Influence of Noninvasive Positive Pressure Ventilation on Inspiratory Muscles

Influence of Noninvasive Positive Pressure ventilation on Inspiratory Muscles· Roger S. Goldstein, M.D., F.C.C.R; Jim A De Rosie, B.Sc.; Monica A. Avendano, M.D., F.C.C.R; and Tom E. Dolmage, M.Sc.

Intermittent positive pressure ventilation reduces inspiratory muscle elechvmyographic activity among patients with restrictive ventilatory failure. It has therefore been suggested that the reduction of energy expenditure at night could result in improved inspiratory muscle function during the day. Reported successes with noctumaI ventilation have not included measurements of inspiratory muscle endurance. We therefore electively ventilated six (Ove female, one male) patients (mean::t SD) aged 36::t 13 years in whom respiratory failure (room air PaCO., 6O::t 13 mm Hg; PaO., 44±11 mm Hg; SaO., 75::t 12 percent) was coosequent on restrictive ventilatory disease (vital capacity, 25::t 7 percent predicted; FEV.IFVC, 81::t 12 percent; totalluog capacity, 4O::t5 percent predicted; MIPav -42::t 10 em 0.0; MEP, 81::t28 em 0.0). Positive pressure ventilation was administered with a customized closely Otting nasal mask attached to a volume-cycled pressure-limited ventilator. Full respiratory poIysomoographic measurements as well as arterial blood gases, pulmonary function, distance walked in six miDutes, and inspiratory muscle endurance were measured at baseline and after 3 and 14 months of ventilation.

patients in whom respiratory failure is consequent on restrictive ventilatory disease experience nocturnal deterioration of their blood gas values, especially during rapid eye movement (REM) sleep} Regular nocturnal mechanical ventilation by effectively preventing these changes can improve their daytime arterial blood gas (ABC) values, exercise tolerance, and sense ofwell-being. 2-6 For both medical and cosmetic reasons, there has been renewed interest in noninvasive mechanical ventilation, and both negative pressure and positive pressure devices have been used successfully in the management of respiratory failure. 7- 13 However, the mechanism by which patients improve remains unclear. A reduction in diaphragmatic and accessory muscle electromyographic (EM C) activity during ventilation has been demonstrated among healthy volunteers lO•14 and in patients· with restrictive ventilatory failure. IO•14 Therefore, it has been postulated that the beneficial effects of ventila-

*From the Departments of Medicine, University of Toronto, West Park Hospitaf, Mount Sinai Hospital, Wellesley Hospital and the Sleep Research Laboratory at the Queen Elizabeth Hospital, Toronto, Ontario, Canada. Manuscript received May_29; revision accepted July 31. Reprintrequuts: Dr: Goldatein, wm lbrk Hospital, 82 Buttonwood, 'lbronto, Ontario, Canada M6M 2]5

408

Ventilation improved saturation (baseline on 0.; SWS 87::t 10, REM 79± 14, ventilator on RIA; SWS 9O::t6, REM 89 ::t 5 percent) and transcutaneous Pea. (baseline on 0.; SWS 85::t26, REM 94::t39, ventilator on RIA; SWS 53±9, REM 58 ± 9 mm Hg). During ventilation, the quantity and distribution of sleep was similar to that observed prior to ventilation. Daytime gas exchange improved as did the sixminute walking test (initial test=4!9::t 120 m, three months after ventilation = 567 ::t 121 m), both of these improvements being sustained at 14 months. Inspiratory muscle endurance measured using a pressure threshold load (mean mouth pressure = 45 percent MIPav) improved from 7.1 ± 3.4 minutes at baseline to 14.8::t7.6 minutes at 3 months, an improvement sustained at 14 months. There was DO change in measured lung volumes or respiratory muscle strength. We conclude that the improvement in nocturnal gas exchange, daytime functioning, and arterial blood gases resulting from nocturnal positive pressure ventilation is associated with an increase in inspiratory muscle endurance sustained at 14 IDOnths. (Cheat 1991; 99:408-15)

tory support may be mediated, in part, by a reduction

in inspiratory muscle work.

