LUNG HYPOPLASIA IN CONGENITAL PVS/De Troyer, Yernault, Englert
12. Friedman WF, Pool PE, Scobowitz D, Seagren SC, Braunwald E: Sympathetic innervation of the developing rabbit heart. Circ Res 33: 25,
1968
13. Lebowitz EA, Novick JS, Rudolph AM: Development of myocardial
sympathetic innervation in the fetal lamb. Pediat Res 6: 887, 1972
14. Graham TP Jr, Lewis BW, Jarmakani JM, Canent RV Jr, Copp MP:
Left heart volume and mass quantification in children with left ventricular pressure overload. Circulation 41: 203, 1970
15. Romero T, Covell L, Friedman WF: A comparison of pressure-volume
647
relations of the fetal, newborn, and adult heart. Am J Physiol 222: 1285,
1972
16. Tsakiris HE, Donald DE, Sturm RE, Wood EH: Volume ejection fraction, and internal dimensions of left ventricle determined by biplane
videometry. Fed Proc 28: 1358, 1969
17. Hirshleifer J, Crawford M, O'Rourke RA, Karliner JS: Influence of
acute alterations in heart rate and systemic arterial pressure on echocardiographic measures of left ventricular performance in normal human
subjects. Circulation 52: 835, 1975
Lung Hypoplasia
in Congenital Pulmonary Valve Stenosis
ANDRE DE TROYER, M.D., JEAN-CLAUDE YERNAULT, M.D.,
AND MARC ENGLERT, M.D.
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
SUMMARY The pulmonary function of ten adult patients
with congenital pulmonary valvular stenosis was investigated.
The patients clearly showed smaller lungs than healthy control
subjects of equivalent age and height; lung elastic recoil pressure
was normal at any given percentage of measured total lung
capacity, indicating that postnatal parenchymal damage is not
the cause of the small lungs. The lung diffusing capacity for
carbon monoxide was reduced, reflecting the anatomical alterations
of the pulmonary vascular bed. Finally, the maximal flow-static
recoil curves showed a fixed (not dynamic) reduction of airway
dimensions: the critical transmural pressure in the collapsible flowlimiting segment (Ptm') was normal, but the conductance of the S
segment was lowered. These abnormalities most likely reflect inadequate development of the lung and suggest that pulmonary blood
pressure may be an important determinant of lung growth in the
postnatal period.
THE POSTNATAL DEVELOPMENT OF THE LUNG
has been the subject of extensive research in the last 20 years.
Investigators generally agree that most of the alveoli appear
in the postnatal period, but the age at which alveolar multiplication ceasesis still debated. Earlier data supported the
view that alveolar multiplication stopped at the age of eight
years,1'8 or even by the end of the first year of life.4 In contrast, recent morphometric investigations seem to indicate
that alveolar multiplication goes on throughout childhood,
and does not cease completely before somatic growth
stops.5-7 This latter view is supported by recent studies of
lung mechanics during growth.8
Moreover, the factors affecting lung growth in the postnatal period are not well understood, as discussed by Thurlbeck in a recent and extensive review.9 Until now, the
amount of blood flow through the lung has not been
considered an important determinant of parenchymal
development.9 This conclusion was based only on morphologic findings made in a few cases of congenital lobar overinflation.10 11 Human lung growth in conditions of abnormal
pulmonary blood flow and pressure has not been studied.
The present work reports the investigation of lung mechanics
in ten patients with congenital pulmonary valvular stenosis
in order to elucidate the role of pulmonary hemodynamics in
lung growth during the postnatal period.
Material and Methods
Lung mechanics were measured in ten adult nonsmoking
patients with congenital pulmonary valvular stenosis, four
men and six women whose ages ranged from 16 to 34 years
(mean ± SEM 22 ± 2 years). The results were compared
with those obtained in ten healthy young subjects of equivalent age and height, who had no clinical, radiographic or
functional evidence of respiratory disease. All patients had a
well-documented congenital pulmonary valvular stenosis;
the valvular stenosis was mild in one subject, moderate in
three and severe in six, based on the criteria used by Johnson
and co-workers.'2 None of the patients had a history of lung
disease; all patients but one had a normal cardiothoracic index on chest X-ray. In three patients, the pulmonary valvular stenosis was associated with a small right-to-left shunt,
due to a ventricular septal defect in one case, and to a patent
foramen ovale in two cases.
