1228 TTO, Nasal CPAP and Nasal 02 in OSA (Famey et a!)

Transtracheal Oxygen, Nasal CPAP andNasal Oxygen in Five Patients withObstructive Sleep Apnea*Robertj Farney, M.D., F.C.C.P;James M. Walker, Ph.D.;

Jeffrey C. Elmer, M.D., F.C.C.P; VincentA. V�scomi, M.D., FC.C.P;

and R. Jon Ord, M.D.

The effect oftranstracheal oxygen administration by meansof a 9-French (2.7 mm) percutaneous catheter was assessed

in five patients with severe obstructive sleep apnea. Wehypothesized that the delivery of oxygen below the site ofairway obstruction should reduce the arterial oxygen de-saturation during apneas and hypopneas, thereby increas-ing respiratory stability. Standard sleep and respiratory

measurements were recorded in these subjects with all-night polysomnography on nonconsecutive nights during

four experimental conditions: room air (BL), nasal contin-uous positive airway pressure (CPAP), nasal 0 (NC Os),

and transtracheal O� (TT Os). In three of these subjects,room air was infused (TT BA) at flow rates comparable toTT 0,. Compared with baseline room air measurements,

TT 0, not only significantly increased the SaO nadir from70.4 percent to 89.7 percent (p<O.Ol), but it also reducedthe frequency of sleep apnea/hypopnea from 64.6 to26.2/h sleep (p<O.Ol). NC O� ameliorated desaturation

during apnea/hypopnea (mean SaO, nadir, 86.2 percent;

p<.o1) but did not significantly alter frequency (59.0/h

sleep). Nasal CPAP was the most effective means of reducing

sleep apnea/hypopnea (13.8/h sleep) but did not abolish

desaturations when apneas occurred (mean Sa05 nadir,80.0 percent). Compared with oxygen, transtracheal infu-

sion of room air appeared to be somewhat effective;

however, the small number ofstudies with TT BA precludedstatistical analysis. We believe that TT O� is superior to NC02 for some patients with obstructive sleep apnea becausecontinuous oxygen flow below the site of airway obstruction

more reliably prevents alveolar hypoxia and respiration isstabilized. Infusion of air or oxygen through the trachealcatheter flow may also increase mean airway pressure andreduce obstructive apnea similar to nasal CPAP. We con-dude that TT O� may be an effective alternative mode oftherapy for some patients with severe sleep apnea/hypopnea

when nasal CPAP is not tolerated or when combined oxygen

and nasal CPAP are required. (Chest 1992; 1O1:122&35)

BLbaseline on room air; etCO,end tidal CO ; NC O,oxygen given via nasal cannula; NREMnonrapiJ eye move-ment; TSTtotal sleep time; TT O,transtracheal oxygen;TT RA= room air administered through catheter

T he purpose ofthis study was to evaluate the efficacy

of transtracheal oxygen (TT O�a) in patients with

severe obstructive sleep apnea. Although therapy with

nasal continuous positive airway pressure (CPAP) is

highly effective in the majority of these patients, the

combined immediate and long-term failure rate meas-

ures 25 to 40 percent.”2 Accordingly, some patients

may receive a tracheostomy or simply oxygen via nasal

cannula. While previous studies have demonstrated

that supplemental oxygen given by either face mask

or nasal cannula (NC O��) attenuates the magnitude of

oxygen desaturation, there is generally only a modest

reduction in apnea frequency.� In addition, some

patients require continuous oxygen therapy as well as

CPAP during sleep. To our knowledge, the frequency

of combined therapy has not been reported, but it is

*From the Intermountain Sleep Disorders Center, LDS Hospital,

and Department of Medicine, University of Utah and Salt LakeClinic, Salt Lake City.Supported in part by a grant from the Deseret Foundation, LDSHospital, Salt Lake City.These data were presented in part at the Annual Meeting,American Thoracic Society, May 10, 1988.

Manuscript received June 3; revision accepted September 3.Reprint requests: Dt� I�zrney, LDS Hospital, Sleep Lab, Salt LakeCity 84143

clear that oxygen plus CPAP is not only more complex

but also more expensive.

