noninvasive face mask ventilation

DOI 10.1378/chest.95.4.865 1989;95;865-870Chest

G U Meduri, C C Conoscenti, P Menashe and S Nair acute respiratory failure.Noninvasive face mask ventilation in patients with

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CHEST I 95 I 4 I APRIL 1989 865

clinical investigations in critical care

Noninvasive Face Mask Ventilation inPatients with Acute Respiratory Failure*Gianfranco Umber-to Meduri, lti. D. , F. C. C . P ;t

Craig C. Conoscenti, M.D.; tPhillip Menashe, Ttf.D.;�

and SreedharNair, M.D., F.C.C.PII

Noninvasive face mask ventilation has been used success-

fully in patients with paralytic respiratory failure. Thisstudy evaluated whether noninvasive face mask ventilation

can be used for patients with acute respiratory failure dueto intrinsic lung disease. Six patients with hypercapnia and

four with hypoxemic acute respiratory failure met clinicaland objective criteria for mechanical ventilation, which wasdelivered with pressure control and pressure support via atightly strapped, clear face mask. No patient terminated

the study because ofinability to deliver adequate ventilation

N oninvasive mechanical ventilation is used success-

fully in patients with acute or chronic paralytic

respiratory failure. Many patients with only moderate

respiratory muscle weakness during the daytime de-

velop severe respiratory failure at night and require

ventilatory support. In recent years, noninvasive pos-

itive-pressure ventilation via the mouth or nose has

partially replaced tracheostomy or the use of negative-

pressure ventilation for this group of patients. Nonin-

vasive positive-pressure ventilation with a face mask

or mouth seal is effective in supporting ventilation for

years; however, it can be associated with complications

such as aerophagia, dehydration ofthe oropharynx, or

bite deformities from the mouth seal.’2 Nose inter-

mittent ventilation administered via a nasal continuous

positive-airway pressure (CPAP) mask and a fitted

foani rubber piece have been equally effective and

better tolerated in patients with neuromuscular dis-

ease, severe kyphoscoliosis, or central hypoventila-

tion.3”

We initiated this study to evaluate whether nonin-

vasive ventilation via a face mask can be used for

*From the Hinds Center for Respiratory Research, Norwalk Hos-

pital, Yale University School of Medicine, Norwalk, CTtAssistant Professor of Medicine, Director of Respiratory Services,

University oflennessee Medical Center University of Tennessee,Memphis; Former Associate Director, Pulmonary Fellowship Pro-gram, Norwalk Hospital, Yale University School of Medicine.

jAttending, Pulmonary Section, Norwalk Hospital.§Senior Pulmonary Fellov�; Norwalk Hospital.

liChief, Section of Pulmonary Medicine, Norwalk Hospital; ClinicalProfessor of Medicine, Yale University School of Medicine.Presented in abstract form at the 54th Annual Scientific Assembly,American College ofChest Physicians, Anaheim, Oct 3-7, 1988.

Manuscript received October 31; revision accepted December 9.Reprint requests: Dr Meduri, 956 Court Avenue, Memphis 38163

or to improve oxygen exchange; three eventually requiredendotracheal intubation. The mask was generally welltolerated. All patients had a nasogastric tube placed onsuction, and none vomited or aspirated. The mean durationof treatment was 33 h (range, 3 to 88). The physiologic

response was considered similar to that which would havebeen achieved with conventionally delivered ventilation.Noninvasive face mask ventilation may have a role inmanaging respiratory failure. (Chest 1989; 95:865-70)

patients with acute respiratory failure from intrinsic

lung disease.

MATERIAL AND METHOD

Patients with acute hypoxemic or hypercapneic respiratory failure

nonselectively entered the study from April 1987 to June 1988 if

they met clinical and physiologic parameters indicating the need

for mechanical ventilation. The protocol was approved by the

Institutional Review Board.

Diagnostic criteria for hypercapnic respiratory failure were severe

difficulty in breathing as expressed by the patient, hypercapnia,

acute respiratory acidosis with a respiratory rate more than 30

breaths/mm, and signs of increased respiratory work such as

intercostal and suprasternal retraction. Intubation was considered

for those patients with COPD only after they failed conventional

aggressive treatment with inhaled and systemic bronchodilators and

IV steroids.