The techniques used for pulmonary function studies have
been described in detail elsewhere.18 14 All pulmonary function tests were carried out with the patient in the sitting position. Vital capacity (VC), total lung capacity (TLC), and
forced expiratory volume in 1 sec (FEV 1) were recorded by
spirometry, in conjunction with measurement of functional
residual capacity (FRC) and of residual volume (RV) by the
helium dilution technique. Lung diffusing capacity for carbon monoxide (DLco) and Krogh's constant (Kco) were
measured by the single-breath method.
Airway resistance (Raw) and plethysmographic FRC were
measured in a constant volume body plethysmograph.
Plethysmographic TLC was calculated by adding the
plethysmographic FRC to the inspiratory capacity obtained
From the Pulmonary and Cardiac Divisions, Department of Internal
Medicine, Saint-Pierre University Hospital, Brussels, Belgium.
Address for reprints: Dr. A. De Troyer, Department of Internal Medicine, Saint-Pierre University Hospital, Rue Haute 322, B-1000 Brussels,
Belgium.
Received March 14, 1977; revision accepted May 6, 1977.
VOL 56, No 4, OCTOBER 1977
CIRCULATION
648
TABLE 1. Anthropometric and Pulmonary Function Data
SEM) in Ten Patients with Congenital Pulmonary
Valve Stenosis
(mean
Control
Parameter
Age (years)
24
6
169
4.74
3.28
1.42
6.16
3.79
79
Sex (F: M)
Height (cm)
VC (liter)
FRC (liter)
RV (liter)
TLC (liter)
FEV 1 (liter)
FEV I/VC (%)
DLco
Patients
2
:4
3
0.37
0.31
0.17
i 0.51
0.29
3
-
(ml.min-'.mm Hg-') 28.0
1.5
0.09
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Kco (min-')
Raw
4.81
(cm H20.1-1lsec-1)
CL (liter-cm H2O-1)
CL/TLC (cm H20-')
1.9 W 0.2
0.234 0.028
0.038 = 0.003
=
22
6
168
3.46
2.70
1.42
4.88
2.73
79
=i 2
: 4
- 3
0.24t
-
O
0.15
0.14
0.30*
0.19t
2
21.5
3.94 4
1.8t
0.27t
0.2
1.8
0.140 0.015t
0.028 + 0.002t
*Significantly different from predicted values (P <0.05).
tP <0.01.
Abbreviations: VC = vital capacity; FRC = functional residual capacity; RV = residual volume; TLC = total lung capacity; FEV 1 = forced
expiratory volume in one second; DLco = diffusing capacity for carbon
monoxide; Kco = Krogh's constant; Raw = airway resistance; CL lung
compliance; CL/TLC = specific compliance.
-
during direct XY recording of the quasistatic expiratory
pressure-volume (PV) curve.8 18,14 Individual PV curves
were constructed as the mean of two to four correctly
recorded curves. The pressure variation between FRC and
FRC + 0.5 liter was used to calculate the expiratory compliance (CL), and specific compliance, defined here as compliance-TLC ratio (CL/TLC).
Maximal expiratory flow-volume (MEFV) curves were
obtained by measuring airflow at the mouth, with a Lilly
type pneumotachograph (the response of which was linear up
to 10 L/sec), and the volume by electric integration of the
flow signal. Maximal flow-static recoil (MFSR) curves were
constructed by plotting maximal expiratory flow (VE max)
expressed in TLC/sec against static transpulmonary
pressure at the same lung volume using MEFV and PV
curves. From the MFSR curves we calculated the slope of
the curve between 80% and 50% TLC, which is the conductance of the S segment (Gs) according to the model described
by Pride and associates.15 We also calculated the intercept on
the pressure axis by extrapolating the MFSR curve to zero
VE max, using the slope between 80 and 50% TLC; this intercept represents the critical transmural pressure (Ptm') of the
collapsible flow-limiting segment.15
Results
The anthropometric data and pulmonary function measurements of patients and control subjects are presented in
table 1. For all the parameters of lung function, no difference appeared between the patients without and those with
right-to-left shunts. The VC, TLC, FEV 1, CL and CL/TLC
were significantly lowered in the patients as compared to
controls. There was no significant difference in RV, FRC,
FEV 1/VC, or Raw. In addition, the patients showed a
significant reduction in diffusing capacity; this reduction was
not due to the reduction in lung volume alone, since Kco was
significantly lowered also.