Reported success using nocturnal positive pressure ventilation by nasal mask has only occasionally included measurements of inspiratory muscle function. Marino and Braun l5 observed an increase in respiratory muscle strength (RMS) after five months ofeither negative or positive pressure ventilation for part of each day (4 to 10 h), and Ellis et al7 observed that after three months of nocturnal positive pressure ventilation, the improvement in daytime ABC values was associated with an improvement in inspiratory muscle strength in four of seven subjects with severe kyphoscoliosis. Accordingly, this study was undertaken to examine the long-term effects of intermittent positive pressure ventilation (IPPV) by nasal mask on inspiratory muscle endurance among patients in whom respiratory failure is secondary to restrictive ventilatory disease. Our findings suggest that following nocturnal ventilation, there is an increase in inspiratory muscle endurance.

PATIENTS AND METHODS Six patients (five female, one male) with respiratory failure consequent upon restrictive ventilatory disease consented to the study. Four patients had idiopathic thoracic restrictive disease (kyphoscoliosis), one patient had postpolio kyphoscoliosis, and one Inftuence of Noninvasive Ventilation on Spiratory Muscles (Goldstein et 81)

patient had neuromuscUlar disease associated with a peripheral neuropathy of undetermined origin. All patients bad required acute ventilatory support on one or more previous occasions. They bad received' close clinical supervision for a number of months d~, which time there had been no spontaneous improvement'iD ·their respiratory condition. Although their nocturnal desaturation could be corrected by administering supplemental oxygen, this bad resulted in unacceptably high levels of Peo. necessitating mechanical ventilatory support. The patients were highly motivated to return to full-time employment and had been referred for respiratory rehabilitation. After initiation of elective ventilation, patients participated in a supervised in-patient multidisciplinary exercise rehabilitation prograDi. This six-week program consisted of twicedaily exercises on a treadmill or individually supervised interval training for five days each week. The program included upper limb endurance training, educational and relaxation classes, but it did not include inspiratory muscle endurance training. Baseline measurements of pulmonary function included standard lung volumes, 80w rates, diffusion, measurements of maximal inspiratory and expiratory pressure, and ABG determinations measured with the patient breathing room air. Inspiratory muscle endurance was measured by pressure threshold loading, a technique first described by Nickerson and Keens lS among healthy volunteers and subsequently reported to be useful in assessing inspiratory muscle function among patients with chronic respiratory disease.17018 A weighted plunger serves as an inspiratory valve and the inspiratory pressure load is determined by the amount of weight applied to the valve. Inspiratory muscle endurance was measured as the endurance time (Tuu) during which the subject could maintain inspiration against 45 percent of maximum inspiratory pressure (MIP) at residual volume (RV). Subjects inspired against a weighted plunger housed in a valve; air 80w occurred when the pressure generated at the airway opening was sufficient to lift the plunger. This threshold pressure had to be sustained throughout inspiration to prevent valve closure. Subjects were given maximal encouragement throughout this test to comply' with the following ventilatory controls: (1) duty cycle (T1f..J at 0.5; (2) respiratory rate ifrJ at resting level; and (3) tidal volume (VT) at 125 percent ofthe previously measured resting value. These parameters were displayed to the patient during each test with an oscilloscope (Tektronix 5223). Subjects varied as to how many practice rons were required before the test was considered technically acceptable. When subjects failed either to match the preset ventilatory controls or to generate the required opening pressure, they came off the mouthpiece, effectively terminating the test. Pressure at the airway

opening was measured with a differential pressure transducer (Validyne Mel). Inspiratory flow was measured with a pneumotachygraph (Fleisch HP 47304A) in series with the inspiratory port. I~iratoryflow was integrated (Gould Integrator Ampli&er 134615-70) to display VT. All variables were recorded on a 16-channel strip chart recorder (Gould ES 1(00). The SaO. was monitored with a pulse oximeter (Ohmeda Biox 37(0) and was maintained at or above 90 percent throughout the test with the administration of supplemental oxygen as neces~ Our clinical test of exercise tolerance was the 6-minute walking test performed under circumstances of maximum encouragement in the hospital corridor. The total distance walked was recorded. The baseline performance was established from the best of three tests performed at the same time each da~ 10 The ABGs were measured both before and after therapy at the same time of the day (late afternoon) while patients breathed room air without ventilatory support.