Diagnostic criteria for hypoxemic respiratory failure included

difficulty in breathing spontaneously as expressed by the patient,

respiratory rate more than 30 breaths/mm, PaO2:F1o2 less than 200,

and signs of increased work of breathing, such as use of accessory

muscles of respiration or Pco2 retention.

Criteria for excluding patients from the study included hemody-

namic and ECG instability (patients with pulmonary edema without

hypotension were included), need for endotracheal intubation to

protect the airways or to manage respiratory secretions, and inability

to properly fit the face mask. Criteria for leaving the study included

patient’s request, hemodynamic or ECC instability, need for intu-

bation to protect the airways or manage secretions, inability to

improve alveolar ventilation or oxygen exchange, and failure to

improve mental status of patients who were lethargic from CO2

retention or agitated from hypoxemia before initiating noninvasive

face mask ventilation.

Each patient used one of two masks: the Snuggy anesthesia and

respiratory mask (No. 8887, Hospitak mc) incorporated a large,

high-compliance, low-pressure inflatable cuff for facial sealing, and

the Downs CPAP mask (9000, Vital Signs Corp) allowed for a larger

mask surface area. A nasogastric tube was inserted before initiating

face mask ventilation and placed on suction.



Patient

No. Diagnosis Age, yr Sex Outcome Survival H pH

Pco,,

mm Hg

Po,,

mm Hg Flo,

PEEP,

cm H2O

RB,

breaths/min

1 COPD/RTI 58 F Excellent S 43 7.10 83 114 0.28 0 362 COPD 78 F Seizure/Intub. S 3 7.25 84 60 0.35 0 443 COPD/CHF 70 M Refused to

continue

NS 88 7.21 93 46 0.32 0 28

4 COPD/RTI 68 M MI/Died NS 16 7.22 92 47 0.24 0 135 COPD/RTI 84 F Excellent S 29 7.39 59 66 0.28 0 406 COPD/RTL’OD 62 F Excellent S 7 7.25 85 59 0.35 0 407 ARDS/Sepsis 32 F Excellent S 71 7.33 52 87 0.70 18 508 ARDS/AIDS-PCP 40 F Excellent S 48 7.42 42 74 0.90 10 409 Cardiac edema 48 F Not tolerated,

intubated

S 20 7.34 34 51 0.50 0 40

10 Cardiac edema 77 M Excellent S 4 7.25 59 73 1.00 0 34

*H = Duration of face mask ventilation; PEEP positive end-expiratory pressure; BE respiratory rate; RTI respiratory tract infection;

OD = overdose; PCP = Pneumocystts carinii pneumonia; S survivor; NS nonsurvivor.

Table 1 -Diagnosis, Outcome, and Baaeline Blood Gas Values oflO Patients with Acute Respiratory Failure0

N. Face Mask Ventilation in Patients with ARF (Modurietal)

All patients received mechanical ventilation using a Servo 900C

Ventilator (Siemens-Elema Corporation). During mechanical venti-

lation, all lung volumes, including exhaled minute ventilation (VE)

and exhaled tidal volume (VT) were measured using the standard

Servo flow monitoring system. Blood gases were measured with a

Radiometer ABL 30 Acid-Base Analyzer (Radiometer Corp). Meas-

urements were made following daily calibration of the acid-base

analyzer using standard testing solutions. Patients received contin-

uous ECG and oximetric monitoring.

The following data were collected: use of the accessory muscles

of respiration, presence of paradoxic abdominal motion, exhaled

volumes, vital signs, baseline pulmonary function testing, duration

of face mask ventilation, causes of exit from the study, and possible

complications.

RESULTS

Ten patients with acute respiratory failure entered

the study (Table 1). Six had COPD with acute venti-

latory failure, and four had refractory hypoxemia of

different etiologies. Two patients who met the entrance

criteria were unable to participate in the study because

of the inability to find a mask that properly fit their

facial contour.

