PULMONARY FUNCTION IN OBESE PERSONS 1'2

By GEORGE N. BEDELL, WILLIAM R. WILSON, AND PAUL M. SEEBOHM

(From the Pulmonary Research Laboratory, Department of Internal Medicine, College of
Medicine, State University of Iowa, Iowa City, Iowa)
(Submitted for publication December 26, 1957; accepted March 6, 1958)

The purpose of this paper is to report a study vanced. One is that the amount of work neces-
of lung function in extremely obese persons. In sary to keep the arterial carbon dioxide pressure
1936, Kerr and Lagen (2) called attention to the (Pco2) at a normal level is too great. A com-
fact that some obese persons develop dyspnea, cya- promise is made which allows the PC02 to rise
nosis, polycythemia, and cardiac failure. They rather than to employ the continuous excess ef-
thought that these signs and symptoms developed fort necessary to keep the Pco2 normal (13, 15).
because of mechanical interference with ventila- Another is that in some persons there is a critical
tion, especially movement of the diaphragm. degree of obesity at which ventilatory insufficiency
Sieker, Estes, Kelser and McIntosh (3) reported appears (12). Still another is that massive obes-
studies in four obese patients and postulated a ity restricts pulmonary ventilation and leads to
cardiorespiratory syndrome peculiar to obese per- alveolar hypoventilation (5, 8, 9).
sons and characterized by somnolence, Cheyne- We decided to study a number of obese persons
Stokes respirations, intermittent cyanosis, and to determine the frequency of various abnormali-
polycythemia. At the same time that Sieker and ties and to investigate the mechanism of alveolar
his associates were working on this problem, hypoventilation. We are reporting studies on 28
Auchincloss, Cook and Renzetti (4) and Weil and obese persons with restudy of 16 following weight
Prasad (5) observed a peculiar type of polycy- loss.
themia associated with obesity. Most of the in-
vestigators previously mentioned have reported METHODS
additional patients characterized by obesity, hy- The patients were selected from the wards and clinics
poxemia, polycythemia and alveolar hypoventila- of the University Hospitals and Veterans Administra-
tion (6-9), and they have been joined by others tion Hospital, Iowa City. We required that all patients
(10-18). Burwell, Robin, Whaley and Bickel- be at least 100 pounds over ideal weight based on height
and size of subject's frame (19). Each patient had a
mann (12) have given the picturesque name complete history, physical examination, roentgenogram
"Pickwickian Syndrome" to this combination of of the chest, and the indicated laboratory tests. Pul-
signs and symptoms. monary function tests were done in the morning after
There is agreement that the cardinal character- the patient had eaten breakfast. The vital capacity, in-
istics of these patients are obesity, alveolar hypo- spiratory capacity and expiratory reserve volume were
measured separately using a Benedict Roth spirometer.
ventilation, and polycythemia. The basic physio- The maximum of at least three trials was recorded. The
logic defect is alveolar hypoventilation. This functional residual capacity of the lungs was measured
leads to arterial hypoxemia and hypercapnia. Ar- in duplicate by the nitrogen washout method of Darling,
terial hypoxemia provokes polycythemia. There- Cournand and Richards (20). Volumes were corrected
to body temperature, ambient pressure, and saturated with
fore, the polycythemia of these patients is no longer water vapor, hereafter called B. T. P. S. Predicted nor-
of a mysterious type but is secondary to hy- mal values for lung volumes were calculated on the basis
poxemia. of the patient's height (21) rather than the body surface
No agreement exists on what initiates alveolar area. Rate, depth and minute volume of ventilation were
hypoventilation. Several theories have been ad- measured while the patient was breathing air, 99.6 per
cent oxygen, and 7.5 per cent carbon dioxide in air.