Sleep Studies

Each patient underwent three overnight sleep studies, one prior to the initiation of positive pressure ventilation, a second while receiving positive pressure ventilation, and a third on the 6rst postventilatory night (no mechanical ventilation) after three months of nocturnal ventilation. Standard sleep variables included the electroencephalogram (EEG), submental electromyogram (EMG), electro-occulogram (EOC), and electrocardiogram (ECG), with sleep stages being scored in 4O-s epochs by standard criteria. II Respiratory movements were monitored by inductive plethysmography (respitrace ambulatory monitoring, Ardsle~ NY). The SaO. was measured with a pulse oximeter (Ohmeda Biox 37(0) and Pcos was measured transcutaneously with a carbon dioxide monitor (Kontron Microgas 7640). Measurements of SaO. were made on an epoch-by-epoch basis, and for each epoch, the highest and lowest values were recorded and the results were expressed as the mean high and mean low values of each sleep stage. Measurements of Peos were made on an epoch-by-epoch basis and were expressed as the mean and highest value for each sleep stage. IPPV Equipment Nasal ventilation was achieved with a volume-cycled portable home ventilator (PLV 100 Life Products). Room air without humidmcation was driven through clear corrugated tubing to the patient via a nose mask. The nose mask was customized with a lightweight sandsplint shell and a Neoprene seal. Each patient underwent at least one daytime laboratory assessment in which resting ventilation was measured by attaching a pneumotachygraph to the expiratory

Table I-Indit>idutJl Pulmona'l/ FUnction Meaaurementa at &aeline and Means ( ± Standard Deviation) at Baaeline, Three Moot'" and 14 Montlu After Ventilation· Subject

Ox

Sex

1 2 3 4 5 6 Baseline 3mo 14mo

ITR ITR NMD ITR PPm ITR

M F F F F F

Age,

Height,

Yr

em

Weight,

kg

29 35 21 57 39 66 36±13

143 132 174 146 153 155 150±16

56 30 51 46 52 81 47±10

VC, %pred

FEVh %pred

FEV/FVC, %

%pred

Vso,

V25, %pred

TLC, %pred

27 21 28 33 15 40 25±7 28±5 30±7

25 20 38 31 12 44 25±10 27±9 29±15

85.7 75.0 100.0 70.0 75.0 88.9 81.1±12.0 82.8± 11.5 74.2± 15.8

34 21 90 23 9 43 35±32 32±29 30±26

27 11 109 13 6 8 33±43 34±42 29±39

36 44 40 47 35 36 4O±5 44±6t 46±5t

*Means based on subjects 1 to 5. Definition of abbreviations: ITR =idiopathic thoracic restriction; NMD =neuromuscular disease; ~PrR = postpolio thoracic restriction; VC = vital capacityi FEV I = forced expiratory volume in 1 s; FEV/FVC = FEV/forced vital capacity; V50 = maximal expiratory 80w at 50 percent of FVC; V25 =maximal expiratory flow at 25 percent of FVC; TLC = total lung capacity measured with a body plethysmograph. tn=4. CHEST I 99 I 2 I FEBRUAR~

1991

409

Table f.-Strength and Endurance at Baaeline, Three Montlu, and 14 Montlu After Nocturnal Ventilation· MIPRv , -cmHIO

MIPnc , -cm HtO

MEe cmHIO

Umin

Pm, %MIPRV

TUM, min

42±10 51±17 47±14

30±7 32±7 28±10

81±28 92±18 84±42

29±22 34±20 39±32

44±13 38±10 49±5

7.1±3.4 14.8±7.6t 17.2±6.3

BaSeline 3mo 14mo

M~

*De6nition of abbreviations: MIPR\· = maximum inspiratory pressure at residual volume; MIPFRc at functional residual capacity; MEP = maximum expiratory pressure; MVV = maximum voluntary ventilation; Pm = mean pressure measured at the mouth during test of inspiratory muscle endurance expressed as %MIPRV ; TUM =endurance time for inspiratory muscle threshold load.

tp
mm Hg; Sa02 75 ± 12 percent) consequent on restrictive ventilatory disease with a reduced vital capacity (VC) and total lung capacity and How rates appropriate to the observed lung volumes (Table 1). Maximum inspiratory pressures at residual volume and functional residual capacity were reduced as was maximum expiratory pressure and maximum voluntary ventilation (Table 2). Although subjects received supplemensaturation tal oxygen during the initial sleep stud~ levels fell substantially, especially during REM sleep '(Table 3). Similarly, the highest values of Pco2 were found during REM sleep (mean high REM = 106 ± 31 mm Hg, Table 4). Subjects consistently displayed a rapid shallow pattern of breathing with a further reduction, especially in rib cage excursion during REM sleep (Fig 1a). During assisted ventilation, subjects were able to breathe room air while maintaining saturation throughout each of the sleep stages at a relatively low ventilator pressure (20 to 25 cm H 20) Fig 2). After 12 weeks of nocturnal ventilation, nocturnal Pco2 and Sa02 without ventilatory support

port of the face mask. Expired 80w was integrated to display volume. Simultaneously the diaphragmatic and sternocleidomastoid EMGs were monitored with surface electrodes. The criteria used for effective ventilatory support were a reduction of at least 50 percent in the EMG signals accompanied by a decrease in Pco. and an increase Sa02 • 10