Hypercapnic Respiratory Failure

Six patients had acute exacerbation ofsevere COPD

with a mean baseline FEY1 of 577 ml. Pulmonary

function test results for the four women and two men

are shown in Table 2. Results for patients 1 and 3 were

obtained 10 years before this admission. The mean

age was 70 (range, 58 to 84 years). The cause of the

acute decompensation was believed to be a respiratory

tract infection in patients 1, 4, and 5; congestive heart

failure in patient 3; a combination of bronchitis and

narcotic overdose in patient 6; and not known in

patient 2.

All patients were in severe respiratory distress, four

were using the accessory muscles of respiration, and

all but one (patient 4) were tachypneic, with a mean

respiratory rate of 34 breaths/mm. All patients failed

to improve despite aggressive treatment with systemic

and inhaled bronchodilators and IY steroids. Three

patients (2, 4, and 6) were lethargic but became alert

and responsive soon after beginning ventilation.

The arterial blood gas drawn before initiating face

mask ventilation showed a pH ranging from 7. 10 to

7.39, with a mean of 7.23, and PCO2 ranging from 58

to 93 mm Hg, with a mean of 82.5. Based on their

clinical or physiologic status, all would have required

intubation and mechanical ventilation. The single

patient with a normal pH (patient 5) was in severe

distress, and it was thought that decompensation was

imminent. Two patients (3 and 6) expressed the will

not to be intubated.

Pressure control ranging from 20 to 30 cm H2O

delivered a TY from 340 to 790 ml with a VE between

Table 2-Pulmonary Function Testing in Patients with COPD0

Patient

No.

FVC, ml

(%)

FEV1, ml

(%)

FEV1/FVC,

(%)

Dsb, m/C&min/mm Hg

(%) RV!FLC, %

it 1,700 (52) 900 (36) 53 NA NA

2 945 (40) 591 (37) 62 NA 65

3t 1,031 (23) 486 (14) 47 9.8 (32) 75

4 1,592 (38)1: 694 (24) 44 9.3 (32) 68

5 760(30) 430(23) 56 NA NA

6 1,074 (38) 752 (36) 70 10.3 (41) 63

*NA = not available.

tPFT obtained 10 years before this admission.

�15% increase in FVC following inhaled bronchodilator.



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90

80

70

60

50

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Time (Hours)

CHE5T/95/4/APRIL 1989 867

Changes in PaCO2 in Six Patientswith Hypercapnic Respiratory Failure

6.3 and 9. 1 . Acceptance ofthe face mask was excellent,

and immediate improvement in the sensation of dysp-

nea was recorded in four patients.

Clinical and physiologic improvements were seen

shortly after beginning face mask ventilation (eg, a

mean fall in respiratory rate of 18 breaths/mm). An

arterial blood gas determination within 1 h of initiating

face masks ventilation showed a mean fall in PCO2 of

18 mm Hg (Fig 1). By the sixth hour, the PCO2 had

fallen by 24 mm Hg and pH had risen by 0.145. Face

mask ventilation lasted from 3 to 88 h (mean, 31 h).

The mask was removed for briefperiods ofrest for the

patients to receive nebulizer treatment with a

agonist agent, to drink water, to expectorate secretions,

or to speak.

Patients 1, 5, and 6 had an excellent response and

an uncomplicated course. The death oftwo patients (3

and 4) was not due to a failure offace mask ventilation.

Patient 3, a 70-year-old man with severe COPD, was

a chronic CO2 retainer who received oxygen therapy

at home and had a history ofcongestive heart failure.

After successful resuscitation at home following car-

diopulmonary arrest, he was admitted intubated. The

following day the patient seif-extubated and expressed

the will not to be reintubated. Twenty-four hours later,

he developed severe respiratory difficulties and aci-

dosis. For four days he tolerated face mask ventilation

well and showed clinical and physiologic improve-

ment. On day 5, after several unsuccessful weaning

trials, he decided not to continue the therapy; 15 hours

later he died.