1 Read by title at the 30th Annual Meeting of the Cen- Expired volumes were collected in a Douglas bag or a
tral Society for Clinical Research, November 1 and 2, Tissot spirometer simultaneously with the drawing of
1957 (1). samples of arterial blood. Volumes were corrected to
2 Supported by a grant from the Iowa Tuberculosis and B. T. P. S. Physiologic dead space was calculated us-
Health Association. ing Bohr's equation. Measured and derived values used
1049
1050 GEORGE N. BEDELL, WILLIAM R. WILSON, AND PAUL M. SEEBOHM

in this calculation are the volume of expired air over a RESULTS

three minute period, the per cent CO, in the expired air,
and the arterial Pco,. Calculation is based on the for- The patients are divided into two groups, de-
mula given by Comroe, Forster, DuBois, Briscoe and pending on arterial oxygen saturation at rest.
Carlsen (22). Uniformity of intrapulmonary distribu- Arterial hypoxemia is considered to be present
tion of inspired gas was checked by the single breath ni-
trogen test of Comroe and Fowler (23) and the measure- when arterial saturation is below 93.2 per cent
ment of the percentage of nitrogen at the end of seven (31). Thirteen patients had normal saturation
minutes breathing of oxygen as described by Cournand, and are considered in Group I. Fifteen patients
Baldwin, Darling and Richards (24). To measure maxi- had arterial hypoxemia and constitute Group II.
mal breathing capacity (MBC), the subject breathed for A. Patients with normal arterial oxygen saturation
15 seconds through a mouthpiece, low resistance valve,
and wide tubing into a Tissot spirometer. Predicted This group consists of 13 patients whose weight
normal values for the MBC were based on age (25). averaged 303 pounds at the time of initial study.
The highest value obtained with three trials was calcu- There were 6 men and 7 women. The age range
lated in liters per minute. Maximal inspiratory (or ex- was 19 to 67 years. The results of pulmonary
piratory) flow rate was measured between 200 and 1,200
ml. of the inspiration (or expiration) according to the function studies in these patients are listed in
method of Danzig and Comroe (26). Diffusion was stud- Tables I and II. Lung volumes were normal.
ied using the single breath carbon monoxide method Mean inspiratory capacity was 92 per cent of pre-
of Ogilvie, Forster, Blakemore and Morton (27). dicted normal; mean expiratory reserve volume
Arterial blood was obtained from the brachial artery was 75 per cent of predicted normal; mean vital
while the semirecumbent subject breathed air, and again
after he had breathed 99.6 per cent oxygen for at least capacity was 89 per cent of predicted normal;
10 minutes. The samples were analyzed for total oxygen mean residual volume was 136 per cent of pre-
content, oxygen capacity, and whole blood carbon dioxide dicted normal; and mean total lung capacity was
content by the manometric technique of Van Slyke and 100 per cent of predicted normal. Mean minute
Neill (28). Blood was rotated with air in a tonometer volume of ventilation was 9.9 liters and mean
at room temperature for 20 minutes before measuring
oxygen capacity. Appropriate corrections were made for minute volume of alveolar ventilation was 6.2
physically dissolved oxygen and for differences in total liters. The physiologic dead space averaged 218
hemoglobin in the content and capacity samples. Direct ml. Distribution of inspired air was slightly un-
measurement of dissolved oxygen was not made, but an even as measured by the single breath nitrogen
approximate calculation was made on the samples col- test, but normal as measured by the less sensitive
lected during the inhalation of oxygen by subtracting the
oxygen capacity from the total oxygen content of such test based on the per cent of nitrogen at the end
blood. Arterial blood pH was measured in a closed of seven minutes of oxygen breathing. Mechani-
Cambridge glass electrode at either 370 C. or, if done at cal tests showed mild abnormalities. The maxi-
room temperature, the pH value was corrected to 370 C. mal breathing capacity was slightly below normal,
using the factor of Rosenthal (29). Plasma carbon the mean value being 87 per cent of predicted nor-
dioxide content and Pco2 were determined from pH, he-
matocrit, oxygen saturation and whole blood carbon mal. The maximal expiratory flow rate averaged
dioxide content using the nomogram of Singer and 212 liters per minute while the maximal inspira-
Hastings (30). tory flow rate averaged 156 liters per minute.
