Long-Term Physiologic Consequences of the Adult Respiratory Distress Syndrome* Harold H. Rotman, M.D., F.C.C.P.;•• Thomas F. Lavelle, ]r., M.D.;t Donald G. Dimcheff, M.D., F.C.C.P.;t. R. ]. VandenBelt, M.D.;§ and JohnG. Weg,M.D.,F.C.C.P.II
Six IUI"Vivon of the adult respiratory distress syndrome
were studied. Measurements were made of lung volnmes, 8ow rates, single-breath diffusing capacity for carbon dioude (Dsb), arterial blood gas levels at rest and during es:erclse, the ratio of pbyslologk dead space to tidal volume (Vo/VT), alveolar-arterial osygen pressure difference (P[A-a](M, and percent shunt (using an assumed arteriovenous osygen content dUierenee). At the time of study, which varied from 3 to 16 months after recovery, we found minor and lneoaslstent JlbnormaHtJes in the lung volnmes (reduced vital capacity in one patient, elevated residual volnme [RV] in two, and redneed RV
There have been few reports ·on the status of pulmonary function in adults recovering from the adult respiratory distress syndrome. One report 1 emphasizes a lingering abnormality of pulmonary function, one 2 relates the function at follow-up to the nature and severity of the causative process, a third 8 shows survivors to have a reduction in diffusing capacity with some loss of elastic recoil, and another shows some survivors to have evidence of restriction. We have studied the long-term physiologic consequences of the adult respiratory distress syndrome in six patients whose illness was severe enough to require mechanical ventilation with positive end-expiratory pressure (PEEP). MATEIUALS AND METHODS
Six adult survivors of the acute respiratory distress syndrome severe enough to necessitate PEEP in their treat• From the Pulmonary Division, Department of Internal Medicine1 University of Michigan Medical Center, and St Joseph's Mercy Hospital, Ann Arbor, Mich. Supported in part by pulmonary academic award 5K07HL70368-05 from the National Heart and Lung Institute. • • Assistant Professor of Medicine and Head, Pulmonary Function Laboratory, University Hospital. tFellow, Pulmonary Disease Division, Department of Medicine. tCiinical Assistant Professor of Medicine. §Clinical Instructor of Medicine and Cardiologist, St. Joseph's Mercy Hospital. II Professor of Medicine and Head, Pulmonary Division. Manuscript received June 26, 1976; revision accepted NovemberS. Reprint requests: Dr. Rotman, University Hospital, Ann Arbor
48109
190 ROTMAN ET Al.
in three) and in the 8ow rates (reduced instantaneous forced upiratory 8ow after 50 percent of the forced vital capacity had been exhaled in two patients). In those tests having to do with transfer of gas, there were more _. normalities, consisting of a decreased Dsb in three patients, an elevated P(A-a:>02 in four, a low resting arterial osygen pressure (Pa02) in two, a decrease in exercise Pil02 in three, an elevated shunt fraction (Qsan/Qt) in three, and an elevated Vn/VT in ooe patient. COnicaDy, at the time of study, the patients all had returned to their status before illness.