Patient 4, a 68-year-old man with severe COPD,

was receiving nocturnal oxygen at home and had a

history of coronary artery disease. He was admitted

with an acute exacerbation and theophylline intoxica-

tion (�Wml level 51.5). Two days after entering the

hospital, he developed severe respiratory difficulties

and lethargy Arterial pH fell from 7.36 to 7.22

60 80 FIGURE 1. Changes in Pco, over time in the group with

hypercapnic respiratory failure.

(respiratory rate, 13 breaths/mm). He responded

quickly and well to face mask ventilation with clinical

and physiologic improvement. Sixteen hours later he

developed acute bradycardia and electromechanical

dissociation. He was intubated but failed to respond

to resuscitation efforts. An arterial blood gas analysis

30 mm before the arrest showed a pH of 7.29, PCO2

of 66 mm Hg, and Po2 of 69 mm Hg. Yital signs and

oximetry results before the event were satisfactory.

(Postmortem study limited to the heart showed a

myocardial infarction.)

One other patient (2) required intubation after she

developed generalized seizure, which is thought to be

secondary to hyponatremia and acute respiratory

alkalosis in patients with a previous history of seizure.

Arterial pH rose from 7.25 to 7.50 with face mask

ventilation and did not correct itselfdespite a decrease

in ventilatory rate.

Hypoxemic Respiratory Failure

The second group consisted offour patients (patients

7 to 10) with acute hypoxemic respiratory failure, two

with adult respiratory distress syndrome (ARDS) and

two with cardiogenic pulmonary edema. Patient 7 had

noncardiogenic pulmonary edema from sepsis. She

was neutropenic and thrombocytopenic 10 days follow-

ing chemotherapy for Wilms’ tumor; the source of

infection was not identified. Patient 8 had AIDS and

developed noncardiogenic pulmonary edema follow-

ing an open lung biopsy examination that diagnosed

the presence of Pneumocystis carinii pneumonia.

Patients 9 and 10 had acute cardiogenic pulmonary

edema. Myocardial infarction was suspected in one

and diagnosed in the other.

Their mean age was 40 years (range, 32 to 77), and

the female-to-male ratio was 3:1. Three patients were

in severe respiratory distress; patient 10 was described

as in moderate distress. All four patients were tachy-



(10)

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00

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Ficun� 2. Change in Po,:FIo, over time in the group

with hypoxemic respiratory failure.

(6)

Table 3-Initial Ventilatory Settings infour Ibtienta with Hypoxemic Respiratory Failure

N. Face Mask %�ntIIatIon m PatIents with ARF (M.dud it a!)

Patient Pressure*

Respiratory Bate,

breaths/mm VT, ml

VE,

(Llmin) Flo,

Positive End-Expiratory

Pressure, cm H,O

7 PS10 46 349 16.1 .70 18

8 PC1O 2U118 290 9.4 1.00 10

9 P520 20 895 17 1.00 5

10 PC18 12/6 835 15 1.00 0

*PS = pressure support; PC pressure control predetermined rate/additional spontaneous rate.

pneic, with a mean respiratory rate of 40 breaths/mm

(range, 34 to 50). The decision to begin mechanical

ventilation in each patient was based on the following

information:

Patient 7 had ventilatory fatigue with respiratory

acidosis (Pco2, 52 mm Hg; respiratory rate, 50 breaths/

mm) and acute change in mental status (agitation and

disorientation) while receiving CPAP of 18 cm H2O by

face mask.

Patient 8 had refractory hypoxemia (Po2 74 mm Hg

on 90 percent FIo2 and CPAP 10 cm H20) and clinical

signs of imminent ventilatory decompensation with

rising PC02.

Patient 9 had a marked increase in an effort to

breathe soon after extubation and two days following

cardiac arrest.

Patient 10 had resistant hypoxemia (Po2, 73 mm Hg

on 100 percent F1o2 by nonrebreathing face mask)

and acute ventilatory decompensation (pH, 7.25; PCO2

50 mm Hg; respiratory rate, 34 breaths/mm, using the

accessory muscles of respiration).