Some of our patients had edema of the legs thought Diffusion studies done in nine patients were
to be caused by congestive heart failure. When these normal.
patients decreased their activity after hospitalization and Six patients were restudied after weight loss.
had appropriate therapy for heart failure, they promptly
lost from 5 to 30 pounds which probably represented wa- These six patients averaged 304 pounds at the
ter loss. Our "initial" studies were done after this rapid time of original study and 252 pounds at the time
loss of water in most cases. When the initial studies of the last study. Weight loss changed the lung
were completed, we placed the patients on an 800 calorie volumes only slightly with the exception of the
diet and later restudied those who lost a significant expiratory reserve volume which increased from
amount of weight. Digitalis, salt restriction, and diu- a mean value of 63 per cent of predicted normal to
retics were used only when indicated. Weight reduction
was best accomplished by continuous hospitalization of
a mean value of 102 per cent of predicted normal.
these patients. When possible, patients were hospitalized Minute volume of ventilation was essentially un-
until they had lost 50 to 100 pounds. In some cases this changed: 10.0 liters before weight loss and 10.2
took six months. liters after weight loss. Mean alveolar ventilation
 PULMONARY FUNCTION IN OBESE PERSONS 1051

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 PULMONARY FUNCTION IN OBESE PERSONS 1053
increased from 6.3 liters to 6.8 liters in five pa- B. Patients with arterial hypoxemia
tients. Alveolar gas distribution was practically
unchanged (the per cent nitrogen after seven min- This group is composed of 15 patients whose
utes of oxygen breathing averaged 0.8 per cent be-
mean weight was 315 pounds and who had arterial
fore weight loss and 1.8 per cent after; the single hypoxemia. There were 12 women and 3 men.
breath nitrogen test averaged 3.1 per cent before Their ages ranged from 39 to 67 years. Ten of
weight loss and 2.2 per cent after weight loss). the 15 patients had clinical or laboratory evidence
Weight loss increased the mean maximal breathing of lung disease. Two women had bronchial
capacity from 79 per cent of predicted normal to asthma; two men had pulmonary emphysema;
one man had multiple pulmonary infarcts; two
96 per cent of predicted normal. Maximal flow
women had pulmonary edema secondary to heart
rates were also increased; the mean expiratory
rate increased from 192 liters per minute to 209 disease; three women had no clinical evidence of
liters per minute and the mean inspiratory rate lung disease but laboratory evidence suggested it.
increased from 171 liters per minute to 190 liters Two women had myxedema, and three women had
per minute.
hypoxemia without evidence of lung disease. The
The results of arterial blood studies in these pa- initials, clinical diagnoses, physical characteristics,
tients are listed in Table III. Mean arterial oxy- and results of pulmonary function tests in these
gen saturation at rest was 96.0 per cent, mean patients are listed in Tables IV and V. The re-
Pco2 was 39 mm. Hg, mean pH was 7.40, and the sults of arterial blood studies are listed in Table
mean hematocrit was 46 per cent. Weight loss VI. Ten patients were restudied after weight re-
in six patients made no change except that the duction. The average initial weight in these 10
hematocrit decreased from a mean value of 46 per patients was 323 pounds and at the time of last
cent to 41 per cent. study it was 251 pounds, a mean loss of 72 pounds.