ment were studied. These survivors were consecutive patients who lived close to Ann Arbor, Mich, and were willing to be studied. The clinical characteristics of these patients and the methods of treabnent are shown in Table 1. Adult respiratory distress was defined in our patients by their worsening picture on analyses of arterial blood gas levels and the increasing amounts of bilateral diffuse infiltrates on chest x-ray films. In all cases the arterial oxygen pressure (Pa0 2 ) before therapy with PEEP was less than 50 mm Hg, with a fractional concentration of oxygen in the inspired gas ( Flo 2 ) of 0.5 or greater. Therapy with PEEP was employed for periods ranging from 2 to 11~ days, and the patients were studied at 3 to 16 months after recovery from the episode. Measurements of the lung volumes were made using an electronic spirometer ( Electromed 800), with the functional residual capacity ( FRC) and the airway resistance ( Raw) being measured in a body plethysmograph (Ohio 3000). The diffusing capacity for carbon monoxide ( Dsb) was detennined by a modification of the single-breath technique, 5 with the alveolar volume being derived from the dilution of the inert gas (helium ) . Flow rates were obtained by electrical differentiation of the volume signal from the spirometer. Detenninations of arterial blood gas levels were made with the patient at rest and undergoing exercise on treadmill 01' bicycle ergometer, using a blood gas analyzer (Radiometer model 27 pH meter) and appropriate electrodes for pH, arterial carbon dioxide tension (PaC0 2 ), and Pa0 2 • These measurements were made with the patient breathing air and also with the patient breathing 100 percent oxygen for the shunt studies. Simultaneous measurement of the concentrations of oxygen and carbon dioxide in the mixed expired gases were also made, using commercially available analyzers ( Beckman infrared C02 analyzer LB-1 and Beckman paramagnetic 02 analyzer E-2) . Expired gas was collected with the patient at rest in the supine position and during the fifth minute of exercise, simultaneously with the drawing of a sample of arterial
CHEST, 72: 2, AUGUST, 1977
Table 1--Ciinical Claaracteri•lic• and Metlaoth of Treatment of Patient. with the Adult Re•piralory Di•treu Syndrome ( ARDS)
Data
Patient 1
Patient 2
Patient 3
Patient 4
Patient 5
Patient 6
M, 31
F, 34
M,27
F, 26
M, 37
M,25
Smoking history
Pipe
20 pack-years
Nonsmoker
Nonsmoker
Nonsmoker
5 pack-years
Cause of ARDS
Mycoplasma pneumonia
Viral pneumonia
Postoperative craniotomy
Aspiration pneumonia
Viral pneumonia
Aspiration pneumonia
Time of study after ARDS, mo
10
9
4
16
3
3
Duration of mechanical ventilation, days
13
2~
3~
11
9
6
Duration of PEEP, days
11~
2
3
5~
5~
175
27
47
231
191
100
No
Yes
Yes
Yes
Yes
Yes
13-17
13
12
12
13-17
13-18
60
50
42
48
41
52
Sex, age (yr)
Duration of Flo.
> 0.4,
hr
Steroid therapy
Tidal volume, ml/kg Peak pressure, em H,O
blood. From the data so obtained, calculations were made of the ratio of physiologic dead space to tidal volume (VD/VT), according to the Bohr relation: Vn VT
=
PaC0 2 PaC0 2
-
-
= (Pa- 47- Pa~~- Pa0 ( Pa - 47 - PaC0 2 760
-
0 2 was also calculated using an assumed respiratory quotient of 0.8, according to the formula/
PaC0 2 0.8
P;;C0 2 PtC0 2
'REsULTS
The shunt fraction ( Qsan/Q,) was calculated according to the equation,e Qsan/Q,
9~
2)
2.3
Pa0 2 ) 2.3
XlOO%
+ 4.5
where Pa is barometric pressure, PaC0 2 and Pa0 2 are expressed in millimeters of mercury, 2.3 is the solubility coefficient of oxygen in plasma. This equation assumes an arteriovenous oxygen content difference of 4.5 volumes percent, an assumption which was necessary since the patients did not undergo catheterization at the time of follow-up study. The alveolar arterial oxygen pressure difference P[A-a]-
We had no opportunity to study these patients prior to the episode of respiratory failure, and so the only possible comparison was with the appropriate predicted normal values.s-to The patients were all young, and none had significant respiratory symptoms before the occurrence of respiratory failure. The abnormalities observed in the lung volumes (Table 2) were minor and consisted of a reduced vital capacity ( VC) in one patient, an elevated residual volume ( RV), in two patients, and a reduced RV in three patients. In the measurements relating to the Bow of air (Table 2), there was a borderline
