Comparative response of right and left ventricles to volume overload

PEDIATRIC CARDIOLOGY

Comparative Response of Right and Left Ventricles To Volume Overload

RAJAMMA

MATHEW,

(Edin) OTTO G. THILENIUS, RENE

A.

Chicago,

ARCILLA,

MBBS, MD, MD,

MRCP

FACC

FACC

Illinois

From the Cardiology Section, Department of Pediatrics, Wyler Children’s Hospital, The University of Chicago Pritzker School of Medicine, Chicago, III. This study was supported in part by a grant (RR-305) from the General Clinical Research Centers Program of the Division of Research Resources, National Institutes of Health, and by a grant from the American Heart Association (#71-658). Manuscript received July 21, 1975; revised manuscript received September 30. 1975, accepted October 29, 1975. Address for reprints: Rene A. Arcilla, MD, Department of Pediatrics, Wyler Children’s Hospital, University of Chicago, 950 E. 59th St., Chicago, Ill. 60637.

The cardiac volume data of 49 normal children were compared wlth those of 23 with secundum atrial septal defect and 24 with patent ductus arteriosus. Significantly smaller ventricular end-diastolic volumes were observed in the normal infants than in older children (right ventricle 53.9 versus 75.5 cm3/m2; left ventricle 46.7 versus 63.6 cm3/m2). “Distensibility” of the right ventricle ( DRV), left ventricle ( DLV) and left atrium increased normally with age. DRv and D Lv were slmllar shortly after birth; thereafter, DRV increased more rapidly than DLv (mean DRv 12.7; mean DLV 7.6 cm3/m2 per mm Hg, P
Angiocardiography provides anatomic details of the heart and great vessels not reproducible by any other method. The excellent radiologic reproduction has enabled estimation of left ventricular,1-5 right ventricular,5-8 left atria14*g-11 and right atrial12 volumes as additional measures of cardiac performance. This approach is especially useful for the comparative analysis of right and left heart function. The purpose of this investigation was to evaluate the response of the ipsilateral (involved) ventricle and of the contralateral (unaffected) ventricle to isolated volume overload of the right or left heart. The pressure and volume data of the right ventricle, left ventricle and left atrium of 23 children with isolated secundum atria1 septal defect and of 24 children with isolated patent ductus were analyzed. These values were compared with similar data obtained from 49 children with normal hemodynamic status. Materials

and Methods

Volume estimation: The methods used to estimate the volume of the ventricles and left atrium have been reported previously.5*g The surface areas of the frontal and lateral images were obtained from the angiocardiograms by planimetry; in addition, the distances from apex to base in the ventricular images and the maximal diameters in the left atria1 images were measured. Volume calculation was by the parallelepiped method for the ventricles5J3 and by the arealength method for the left atrium.g The initial volume estimates were corrected by regression equations specific for each chamber: V, = 0.65 V, + 0.01 (right

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TABLE

ET AL.

I

TABLE

Cardiac Chamber Volumes in Normal Children

Related to Body Surface

r RVEDV Infants (no. = IO) Children (no. = 34) LVEDV Infants (no. = IO) Children LA max fno’ = 3g) infants (no. = IO) Children (no. = 37)

Regression

Area

Comparative Values for Chamber Volume and Ventricular Output in’hlormal Infants and Children (mean + standard error)

Equation Variable

0.75

Vfcm”)

= 60.29

BSA -

2.69

0.94

Vfcm?

= 93.53

BSA -

15.25

0.84

V(cm’)

= 73.65

BSA -

8.85

0.89

Vfcm’)

= 63.77

BSA -

0.16

0.84

Vfcm?

= 47.40

BSA -

4.63

0.87

Vfcm?