TABLE III
Arterial blood studies in obese patients with normal arterial oxygen saturation

02 02 saturation
content 02 Po02 Hema-
Date of (rest) capacity (Rest) 100% 02* (rest) pH tocrit
Patient study vol. % vol. % % % mm. Hg (rest) %
D. C. 15 Nov. 56 15.30 15.43 99.2 100 + 2.27 34 7.44 39
22 Jan. 57 13.69 14.25 96.1 100 + 1.91 39 7.39 34
R. W. 11 Dec. 56 18.14 18.82 96.4 100 + 2.11 33 7.46 53
D. V. 21 May 57 15.95 16.47 96.8 100 + 2.03 42 7.35 41
F. S. 6 Dec. 56 19.70 20.89 94.3 100 + 1.35 36 7.46 51
8 Feb. 57 17.99 17.66 100 + 0.33 100 + 2.70 35 7.41 45
F. P. 18 June 57 19.56 20.52 95.3 100 + 0.87 38 7.39 48
W. B. 26 July 56 18.66 19.07 97.9 100 + 2.56 42 7.39 52
M. F. 11 June 57 18.71 19.39 96.5 100 + 1.56 40 7.34 47
E. T. 23 May 57 15.51 16.18 95.9 100 + 1.83 46 7.34 39
F. H. 6 Dec. 56 17.71 18.92 93.6 100 + 1.20 38 7.44 56
N. S. 31 July 56 20.61 23.03 93.6 33 7.41 52
30 Apr. 57 16.93 17.60 96.2 100 + 1.78 31 7.48 43
J. R. 3 Sept. 57 16.82 17.95 93.7 100 + 1.54 46 7.36 42
5 Nov. 57 17.11 18.41 93.0 100 + 1.73 46 7.35 42
R. G. 3 Dec. 56 18.46 18.71 98.7 100 + 2.34 35 7.41 50
16 May 57 15.05 16.14 93.3 100 + 1.62 37 7.40 41
R. M. 9 Aug. 56 16.78 17.48 96.0 100 + 2.11 37 7.35 40
21 Mar. 57 17.00 17.41 97.7 100 + 1.46 37 7.39 43
Mean, (initial) 13 patients 96.0 39 7.40 46
Mean (before weight loss) 6 patients 95.9 37 7.41 46
Mean, (after weight loss) 6 patients 96.1 38 7.40 41
* Values following + sign refer to ml. 02 per 100 ml. blood in excess of that required to saturate hemoglobin (i.e.,
dissolved 02). Normal value for dissolved 02 is 2.00 ml.
1054 GEORGE N. BEDELL, WILLIAM R. WILSON, AND PAUL M. SEEBOHM

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 PULMONARY FUNCTION IN OBESE PERSONS 1055
TABLE V
Studies of ventilation, respiratory mechanics, and diffusion in obese patients with hypoxemia
Ventilation Mechanical tests
Alveolar gas distribution
Minute volume Maximal Maximal Maximal
Single breathing expiratory inspiratory Diffusion
Physiologic 7 min. breath capacity flow flow ml. CO/
Total Alveolar dead space washout N2 test rate rate mm. Hgl
Patient L. L. ml. (%)* % Nit % Ni4 L./min. %I L./min. L./min. min.

