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© 1984 S. Kargcr AG. Basel
0025-7931/84/0461 -0026 S 2.75/0
Respiration 46: 26-32(1984)
Pulmonary Haemodynamics at Rest and during Exercise in
Patients with Sarcoidosis
Jartusz Gtuskowski, Iwona Hawrylkiewicz, Dobiesfaw Zych. Andrzej Wojtczak,
Jan Zielinski
Second Department of Medicine, Institute of Tuberculosis, Warsaw, Poland
Key Words. Pulmonary sarcoidosis • Pulmonary haemodynamics • Physical exercise •
Lung function data
Introduction
Sarcoidosis is a granulomatous disease
or syndrome of unknown origin. In the
majority of cases it resolves spontaneously
or after steroid therapy. However, in
about 10% of patients the disease is not
treated or, despite treatment, is progress­
ing into a chronic form with development
of diffuse fibrotic changes leading to re­
spiratory failure and pulmonary hyperten­
sion [I, 17].
It is well known that in patients with
sarcoidosis there is no close correlation
between radiological changes and disturb­
ances in pulmonary function. Small gran­
ulomas, barely discernible on chest radio­
grams, disseminated in the lung parenchy­
ma, can sometimes produce greater pul­
monary functional impairment than easily
visible infiltrations [14]. It seems probable
that the same is true as far as the involve­
ment of pulmonary vessels in granuloma­
tous lesions is concerned. Pulmonary
function in sarcoid patients has been stud­
ied extensively [8-11, 13], but there are few
works on pulmonary circulation. They
were based on a small number of patients
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Abstract. Pulmonary haemodynamics at rest and during exercise was studied in 30
patients with histologically confirmed sarcoidosis. All subjects were divided into three
groups according to the stage of the disease assessed by radiological image of pulmon­
ary lesions. At rest, in stage I and II patients, the mean pulmonary pressure (P.\p) was
normal. In stage III patients, a slight pulmonary hypertension was found. During exer­
cise, a rise in Pap in stage I and II subjects was within the normal limits for a given work­
load, although in individual stage II subjects a rise in PAp was abnormally high. In all
stage III patients a rise in Pap was pathologically elevated.
27
Pulmonary Haemodynamics in Patients with Sarcoidosis
Table I. Pulmonary function in studied patients
Variables
Stage 1
Stage 11
Stage 111
Statistical
significance
of differences
VC, litres
5.0 ±0.9
4.5 ± 1.5
3.4 ± 1.5
1-11
NS
I-II1 p< 0.0l
I1-I1I NS
VC % N
96 ± 10
91 ±22
68 ±24
l-II
NS
I-III p< 0.0l
I1-1II p < 0.05
FEV,, litres
4.0 ± 0.7
3.4 ± 1.1
2.3 ± 1.2
I-II
NS
I-III p< 0.0l
II-III NS
FEV,, % N
80 ±9
78 ± 12
68 ± 14
l-II
NS
I-III p < 0.05
II-III NS
CJ)n. ml/cm H ,0
218 ± 67
179 ±49
122 ± 58
l-II
NS
I-III p<0.01
II-III p < 0.05
C„, ml/cm H, O
229 ±58
202 ± 56
152 ±72
l-II
NS
l-IIl p < 0.05
II-III NS
39 ± 17
34 ± 14
39 ± 13
P« nu»'Cm H ,0
I-II
NS
I-III NS
II-III NS
VC = Vital capacity: VC % N = vital capacity, % of normal value; FEV, = forced expiratory volume in I s:
FEV, % N “ forced expiratory volume in I s, % of predicted value; Cdyn —dynamic compliance; C„ = static
compliance; P„ max= static elastic recoil pressure; NS = differences not significant. Mean values ± SD.
Material and Methods
Pulmonary haemodynamics at rest and during
exercise were studied in 30 patients with histological­
ly confirmed sarcoidosis. Diagnosis was established
by different biopsy techniques (lymph node, bron­
chial mucous membrane, lung tissue) an d /o r by pos-
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studied at a rather late stage of the disease
[4 , 12, 15, 16].
The aim of this investigations was to
study pulmonary circulation at rest and
during exercise in different stages of pul­
monary sarcoidosis.