Table 2-Meaurementl of Y olume, Fl0111, and Ca Tran~fer after the Adult Rupirator;r Diltru• Syndrome
Measurement
Patient 1
VC, ml (percent predicted) 4,326 (87) FRC, ml (percent predicted) 3,060 (84) RV, ml (percent predicted) 1,618 (77) TLC, ml (percent predicted) 5,944 (84) FEVt/FVC% 77 FEF50%, L/min (percent predicted) 246 (85) 1.2 Raw, em H,O/L/sec Resting PaO., mm Hg* 97 Resting PaCO,, mm Hg* 30 Resting P(A-a)O,, mm Hg* 12 Exercise PaO,, mm Hg* 84 Resting Vn/VT, percent* 44 Resting Dsb, rnl/mm Hg/min 25.3 (90) (percent predicted) Resting Qsan/Q,, percent 9
Patient 2
Patient 3
Patient 4
Patient 5
Patient 6
3,950 (108) 3,760 (147) 2,095 (126) 5,710 (107) 84 240 (105 1.4 69 33 39 89
3,650 (71) 3,745 (102) 2,895 (141) 6,545 (91) 79 264 (81) 1.8
2,700 (94) 1,610 (62) 1,085 (69) 3,760 (85) 81 138(56) 4.1
84
90
34 19
34 9 81 27
4,350 (83) 3,745 (102) 2,145 (96) 6,640 (89) 81 240 (83) 1.7 98 25 14 101 32
4,726 (102) 3,150 (74) 1,568 (72) 6,277 (80) 87 186 (69) 2.5 86 30 19 93 30
19.4 (64) 3
13.7 (59) 5
15.9 (58) 9
33.1 (110) 12
14.0 (75) 4
*Values during breathing of air.
CHEST, 72: 2, AUGUST, 1977
LONG-TERM PHYSIOLOGIC CONSEQUENCES OF ARBS 191
decrease in the ratio of the forced expired volume at one second ( FEV1) over the forced vital capacity ( FVC) (ratio expressed as a percentage) in one patient a reduced instantaneous forced expired flow after 50 percent of the FVC has been exhaled ( FEFSO$) in one patient, and an increased Raw in one patient. More striking were the changes found in those measurements having to do with the transfer of gas (Table 2). Three of the six patients had an abnormally low Dsb, and four had an abnormal P( A-a )02. Two patients had a low resting Pa02, and in two of the five who could exercise, there was a decrease in Pa02 with exercise. Three patients had an elevated Qsan/Q,· and one of the four in whom Vn/VT was determined had an elevated value. Statistical analyses were done by the Student's t-test 11 No measured value was significantly different from the predicted normal value by either test. DISCUSSION
In previously published studies, the most Consistent and lasting abnormality was in some aspect of the transfer of gas. 1·3 This was usually manifest as a decrease in Dsb and an elevated Vn/VT. Of interest is that these are the same abnormalities one would expect in many of the antecedent diseases,12·13 as well as in more fully developed oxygen toxicity. 14 In the present study the physiologic abnormalities detected in survivors of an episode of the adult respiratory distress syndrome severe enough to require mechanical ventilation and PEEP were trivial. The patients were all young and healthy before the episode of respiratory failure, and while these were not the bases for their selection, they make the comparison of their physiologic measurements with normal values valid. Some clinical features are worth pointing out, although because of the small numbers, statistical correlation would be invalid. In defining the population under study, we required bilateral, diffuse, and worsening infiltrates on the chest x-ray films. Follow-up chest x-ray films after recovery showed complete or almost complete clearing of the infiltrates in all of the patients, with the only persisting abnormality being some fibrous stranding remaining in two patients (patients 3 and 6). Clinical followup after recovery revealed that there was fatigue and malaise for varying periods, but no correlation could be identified between these symp-
192 ROTMAN ET AL
toms and any measurement of pulmonary function, therapeutic maneuver, or antecedent condition. We conclude that if patients survive an episode of the adult respiratory distress syndrome requiring mechanical ventilatory support and PEEP, some physiologic abnormalities may persist, but they are very mild. ACKNOWLEDGMENTS : We wish to thank Dr. David R. Dantzker for his review of the manuscript and helpful suggestions. REFERENCES