A. H. 10.2 7.5 161 (32) 3.8 7.0 41 46 55 82

6.8 3.5 143 (49) . 2.3 1.5 41 46 63 109
I. K. 9.3 3.6 242 (68) 5.0 1.8 33 45 34 63
7.5 3.2 204 (69) 4.0 2.5 42 57 26 146 25
6.8 3.3 135 (52) 1.5 2.8 37 50 22 162 27
10.3 5.9 165 (44) 2.2 2.4 42 57 45 182
8.4 4.1 183 (44) 1.8 4.5 45 61 53 154 26
W. C. 7.4 4.0 153 (52) 13.2 6.5 32 36 34 111
7.6 4.1 209 (55) 2.1 5.3 46 51 97 140
W. B. 7.6 3.3 272 (65) 0.7 8.5 51 47 72 109
11.7 5.9 363 (50) 0.3 3.3 66 61 105 143 18
H. B. 6.4 1.9 150 (78) 25 23 35 83
F. W. 7.3 4.4 223 (40) 2.5 1.5 75 101 122 167 12
I. F. K. 6.2 5.0 97 (31) 1.9 0.5 48 65 158 75 12
8.0 5.2 153 (35) 1.8 0.9 84 113 214 188 35
L. R. 8.5 2.6 126 (70) 1.3 1.3 70 95 46 64 10
10.6 4.4 295 (59) 0.4 0.8 111 135 286 125 15
K. P. 7.7 3.7 200 (42) 1.7 2.2 57 64 207 136 20
E. B. 10.0 1.8 2.5 57 78 47 88
9.0 4.1 221 (54) 1.5 6.0 40 54 43 61
A.L. 7.0 3.2 165 (59) 7.0 27 30 31 86
9.0 6.3 121 (30) 6.3 6.3 43 37 59 128
O. R. 7.3 4.0 145 (40) 1.4 6.5 40 45 110 154 15
9.0 6.0 300 (33) 0.2 3.9 79 89 188 115 16
H. H. 7.1 3.9 128 (45) 0.2 0.5 45 61 250 188 34
10.6 5.4 208 (9) 0.4 1.6 97 131 285 220 27
A. D. 10.5 4.8 329 (54) 0.4 1.5 83 113 231 160 20
M. F. 8.0 5.0 214 (48) 1.0 0.9 105 142 250 97 19
* Per cent of vital capacity.
t Normal values for seven minute nitrogen washout are less than 2.5 per cent N2.
$ Normal values for single breath nitrogen test are less than 1.5 per cent N2.
§ Per cent of predicted value based on age (25).
The asthmatic patients had reduced vital capaci- changed from 66 to 44 mm. Hg. This patient has
ties, normal or increased residual volumes, uneven been studied five times over a period of 14 months;
distribution of inspired air, diminished maximal the studies demonstrate gradual progressive im-
breathing capacities and maximal flow rates, ar- provement with continued weight loss (see Tables
terial hypoxemia, and carbon dioxide retention. IV, V, and VI).
Following weight loss of 109 pounds, Patient The two patients with pulmonary emphysema
A. H. was unimproved as measured by pulmonary had reduced vital capacities, increased residual
function studies and arterial blood studies. Pa- volumes, uneven distribution of inspired air, re-
tient I. K. lost 149 pounds. She had the follow- duced maximal breathing capacities, and maximal
ing evidence of improvement: Vital capacity expiratory flow rates, hypoxemia, and carbon
changed from 51 per cent to 87 per cent of pre- dioxide. retention. Following weight loss of 26
dicted normal, arterial oxygen saturation in- pounds, Patient W. C. had improvement in ar-
creased from 90 per cent to 98 per cent and Pco2 teria). oxygen saturation, decrease in carbon diox-
1056 GEORGE N. BEDELL, WILLIAM R. WILSON, AND PAUL M. SEEBOHM

ide retention, more even distribution of inspired ventilation was 1.9 liters per minute, and the re-
air, and improvement in the measurements of sults of tests of mechanical function were abnor-
mechanical function. This man was probably mally low. The diagnosis of multiple pulmonary
benefited in part also by phlebotomy, salt restric- infarcts was proved at necropsy.