We were interested in assessing the short-term

effects of administration of oxygen below the site of

airway obstruction by means of a 9-French (2.7 mm)

transtracheal catheter (TT 02) that was recently de-veloped for patients with chronic lung disease.� We

hypothesized that alveolar hypoxia would be prevented

during apnea ifthe catheter flow rate exceeded oxygen

consumption. Although ventilation/perfusion mis-

matching and increased venous admixture may accom-

pany obstructive apneas, increasing the alveolar Po2

should ameliorate arterial hypoxemia, stabilize respi-

ratory control, and reduce the frequency of apnea.�”

Consequently, both the time spent apneic and hypoxic

would be reduced.

Using all-night polysomnography, we compared TT

02 with nasal CPAP and NC 02 in its ability to reduce

oxygen desaturations and obstructive apnea. In some

ofthese patients, we also measured the effects of room

air administered through the catheter (FT RA) since

infusion of gas beneath the site of airway obstruction

could increase the airway pressure and exert a similar

effect as CPAP. We report herein the first study in

which these three modalities and room air have been

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Table 1-Study Population

CHEST I 101 I 5 I MAY, 1992 1229

Patient/Sex/Age, yr

Height,

cm

\�ight,

kg

PaO,,

mm HgSaO,,

%

HB,

g/dlPaCO2,

mm Hg pH SAHI

Additional

Diagnoses

1/Fi�l0 157 106 90 14 � 37 7.47 35

21M157 183 135 62 93 17 31 7.50 50 CB

a’M/48 183 147 71 93 15 40 7.41 74 CB

431/47 167 116 58 88 16 43 7.43 78

5fM/37 188 206 49 82 15 45 7.43 86

*SAHI = sleep apnea plus hypopnea index competed as total apneas and hypopneas/total sleep time in hours; CB chronic bronchitis

compared in sleep apnea patients with polysomnog-

raphy using one therapeutic condition across the night.

Rd� Ib�on

METHODS

Five patients with severe obstructive sleep apnea were selected

to participate in this study because they were either noncompliantwith nasal CPAP or also required supplemental oxygen 24 K/day.

All had been previously tested by means of all-night polysomnog-

raphy with and without nasal CPAP The anthropometric and

baseline arterial blood gas data for the patient population arepresented in Thble 1. Male subjects predominated (4’S) and two

subjects had chronic bronchitis secondary to cigarette smoking.

Study Protocol

The research protocol was approved by the Institutional ReviewBoard and informed consent was Obtained. Following selection from

patients with previously documented sleep apnea, subjects wererestudied with polysomnography on nonconsecutive nights using

the following experimental conditions: baseline on room air (BL),

nasal CPA1� NC 0, TT 0,,, and Tf BA (three patients only). The

sequence oftests, intervals between studies, and ultimate therapeu-tic levels used in each case are shown in lhble 2. An unusually long

interval occurred in one subject (No. 3) who had been tested onCPAP three months before his repeated baseline polysomnogram.

This person� testing was delayed because he temporarily movedout of state. Not only was he completely intolerant of nasal CPAP,

but he also had severe sleep apnea on baseline testing subsequent

to the CPAP trial (sleep apnea plus hypopnea index 74/h sleep).A transtrachealeatheter(SCOOP)was placed using the technique

described by Christopher et al. Ifpossible, one week was allowed

for the subjects to become accommodated to the catheter beforerestudying with TT O�. Since experimental data were also beingused for clinical decision making, maximal levels ofnasal CPAP andoxygen were arbitrarily set that would be practical to continue afterthe study. Nasal CPAP was adjusted in approximate increments of

2.5 cm H,O pressure up to a maximum of 15 cm H,O. Oxygen flow

rates were adjusted in approximate increments of 1 IJmin using a

pediatric flowmeter up to a total flow of 6 IJmin. Oxygen or nasal

CPAP was titrated as quickly as possible, generally within the first

hour following the initiation ofsleep to a target Sa02 of9O percent,

after which therapeutic levels remained constant. If desaturationsdeveloped after the initial titration period, fur example, with rapid

eye movement (REM) sleep, no changes in therapy were made so

that the experimental condition would remain constant throughout

the night.