In figure 1, the mean PV curve obtained in the patients is
compared to that obtained in the control subjects. The graph
demonstrates clearly that the PV curve of the patients was
reduced on its volume axis: for any given transpulmonary
pressure there was a decrease in absolute lung volume. However, when volume was expressed as a fraction of measured
TLC (fig. 2), the curve was identical to the normal one.
6
100l
-
5
-J
-
-j
w
3
0
80
I.
I0
4
-.
60
-J
3
0
40 .
* NORi4L |
|o
PATIENTSI
2$1'
0
10
20
Pst (1)
30
(cm H20)
FIGURE 1. Relationship oflung volume in absolute value to static
recoil pressure of the lung (P st (1)) in patients with congenital
pulmonary valvular stenosis, and in normal subjects. Each bar
represents ± I SEM.
10
20
Ps t ( j)
30
(cm H20 )
FIGURE 2. Relationship of lung volume in percent of measured
total lung capacity (TL C) to static recoil pressure of the lung (P st
(1)) in patients with congenital pulmonary valvular stenosis, and in
normal subjects. Each bar represents ± I SEM.
649
LUNG HYPOPLASIA IN CONGENITAL PVS/De Troyer, Yernault, Englert
8
[
8
7
7
6
[
5
[
6
0
-J
J
4
5
x
3
<4
[
>
3I~
1
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
2
Io PATlENT
"I
0
60
70
80
VOLUME (% TLC)
FIGURE 3. Relationship of maximal expiratoryflow (PE max) to
lung volume in patients with congenital pulmonary valvular
stenosis, and in normal subjects. Each bar represents ± I SEM.
50
The relationship between VE max and lung volume is
presented in figure 3. At any given volume between 80 and
50% TLC, VE max was clearly decreased (P < 0.005); as
shown in figure 4, this reduction in airflow could not be accounted for by the loss of lung volume alone.
The relationship between VE max and lung static recoil is
presented in figure 5. In order to correct for differences in
lung size between patients and control group, VE max was
divided by TLC (VE max, TLC/s). The mean plots between
80 and 50% TLC are remarkably linear, both in patients and
in controls. The graph demonstrates that at any given driving pressure, flow rates in the patients were lower than normal (P < 0.02 or less), and moreover, the slope was steeper
in the control subjects than in the patients. The Gs (mean ±
SEM) in the control group was 0.079 ± 0.004 TLC per sec per
cm H20; it was below the normal range in seven of the
patients (mean ± SEM: 0.061 ± 0.009 TLC per sec per cm
H20), and the difference between the groups was significant
(P < 0.05). In contrast, Ptm' was within normal limits in all
patients, and the mean value of the intercept on the pressure
axis was similar to that obtained in normal subjects (-3.03
i1.
0 L-7/--I,e
.
50
80
70
60
VOLUME (% TLC pred.)
Relationship of maximal expiratoryflow (PE max) to
40
FIGURE 4.
lung volume expressed in percent ofpredicted total lung capacity
(TLC) in patients with congenitalpulmonary valvularstenosis, and
in normal subjects. Each bar represents ± I SEM.
patients thrombi are frequently found in pulmonary arteries.20' 21 A reduction of available capillary bed, and thereby a decreased lung diffusing capacity, could thus be expected.
In contrast, the alterations observed in mechanical lung
properties were unexpected since anatomical studies
reported the lung parenchyma to be normal in patients with
VEMAX
(T LC /S)1'5
1,0
cm H20).
Discussion
Lung function in patients with pulmonary valvular
stenosis has not been studied extensively. Only isolated cases
have been reported, and the data are poor and conflicting'6 '8: dynamic compliance has been reported to be normal6', 17 or low,'8 but other lung mechanical properties have
not been investigated.
The decrease in diffusing capacity found in our group of
patients is not surprising: a reduction both in number and in
caliber of preacinar and intraacinar arterioles has been
described in pulmonary valvular stenosis,'9 and in adult
0,51
_-,
A
-5
a
0
5
10
Pst(l) (cm
15
H20)
FIGURE 5. Relationship of volume-corrected maximal expiratory flow (V,E max) to lung static recoil (P st (1)) in patients with
congenital pulmonary valvular stenosis, and in normal subjects.