The initial ventilatory settings in this group are

given in Table 3. Patient 8 initially experienced a

moderate degree of anxiety from having a tight-fitting

mask; the anxiety slowly improved. Patient 9 tolerated

the mask well initially but after 20 h became uncom-

fortable and was finally intubated, despite adequate

oxygen tension (Po2, 122 mm Hg on 40 percent FIo�).

This was the only patient who required intubation

because of an inability to tolerate the face mask.

7006005004003002001 801 601 401 201 00

9080#{149}7060

The mean PaO2:F1o2 before initiating face mask

ventilation was 95 mm Hg and increased to 192 mm

Hg at the first hour and to 261 mm Hg after 6 h, with

a mean increase of 97 and 167 mm Hg, respectively

(Fig 2). The mean duration of face mask ventilation

was 36 h (range, 4 to 71). After initiating face mask

ventilation, the respiratory rate halved in the subgroup

with cardiogenic edema, from a mean of 38 to of 19.

In the subgroup with ARDS, the respiratory rate did

not change, which may have resulted from our inability

to deliver a higher tidal volume or from intrinsic lung

disease. Significant oxygen desaturation was seen in

these two patients if the mask was removed for even a

brief period, while they were receiving high positive

end-expiratory pressure (PEEP).

The only observed complication was the develop-

ment of the nasal bridge abrasion at the site of mask

. application in patients 7 and 8. The abrasion healed

spontaneously in a few days.

DISCUSSION

Mechanical ventilation is a lifesaving support meas-

ure for patients with respiratory failure. Its primary

purposes are to achieve adequate alveolar ventilation

and to improve oxygen exchange. Traditionally, insert-

ing an endotracheal tube is needed to deliver the

mechanical tidal breath. Complications can result from

the intubation procedure, either while the tube is in

place or after ti”2

Pa02/Fj02 in Four PatientsWith Hypoxemic Respiratory Failure

012345678910 15 25 35 45 55lime ( Hours)



FIGURE 3. View of the face mask and ventilator.

CHEST I 95 I 4 I APRIL, 1989 869

Placement of a tube in the oral cavity and the

inability of patients to verbalize are associated with a

great degree of discomfort and anxiety that can neces-

sitate the use of sedatives or paralyzing agents to

control them . In recent years, new noninvasive mo-

dalities have been developed to improve alveolar

ventilation and oxygenation in patients with respira-

tory failure. Patients with respiratory failure from

neuromuscular disorders and without significant in-

trinsic lung disease have been successfully ventilated

nonmnvasively through a face mask’2 or a nose mask,�’#{176}

thereby avoiding or postponing for years the need for

tracheostomy.

CPAP applied noninvasively through a face or nose

mask has been used successfully to correct refractory

hypoxemia in patients with cardiogenic’3 and noncar-

diogenic pulmonary �4�6 Retention of CO2 has

occasionally been a limiting factor for this technique,

however.

Ten patients nonselectively entered this study. Six

had severe COPD with acute hypercapnic respiratory

failure and four had hypoxemic respiratory failure

from cardiogenic and noncardiogenic pulmonary

edema. All patients met objective or clinical criteria

indicating the need for mechanical ventilation. Face

mask ventilation rapidly ameliorated dyspnea and

reduced respiratory rates.

The use of a tight-fitting mask was well tolerated;

only one patient stopped using the mask after 20 h

because of discomfort. Only two patients developed

abrasions on the nasal bridge, and they healed spon-

taneously; this was the only obvious complication noted

in this group. A nasogastric tube was inserted in all

patients before beginning face mask ventilation. This

tube resulted in leaking air where the tube exited

from the mask, but no patient developed abdominal

distention secondary to aerophagia or gaseous insuffla-

lion, and no vomiting occurred. We did not observe

obvious aspiration clinically or radiographically.

Three patients, lethargic from CO2 retention (pa-

tients 2, 4, and 6), became alert and oriented after

beginning face mask ventilation. One patient (7) with

refractory hypoxemia was acutely agitated and disori-

ented before treatment and became comfortable and

oriented soon after beginning ventilation.