Noctum6l~ Nasal ventilation was started during the day under no supervision of a respiratory therapist. The time during which a patient received ventilatory support was increased gradually over several days. When the patient could tolerate several hours of ventilation, daytime ventilation was discontinued and nighttime ventilation commenced. The duration of ventilation was increased until patients could tolerate 6 h each night for at least six nights each week. On the initial nights, nocturnal SaO. and Pco2 were monitored continuously. All baseline measurements were repeated eight weeks following hospital discharge (equivalent to 12 to 14 weeks of ventilation and again following 14 months ofventilation). Statistical analysis between baseline and the initial post intervention measurements was by paired t test with an alpha ofO.OS. RESULTS

Each of the subjects had respiratory failure (mean±SD: PaC02 , 6O±13 mm Hg; Pa02 , 43±11

Table 3-Chygen Saturation During Sleep at Baaelirae Uraaaimd, During Vmtilation, and on the Fint p ~ Night FollotDitag 12 ~b afNocturnal Ventilation

ID

High

Baseline (oxygen)

94 1 93 2 94 3 92 4 95 5 93 6 94±1 Mean Ventilation (room air) 92 1 95 2 98 3 97 4 95 5 95 6 95±2.3 Mean Postventilation (room air) 94 1 97 3 94 4

Low 94 89 94 46

84 87 81±20 91 88 93

86

High 94.5 92.0 93.0 86.5 92.0 92.5 92±3 90.5 94.5 97.5

95.5

Low

High

Low

High

Low

93

89 92 79 79 91 92 86±7

77 68 70 44 84

94.0 68.0 92.0 57.0 85.5 85.0 79±16

93 93

91±4

87 87 81±13

90.0

89

89 86 91 85 89 76 88±2 83 91 88

97 95

88.5 92.5

83.5

87 9O±3

97.0 94.5 95±2.8

89.0 84.5 89±3

70 89 75

90.5 95.5 92.0

72.0 83.5 77.0

93

REMS

SWS

Stage 1 and 2

Awake

93

94 91 84

93

97 96 93 93

94±3 90 93

92

69 90 65

80

69±15

93

87 84 85

93±3

90

86 87 84±3

96

34

89 97 94 92

80

65 65

ID = patient identification; SWS = slow wave sleep; REMS = rapid eye movement sleep.

410

Influence of NoninvasMt ventilation on Spiratory Muscles (Goldstein et 81)

lJnM8isted - 0, 2l.Jnin

RC

ABO-----·-

v,

1l[

5.

FIGURE 1. Recorder tracing in a patient with kyphoscoliosis (subject 2). The channels show from top to bottom: electroencephalogram (EEG), electroocculogram (EOG), submental electromyogram (EMG), electrocardiogram (ECG), excursion of the rib cage (RC), the abdomen (ABO), and the sum (VT) and arterial saturation (SaOJ. The panel shows unassisted ventilation while receiving supplemental oxygen at 2 Umin via nasal prongs. Note that the pattern of breathing is rapid and shallow with little rib cage excursion. During REM sleep there is a further reduction in rib cage excursion associated with ~ reduction in the abdominal excursion resulting in hypoventilation to the point of central apnea.

were noted to have improved as compared with the initial measurements. However, the values recorded were clearly worse than those recorded during ventilation (1ables 3 and 4). The quality and quantity of sleep were not adversely affected by the nasal mask, although four of five patients in whom a complete night's sleep could be measured showed a reduction in slow wave sleep and an increase in REM sleep

(Table 5). All patients complied with the treatment for three months, and follow-up measurements were completed for five subjects at 14 months; the other subject (subject 6) expressed important family problems and did not present for the 14-month follow-up. Following three months of nightly ventilation, there was no ch~ge in measurements ofpulmonary function or in respiratory muscle strength (Table 1). There was,

Al8lllldRA AWAKE

EEG EOG

~~~~~~~~~~~~

~~~~~~~~~~~~

•

~

~ +J.44·J,4J,J.-J,Jrl4 i

"· ,,. ~ ,.,1

J. ~ ~ J. i ~ ~ ~4 {~~

~ ~ ~ ~ ~ ~

AC

v,

ASO------------1L[

J\J\AAAIV 51.

