six children during periods following BP and was associated with short episode of drop in tcf'co, (Fig 3). In the remaining cases, the highest tcPo 2 occurred during nonapneic episode of drop in tcP02 (Fig 4). There was no significant relationship between the maximal increase in tcf'oo, during sleep and the awake PaC0 2 • DISCUSSION

The present study examined respiration during sleep in a group of children with COPD. In this population, we recorded the frequency of BPs, which were shown to be obstructive in a large proportion of cases. Episodes of drop in teP02 and of increase in tcf'co, occurred both following BP periods and far

1

0' ao[ -b- : c0)70 E

• E 70[

~

oS

50[

from such periods. Furthermore, paradoxic inward rib cage motion was observed in these patients. Our patients were studied throughout a single night. Thus, despite the fact that all of them were accustomed to the laboratory from previous awake testings, the socalled "first night effect" on the organization of sleep cannot be excluded." The time spent in REM sleep was lower than in normal children." though it is not dissimilar to the adolescent range." Absence of REM sleep in two cases and short period of REM sleep in some COPD children were probably due to a sleep time which did not include the last part of the night and/or to the "first night effect.?" When considering the total time of BPs as a percentage ofTST, as well as the number of pauses greater than five seconds, our patients experienced more BPs than healthy children.!" However, the number of BPs longer than ten seconds, as well as the mean duration and the maximal duration of BPs, were in the normal range.!" As has been found in COPD adults," BPs were more frequent in REM sleep than in the other sleep stages. Episodes of periodic breathing have been reported to be rare in a normal population," whereas some of our COPO children had a large number of such episodes. In contrast to healthy children," our patients did not have exclusively central Bp, but both central and obstructive BP (OBP) as has been shown in COPO adults. 24 The percentage ofOBP in our patients was related to the degree of awake airways obstruction.

Imin

........

---------------------

4. Changes in transcutaneous partial pressure of co. (tcPeoJ and ofO, (tcPoJ for case 3. The arrow indicated the change in sleep stages from stage 3-4 to REM sleep. During REM sleep, tcf'o, decreased and stayed low for several minutes, associated with an increase in tcPeosFIGURE

CHEST I 87 I 2 I FEBRUARY, 1985

171

The occurrence of OBP during sleep appears to result from an imbalance between chest wall and upper airway muscles due to the increase in the chemical stimulation." In normal subjects, sleep decreases airway patency because of secretions, 26 increase in the airway smooth muscle tone," and increase in the upper airway resistance. 6.28 In chronic obstructive pulmonary diseases, similar events occur, the resulting increase in airway obstruction worsens gas exchange and leads presumably to control instability which produces OB~25

In our COPO children, anomaly of the coupling between the abdomen and the rib cage was observed with paradoxic inward rib cage motion (PIRC). Such abnormal movements are known to occur in the newborn'":" because of a decrease in intercostal muscle tone during sleep and a high chest wall compliance, whereas PIRe is not observed in normal adolescents whose rib cage has become rigid." The PIRC has been reported during sleep in children with enlarged tonsils" and in asthmatic adolescen ts'" as in our patients. In COPO children, PIRC during sleep may be explained by the increase of the work of breathing and the mechanical disadvantage of the diaphragm;" in addition to the sleep intercostal muscle hypotonia. Since chest wall compliance decreases with age, a greater frequency of PIRC could be expected in the youngest children. We did not observe an age dependence of PIRC possibly because of the small number of very young children in our group of patients. Gas exchange efficiency was monitored with transcutaneous O 2 and CO 2 electrodes. The validity of the measurements in children has previously been demonstrated. 20 •33 ,34 The tcf'oo, was not corrected for arterial CO 2 tension because of the large individual variations of tcPco/arterial Pco 2 ratio.":" The COPO children experienced more episodes of drop in tcf'o, (OP) than healthy children.'" these episodes occurred most frequently during REM sleep, as has been shown in adults with asthma" and COPO. 23 The mean maximal drop in O 2 saturation of our COPO children, corresponding to the mean maximal drop in tcPo 2 , was greater than in normal childrerr':" and adolescents," reaching the range reported in asthmatic children, 3.4 in cystic fibrosis,":" and asthmatic" adolescents. A preceding breathing pause explained a large amount of episodes of drop in tcPo 2 • The few such episodes occurring far from apneic events were possibly due to fall in lung volume" and worsening of the ventilationperfusion distribution" as shown in COPO adults. Furthermore, the concurrent increase of tcf'oo, with drop in tcf'o, indicates alveolar hypoventilation.":" There have been no other reported sleep studies on tcf'co, in normal or sick children, and thus, our data cannot be compared with others. In COPD adults, arterial Pco, has been shown to increase during 172