tion, and mercurial diuretics. Patient W. B. lost Patients I. F. K. and F. W. who had pulmo-
57 pounds in weight and improved similarly. His nary edema and L. R. and K. P. who had myx-
arterial oxygen saturation and Pco2 returned to edema had similar results. They had reduced
normal. vital capacities, normal or reduced residual vol-
The patient with multiple pulmonary infarcts umes, and reduced total lung capacties. All four
had severe hypoxemia and carbon dioxide reten- had normal distribution of inspired air but low
tion. On breathing 99.6 per cent oxygen for 10 diffusing capacities. Tests of mechanical func-
minutes, his arterial blood did not become fully tion were normal or only slightly impaired. All
saturated indicating that a sizable amount of blood four patients had arterial hypoxemia and three
was not coming into contact with ventilated alveoli patients had carbon dioxide retention. Following
before entering the left heart. His vital capacity weight loss of 72 pounds, I. F. K. had normal ar-
was 24 per cent of predicted normal, his alveolar terial oxygen saturation, increased vital capacity
TABLE VI
Arterial blood studies in obese paients with hypoxemia

02 02 saturation
Date of
content
(rest)
02
capacity (Rest) 100% 02*
Poo2
(rest) pH
Hema-
tocrit
Patient study Vol. % Vol. % % % mm. Hg (rest) %
A. H. 14 June 56 14.39 17.96 80.1 100 + 0.45 52 7.36 49
21 Feb. 57 15.21 21.38 71.1 96.5 59 7.30 62
I. K. 18 Sept. 56 16.65 18.45 90.2 100 + 1.22 66 7.26 58
7 Jan. 57 18.44 19.98 92.3 100 + 1.56 50 7.37 48
18 Mar. 57 17.80 18.44 96.5 100 + 1.81 48 7.35 46
28 May 57 17.30 17.27 100 + 0.03 100 + 2.15 39 7.42 43
12 Nov. 57 15.97 16.25 98.3 100 + 2.33 44 7.38 41
W. C. 21 Sept. 56 20.29 24.86 81.6 100 + 2.56 63 7.31 72
25 Oct. 56 19.16 20.21 94.8 100 + 1.77 50 7.34 52
W. B. 28 Nov. 56 20.16 23.41 79.3 100 + 0.06 51 7.38 65
23 Apr. 57 16.57 16.66 99.5 100 + 2.50 42 7.37 45
H. B. 13 Dec. 56 6.68 17.88 37.4 89.4 98 6.99 so
F. W. 24 June 57 14.85 17.44 85.2 100 + 0.91 47 7.38 47
I. F. K. 24 Jan. 57 17.56 19.54 89.9 100 + 1.77 32 7.53 50
6 Aug. 57 16.48 17.40 94.7 100 + 1.10 40 7.39 40
L. R. 14 Mar. 57 12.34 15.01 82.2 100 + 1.70 54 7.31 41
21 Nov. 57 13.96 14.64 95.4 42 7.36 37
K. P. 3 Sept. 57 12.99 14.33 90.6 100 + 0.75 49 7.34 37
E. B. 8 Dec. 55
19 Apr. 56 12.55 13.98 89.8 100 + 1.32 45 7.37 36
A. L. 16 Feb. 56 9.25 17.78 52.0 100 + 1.49 70 7.37 53
6 Mar. 56 18.23 22.08 87.3 46 7.39 60
0. R. 15 Aug. 57 13.97 18.30 76.3 100 + 1.60 48 7.36 50
15 Oct. 57 16.27 18.83 86.4 100 + 1.00 48 7.36 51
H. H. 7 Mar. 57 14.99 16.54 90.6 100 + 0.71 45 7.36 41
15 July 57 15.45 15.46 99.9 100 + 1.90 44 7.36 39
A. D. 27 Aug. 57 15.56 16.80 91.4 100 + 0.96 45 7.39 40
M. F. 27 June 57 17.19 18.60 92.4 100 + 1.49 40 7.38 43
* Values
following + sign refer to ml. 02 per 100 ml. blood in excess of that required to saturate hemoglobin (i.e.,
dissolved 02). Normal value for dissolved 02 is 2.00 ml.
 PULMONARY FUNCTION IN OBESE PERSONS 1057
and residual volume, and improvement of maxi- In 28 we found 10 who had alveolar hypoventila-
mal breathing capacity and maximal flow rates. tion as manifested by increased arterial Pc2.