Each bar represents ± I SEM.
650
CIRCULATION
VOL 56, No 4, OCTOBER 1977
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congenital pulmonary valve stenosis.21 The current data
clearly demonstrate, however, that those patients have
smaller lungs than normal subjects of similar height and age.
Analysis of the PV curves indicates that postnatal parenchymal damage is not the cause of the small lungs. Indeed,
there is an essential difference between subjects with small
lungs due to parenchymal injury (for instance, in diffuse pulmonary fibrosis) and those with the same small lungs but
without parenchymal damage. In the former case, the subject has a chest wall which is appropriate for a larger lung
hemodynamics are not important determinants of human
postnatal lung growth is not supported by the results of the
current study. Indeed, from our data, it appears that an inflow obstruction, resulting in low intravascular pressure, prevents the normal development of lung parenchyma and
peripheral bronchial system. The hypothesis that the valvular heart disease and lung hypoplasia are independent
malformations, without cause-and-effect relationship, is
possible but seems very unlikely.
and the effect on the PV curve will be the same as a true increase in muscle strength: then, because of the greater
mechanical advantage of the inspiratory muscles, a supernormal maximum distending pressure can be applied to the
lungs so that P st (1) max is abnormally high, and in addition, when the PV curve is plotted as percent of the actual
TLC, the curve lies to the right of the predicted one, at least
at high lung volumes.22 25 In contrast, subjects with small but
normal lungs have a chest wall appropriate for the small
lungs; P st (1) max is then normal and the PV curve, when
plotted as percent of the actual TLC, is normal. This is the
pattern observed in our patients (fig. 2), and is consistent
Acknowledgment
with anatomical studies that failed to demonstrate any abnormality in the alveolar wall of patients with congenital
pulmonary valvular stenosis.2' It seems, thus, very likely that
the small lungs of these patients result from a growth failure
of the lung parenchyma. Whether this is due to a decrease in
number or in size of functional units cannot be definitely
assessed, since no morphometric data are available. Nevertheless, the low values obtained for specific compliance
would mean that the ratio of lung tissue to air per unit lung
volume is increased, i.e., that the number of alveoli per unit
volume is higher than normal. On theoretic grounds, it thus
may be speculated that the alveoli are decreased more in size
than in number.
In addition to alveoli, the small airways of patients with
congenital pulmonary valvular stenosis also appear to be
affected by growth failure. Indeed, the volume-corrected
MFSR curve shows that, at any given driving pressure, the
airflow is lower than normal. There is, thus, a greater than
normal upstream resistance (absolute value of VE max
divided by the value of P st (1))26 during forced expiration.
Since Raw is normal, obstruction to airflow must be located
in the small peripheral bronchioles.27' 28 Further analysis of
MFSR curves in terms of A VE max/A Pst (1) slope and of
the intercept of this slope on the static recoil axis (Ptm') supports the presence of a fixed (not dynamic) reduction of airway dimensions in our patients It is to be noted here that the
values obtained both for Gs and for Ptm' in our normal subjects are very close to those previously reported.29 90 The
Ptm' of the patients is similar to those of normal subjects,
which implies that the compliance of the bronchial wall (collapsible flow-limiting segment) is normal. In contrast, the
lowered Gs means that the cross-sectional area of airways at
the equal pressure points is smaller than normal. All of the
patients being nonsmokers, it
seems reasonable to assume
that this reduction in airway dimensions is also a consequence of underdevelopment of the lung. We are unable to
determine whether this is due to a reduction in the number or
in the caliber of parallel airways.
The commonly accepted assumption that pulmonary
We gratefully acknowledge the excellent technical assistance of Mrs. H.
Malrait, J. Bourbigot, and C. Van de Zande; and the secretarial work of
Mrs. B. Noel.
Appendix
Definitions and Abbreviations of Terms of Pulmonary Mechanics
Lung elaslic recoil pressure (P st (1)): the difference between the alveolar
and the pleural pressures at a specified lung volume measured under static
conditions. P st (1) max is the elastic recoil pressure of the lung at total lung
capacity.
Lung compliance (CL): the change in lung volume produced by a unit
change in lung elastic recoil pressure.
Specific compliance: compliance per unit of lung volume.