Gtuskowski/Hawrytkiewicz/Zych/Wojtczak/Zieliñski
28
Table
cice(B)
II.
Blood gases and haemodynamic data in studied patients, at rest (A) and at the 7th min of exer-
B
A
B
A
B
Statistical
significance of
differences
X 89
SD ± 15
141
22
84
13
142
29
91
10
139
18
all differences
not significant
X 19
SD ± 3
27
5
17
5
29
10
24
II
46
21
IB-IIIB p <0.05
X 5.95
SD ±2.I
_
-
10.89
5.5
_
-
6.25
2.8
_
mm Hg
-
I A—111A p<0.05
11A—111A p <0.05
P a0 2,
mm Hg
X 84
SD±6
85
8
81
10
87
9
81
8
69
12
IB-IIIB p <0.01
IIB-IIIB p < 0.01
PaCO„
mm Hg
X 33
SD ± 4
34
4
33
6
34
6
36
5
40
6
IB-IIIB p <0.05
Cl,
1/min/nF
X 4.3
SD+1.6
10.6
3.7
3.8
1.6
9.5
4.0
4.8
1.4
10.2
3.9
all differences
not significant
Variables
Stage
A
Heart rate
beats/min
r AP»
mm Hg
4 f* A IV
Stage
1
Stage
11
111
itive Kveim test. All subjects were divided into three
groups of 10 patients each, according to the radiolog­
ical stage of pulmonary lesion (stage I - bilateral hi­
lar lymphadenopathy, stage il - hilar lymphadenopathy + pulmonary infiltration, stage II! -pulm onary
infiltration with or without fibrosis).
There were 26 men and 4 women in the group
studied, aged from 21 to 59 years, mean age in stage I
- 32.4 years, in stage 11 - 33.5 years and in stage 11140.7 years. None of the patients suffered from
systemic hypertension or any other disease. In all
subjects pulmonary function tests were performed,
comprising measurements of vital capacity (VC),
forced expiratory volume in I s (FEV,), FEV,%VC
ratio, static and dynamic compliance (C„ and Cdy„)
and static elastic recoil pressure (P„ m„). Spirography
was done using a dry spirometer (Vitalograph). Nor­
mal values were those of Berglund et al. [2]. Pulmon­
ary mechanics were measured in a constant-volume
body pletliysmograph (Bodytest, Jaeger).
Pulmonary artery catheterization was carried out
by the floating catheter method [6] in the supine posi­
tion. Pulmonary arterial, right ventricular and right
atrial pressure were measured with a 746 SiemensElema pressure transducer and recorded simultane­
ously with an ECG lead on a Mingograph 34 recor­
der. The hydrostatic zero level was at 5 cm below the
sternal angle. Arterial and mixed venous oxygen,
carbon dioxide, tension and pH were measured by
Radiometer microelectrodes. Minute ventilation and
oxygen consumption were measured with an auto­
matic gas analyser (Metabolic Measurement Cart,
Beckman). Cardiac output was calculated according
to the Fick principle.
The initial haemodynamic measurements were
taken after 10 min of resting and repeated at the 7th
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P.vp = Mean pulmonary artery pressure; APap = inspiratory to expiratory fluctuation of pulmonary arterial diastolic pressure; P a02= arterial oxygen tension; PaC 02=■arterial casbon dioxide tension; Cl = cardiac
index.
29
Pulmonary Haemodynamics in Patients with Sarcoidosis
Results
Details of lung function data in the
three groups studied are presented in table
1. Vital capacity was normal in stage I of
pulmonary sarcoidosis, slightly lowered in
stage II and markedly decreased in stage
III. The same applied to the forced expira­
tory volume in 1 s. Dynamic and static
pulmonary compliance were normal in
stage I patients, borderline in stage II pa­
tients and lowered in stage III patients.
Static elastic recoil pressure was slightly
elevated in all stages. There was a consid­
erable scatter of individual values. Statisti­
cal analysis showed significant differences
for all variables between stages I and III
and for some indices between stages II
and III.