= 37.58

BSA -

0.90

ventricle); V, = 0.77 V, + 1.17 (left ventricle); and V, = 1.143 V, + 0.14 (left atrium) where V, = corrected volume and V, = initial estimate. These equations have been derived from in vitro studies relating true volumes of casts made of the heart to the volumes estimated from the radiologic imagesgJ3 The angiocardiograms were obtained in the frontal and lateral projections using Phillips biplane, dual mode (5 and 9 inch [12.7 and 22.9 cm]) cesium iodide image intensifier tubes with fixed tube to film distances of 81 cm in the frontal projection and 89 cm in the lateral projection. A Datacor system facilitated timing of each X-ray exposure through display of the electrocardiogram and pressure-pulse curve in the tine film. The electrocardiogram and pressure curves were also recorded on paper at speeds of 50 or 75 mm/set. Different correction factors for X-ray magnification were used for the three chambers depending on their respective distances from the X-ray grids.14 Protocol: The infants were studied without sedation; the older children were given Demerolo and Vistarila intramuscularly (1.5 to 1.8 mg/kg body weight of each, up to 50 mg) for premeditation. For the Fick cardiac output calculations, oxygen consumption was determined only in 10 children in the normal group, in 5 of those with atria1 septal defect and in none of those with patent ductus arteriosus; in the rest, normal oxygen consumption15 was assumed. Cineangiocardiography was performed after cardiac catheterization; 35 mm movie cameras were used at filming rates of 80 frames/set in the infants and 64 frames/set in the older children. Renografin 76’s’ in a dose of 1.0 to 1.5 ml/kg was used as the contrast medium. For the right ventricular analysis, the contrast material was injected into the right atrium to avoid ventricular arrhythmias that otherwise frequently occur during high pressure injection into the ventricles. A second injection of contrast medium was usually made into the pulmonary trunk for diagnostic purposes or better visualization of the left ventricle, or both. At least 10 minutes was allowed between injections. In 15 children with atria1 septal defect and in 21 with patent ductus arteriosus, the right atria1 angiocardiograms were of sufficient contrast to enable border delineation of the left atrium and left ventricle as well. In the remaining patients, the left heart volume analyses were derived from the pulmonary angiograms. The heart rates at the time of right and left

August 1976

Heart rate fbeats/min) RVEDV (cm3/m2) RVO fliter/min par m2) LVEDV (cm3/mz) LVO (literlmin par m*) LAmax km3/mZ)

BSA = body surface area fin m’); LAmax = left atrial maximal volume;.LVEDV = left ventricular and-diastolic volume.; r = correlation ;;f?uff;;ent; RVEDV = rrght ventrrcular end-diastolrc volume; V =

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Children (2 to 19 vr) 106.21 + 2.57 (no. = 39) 75.48 I? 2.26 (no. = 34) 4.83 * 0.25 (no. = 34)

Infants (4 days to 14 mo) i 5.4 = 10) k 3.14 = IO) t 0.24 = IO)


63.56 + 1.83 (no. = 39) 4.77 * 0.19 (no. = 37)

46.67 + 3.28 (no. = IO) 4.22 + 0.22 (no. = 9)


36.63

33.82

+ 1.13

(no. = 34)

135.5 (no. 53.86 (no. 4.2 (no.

P Value

i- 2.37


NS

NS

(no. = IO)

= left ventricular LA max = left atrial maximal volume; LVEDV and-diastolic volume; LVO = left ventricular output (systemic blood flow); NS = not significant; f value = level of significance (t test); RVEDV = right ventriculaT end-diastolic volume; RVO = right ventricular output (pulmonary blood flow).

heart opacification were essentially identical during the atria1 angiograms; the heart rates during the pulmonary angiograms did not differ by more than 10 beats/min from those during the corresponding atria1 angiograms. Case material: The 23 infants and children with atria1 septal defect ranged in age from 0.3 to 14.6 years (mean 5.4), and the 24 with patent ductus arteriosus from 2 weeks to 9 years (mean 3.4 years). The diagnosis was surgically confirmed in all but seven of the former and two of the latter who are still awaiting surgery. The left to right shunt was localized by hydrogen inhalation curves, blood oxygen analyses and selective angiocardiography. No patient had congestive heart failure or a right to left shunt. There was no associated valvular stenosis or regurgitation. Postoperative clinical evaluation revealed normal cardiac findings. The cardiac chamber volumes of 49 children with normal cardiac catheterization findings were also analyzed. These children were referred for hemodynamic evaluation because of suspected organic heart disease or unusual chest roentgenographic findings (vascular ring, mediastinal or pulmonary mass, pericardial cyst, for example) requiring supplementary angiographic studies. Patients with demonstrable cardiac abnormality, even though mild, and those with previous cardiac surgery were excluded from this group. The angiocardiograms were obtained similarly, with injection of contrast medium into the right atrium. Border delineation of the left heart chambers was made from these angiograms. These normal data represent an expansion of our previous study.14 Determinations: Technically poor cineangiocardiograms showing poor contrast, subject motion or arrhythmia were not analyzed. The end-diastolic volume, end-systolic volume, stroke volume and ejection fraction of the right and left ventricles and left atrial maximal volume were determined. Right and left ventricular output measurements were obtained by multiplying the respective stroke volume by heart rate. Ejection fraction was represented by the ratio between stroke volume and end-diastolic volume. In both atria1 septal defect and patent ductus arteriosus, the difference between the right and left ventricular output values represented shunt flow per

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Stroke Volume

End-Diastolic Volume

Y= 1.23 X -1.98 r = 0.96 p< 0.001

FIGURE 1. Comparison of right and left ventricular end-diastolic and stroke volumes in normal children. Regression lines have been drawn.