Diffusion returned to normal. Patient L. R. lost Five other obese persons had hypoxemia not as-
143 pounds and in addition received dessicated sociated with alveolar hypoventilation. Alveolar
thyroid for myxedema. Repeat studies demon- hypoventilation was associated with myxedema or
strated normal arterial oxygen saturation, normal lung abnormalities including bronchial asthma,
Pco2, only minor changes in lung volumes, in- emphysema, infarction, edema, and lung disease
creased alveolar ventilation, and improvement in of unclassified type. Others (32, 33) have re-
the maximal breathing capacity and maximal flow ported alveolar hypoventilation in obese patients
rates. Diffusion returned toward normal. Pa- who had normal lungs but who were thought to
tients F. W. and K. P. have not been restudied. have a lesion of the medullary respiratory center.
Three patients (E. B., A. L. and 0. R.) had Disorders of the muscles of respiration such as
laboratory evidence of lung disease of unclassified poliomyelitis could produce an abnormal ventila-
type resembling pulmonary emphysema. They tory response in obese persons and be associated
had reduced vital capacities, normal or increased with alveolar hypoventilation. We have no such
residual volumes, uneven distribution of inspired cases but no doubt they exist.
air, reduced maximal breathing capacities, and se- The existence of alveolar hypoventilation in any
verely reduced maximal flow rates with the ex- patient must be caused by lung disease, malfunc-
piratory flow rates being reduced out of propor- tion of the chest bellows, inadequate neuro-mus-
tion to the reduction in inspiratory flow rates. cular coordination, or a central nervous system
Diffusion was low in the one patient in whom it lesion. The physiologic problem in the obese pa-
was measured. Study of the patients' arterial tient with hypoventilation is to identify in which
blood revealed hypoxemia and carbon dioxide re- of these four areas lies the derangement of func-
tention. All three patients have beep restudied tion. Others have advanced the following theory
after weight loss. Weight loss varied from 31 to explain alveolar hypoventilation in obese people
pounds in Patient E. B. to 46 pounds in Patient who have normal lungs. In the obese individual
A. L. In two patients the vital capacity increased. the work of breathing is increased (16, 34). Some
The residual volume was unchanged in two pa- increased work of breathing can be tolerated, but
tients but increased in one patient. Alveolar ven- when obesity reaches a certain point the work of
tilation increased in all three patients. All three breathing becomes excessive and the patient ad-
patients still have evidence of uneven distribution justs to suboptimal ventilation by development of
of inspired air. After weight loss, two patients a refractory medullary state, thereby permitting
were improved as measured by the maximal alveolar hypoventilation. When weight is re-
breathing capacity test; the other patient did worseduced, the work of breathing is reduced, normal
on retesting. Maximal flow rates continue to be medullary activity reappears, and the alveoli are
abnormal in all three patients. The diffusing ca- properly ventilated. No one has demonstrated
pacity has not changed in the one patient in whom the point at which the work of breathing becomes
this was studied. Study of the arterial blood in so excessive that alveolar hypoventilation is pre-
two patients before and after weight loss demon- ferable to a further increase in the work of breath-
strated improved oxygen saturation in both, and ing. Our group of obese patients with normal
a fall in Pco2 toward normal in one. lungs consists of people between the ages of 19
Three patients (H. H., A. D. and M. F.) had and 67 years and weighing as much as 382 pounds.