1 Downs JB, Olsen GN: Pulmonary function following adult respiratory distress syndrome. Chest 65:92-93, 1974 2 Lakshminarayan S, Stanford RE, Petty TL: Prognosis after recovery from adult respiratory distress syndrome. Am Rev Respir Dis 113:7-16, 1976 3 Yemault JC, Englert M, Sergysels R, et al: Pulmonary mechanics and diffusion after 'shock lung.' Thorax 30: 252-257, 1957 4 Klein JJ, van Haerigen JR, Sluiter HJ, et al: Pulmonary function after recovery from the adult respiratory distress syndrome. Chest 69:350-355, 1976 5 Ogilvie CM, Forster RE, Blakemore WS, et al: A standardized breath-holding technique for the clinical measurement of the diffusing capacity in the lung for carbon monoxide. J Clin Invest 36:1-17, 1957 6 Holman CW, Muschenheim C : Bronchopulmonary Diseases and Related Disorders. Hagerstown, Md, Harper and Row, 1972, p 64 7 Comroe JH Jr, Forster RE II, Dubois AB, et al: The Lung: Clinical Physiology and Pulmonary Function Tests (2nd ed). Chicago, Year Book Medical Publishers, 1962, p335 8 McGrath MW, Thomson MJ: The effect of age, body size and lung volume change on alveolar-capillary permeability and diffusing capacity in man. J Physiol (London) 146: 572-582,1959 9 Goldman HI, Becklake MR: Respiratory function tests : Normal values at median altitudes and the prediction of normal results. Am Rev Tuberc 79:457-467, 1959 10 Kory RC, Callahan R, Bonan HG, et al: The Veterans Administration-Army cooperative study of pulmonary function: 1. Clinical spirometry in normal men. Am J Med 30:243-258, 1961 11 Colton T: Statistics in Medicine. Boston, Little, Brown, andCo,1974 12 Moore FD, Lyons JH, Pierce EC: Post-traumatic Pulmonary Insufficiency: Pathophysiology of Respiratory Failure and Principles of Respiratory Care after Surgical Aspirations, Trauma, Hemorrhage, Bums and Shock. Philadelphia, WB Saunders Co, 1969, p 125 13 Burke JF, Pontoppidan H, Welch CE : High output respiratory failure: An important cause of death ascribed to peritonitis or ileus. Ann Surg 158:581-595, 1963 14 Barber RE, Lee J, Hamilton WK: Oxygen toxicity in man: A prospective study in patients with irreversible brain damage. N Eng! J Med 283 :1478-1484, 1970
CHEST, 72: 2, AUGUST, 1977
Six IUI"Vivon of the adult respiratory distress syndrome
were studied. Measurements were made of lung volnmes, 8ow rates, single-breath diffusing capacity for carbon dioude (Dsb), arterial blood gas levels at rest and during es:erclse, the ratio of pbyslologk dead space to tidal volume (Vo/VT), alveolar-arterial osygen pressure difference (P[A-a](M, and percent shunt (using an assumed arteriovenous osygen content dUierenee). At the time of study, which varied from 3 to 16 months after recovery, we found minor and lneoaslstent JlbnormaHtJes in the lung volnmes (reduced vital capacity in one patient, elevated residual volnme [RV] in two, and redneed RV
There have been few reports ·on the status of pulmonary function in adults recovering from the adult respiratory distress syndrome. One report 1 emphasizes a lingering abnormality of pulmonary function, one 2 relates the function at follow-up to the nature and severity of the causative process, a third 8 shows survivors to have a reduction in diffusing capacity with some loss of elastic recoil, and another shows some survivors to have evidence of restriction. We have studied the long-term physiologic consequences of the adult respiratory distress syndrome in six patients whose illness was severe enough to require mechanical ventilation with positive end-expiratory pressure (PEEP). MATEIUALS AND METHODS
Six adult survivors of the acute respiratory distress syndrome severe enough to necessitate PEEP in their treat• From the Pulmonary Division, Department of Internal Medicine1 University of Michigan Medical Center, and St Joseph's Mercy Hospital, Ann Arbor, Mich. Supported in part by pulmonary academic award 5K07HL70368-05 from the National Heart and Lung Institute. • • Assistant Professor of Medicine and Head, Pulmonary Function Laboratory, University Hospital. tFellow, Pulmonary Disease Division, Department of Medicine. tCiinical Assistant Professor of Medicine. §Clinical Instructor of Medicine and Cardiologist, St. Joseph's Mercy Hospital. II Professor of Medicine and Head, Pulmonary Division. Manuscript received June 26, 1976; revision accepted NovemberS. Reprint requests: Dr. Rotman, University Hospital, Ann Arbor