0 .

minute. The ratio between ventricular end-diastolic volume and end-diastolic pressure was also used as a rough index of “ventricular distensibility.” The ratio of left atria1 maximal volume to the corresponding peak V wave pressure, obtained from pulmonary capillary wedge or direct left atria1 recordings, was likewise used to represent “atria1 distensibility.” More elaborate indexes of chamber distensibility such as Avolume/Apressure were not derived since the pressures were obtained by a liquid-filled catheter-transducer system with limited frequency response.

TABLE

III

Normal Angio PBF

Normal Data The patients were 10 infants aged 4 days to 14 months aged 2.3 to 19.4 years (mean 8.2). Good correlation between right ventricular end-diastolic volume, left ventricular end-diastolic volume or left atria1 maximal volume and body surface area was observed. The respective correlation coefficients (r) and regression equations are shown in Table I. When corrected for body surface area, the ventricular volumes in the infant group were smaller than those in the older children (Table II). The stroke index in the former (31.9 f 2.11 cm3/m2 [mean f standard error]) was also smaller than that in the latter (45.2 f 1.43, P
-Infants (0.1-1.2 yrs) -Children (2-19yrs)

Comparison of Angiographically Pulmonary and Systemic Blood

SBF

Results

and 39 children

Left Ventricle (ml)

Left Ventricle (cm31

and Fick-Derived Flow Values PDA

ASD Fick

4.86 4.65 (no. = 42) r = 0.86 P
Angio

Fick

8.82 7.19 (no. = 21) i- = 0.79 P
Angio

Fick

8.49 6.63 (no. = 231 r = 0.77 P
Angio = angiographically derived value; ASD = atrial septal defect; Fick = value derived with the Fick method; P = level of significance; PBF = pulmonary blood flow (liters/min per m’); PDA = patent ductus arteriosus; r = correlation coefficient; SBF = systemic blood flow (liters/min per mZ).

Effect of age: Figure 2 shows the right and left ventricular end-diastolic volume/pressure ratios plotted against age. Increasing distensibility with age was more evident in the right than in the left ventricle as shown by the respective regression lines. The initial segments of these lines were comparable shortly after birth; however, that of the right ventricle rose rapidly during the first year (Fig. 2, left) followed by a less steep slope thereafter (Fig. 2, right). The left ventricular regression line assumed a nearly uniform and less rapid increase with age. Mean distensibility index of the right ventricle was 12.7 f 0.08 cm3/m2 per mm Hg whereas that of the left ventricle was 7.8 f 0.47 (P
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with heart rate was negative. The regression formulas for predicting the normal maximal volumes of the right ventricle, left ventricle and left atrium, based on the present data, are shown in Table IV.

39.6 f 4.5 versus 49.7 f 5.2 cm3, P
Right Ventricular Volume Overload (Atrial Septal Defect) The changes in the end-diastolic volume of the ipsilateral right ventricle and contralateral left ventricle are shown in Figure 4, in which the observed and corresponding predicted normal values are plotted against body surface area. As shown by the regression lines, significant right ventricular enlargement was present (mean 91.4 f 10.8 versus 54.9 f 6.0 cm3, P
CHjnL_03R2fN

‘N:%P n

. 25~

6r

.

Y= 0.91 x + 4.7

Infants . - Children 0 -

4-

x z a \ ,_.

Y=2.6X+1.4 r =0.73

I .o

-I 2.0

Y= 0.21 x + 0.99 r = 0.77 p< 0.001 n=18

5

I 0

2-

;: E

0

4

Age (yrs)

6

16

12

20

Age (yrs)

10

0

- right ventricle o - left ventricle l

20

Age (yrs)

FIGURE 2 (lefl and center). Ventricular “distensibility” in nofmal infants and children, plotted against age. Solid line is the regression line for the right ventricle, and the dashed I/ne that for the left ventricle. The infant group (left panel) has a steep right ventricular regression slope also represented by the long-short dashed line (right panel). Note the dual slopes of the right ventricular regression line not observed in the left ventricular regression. EDV/EDP = ratio between end-diastolic volume and pressure. FIGURE 3 (right). Lefi atrial “distensibility” in normal infants and children, plotted against age. Increasing left atrial distensibility with age is shown by the regression line. LAmax = left atrial maximal volume.