FIGURE 2. Recorder tracing from the same subject as in Figure 1. The subject is now breathing room air and receiving intermittent positive pressure ventilation via a nasal mask. Abbreviations are as in Figure 1 (Pvent = pressure generated by positive pressure ventilator). Note that during wakefulness, slow wave sleep, and REM sleep, tidal volume is increased as compared with that of the control night and saturation remains close to 95 percent. CHEST I 99 I 2 I FEBRUAR~

1991

411

Table 4- 7rGtIICUItJneoua CO. During Sleep at BGNUtae Unauimd, during Ventilation, and on the First p ~ Night FollotDing 11 l*eb of Nocturnal VenIiltJtion Stage 1 and 2

Awake

ID

Mean

Baseline (oxygen)

1

59

2

122

3

:s

6 Mean

~ntilation

1

2

3 4 5

6 Mean

Mean

High

62

63.5 129.0 91.5 69.5 82.5 49.0 87±26

66.5 152.0 101.0 BO.5 92.5 53.0 99±33

41 56±6*

44.0 43.5 51.5 62.0 58.5 39.5 52±8

49.0 44.5. 58.0 67.0 62.0 42.5 56±9

58 53 65

51.5 53.0 63.5

61.5 55.5 66.5

79

67 70 49 83±26 (room air) 43 45 55 52 51

lOB 54

l00±33 51 50 58 61 62

39

49±5*

Postventilation (room air)

51

1 3 4

High

148 105

96

4

48

63

SWS Mean

REMS High

68

Mean

High

69

75 151 110 77 115 57 106±31.3

69

120

92 70 88 50 88±21

137 99

139 103

99

lOB

76

51 96±27

50

52 47

48

54

47

62 62 41 54±8* 50 54

63

68

54

97±30 49 47 54 64 64

68

62 44

57±8*

56±S*

54 57 64

55 68

56

55 50 60

70 65 6O±S* 62 58 70

·Signmcantly different from baseline (p<0.05). Abbreviations as in Table 3.

plete measurements were obtained had saturation levels at or above 90 percent while breathing room air. Subject 1 did not consent to repeat ABC measurements at three months, and subject 6 was unavailable at 14 months, as stated above. Patients reported an increased sense of well-being and an increase in their ability to carry out functional activities. Four patients were able to resume work on

however, a marked increase in inspiratory muscle endurance at three months that was maintained at 14 months. Inspiratory muscle endurance was measured at the same mean mouth pressure expressed as a percentage of MIP at baseline and at three and 14 months after nocturnal ventilation. Daytime ABC values improved at three and 14 months (Table 6). At 14 months, three of the four subjects in whom com-

Table 5-QualiIv mtd Quantity of Sleep at Btaeline, during Ventilation, mtd on the Fint PoBtventilatory Night Following 12 weeb o/Nocturnal VenIiltJtion

ID Baseline

1

2

3 4

5 ~

Mean Ventilation

1

2

3 4 5 6 Mean

Total Thne Asleep, (min)

min

SWS

REMS

189 105 179 241

7 19 63

145 157±69

74 212 127 67 150 55 126±60

32 58 3O±21

2m

259 162 195 183 61

68 78 112 67 109

59 142 92 35

333±90

172±72

87±22

73±45*

336 390 440

146 169

101

272 337 370 337 250 258 313±50 366 302 450 343

Postventilation

1 3 4

Stages

1 and 2.

69

294

98

16

28

38

88

121

84

Sleep Efficiency

70 85 96 77 65 70 79±12 76

Movement

Arousals.

per Hour 20

7 26 19 13 7 17±7 25

78 66

23 8 18 2

77±11

15±10

88

13 31 21

69 95

83 91

·Significantly different from baseline (p<0.05).