Flow-limiting segment: that segment of the bronchial tree which collapses
during forced expiration when its transmural pressure reaches a critical value
(Ptm'), so that expiratory flow is limited despite further increase in driving
pressure.
Conductance of the S segment (Gs): conductance of the airway segment
which extends from the alveoli to the flow-limiting segment.
References
1. Weibel ER: Morphometry of the Human Lung. New York, Academic
Press, 1963
2. Dunnil MS: Postnatal growth of the lung. Thorax 17: 329, 1962
3. Davies G, Reid L: Growth of the alveoli and pulmonary arteries in childhood. Thorax 25: 669, 1970
4. Hieronymi G: Ober den durch das Alter bedingten Formwandel menschlicher Lungen. Ergeb Allg Pathol Anat 41: 1, 1961
5. Emery JL, Wilcock PF: The post-natal development of the lung. Acta
Anat (Basel) 65: 10, 1966
6. Nakamura T, Takizawa T, Morone T: Anatomic changes in lung parenchyma due to aging process. Dis Chest 52: 518, 1967
7. Thurlbeck WM, Angus GE: Growth and aging of the normal human
lung. Chest 67: 3S, 1975
8. Baran D, Yernault JC, Paiva M, Englert M: Static mechanical lung
properties in healthy children. Scand J Resp Dis 57: 139, 1976
9. Thurlbeck WM: Postnatal growth and development of the lung. Am
Rev Resp Dis 111: 803, 1975
10. Hislop A, Reid L: New pathologic findings in emphysema in childhood:
I. Polyalveolar lobe with emphysema. Thorax 25: 682, 1970
11. Hislop A, Reid L: New pathologic findings in emphysema in childhood:
II. Overinflation of a normal lobe. Thorax 26: 190, 1970
12. Johnson LW, Grossman W, Dalen JE, Dexter L: Pulmonic stenosis in
the adult. Long-term follow-up results. N Engl J Med 287: 1159, 1972
13. Yernault JC, Englert M: Static mechanical lung properties in young
adults. Bull Physiopath Resp (Nancy) 10: 435, 1974
14. De Troyer A, Yernault JC, Englert M: Mechanics of breathing in
patients with atrial septal defect. Am Rev Resp Dis 115: 413, 1977
15. Pride NB, Permutt S, Riley RL, Bromberger-Barnea B: Determinants
of maximal expiratory flow from the lungs. J Appl Physiol 23: 646, 1967
16. Pryor WW, Hickam JB, Page EB, Sieker HO: Factors influencing
pulmonary compliance in heart disease. Am J Med 1.: 149, 1955
17. Haughton V: Changes in pulmonary compliance in patients undergoing
cardiac surgery. Dis Chest 53: 617, 1968
18. Verstraeten JM, Verstraeten J, Pannier R: La compliance pulmonaire
chez les sujets adultes presentant une cardiopathie cong6nitale. Arch
Mal Coeur 57: 1409, 1964
19. Haworth SG, Reid L: The pulmonary vasculature in congenital heart
disease. Proc of the 1st International Congress on Cardiac Lung,
Florence, 1976
20. Rich AR: A hitherto unrecognized tendency to the development of widespread pulmonary vascular obstruction in patients with congenital
pulmonary stenosis. Bull Johns Hopkins Hosp 82: 389, 1948
21. Damman JF Jr, Ferencz C: The significance of the pulmonary vascular
BLOOD PRESSURE INSTRUMENTS FOR CHILDREN/Webber et al.
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26.
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the heart in which there is pulmonary stenosis. Am Heart J 52: 7, 1956
Ostrow D, Cherniak RM: Resistance to airflow in patients with diffuse
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Yernault JC, De Jonghe M, De Coster A, Englert M: Pulmonary
mechanics in diffuse fibrosing alveolitis. Bull Physiopath Resp (Nancy)
11: 231, 1975
Gibson GJ, Pride NB: Lung distensibility in pulmonary fibrosis. Bull
Physiopath Resp (Nancy) 9: 1250, 1973
Gibson GJ, Pride NB: Lung distensibility. The static pressure-volume
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Mead J, Turner JM, Macklem PT, Little JB: Significance of the rela-
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651
tionship between lung recoil and maximum expiratory flow. J AppI
Physiol 22: 95, 1967
Macklem PT, Mead J: Resistance of central and peripheral airways
measured by a retrograde catheter. J Appl Physiol 22: 395, 1967
Hogg JC, Macklem PT, Thurlbeck WM: Site and nature of airway
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Leaver DG, Tattersfield AE, Pride NB: Contributions of loss of lung
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A Study of Instruments
in Preparation for a Blood Pressure Survey of Children
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LARRY S. WEBBER, PH.D., A. WOUTER VOORS, M.D., DR.P.H.,
THEDA A. FOSTER, M.S., AND GERALD S. BERENSON, M.D.