In our laboratory, independent simultaneous recording of the

SaO, at slow paper speed (20 cm/li) has been a convenient method

of titrating CPAP When respiratory disturbances occur at our

elevation, desaturations or oscillations of the SaC), almost alwaysresult.”The Sa02 pattern thereby provides a reproducible endpointthat may be less subject to observer error and artifactual changes

compared with the detection of hypopneas, for example. Further-

more, since a major therapeutic objective was to maintain the Sa01

at a physiologic level, the SaC)1 of9O percent was chosen as the end

point (for both CPAP and 0,, trials). Consequently, therapy was not

specifically adjusted to eradicate apneas and hypopneas. In three

subjects, room air (IT BA) was administered through the catheter

and compared with TT 0, at identical flow rates (3 L/min). Patient

5, who was restudied seven months after his original TT O� test,

underwent a second night of testing with TT 0, with a resultantdecrease in his 0, requirements to 3 Iimin.

Sleep and Respiratonj Measurements

Fblysomnographic recordings included standard placements forcontinuous monitoring of central and occipital electroencephalo-

gram (C3/C4 and 0IA�2), horizontal electro-oculogram, and sub-mental and anterior tibialis electromyogram. Mrflow at the nose

and mouth was sensed by measurement of end tidal CO2 (etCO,)

(Biochem MicroSpan Capnograph). Qualitative tidal volume (VT),

thoracic excursion, and abdominal excursion were recorded by

inductive plethysmography (Bespigraph). Qualitative diagnostic

Table 2-Sequence ofPolysomnography and 7�eatment Conditions

Case Study 1 Interval Study 2 Interval Study 3 Interval Study 4 Interval Study 5 Interval Study 6

1 CPAP 6 days BL 2 days NC O� 2 mo TT O� . . . . . . . . . ...

10 cm 1 Iimin 1 L/min

2 NC 0 5 days CPAP 1 day BL 34 days �VF 0, . . . . . . . . . ...

5IJmin 10cm 3IJmin

3 CPAP 3 mo BL 7 days NC 0, 1 day TT 0, 6 days TT RA . . . ...

15cm 6L/min 3L/min 3L/min

4 BL 2 days NC O�

2.5 IJmin

3 days CPAP

15 cm

26 days TT 0,

2 L/min

9 mo TT O�

3 IJmin

37 days ‘FT BA

3 IJmin

5 BL 7 days NC 02

6 L/min

7 days CPAP

15 cm

6 days TT 0,

6 Iimin

7 mo TT 0,

3 Llmin

8 days TT BA

3 L/min

*BL = baseline polysomnography; CPAP nasal continuous positive airway pressure; numbers underneath define final level of pressure in cm

H,O; NC O,nasal cannula oxygen; numbers underneath refer to final oxygen flow; TT O�’ transtracheal oxygen; numbers underneathrefer to final oxygen flow; TT RA=transtracheal room air; numbers underneath refer to flow ofroom air through transtracheal catheter.

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Table 4-Means and Standard Deviations ofLength (a) and Arterial Oxygen Desaturation (Percent)for Apneasand Hypopneaa across All Conditions�

Baseline NC 0, CPAP TT 0,

Length, sCentral apnea 16.9± 10.1 19.6± 13.3 12.1 ±3.1 23,0±23.0Obstructive apnea 27.6± 10.6 28.6± 10.9 24.9± 14.0 28.9± 13.3

Hypopnea 20.8±11.9 28.2±13.0�! 12.8±3,9!E 26.2±13.8

Apneas and hypopneas 26.1 ± 10.6 28.9± 10.8 21.9± 13.8 26.3± 13.5

Mean nadir desaturation, %Centralapnea 69.7±21.8”� 85.0±14.5 81.4±12.5 89.4±5.7

Obstructive apnea 69.4 ± 12.2�1i!i 85.5 ± 5.9 77�3 ± 16.9 89.2 ± 5.0

Hypopnea 72.0±13.3�E�!�i 87.9±4.4 86.7±9,1 90.2±4.0

Apneasandhypopneas 70.4±12.3�9�i! 86.2±5.6 80.0±12.9� 89.7±4.6

from baseline p<O.05 and p<O.Ol, respectively; ‘��differs from NC 0, p<O.05 and p<O.Ol, respectively; cP.�djffers

from nasal CPAP p<O.05 and p<O.Ol, respectively; �‘!Zdiffers from iT 0, p<O.05 and p<O.Ol, respectively.

Table 3-Means and Standard Deviationsfor Apnea and Hypopnea Indices across All Conditions�

1230 1-To. Nasal CPAP and Nasal 0, in OSA (Famey et a!)