48109
190 ROTMAN ET Al.
in three) and in the 8ow rates (reduced instantaneous forced upiratory 8ow after 50 percent of the forced vital capacity had been exhaled in two patients). In those tests having to do with transfer of gas, there were more _. normalities, consisting of a decreased Dsb in three patients, an elevated P(A-a:>02 in four, a low resting arterial osygen pressure (Pa02) in two, a decrease in exercise Pil02 in three, an elevated shunt fraction (Qsan/Qt) in three, and an elevated Vn/VT in ooe patient. COnicaDy, at the time of study, the patients all had returned to their status before illness.
ment were studied. These survivors were consecutive patients who lived close to Ann Arbor, Mich, and were willing to be studied. The clinical characteristics of these patients and the methods of treabnent are shown in Table 1. Adult respiratory distress was defined in our patients by their worsening picture on analyses of arterial blood gas levels and the increasing amounts of bilateral diffuse infiltrates on chest x-ray films. In all cases the arterial oxygen pressure (Pa0 2 ) before therapy with PEEP was less than 50 mm Hg, with a fractional concentration of oxygen in the inspired gas ( Flo 2 ) of 0.5 or greater. Therapy with PEEP was employed for periods ranging from 2 to 11~ days, and the patients were studied at 3 to 16 months after recovery from the episode. Measurements of the lung volumes were made using an electronic spirometer ( Electromed 800), with the functional residual capacity ( FRC) and the airway resistance ( Raw) being measured in a body plethysmograph (Ohio 3000). The diffusing capacity for carbon monoxide ( Dsb) was detennined by a modification of the single-breath technique, 5 with the alveolar volume being derived from the dilution of the inert gas (helium ) . Flow rates were obtained by electrical differentiation of the volume signal from the spirometer. Detenninations of arterial blood gas levels were made with the patient at rest and undergoing exercise on treadmill 01' bicycle ergometer, using a blood gas analyzer (Radiometer model 27 pH meter) and appropriate electrodes for pH, arterial carbon dioxide tension (PaC0 2 ), and Pa0 2 • These measurements were made with the patient breathing air and also with the patient breathing 100 percent oxygen for the shunt studies. Simultaneous measurement of the concentrations of oxygen and carbon dioxide in the mixed expired gases were also made, using commercially available analyzers ( Beckman infrared C02 analyzer LB-1 and Beckman paramagnetic 02 analyzer E-2) . Expired gas was collected with the patient at rest in the supine position and during the fifth minute of exercise, simultaneously with the drawing of a sample of arterial
CHEST, 72: 2, AUGUST, 1977
Table 1--Ciinical Claaracteri•lic• and Metlaoth of Treatment of Patient. with the Adult Re•piralory Di•treu Syndrome ( ARDS)
Data
Patient 1
Patient 2
Patient 3
Patient 4
Patient 5
Patient 6
M, 31
F, 34
M,27
F, 26
M, 37
M,25
Smoking history
Pipe
20 pack-years
Nonsmoker
Nonsmoker
Nonsmoker
5 pack-years
Cause of ARDS
Mycoplasma pneumonia
Viral pneumonia
Postoperative craniotomy
Aspiration pneumonia
Viral pneumonia
Aspiration pneumonia
Time of study after ARDS, mo
10
9
4
16
3
3
Duration of mechanical ventilation, days
13
2~
3~
11
9
6
Duration of PEEP, days
11~
2
3
5~
5~
175
27
47
231
191
100
No
Yes
Yes
Yes
Yes
Yes
13-17
13
12
12
13-17
13-18
60
50
42
48
41
52
Sex, age (yr)
Duration of Flo.