412

InIk.Ba of Not...... YenIIation on SpIndory Mu8cIe8 (GoldsteIn at aI)

Table 6-lradicidual ArteritJl Blood GGI Value. Meaaured Vraaaiated, Recumbent, and Breathing Boom Air at &aeUne, Three MontIaa, and 14 Mont'" After Noctumal Ventilation by Intermittent PoaiOOe Preaure Through NtllltiLMaalc Subject Baseline 1 2 3 4 5 6 3mo 1 2

3 4 5

6

14mo 1 2 3 4 5

Pcol , mmHg

POI' mmHg

Saturation,

pH

7.44 7.44 7.28 7.42 7.40 7.43

47 66 81 54 64 50

36 28 42 60 45 50

73 57 66 90 81 85

7.38 7.35 7.36 7.41 7.46

48 49 56 56 42

56 73 58 51 57

87 92 87 85 90

7.41 7.37 7.37 7.35 7.38

39 55 46 60 58

65

92 85

53 82 65

56

%

96 90 87

6

a full-time basis and two resumed their full-time household activities. None of the subjects has been readmitted to hospital for respiratory failure and all have discontinued treatment with diuretic medications. There was an improvement in their six-minute walking test (mean ± SD initial test =: 429 ± 120 m; three months = 567 ± 121 m; 14 months = 569 ± 83 m). Measurements at three months were significantly different from baseline (p<0.05). DISCUSSION

Long-term nocturnal mechanical ventilation in pa-' tients with restrictive respiratory failure will prevent the nocturnal worsening of their gas exchange and improve their daytime ABG values. Intermittent positive pressure breathing through a closely fitting nasal mask is an effective way to assist ventilation among this population. Despite the mask and associated straps, the quantity and distribution of sleep in our experience is no worse than that measured on the initial night prior to ventilation. The mechanism by which this clinical improvement occurs remains unclear. Rochester et al 14 measured a significant reduction in diaphragmatic and accessory muscle EMG activity when patients were ventilated with a negative pressure device. Given that most patients have either a marked increase in their work of breathing, weakness of the respiratory muscles, or a combination of both,14.22.23 they reasoned that the beneficial effects of ventilation are mediated, in part,

by a reduction in inspiratory muscle work, thus improving the daytime function of the inspiratory muscles and contributing to the observed clinical improvement. Carrey et al lO investigated the effects of positive pressure ventilation on inspiratory muscle activity in three normal subjects, four patients with restrictive ventilatory failure, and five patients with obstructive ventilatory failure. During ventilation, phasic diaphragmatic EMG amplitude decreased to below 10 percent of control measurements in each group. These reductions in inspiratory muscle activity were associated with positive intrathoracic pressure swings on inspiration in all subjects. Therefore, Carrey et al reasoned that nocturnal ventilation should improve daytime inspiratory muscle performance. Howev~r, few studies have measured inspiratory muscle function. Marino and Braun15 used negative or positive pressure ventilation in 35 patients, some of whom had par~nchymal disease, and observed an improvement in their respiratory muscle strength (RMS) and their maximal voluntary ventilation. Ellis et al7 reported an improvement in RMS in four oftheir subjects receiving positive pressure ventilation. We therefore explored the influence of IPPV on RMS and inspiratory muscle endurance. The RMS did not change among our subjects (Table 2) despite repeated measurements at regular intervals, nor did we observe changes in lung volumes except in one patient (idiopathic neuromuscular disease) in whom the inspiratory capacity increased from 0.6 to 1 L. These findings are consistent with our previous worJc9 in which neither standard measurements oflung function nor RMS changed following two months of nocturnal negative pressure ventilation. They are, however, at variance with the increases in MIP observed by Marino and Braun15 (MIP - 28 ± - 17 em H 20 to - 45 ± - 23 cm H 20) follOwing ventilatory support for several hours each day. Our findings are also at variance with those reported by Ellis et al7 in patients with kyphoscoliosis. After three months of nocturnal ventilation, one patient had a fourfold improvement in MIP with no c~ge in VC and another had a threefold improvement with a 20 percent increase in VC. We measured inspiratory muscle endurance against a pressure threshold load, a method originally described by Nickerson and Keens 16 and subsequently used to measure endurance among healthy elderly subjects and patients with chronic obstructive pulmonary disease (COPD) undergoing inspiratory muscle endurance training.17.18 We set the pressure threshold load constant at 45 percent MIPRv (55 percent MIPFRc) and measured endurance time. We have previously reported the magnitude of variability of this test to be ± 1.26 minutes}9 Thus, the improvement that we observed from an initial endurance time CHEST 199 I 2 I