Baseline NCO2 CPAP TTO,

NREM

Central apnea 1.3± 2.8 1.4± 2.0 2.1 ±2.9 0.0±0.0

Obstructive apnea 36.0± 19.7�!�i 40.7± 15.7E!!i 1.3 ± 1.9 5.88±8.1

Hypopnea 27.9±20.7 19.5± 19.0 25±3.8� 20.6± 18.8

Apneas and hypopneas 65.3±21.4�!i� 61.6± 10.7�!�i 5.9±5.6� 26.6±22.8

REM

Central apnea 7.7± 12.4 8.9± 13.9 10.0± 17.6 2.5± 3.3

Obstructiveapnea 35.4±20.9� 33.7±26.0� 11.3±10.5 4.4±4,0

Hypopnea 21.2±18.7 6.2±5.5 9.1±18.6 16.6±14.3

Apneas and hypopneas 64.4 ± 29,6�”� 48.8 ± 20.3 30.3 ± 17.6 23.5 ± 13.2

Total sleep time

Centralapnea 2.1±4.0 2.3±2,7 3.8±5.8 0.4±0.4

Obstructive apnea 35.7± 18,6�i 39.0± 15.&!�i 4.1 ±3.9 5.7±7.5

Hypopnea 26.7±20.5 17.7±17.3 6.0±11.0 20,1±16.9

Apneas and hypopneas 64.5 ± 21.5E�i 59.0± 11.3E!�LE 13.8 ± 10.0 26.2 ± 20.7

*BLRLd�ffe� from baseline p<O.05 and p<O.Ol, respectively; Nc.��Ijff�� from NC 02 p<O.05 and p<0.Ol, respectively; �

from nasal CPAP p<O.05 and p<O.Ol, respectively; “�i=differs from TT 02 p<O.05 and p<O.Ol, respectively.

calibration was performed according to the manufacturer’s specifi-

cations. Continuous arterial oxygen saturation was obtained by

finger oximetry (Ohmeda 3700). All variables, including the electro-

cardiogram, were recorded on a 12-channel polysomnograph (Ni-

hon-Kohdon). Subjects were studied in the Intermountain Sleep

Disorders Center at LDS Hospital, Salt Lake City, Utah, at an

elevation of 1 ,400 m.

Data Analysis

Using standard criteria,’3’4 records were analyzed manually for

sleep stages and respiratory events without knowledge of treatment

condition. Apneas were defined by an 80 to 100 percent reduction

in the airflow signal (etCO,) compared with baseline, whereas

hypopneas were defined as a 50 to 80 percent reduction. The

occurrence and duration of respiratory events were corroborated

by concurrent changes in VT. However, arterial oxygen desaturationswere not required to define an apnea or hypopnea since desatura-

tions were attenuated by oxygen administration. Almost all apneas

and hypopneas were terminated by briefelectrophysiologic arousals.

By definition, all apneas and hypopneas lasted at least 10 s.

Obstructive apneas were indicated by the presence of respiratory

effort or paradoxic thoracic-abdominal motion while central events

were defined by the absence of any apparent respiratory effort. If

there were both central and obstructive components to a respiratory

event, an event was defined as mixed. Since there were few pure

obstructive apneas for meaningful analysis and since there is no

evidence that mixed and obstructive apneas have unique patho-

physiologic mechanisms or clinical consequences, mixed and ob-

structive apneas were grouped together as obstructive. Hypopneas

were not differentiated as obstructive or central. The frequencies

for apneas and hypopneas were defined for nonrapid eye movement

(NREM), rapid eye movement (REM), and total sleep time (TST).

The sleep apnea index was computed as the total of all apneas

divided by TST in hours. The sleep hypopnea index and the sleep

apnea/hypopnea index were computed similarly.

Data obtained during the initial oxygen or CPAP titration period

were excluded from the analysis. Means and standard deviations

were determined on the following parameters: apnea index, hypo-

pnea index, apnea/hypopnea index, SaO, nadir during respiratory

events, duration of apneas and hypopneas, TST, sleep efficiency

(TST/total recording time X 100), electrophysiologic arousals perhour of sleep, number of awakenings, percentage of stage REM,

and percentage of stage 1 to 4 NREM sleep. One-way analysis of

variance with repeated measurements was performed on the data.