The mean duration of face mask ventilation was

33 h (range, 3 to 88 h). No patient left the study

because of failure to achieve adequate oxygenation or

ventilation. Three patients eventually required endo-

tracheal intubation: patient 2 after generalized sei-

zures, patient 4 during cardiopulmonary resuscitation,

and patient 9 because of discomfort from the tight-

fitting mask. Two patients died. Patient 3 refused to

continue after four days of successful ventilation and

died 15 h after discontinuing ventilation. Patient 4 had

a sudden, unexpected cardiac arrest, and an autopsy

showed a myocardial infarction.

The physiologic response to face mask ventilation

was considered satisfactory in all patients (Fig 3). In

the hypercapnic group, mean Pco, was reduced by 18

and 24 mm Hg at the first and sixth hours of ventilation,

respectively, while the mean respiratory rate fell by

18 breaths/mm. Patients also experienced a marked

amelioration of dyspnea and decreased effort to

breathe. Overcorrection of respiratory acidosis (from

pH 7.25 to 7.50) was, in part, responsible for the

development ofgeneralized seizures in patient 2, who

had hyponatremia.

The patients with COPD and hypercapnia had the

advantage of being able to remove the mask for brief

periods (10 to 15 mm) during which they could drink

fluids, verbalize, receive nebulized �3-agonist agents,

or expectorate secretions. Weaning from face mask

ventilation was achieved by prolonging the periods off

the mask, while the patients received additional F1o2

by nasal cannula or a Yenturi mask. Noninvasive face

mask mechanical ventilation was successful in achiev-

ing adequate alveolar ventilation and correcting the

respiratory acidemia (mean rise in pH at 6 h was

0. 145) while allowing the respiratory muscles to rest.

Compared with mechanical ventilation delivered via

an endotracheal tube, face mask ventilation had the

advantage of being noninvasive and more comfortable

to the patients. It can be used also in an earlier stage

of ventilatory decompensation while medical manage-

ment is initiated. Because of the risk of aspiration, we

think that face mask ventilation should not be contin-

ued in patients who are lethargic and whose mental

status fails to improve after beginning ventilation.

In the group with hypoxemia and low lung compli-

ance, face mask ventilation satisfactorily improved gas

exchange and effective alveolar ventilation. Patients 7

and 8 had ARDS with refractory hypoxemia and

ventilatory insufficiency (tachypnea and PCO, reten-

tion) while receiving CPAP delivered by a face mask.

In patient 7, tachypnea and the sensation of dyspnea



870 Face Mask Venthation in Patents with ARF (Medun at a!)

were corrected by instituting face mask ventilation;

however, the PaO2:F1o2 ratio did not improve for

24 h. Patient 8 experienced a rapid improvement in

oxygen exchange that permitted a reduction in FIo2

from 0.9 to 0.5 in 13 h, while the PEEP remained

constant at 10 cm H2O. A significant and rapid im-

provement in PaO2:FIO2 ratio was also seen in the two

patients with cardiogenic pulmonary edema.

Face mask ventilation was used in a small hetero-

geneous group ofpatients with acute respiratory failure

due to intrinsic lung disease. This procedure appears

to produce physiologic improvements similar to those

in intubated patients receiving mechanical ventilation.

The mask was well accepted and tolerated for pro-

longed periods of time without significant complica-

tions. While this preliminary report on a new mode

of noninvasive mechanical ventilation is encouraging,

a much larger study is necessary before firm conclu-

sions and recommendations can be reached.

ACKNOWLEDGMENT: The authors wish to thank the respiratorytherapists and the Pulmonary attendings of Norwalk Hospital fortheir dedication and enthusiasm that have made this study possible.We would like to acknowledge the assistance of Dr. Norman Soskeland Dr. David Armbruster in editing the manuscript, Nancy Smithand Vicky Franke for secretarial support, and Denis Selmont, PhD,for organizing Tables 1-3.

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DOI 10.1378/chest.95.4.865 1989;95; 865-870Chest

G U Meduri, C C Conoscenti, P Menashe and S NairNoninvasive face mask ventilation in patients with acute respiratory failure.

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