Haemodynamic and blood gases data
at rest and on exercise are presented in
table II. Exercise heart rate equalled the
predicted submaximal. Arterial oxygen
tension (PaCK) at rest was normal in all
subjects. During exercise there was no
change in PaC>2 in stage I and an increase
of 6 mm Hg (0.78 kPa) in stage II was ob­
served. In stage III PaCb decreased by
12 mm Hg (1.56 kPa). Arterial carbon di­
oxide tension was normal at rest in all
stages. It slightly increased on exercise in
stage III patients. Mean pulmonary pres­
sure ( P a p ) at rest was normal in almost all
stage I and II patients. Only 2 patients, 1
from stage I and 1 from stage II, had PAp
higher than 20 mm Hg (2.6 kPa). In 5 pa­
tients from stage III, a slight pulmonary
hypertension was found.
On exercise, the rise in PAp was within
normal limits for a given workload in
stage I and II subjects although in 3 cases
with stage II of the disease a rise in PAp
was abnormally high by 16 mm Hg,
(2.08 kPa); 20 mm Hg, (2.6 kPa), and
21 mm Hg, (2.73 kPa). In all patients with
stage 111, a rise in PAP was abnormally
high, above 10 mm Hg ( 1.3 kPa).
Inspiratory to expiratory fluctuations
of pulmonary arterial diastolic pressure (A
PApD) in stage I and II patients were
slightly higher than in healthy people. In
all stage III subjects, they were abnormal­
ly high.
Discussion
This study confirmed previous reports
[8-11] that there is no definite correlation
between radiological changes and disturb­
ances in pulmonary function, lung me­
chanics and pulmonary gas exchange in
patients with sarcoidosis. This is especially
expressed in stages 1 and II of the disease.
It appears that the same applies to the pul­
monary circulation. The results presented
suggest that in stage I of pulmonary sar­
coidosis, pulmonary circulation at rest is
normal, and the capacity of pulmonary
vascular bed assessed by the reaction to a
submaximal exercise remains intact. The
same was found in the majority of patients
with stage II of pulmonary sarcoidosis.
Nevertheless, in that stage we found 3 pa­
tients with a markedly abnormal reaction
of the pulmonary circulation to exercise. It
is interesting that lung compliance was ab­
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min of submaximal exercise on a bicycle ergometer.
The exercise workload was adjusted previously to
achieve a steady heart rate ranging between 80 and
90% of predicted maximal heart rate [3], Results were
statistically analyzed using Student’s t test.
Gtuskowski/Hawrylkiewicz/Zych/Wojtczak/Zielinski
normal in only 1 of them. Depending on tension and 2 further patients showed post­
the localisation of sarcoid lesions in rela­ exercise pulmonary hypertension.
Increased inspiratory to expiratory
tion to the anatomical structures import­
swings
of pulmonary arterial diastolic
ant for the alveolar ventilation and perfu­
sion, pulmonary function and pulmonary pressure found in the majority of our sub­
circulation can be more or less impaired. jects suggest that it is a sensitive sign of
This may explain the lack of correlation elevated elasticity of the lung. Fluctua­
between disturbances of pulmonary func­ tions of instantaneous pulmonary arterial
tion and the state of the pulmonary circu­ pressure closely follows intrathoracic
pressure changes exerted to inflate the
lation.
In most of the patients in stage III of lung on inspiration. In healthy people
sarcoidosis, there were signs of restricted they do not exceed 4 mm Hg (0.52 kPa).
pulmonary circulation. Even in subjects in They equalled around 6 mm Hg (0.72 kPa)
whom PAp at rest was normal, an increase in our stage I and II patients, suggesting
in PAp during exercise was abnormally that even in stage I of sarcoidosis there can
high, confirming severe limitation of the be infiltrations in the lung parenchyma in­
pulmonary vascular bed. In I extreme case visible on radiogram. Our findings are in
Pap increased up to 100 mm Hg (13 kPa), keeping with the data of Radwan et al. [14]
in 2 others to 50 mm Hg (6.5 kPa) and who found decreased compliance and in­
56 mm Hg (7.28 kPa), respectively. Our re­ creased static recoil pressure in patients
sults are in keeping with those of other au­ with stage I of sarcoidosis. In stage III res­
thors. McClement et al. [12] in 2 out of 8 piratory pressure swings were highly ab­
patients with stage 11 of sarcoidosis found normal which corresponds with severely
moderate pulmonary hypertension. Svan- impaired lung mechanics.