When a significant F test was obtained, a Duncan’s multiple range

test was used to compare specific means. Statistical comparisons

were not performed on TT BA data because of the small number of

subjects.

REs ULTS

There were no procedure-related complications in

these subjects such as hemorrhage, subcutaneous

emphysema, pneumothorax, or infection. When the

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Table 5-individual Valuesfor Apneas, Hypopneas, and Sa05 Nadir across All Conditions�

CHEST I 101 I 5 I MAY, 1992 1231

Baseline NC� 0, CPAP TTO,

Case No. Al HI

SaO,

Nadir, % Al � HI � �

SaO,

Nadir, % Al HI

SaO,

Nadir, % Al HI

SaO,

Nadir, %

1

2

3

4

5

Mean

SD

34.513.5

51.1

23.2

66.9

37.8

±21.4

0.0

36.423.3

55.0

19.0

26.7

±20.5

86.2

73.2

73.7

66.4

52.6

70.4

±12.3

37.3

36.5

54.2

22.9

55.7

41.3

±13.7

9.3

11.6

7.0

48.5

12.2

17.7

±17.3

92.5

90.5

84.5

85.1

78.3

86.2

±5.6

1.9

8.6

2.2

11.2

15.3

7.8±5.9

0.0

0.0

25.3

0.0

4.5

6.0

±11.0

86.8

87.1

92.7

71.9

61.6

80.0±12.9

0.7

4.0

19.1

2.6

4.3

6.1

±7.4

4.1

17.9

30.8

43.1

4.6

20.1

±16.9

94.389.1

93.0

89.5

82.6

89.7

±4.6

*AI = apnea index computed as total apneas/total sleep time in hours; HI hypopnea index computed as total hypopneas/total sleep time in

hours.

study was completed, all patients elected to continue

using TT 02 rather than use alternative therapies.

Objective studies to assess the state of daytime sleep-

mess were not performed in this study. However,

subsequent clinical interviews revealed that these

subjects felt more alert and snoring was reportedly

diminished with TT 02.

Respiratory Parameters

The results of standard respiratory parameters are

shown in Tables 3 through 5.

Arterial Oxygen Saturation: Compared with room

air breathing, all treatment conditions improved SaO2.

With TT 02, the Sa02 was almost always maintained

at about 90 percent with oximetric patterns suggesting

respiratory 12 Oxygen therapy via nasal can-

nula also increased the SaO2 level, but respiratory

instability was evident by persistent fluctuations. The

Sa02 desaturation during NC 02 was greater than with

TT 02 but did not reach statistical significance.

Although the Sa02 was usually maintained near 90

percent with CPAP, respiratory disturbances, partic-

ularly during REM sleep, resulted in substantial

desaturations (mean Sa02 nadir during REM sleep,

78.5 percent, and during NREM sleep, 83.7 percent).

Representative recordings of the SaO2 from patient

5 are shown in Figure 1 . This subject presented with

typical symptoms of extremely loud snoring and ex-

cessive sleepiness associated with marked peripheral

edema, obesity, and alveolar hypoventilation. While

breathing room air, the apnea/hypopnea index meas-

ured 85.9/h Sleep and the mean oxygen desaturation

was 52.6 percent. Treatment with nasal CPAP reduced

the frequency of respiratory disturbances effectively

but due to baseline hypoxia, the oxygen saturation

was not adequately corrected (mean nadir, 61.6 per-

cent). Oxygen via nasal cannula resulted in a substan-

tial increase in SaO2 but there were still frequent

apneas, hypopneas, and arterial oxygen desaturations.

Transtracheal oxygen not only reduced the frequency

ofall respiratory events but also provided a satisfactory

SaO2. Paired transtracheal oxygen and room air studies

were performed seven months following the initial

studies (Fig 1 through 3).

ApnealHypopnea Frequency: Table 5 shows the

individual data for each patient. The frequency of

apneas and hypopneas was most effectively reduced

by means ofCPAP (apnea/hypopnea index 13.8/h sleep

vs baseline of64.6/h sleep) while the effects ofTT 02

were more variable. Despite the stable appearance by

oximetry, moderately frequent hypopneas were pres-

ent with TT 02 in some patients (hypopnea index

20. L/h sleep). However, the effect of TT 02 on apnea

index (6. lj’h sleep) was equivalent to CPAP Although

there was a trend, the apnea/hypopnea index was not

significantly reduced with NC 02 compared with room

air.