SUMMARY In preparation for the measurement of blood
pressure in children of a total geographic community, several
preliminary studies of the validity and reliability of various methods
and instruments for indirect blood pressure measurements were performed. These studies included Graeco-Latin Square designs, examination of children in a field setting, and assessments of the
replicability of reading automatically recorded blood pressures.
Each of the studies was designed to monitor the validity and
replicability of instruments, methods, and observers. Controlling for
subject, we computed biases due to instrument, method and observer
and, where possible, eliminated them in the ensuing studies. One
automatic instrument, the Physiometrics recorder, was selected and
used in conducting epidemiologic studies where it complements the
measurements by the mercury sphygmomanometer.
THE IMPORTANT ROLE OF MASS SURVEYS in
detecting individuals with hypertension has stimulated an interest in improving techniques and instruments for measuring indirect blood pressure. As new technology is applied,'
new insights are gained into the pathophysiology of blood
pressure control,2 furthering the need for improved methods
that will obtain valid and reliable indirect measurements.
Although automatic instruments could reduce such factors
as examiner fatigue and observer bias in measuring blood
pressure, a recent report suggests8 that the available instruments are not adequate for use in epidemiologic studies.
Our studies do not support this conclusion.
In preparing for an extensive survey of cardiovascular risk
factors in children, we investigated the currently available
automatic blood pressure instruments for measurement
reliability. The mercury sphygmomanometer was considered
the general reference instrument since it is so widely used by
physicians; however, several questions were posed: 1) Are
there differences among commonly used instruments that are
comparable to the standard mercury sphygmomanometer?
2) Do examiners using the same instruments on the same
subjects obtain different measurements? 3) Which instruments would be most satisfactory for studying children,
especially in a large survey? 4) In a complete field setting,
will the measurements be similar to those obtained under a
rigidly controlled statistical design? 5) Can the graphic recordings of automatic measuring devices be interpreted without reader bias? 6) Can differences among equally trained
readers be explained?
From the Departments of Medicine, Public Health and Preventive
Medicine, and Biometry, LSU Medical Center, New Orleans, Louisiana.
Supported by funds from the National Heart and Lung Institute,
Specialized Center of Research - Arteriosclerosis (SCOR-A), HL 15103.
Address for reprints: Gerald S. Berenson, M.D., Department of Medicine
(SCOR-A), LSU Medical Center, New Orleans, Louisiana 70112.
Received April 14, 1977; accepted May 6, 1977.
Materials and Methods
In these studies a number of instruments were used in
several experimental designs (table 1). We used as many
automatic instruments as became available. A recent
catalogue of all available automatic instruments has been
published,' which gives particulars concerning the instruments.
Arteriosonde 1216. The Arteriosonde registers phonosound Korotkoff signals detected by an ultrasonically produced Doppler principle. Systolic and diastolic pressures are
registered directly on vertical mercury columns when the
falling mercury automatically stops at these levels." 6
Bonn (Sela Electronics Co.). This instrument converts
Korotkoff sounds into visual or sonic signals but does not
produce a permanent record. The transducer is a
phonosound microphone.
Kass-Zinner (Boston) Automatic Recorder. Korotkoff
sounds, detected by phonosound microphone, are recorded
on electrocardiographic paper moving at a constant speed.
As in the Narco Physiograph, these sounds are superimposed
on the cuff pressure curve, which is calibrated by reference
standard square waves."
Mercury Sphygmomanometer (Baumanometer). We used
Lung hypoplasia in congenital pulmonary valve stenosis.
A De Troyer, J C Yernault and M Englert
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Circulation. 1977;56:647-651
doi: 10.1161/01.CIR.56.4.647
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1977 American Heart Association, Inc. All rights reserved.
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