sleep,":" as was observed in the present study. The maximal changes during sleep of tcf'co, were not correlated to awake blood gas levels, as has been found in COPO adults. 37 In conclusion, we have shown that during sleep, COPO children experienced more abnormal respiration and gas exchange than have been reported in healthy children. These results could have important implications. Hypoxemia during the period of lung growth is known to alter postnatal vascular development. In children with cystic fibrosis, a decrease in the number of arteries per unit area of lung section, correlated with right ventricle hypertrophy, has been reported." Furthermore, all these patients had an increase in pulmonary arterial muscle and peripheral extension of arterial muscle. Hypoplasia and remodelling of the pulmonary circulation have a possible effect on the development of cor pulmonale." Thus, in children with COPO, appropriate preventative treatment of respiratory abnormalities during sleep needs to be explored further. Physiotherapy and drug management of bronchial obstruction preceding sleep, nocturnal O 2 therapy and/or nasal continuous positive airway pressure should be considered. REFERENCES 1 Guilhaume A, Benoit O. Pauses respiratories au cours du sommeil chez l' enfant normal. Observation de 3 cas pathologiques. Rev Electroenceph Neurophysiol Clin 1976; 116: 116-23 2 Carskadon MA, Harey K, Dement WC, Guilleminault C, Simmons FB, Anders TA. Respiration during sleep in children. West J Med 1978; 477:447-81 3 Chipps BE, Mak H, Schuberth KC, Talamo JH, Menkes HA. Nocturnal oxygen saturation in normal and asthmatic children. Pediatrics 1980; 65:1157-60 4 Smith TF, Hudgel DW. Arterial oxygen desaturation during sleep in children with asthma and its relation to airway obstruction and ventilatory drive. Pediatrics 1980; 66:746-51 5 Tabachnik E, Muller NL, Bryan AC, Levison A. Changes in ventilation and chest wall mechanics during sleep in normal adolescents. J Appl Physiol Respir Environ Exer Physiol1981; 51:557-63 6 Guilleminault CH, Winkle R, Korobkin R, Simmons B. Children and nocturnal snoring: evaluation of the effects of sleep related respiratory resistive load and daytime functioning. Eur J Pediatr 1982; 139:165-71 7 Guilleminault C, Eldridge FL, Simmons B, Dement WC. Sleep apnea in eight children. Pediatrics 1976; 58:23-30 8 Brouillette Rl: Fernbach SK, Hunt CEo Obstructive sleep apnea in infants and children. J Pediatr 1982; 100:31-40 9 Frank Y, Kravath RE, Pollad CE Weitzman E. Obstructive sleep apnea and its therapy: clinical and polysomnographic manifestations. Pediatrics 1983; 71:737-41 10 Tabachnik E, Muller NL, Levison H, Bryan AC. Chest wall mechanics and pattern of breathing during sleep in asthmatic adolescents. Am Rev Respir Dis 1981;124:169-273 11 Francis PW, Muller NL, Gurwitz D, Milligan DW, Levison H, Bryan AC. Hemoglobin desaturation: its occurrence during sleep in patients with cystic fibrosis. Am J Dis Child 1980; 124:734-40 Sleep in Children with COPO (Gaultier et aI)

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