We have considered the possibility that the treat-

Table 6-Means and Standard Deviationafor Sleep %hriables across All COndItIOnS

Baseline NC 0, CPAP TT 0,

Total sleep time, h 6.7±0.8 6.8±0.6 5.6± 1.4 6.8±0.9

Stage 1 NREM, % 20.4± 12.3 10.9±6.0� 13.6±5.P’ 11.1 ±3.9�Stage 2 NREM, % 64.6±7.2 74.6±8.1 48.8± 19.6B���Ei� 72.6±3.2

Stage 3 and 4 NREM, % 0.5±0.6 0.3±0.5 8.9± � 1.8±2.6

REM, % 15.1±6.0 14.5±4.8 29.2±10.8��’� 14.9±4.7Sleepeffidenc�� % 88.6±6.2 90.7±5.8 84.9±12.0 90.4±7.5

Arousal index, 74.0±46.1 53.5±29.9 21.9±9.4!!� 41.5±28.P’-

events/h

*BLBL�jff�� from baseline p<O.05 and p<O.Ol, respectively; � differs from NC 0, p<O.05 and p<O.Ol, respectively; �!i=differs

from U 0, p<O.OS and p<O.Ol, respectively.

Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21644/ on 06/03/2017

60

40�

66.9 85.9

80

60

40

I00

::T�T�0�frf�r :�5.5 20.0 40

100 N-CPAP(I5cm)

� 00

80

60

40

� 00

80

60

40#{149}

55.7 67.9

80

60

40

80

60

40

SAl SAHI

4.3 8.9

- 100

. 80

- 60

- 40

80

60

40

SAl

I 4.2

SAHI

49.5

l00

80

60

40

I00

80

60

40

SAl SAHI

3.9 0.7

I I I I I I I I

2 3 4

TIME (hours)

FIGURE 1. Oximetric recordings from patient 5. The SaO, recorded from the second to fourth hour of eachexperimental condition are shown. The more severe desaturations in each panel are related to REM sleep.

PATIENT 5 00

1232 1-To. Nasal CPAP and Nasal O� k� OSA (Fameyetal)

2

0

I-

(I,

2

u-i>-

0

ment conditions may have led to artifactual changes

in respiratory scoring. However, the concordance

between measurements of etCO2, VT, chest wall

excursion, and abdominal excursion in association with

electrophysiologic arousals at the termination of res-

piratory events indicates that their frequency and

duration were not underestimated. Note that the

changes in the arousal index paralleled changes in

apnea plus hypopnea index (Tables 3 and 6).

Duration of Apnea/Hypopnea: None of the treat-

ments resulted in a significant increase in duration of

apnea compared with the baseline room air condition.

However, there was a significant difference in the

hypopnea duration (p’(0.01) between the CPAP and

02 conditions as a result of decreased duration during

CPAP.

Transtracheal Room Air Studies: The effects of

administering room air via the transtracheal catheter

on apneas, hypopneas, and oxygen desaturation are

shown in Figures 2 and 3. Since apneas and hypopneas

did not result in consistent differences in desaturation,

mean SaO2 values for all respiratory events are plotted.

Compared with baseline studies, TT BA resulted in a

slight increase in the Sa02 nadir and a mild reduction

in frequency of apneas and hypopneas (apnea plus

hypopnea index: BL, 79.5; TT BA, 66.7; TT 02, 39.9).In one case (No. 5), the apnea index was markedly

decreased with TT BA but there were frequent

hypopneas associated with substantial oxygen desatu-

rations (Figs 1 through 3). In two subjects, frequent

hypopneas were also observed with TT 02, but the

overall Sa02 was about 90 percent (mean nadir, 88.7

percent).

Sleep Variables: Table 6 shows means and SDs for

standard sleep parameters across experimental con-

ditions. In general, sleep architecture was more nor-

mal during CPAP The percentage of REM and stage

3/4 sleep increased, whereas the percentage of stage 2

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APNEA + HYPOPNEA INDEX

-----APNEA INDEX

5

43

5”

3a�----��

0�UiUi-JU)

=

U)I-.zUi>Ui

0I-

a.U)Ui

00-

90

80

70

60

50

40

30

20

0

0-

4 �

BASELINE TTRA

STUDY CONDITIONS

3

4

5

90-

c,%J0c� 80-

z

2 70-F-.�

� 60-

U)

� 50-

0 40--i

tr 30-UiI-

I I I

BASELINE TTRA ITO2

STUDY CONDITIONS

Ficuax 3. Mean Sa02 nadir during apneas and hypopneas of three

subjects while receiving either room air or oxygen via transtrachealcatheter at comparable flow rates.