> 0.4,
hr
Steroid therapy
Tidal volume, ml/kg Peak pressure, em H,O
blood. From the data so obtained, calculations were made of the ratio of physiologic dead space to tidal volume (VD/VT), according to the Bohr relation: Vn VT
=
PaC0 2 PaC0 2
-
-
= (Pa- 47- Pa~~- Pa0 ( Pa - 47 - PaC0 2 760
-
0 2 was also calculated using an assumed respiratory quotient of 0.8, according to the formula/
PaC0 2 0.8
P;;C0 2 PtC0 2
'REsULTS
The shunt fraction ( Qsan/Q,) was calculated according to the equation,e Qsan/Q,
9~
2)
2.3
Pa0 2 ) 2.3
XlOO%
+ 4.5
where Pa is barometric pressure, PaC0 2 and Pa0 2 are expressed in millimeters of mercury, 2.3 is the solubility coefficient of oxygen in plasma. This equation assumes an arteriovenous oxygen content difference of 4.5 volumes percent, an assumption which was necessary since the patients did not undergo catheterization at the time of follow-up study. The alveolar arterial oxygen pressure difference P[A-a]-
We had no opportunity to study these patients prior to the episode of respiratory failure, and so the only possible comparison was with the appropriate predicted normal values.s-to The patients were all young, and none had significant respiratory symptoms before the occurrence of respiratory failure. The abnormalities observed in the lung volumes (Table 2) were minor and consisted of a reduced vital capacity ( VC) in one patient, an elevated residual volume ( RV), in two patients, and a reduced RV in three patients. In the measurements relating to the Bow of air (Table 2), there was a borderline
Table 2-Meaurementl of Y olume, Fl0111, and Ca Tran~fer after the Adult Rupirator;r Diltru• Syndrome
Measurement
Patient 1
VC, ml (percent predicted) 4,326 (87) FRC, ml (percent predicted) 3,060 (84) RV, ml (percent predicted) 1,618 (77) TLC, ml (percent predicted) 5,944 (84) FEVt/FVC% 77 FEF50%, L/min (percent predicted) 246 (85) 1.2 Raw, em H,O/L/sec Resting PaO., mm Hg* 97 Resting PaCO,, mm Hg* 30 Resting P(A-a)O,, mm Hg* 12 Exercise PaO,, mm Hg* 84 Resting Vn/VT, percent* 44 Resting Dsb, rnl/mm Hg/min 25.3 (90) (percent predicted) Resting Qsan/Q,, percent 9
Patient 2
Patient 3
Patient 4
Patient 5
Patient 6
3,950 (108) 3,760 (147) 2,095 (126) 5,710 (107) 84 240 (105 1.4 69 33 39 89
3,650 (71) 3,745 (102) 2,895 (141) 6,545 (91) 79 264 (81) 1.8
2,700 (94) 1,610 (62) 1,085 (69) 3,760 (85) 81 138(56) 4.1
84
90
34 19
34 9 81 27
4,350 (83) 3,745 (102) 2,145 (96) 6,640 (89) 81 240 (83) 1.7 98 25 14 101 32
4,726 (102) 3,150 (74) 1,568 (72) 6,277 (80) 87 186 (69) 2.5 86 30 19 93 30
19.4 (64) 3
13.7 (59) 5
15.9 (58) 9
33.1 (110) 12
14.0 (75) 4
*Values during breathing of air.