FEBRU~

1991

413

of 7 minutes to 13 minutes at three months and 17 minutes at 14 months likely reHects a real improvement of inspiratory muscle function. It may be of interest that patients with COPD in a randomized controlled six-week trial of inspiratory muscle endurance training sustained an improvement of similar magnitude (approximately seven minutes).19 One might therefore speculate that inspiratory muscle endurance could be further increased with a combination of rest and exercise, but to our knowledge, possible clinical benefits of such an approach have not been evaluated. 14 Although it is conceivable that the inspiratory muscles recovered from a state of chronic fatigue, we have not provided conclusive evidence ofthe existence of such fatigue. It is possible that the inspiratory muscles benefited from the improvement in Sa02 and pH that resulted from the improved nocturnal gas exchange (Thbles 3 and 4).25.96 In addition to the beneficial effects ofrest and better gases on inspiratory muscle function, nocturnal mechanical ventilation may reduce the daytime work of breathing by preventing peripheral atelectasis and the consequent decrease in lung compliance. 22 Another consequence of improved nocturnal gas values may be a resetting of central control to increase chemosensitivity and a reduction in body bicarbonate pool. Such changes are difficult to measure and in three ofour subjects, we found both the peripheral!7 and the central18 chemoreHexes to remain well below the normal range at 14 months despite the improvement in daytime ABG values. A single case report:J9 in a patient with central alveolar hypoventilation treated with nocturnal ventilation showed that the hypercapnic response returned to normal after ten days of ventilation and the hypoxic response returned to normal after three months. Clearly, the interactions between changes in central control, lung compliance, and inspiratory muscle endurance require further study. By the third week of hospital admission when nocturnal mechanical ventilation was well established, the subjects were able to participate in a supervised exercise rehabilitation program. Thus, the improvement in exercise tolerance was likely inHuenced by both the nocturnal ventilatory support and the daytime exercises.. Although these patients had been initially referred for respiratory rehabilitation, they were too clinically unstable with refractory cor pulmonale, chronic fatigue, and daytime somnolence to participate in the rehabilitation program. Nocturnal ventilatory support was critical in maximizing their exercise tolerance and sense of well-being. In conclusion, patients with restrictive ventilatory failure may be adequately ventilated noninvasively with a closely fitting customized nasal mask attached to a positive pressure ventilator. Nocturnal gas ex414

change, daytime function, and daytime ABG values improved. This improvement was associated with an improvement in inspiratory muscle endurance three months after nocturnal ventilation that was sustained at 14 months. Four of the six subjects returned to £011time employment and two subjects resumed their household responsibilities on a full-time basis. ACKNOWLEDGMENT: This study was supported by a grant from The Physicians Services Incolp)rated Foundation. The authors acknowledge, with appreciation, the technical support provided by J. Popkin and R. Rutherford in carrying out the sleep studies. The authors acknowledge the assistance of D. Mills in preparing this manuscript.

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17 Clanton TL t Dixon G t Drake Jt Gadek JE. Inspiratory muscle conditioning using a threshold loading device. Chest 1985;

87:62-6 18 Larsen JL t Kim MJt Sharp fTt Larsen DA. Inspiratory muscle training with a pressure threshold breathing device iD--pdie1ltI with chronic obstructive pulmonary disease. Am Rev Respir Dis 1988; 138:689-96 19 Goldstein Rt De Rosie Jt Long St Dolmage Tt Avendano MA. Applicability of a threshold loading device for inspiratory muscle testing and training in patients with COPD. Chest 1989; 96:56471 20 Mungall IPFt Hainsworth R. Assessment of respiratory function in patients with chronic obstructive airways disease. Thorax 1979; 134:254-58 21 RechtschafFen At Kales At eds. A manual of standardized terminology, techniques and scoring system for sleep states of human subjects. Bethesdat Md: National Institutes of Healtht 1968 t NIH publication 204 22 Bergofsky EH. Respiratory failure in disorders of the thoracic cage. Am Rev Bespir Dis 1979; 119:643-69 23 Braun NMTt Arora NS t &chester DF. Respiratory muscle and

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Pediatric Lung Disease Conference The Nemours Children's Clinic, Jacksonville, Florida, will present this conference in St. Petersburg, April 19-21. Contact: Paul ICehrli, Nemours Children's Clinic, PO Box 5485, Jacksonville 32247-5485 (904: 390-3638).

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