CHEST/lOl /5/MAY, 1992 1233

Ficuns 2. Apnea and hypopnea indices of three subjects while

receiving either room air or oxygen via transtracheal catheter at

comparable flow rates. Subjects 4 and 5 were tested nine and seven

months, respectively, after their original evaluations.

NREM sleep decreased in the CPAP condition as

compared with other conditions. There was a corre-

spondence between the effectiveness of respiratory

therapy and changes in sleep parameters. The number

of arousals decreased significantly with both CPAP

and TT 02 administration as compared with the

baseline study. Treatment with TT 02 resulted in the

next greatest reduction in apnea plus hypopnea index

to 26.2 (± 20.7) with a corresponding reduction in the

arousal index to 41 .5(± 28. 1). Treatment with NC 02

had the least impact on both respiratory parameters

and frequency of arousals. Stage 1 NREM sleep was

reduced (p<O.05) in all treatment modalities. There

were no significant increases in sleep efficiency be-

tween baseline and treatment conditions, possibly due

to the relatively high sleep efficiency (88.6 percent)

on the baseline condition.

DIScUSsIoN

The most important observation from this study is

that transtracheal oxygen maintained a physiologically

adequate Sa02 and reduced the frequency of sleep-

disordered breathing in these patients with severe

sleep apnea. In this study, a pragmatic end point (SaO2

of 90 percent) was selected because of previous

experience.’2 Greater reductions in apnea and hypo-

pnea frequency may have been demonstrated if the

measurement of airflow, tidal volume signal, and/or

electrophysiologic arousals had been used. Our results

are consistent with other more limited studies showing

marked reductions in the apnea/hypopnea index with

TT 02 � Because TT 02 was effective

and well tolerated, the need for tracheostomy was

eliminated. Oxygen via nasal cannula was found to be

the least effective form oftherapy in the present study.

As expected, the frequency of periodic breathing was

most effectively reduced by CPAP. Except when there

was significant hypoxia during wakefulness, CPAP also

resulted in desirable SaO2 levels.

One of the most intriguing questions raised by this

study concerns the mechanism of TT 02 on reducing

respiratory instability, and in particular the s!et�p

apnea index. In some cases, the reduction in bothapneas and hypopneas was dramatic (Fig 1). In other

cases, there were residual respiratory events that were

predominantly hypopneas but without significant de-

saturation. Thus, even when respiratory disturbipces

were not completely eliminated by TT 02, the more

severe grades of obstruction appear to have been

reduced which ameliorated oxygen desaturation.TI 02 Information concerning the effect of either nasal or

transtracheal oxygen therapy in patients with sleep

apnea is ljmjted.3-5,15-’7 Various mechanisms have been

proposed for the salutary effect ofoxygen on eliminat.

ing or reducing periodic breathing#{176}”#{176}that include the

following: (1) a direct stimulation ofthe central nervous

system; (2) reduction of upper airway resistance; and

(3) stabilization of chemical feedback by reduction of

peripheral chemoreceptor activity. According to mod-

els of the respiratory control system that incorporate

negative feedback, ventilatory instability is directly

I00-,

20-

10-

0-

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1234 TTO, Nasal CPAP and Nasal 02 in OSA (Fameyetal)

correlated with hypoxia, hypercapnia, reduced lung

02 and CO2 storage volumes, and increased gain of

the peripheral chemoreceptors.”

An additional mechanism may be operative with TT

02. As a result of continuous oxygen flow through the

catheter, an increase in the mean airway pressure

might develop sufficient to maintain airway patency

similar to the effect of nasal CPAP Increased airway

pressure may also increase functional residual capacity,

which has been shown to enlarge pharyngeal cross-

sectional area in patients with obstructive sleep ap-

18 Transtracheal room air at comparable flow rates

to TT 02 resulted in slight improvement in both apnea/

hypopnea index and Sa02 nadir compared with base-

line data. The transtracheal room air studies were

interesting but unfortunately inconclusive because of

the small number and because the infusion of room

air still provides oxygen, albeit at a lower concentration

than TT 02. Thus, the effect of oxygen could not be

completely separated from increased airway pressure.