We have not been measuring the pul­
borg and Holmgren [16] in 37 patients with
sarcoidosis studied pulmonary circulation monary wedge pressure which influences
at rest and during submaximal exercise. the pulmonary artery mean pressure but
Resting PAp in stages 1 and II patients was there was no evidence that the earlier
normal. The reaction to exercise in all could be elevated. Although sarcoidosis of
stage 1 patients and in most patients with the heart seems to be more frequent that
stage II was also normal. Some patients commonly believed [5], it features mainly
with stage III had resting pulmonary hy­ as conduction defects [20], None of our
pertension. In almost all those patients, patients had heart enlargement or ECG
they observed an abnormal reaction of the changes suggesting sarcoidosis of the
heart.
pulmonary circulation to exercise.
They were also free of any other heart
Emirgil et al. [4] also found in the ma­
jority of their patients with stage III of sar­ disease. We could assume that pulmonary
coidosis resting pulmonary hypertension wedge pressure in our patients was nor­
and an abnormally high rise in PAp during mal. The mean decrease of PaC>2 during
exercise. Recently, Rizzato et al. [15] in 2 exercise in our patients with stage III by
out of 4 patients with stage III of sarcoid­ 12 mm Hg (1.56 k Pa) suggests severe im­
osis have found resting pulmonary hyper­ pairment of pulmonary gas exchange due
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30
to fibrotic changes in the lung parenchy­
ma [8, 11]. The reaction to exercise ex­
pressed as a rise in PAP and a fall in PaCb
observed in patients with stage III of sar­
coidosis was similar to that reported in pa­
tients with idiopathic pulmonary fibrosis
[7, 18, 19].
The most interesting findings seem to
be our observations of pulmonary haemo­
dynamics in patients with stage II of the
disease. Our results suggest that in spite of
a similar lung involvement assessed by
chest radiogram in patients with stage II
of sarcoidosis there are markedly ex­
pressed differences in haemodynamic da­
ta, especially during exercise. It seems that
these differences do not depend on the
severity of disturbances of pulmonary
function, but are probably due to differ­
ences in localisation of sarcoid granulo­
mas in relation to pulmonary artery pe­
ripheral branches [21 ].
In most centres the indication for ster­
oid therapy is the degree of limitation of
pulmonary function [1, 8-13]. We believe
that evaluation of pulmonary haemody­
namics in patients with borderline indica­
tion for treatment may contribute valuable
information helping to make a proper de­
cision.
References
1 Battesti. J.P.: Georges, R.: Basset, F.; Saumon,
G.: Chronic cor pulmonale in pulmonary sarcoid­
osis. Thorax 33: 76-86(1978).
2 Berglund. E.; Birath. G.: Bjure, J.; Grimby, G.;
Kjellmer, I.; Sandquist, L.: Soderholm, B.: Spirometric studies in normal subjects. Acta med.
scand. 173: 185-206(1963).
3 Borg, G.; Linderkolm, H.: Perceived exertion and
puls rale during graded exercise in various age
31
groups. Acta med. scand., suppl. 472, pp. 194-204
(1967).
4 Emirgil, C.; Sobol, B.: Herbert, W.; Trout, K.:
The lesser circulation in pulmonary fibrosis sec­
ondary due to sarcoidosis and its relationship to
respiratory function. Chest 60: 371-378(1971).
5 Fleming, H.A.: Sarcoid heart disease: a review
and an appeal. Thorax 35: 641-643 (1980).
6 Grandjean, T.: Une microtechnique du cathété­
risme cardiaque droit praticable au lit du malade
sans contrôle radioscopique. Cardiologia 51:
184-192(1967).
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at rest and on exercise in patients with idiopathic
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IS: 403-410(1982).
8 Kowalski. J.; Grçbska, E.; Lung elasticity in dis­
seminated lesions. Gruzlica 43: 813-823 (1975).
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Pulmonary Haemodynamics in Patients with Sarcoidosis
GIuskowski/Hawrytkiewicz/Zych/Wojtczak/Zielihski
16
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Received: November 30, 1982
Accepted: August 4, 1983
Jan Zielinski, MD,
II Klinika Chorob Wewnetrznych.
Instytut Gruzlicy,
Plocka 26,
01-138 Warsaw (Poland)
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