arterial hypoxemia without evidence of lung dis- None of these persons had alveolar hypoventila-
ease. Patient H. H. lost 41 pounds in weight. tion. Our obese persons with normal lungs toler-
This was associated with a return of arterial oxy- ated the increased work load satisfactorily. We
gen saturation to normal. believe that the obese patient with normal lungs
and a normal respiratory center may be able to
DISCUSSION move his chest enough to provide adequate ven-
We sought to determine the frequency and na- tilation. However, we still must deal with the
ture of alveolar hypoventilation in obese persons. mechanism of production of alveolar hypoventila-
1058 GEORGE N. BEDELL, WILLIAM R. WILSON, AND PAUL M. SEEBOHM

tion in obese patients without disease of the lungs. mentioned which is transient, which results in
Is it possible that obesity alone, by putting a se- temporary hypoventilation, and which eventually
vere load on the respiratory bellows, leads to a clears up regardless of whether or not the patient
derangement of the respiratory center? Whether loses weight. This mechanism, a transient lesion
obesity alone is enough to produce such a lesion in one of these four areas, for example a pulmo-
we cannot say. We have no evidence to support nary infarct or edema of the medullary respira-
the theory that it does. Nor can we say categori- tory center, could explain some of the cases re-
cally that it doesn't. If such patients exist we have ported by others. Then, too, some of the patients
not studied one, although we have searched dili- reported by others were studied incompletely and
gently for one. thus the possibility of lung disease was not ex-
We suspect that the increased work of breath- cluded. Other patients had "complete" studies,
ing when associated with even mild lung disease, but this implies only that all available tests were
malfunction of the muscles of respiration, or a done. Lung disease can exist in the presence of
central nervous system lesion is enough to pro- normal "complete" pulmonary studies.
duce alveolar hypoventilation and the events which Necropsies have been done on several patients.
follow. Others have shown that weight loss re- One patient had mild emphysema (17), one pa-
duces the work of breathing (16) and improves tient had bronchopneumonia (13), one patient
alveolar ventilation. We believe that this mecha- had extensive thrombi in the pulmonary trunk and
nism is responsible for the improvement in lung pulmonary arteries with infarction of the lower
function in our obese patients who lost weight. lobe of the right lung (15), and one patient had
However, weight reduction alone does not cor- pulmonary artery atherosclerosis, focal areas of
rect underlying lung disease. One of our asth- atelectasis, and recent pulmonary infarction (35).
matic patients (A. H.) lost weight but discon- The patient studied by us (H. B.) who died had
tinued her cortisone. At this point pulmonary extensive pulmonary infarction.
function tests showed that she was worse than Two of our patients with alveolar hypoventilation
before weight reduction. had myxedema. These patients may have had
Three of our patients had laboratory evidence of pulmonary edema to explain reduced vital ca-
lung disease of unclassified type. This lung dis- pacity, reduced diffusing capacity, and hypoxemia.
ease was characterized by reduced vital capacity, The mechanism of production of hypercapnia is
normal or increased residual volume, uneven dis- unknown; however, we can postulate a myxede-
tribution of inspired air, reduced maximal breath- matous lesion involving the muscles of respiration
ing capacity, reduced maximal flow rates with the or the central nervous system to produce alveolar
expiratory flow rate being reduced out of pro- hypoventilation.
portion to the reduction in the inspiratory flow Three patients had hypoxemia without evi-
rate, and diminished diffusing capacity. Follow- dence of lung disease. The most reasonable ex-
ing weight loss, all three patients continued to planation for hypoxemia in these persons is that
have uneven distribution of inspired air and ab- they had a disturbance in ventilation perfusion
normal mechanical tests. These persistent ab- ratios, either mixed venous blood perfusion of
normalities are consistent with a structural defect underventilated lung areas or overperfusion of
similar to that seen in local and diffuse pulmonary normally ventilated lung areas. Some support for
emphysema, although clinical evidence of either this comes from the fact that two of the three failed
condition was not present. In these patients the to come to full values for oxygen saturation after
pulmonary abnormalities were mild in degree but breathing 99.6 per cent oxygen for 10 minutes.
they were associated with hypoxemia and carbon The third patient has an arterial saturation of
dioxide retention. Pulmonary insufficiency could 92.4 per cent while breathing room air. This is
be reversed by weight reduction but evidence of just below the normal range. These patients did
lung disease persisted. not develop the "Pickwickian Syndrome" as al-
A possibility exists that the obese patient may veolar hypoventilation was not present.
have a lesion in one of the four areas previously Several of our patients clinically resembled the
 PULMONARY FUNCTION IN OBESE PERSONS 1059
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