Based on the present study and consistent findings

by other investigators, we believe that TT 02 exerts

its major effect by stabilizing chemoreceptor activity

and by reducing the central component of apnea,

although increased airway pressure may play a role.

The superiority of TT 02 over NC 02 most likely

stems from the more reliable delivery of oxygen to

the alveolar gas compartment when upper airway

occlusion is present.

Previous investigators have demonstrated that oxy-

gen via nasal prongs or face mask consistently reduces

both the severity of oxygen desaturation and the

frequency of apnea in patients with obstructive sleep

apnea syndrome.35 Because ofdifferent study designs,

it is difficult to compare our results.

We were concerned that oxygen therapy would

prolong the duration ofrespiratory events and increase

accumulated apnea time.3’5”5”9’�#{176} However, our data

and those of Chauncey and Aldrich’6 did not indicate

that oxygen therapy by transtracheal catheter or nasal

cannula significantly increased the duration of apneic

events. In contrast to some studies,�9m our subjects

were examined using one steady-state treatment mo-

dality throughout the entire sleep period, which we

believe may provide more realistic data.

It is conceivable that the order of the studies or

intervals between tests may have biased these results.

Long-term use ofCPAP has been shown to change the

ventilatory response to C02,2’ which could possibly

also modify the extent of obstructive sleep apnea. It

is unlikely that the prior use ofCPAP was a confound-

ing factor in this study because these patients were

selected on the basis of being poorly compliant with

CPAP and none was using this therapy regularly.

Transtracheal oxygen studies were delayed in several

patients because of scheduling conflicts and one pa-

tient (No. 1) received oxygen via nasal cannula. Gold

et al� have demonstrated that long-term oxygen ther-

apy has no effect on apnea frequency beyond the

period ofadministration. Therefore, the use of oxygen

before TT 02 studies would not likely skew the results.

Finally, the order oftests preceding TT 02 studies was

randomized so that there would be no consistent effect

from any therapy.

Nasal CPAP is the optimal therapy for immediately

eliminating obstructive apneas and normalizing sleep

architecture in the majority of patients. However,

some will be intolerant of nasal CPAP and others may

require concomitant and continuous use of oxygen.

This study suggests that TT 02 may be a viable

therapeutic alternative. When supplemental oxygen

was required in addition to CPAP, transtracheal oxygen

was successfully used as a single modality, thus reduc-

ing complexity and treatment expense.

We did not address potential long-term complica-

lions of transtracheal catheter therapy nor did we

evaluate other catheter systems. Chronic therapy with

TT 02 could be complicated by mucosal ulcerations

and infection. Transtracheal oxygen therapy requires

frequent cleaning and the catheter can be easily

occluded by mucus in patients with heavy secretions.

Some of the subjects in this study may not be

representative of the majority of patients with severe

sleep apnea. All were more difficult to treat than usual

which, in fact, was the specific reason for considering

them for an experimental treatment. Two had chronic

bronchitis and all were studied at moderately high

elevation. Nevertheless, we do not believe that these

considerations seriously detract from the main thrust

ofthis article, which is that TT 02 may be useful when

other modalities of therapy are not successful or are

impractical. Given the success of TT 02 in these

patients, transtracheal oxygen therapy may also be

beneficial in less severe cases, although additional

subjects should be studied before such conclusions

can be drawn. In some subjects, hypopneas may still

be present but perhaps the single most significant

physiologic consequence, hypoxia, can be prevented.

The frequency of arousals was also reduced with

transtracheal oxygen but further studies are necessary

to determine the long-term effects on sleep architec-

ture and daytime symptoms as well as to better define

the role ofairway pressure.

ACKNOWLEDGMENTS: The authors wish to thank Kathy Bradleyfor her invaluable assistance and patience in the preparation of thismanuscript, William Clark and Jan Kramer for their technicalexpertise with polysomnography, Julian Maack for medical illustra-lions, Alan Abdulla, M.D. , for his contributions in the initialstudies, and Alan H. Moms, M.D. , Robert 0. Crapo, M.D., andArthur S . Slutsky, M . D. , for their critical reviews and suggestions.

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