CHEST, 72: 2, AUGUST, 1977
LONG-TERM PHYSIOLOGIC CONSEQUENCES OF ARBS 191
decrease in the ratio of the forced expired volume at one second ( FEV1) over the forced vital capacity ( FVC) (ratio expressed as a percentage) in one patient a reduced instantaneous forced expired flow after 50 percent of the FVC has been exhaled ( FEFSO$) in one patient, and an increased Raw in one patient. More striking were the changes found in those measurements having to do with the transfer of gas (Table 2). Three of the six patients had an abnormally low Dsb, and four had an abnormal P( A-a )02. Two patients had a low resting Pa02, and in two of the five who could exercise, there was a decrease in Pa02 with exercise. Three patients had an elevated Qsan/Q,· and one of the four in whom Vn/VT was determined had an elevated value. Statistical analyses were done by the Student's t-test 11 No measured value was significantly different from the predicted normal value by either test. DISCUSSION
In previously published studies, the most Consistent and lasting abnormality was in some aspect of the transfer of gas. 1·3 This was usually manifest as a decrease in Dsb and an elevated Vn/VT. Of interest is that these are the same abnormalities one would expect in many of the antecedent diseases,12·13 as well as in more fully developed oxygen toxicity. 14 In the present study the physiologic abnormalities detected in survivors of an episode of the adult respiratory distress syndrome severe enough to require mechanical ventilation and PEEP were trivial. The patients were all young and healthy before the episode of respiratory failure, and while these were not the bases for their selection, they make the comparison of their physiologic measurements with normal values valid. Some clinical features are worth pointing out, although because of the small numbers, statistical correlation would be invalid. In defining the population under study, we required bilateral, diffuse, and worsening infiltrates on the chest x-ray films. Follow-up chest x-ray films after recovery showed complete or almost complete clearing of the infiltrates in all of the patients, with the only persisting abnormality being some fibrous stranding remaining in two patients (patients 3 and 6). Clinical followup after recovery revealed that there was fatigue and malaise for varying periods, but no correlation could be identified between these symp-
192 ROTMAN ET AL
toms and any measurement of pulmonary function, therapeutic maneuver, or antecedent condition. We conclude that if patients survive an episode of the adult respiratory distress syndrome requiring mechanical ventilatory support and PEEP, some physiologic abnormalities may persist, but they are very mild. ACKNOWLEDGMENTS : We wish to thank Dr. David R. Dantzker for his review of the manuscript and helpful suggestions. REFERENCES
1 Downs JB, Olsen GN: Pulmonary function following adult respiratory distress syndrome. Chest 65:92-93, 1974 2 Lakshminarayan S, Stanford RE, Petty TL: Prognosis after recovery from adult respiratory distress syndrome. Am Rev Respir Dis 113:7-16, 1976 3 Yemault JC, Englert M, Sergysels R, et al: Pulmonary mechanics and diffusion after 'shock lung.' Thorax 30: 252-257, 1957 4 Klein JJ, van Haerigen JR, Sluiter HJ, et al: Pulmonary function after recovery from the adult respiratory distress syndrome. Chest 69:350-355, 1976 5 Ogilvie CM, Forster RE, Blakemore WS, et al: A standardized breath-holding technique for the clinical measurement of the diffusing capacity in the lung for carbon monoxide. J Clin Invest 36:1-17, 1957 6 Holman CW, Muschenheim C : Bronchopulmonary Diseases and Related Disorders. Hagerstown, Md, Harper and Row, 1972, p 64 7 Comroe JH Jr, Forster RE II, Dubois AB, et al: The Lung: Clinical Physiology and Pulmonary Function Tests (2nd ed). Chicago, Year Book Medical Publishers, 1962, p335 8 McGrath MW, Thomson MJ: The effect of age, body size and lung volume change on alveolar-capillary permeability and diffusing capacity in man. J Physiol (London) 146: 572-582,1959 9 Goldman HI, Becklake MR: Respiratory function tests : Normal values at median altitudes and the prediction of normal results. Am Rev Tuberc 79:457-467, 1959 10 Kory RC, Callahan R, Bonan HG, et al: The Veterans Administration-Army cooperative study of pulmonary function: 1. Clinical spirometry in normal men. Am J Med 30:243-258, 1961 11 Colton T: Statistics in Medicine. Boston, Little, Brown, andCo,1974 12 Moore FD, Lyons JH, Pierce EC: Post-traumatic Pulmonary Insufficiency: Pathophysiology of Respiratory Failure and Principles of Respiratory Care after Surgical Aspirations, Trauma, Hemorrhage, Bums and Shock. Philadelphia, WB Saunders Co, 1969, p 125 13 Burke JF, Pontoppidan H, Welch CE : High output respiratory failure: An important cause of death ascribed to peritonitis or ileus. Ann Surg 158:581-595, 1963 14 Barber RE, Lee J, Hamilton WK: Oxygen toxicity in man: A prospective study in patients with irreversible brain damage. N Eng! J Med 283 :1478-1484, 1970
CHEST, 72: 2, AUGUST, 1977