TABLE Multiple

IV Regression

Chamber

Equations

for Predicting

Normal

Chamber

Volumes

In Children*

Regression Equation

(cm3)

I.2

95% Confidence Limits (f 2 SD) i- (o/o)

A. Infants RVEDV LVEDV LAmax

V = 12.46 (age) - 0.029 (ht) + 1.74 (wt) + 0.070 (HR) - 7.65 = 10.61 (age) - 0.336 (ht) + 1.77 (wt) - 0.046 (HR) + 26.43 = 3.09 (age) - 0.117 (ht) + 0.93 (wt) - 0.103 (HR) + 24.89

0.96 0.88 0.92

86114 71-129 64136

0.90 0.84 0.83

6867 65 -

6. Children RVEDV LVEDV LA,,,

V = 2.03 = 4.22 = 2.74

(age) + 0.291 (age) - 0.329 (age) - 0.268

(ht) + 1 .I9 (wt) + 0.009 (HR) - 11.44 (ht) + 1 .OO (wt) - 0.178 (HR) + 62.03 (ht) + 0.57 (wt) - 0.034 (HR) + 34.73

132 133 135

“Data based on 10 infants and 39 children; using age in years, height (ht) in centimeters, weight (wt) in kilograms, and heart rate (HR) in beats per minute. 195% confidence limits = ? 2 standard deviations (SD) for range of observed/predicted X 100 (%). = left ventricular end-diastolic volume; rz = multiple correlation coefficient; RVEDV = right venLA max = left atrial maximal volume; LVEDV tricular end-diastolic volume; V = volume.

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VENTRICULAR

by the Fick method (Q, and Qs, respectively) revealed good correlation (Table IV). The mean Quv/Q~v ratio was 2.09 f 0.14, and the Fick derived QP/Qs ratio was 2.10 f 0.16. The end-diastolic volume/pressure ratios of the right ventricle were significantly higher than those of the normal children. The mean “distensibility” index was 18.5 f 1.4 cm3/m2 per mm Hg compared with 12.7 f 0.08 for the normal children (P <0.0005). Similar data for the left ventricle obtained from nine subjects revealed a mean value of 5.49 f 0.56 cms/m2/mm Hg compared with 7.2 f 0.47 for the normal (P = not significant). The mean left atria1 maximal volume was 46.6 cm3/m2; this was significantly greater than the predicted normal value of 35.9 cm3/m2 (P
Right

200

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percent observed/predicted normal values and were plotted against the angiographically derived pulmonary/systemic flow ratio (QnvlQ~v). As shown by the respective regression lines, the right ventricle remained large and increased further with increasing shunts. In contrast, left ventricular size tended to be low normal with small shunts and decreased at Qnv/Q~v ratios of >2.0. Left atria1 size was increased, and also tended to increase further with increasing shunts. Left Ventricular Arteriosus)

Volume Overload

(Patent

Ductus

The changes in the end-diastolic volume of the ipsilateral left ventricle and contralateral right ventricle are shown in Figure 7, in which the observed and predicted normal values are plotted against body surface area. The regression lines indicate that the left ventricle was significantly enlarged. The mean end-diastolic volume was 86.96 f 4.86 cm3/m2 compared with the predicted normal value of 63.0 f 2.35 (P
Ventricle

Left

Ventricle

r = 0.95 Y= 151.7

x -18.1 /

150-

/

/

1’ ; Y 2 w

IOO-

&

FIGURE 4. Right and left ventricular end-diastolic volumes (RVEDV and LVEDV) plotted against body surface area (BSA) in atrial septal defect. The predicted normal for each observed value, using the equations in Table IV for derivation, has also been plotted for comparison. The solid line is the regression line of the observed values and the dashed line that of the predicted normal values.

50 Y=88.4

x -8.9

0

I 20

1.0 BSA

10

Cm’)

BSA Observed PredIcted

Atrlal

Septal

Value Value

20 Cm’)

. o ----

Defect

Patent

Ductus

Arterlosus

IOC r = 0.97 Y = 63

I x -103

FIGURE 5. Maximal left atrial volume (LAmax) plotted against body surface area (BSA) in atrial septal defect (left) and patent ductus arteriosus (right). The predicted normal value for each observed value, derived from the equations in Table IV. is also shown. The solid line shows the regression of the observed values and the dashed line that of the predicted normal values.

Y=525

x-63

BSA (m’) Observed Value .Predicted Normal o----

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2.95 cm3/m2) did not differ in size from the predicted normal value (mean 69.4 f 2.48, P = not significant). The ejection fraction of the left ventricle was 0.67 f 0.01 and that of the right ventricle 0.55 f 0.02. Neither differed significantly from the normal value. Left atria1 enlargement was observed as expected (Fig. 5, right). The mean left atrial maximal volume was 52.5 f 2.65 cm3/m2 compared with the predicted normal value of 36.2 f 1.66 (P
PotentDuctusArteriosus

Atrial Septal Defect (secundum)

300-

30a0

0 z

z

E s

.

-

200

.

3

. .

A+--

+A*

***-

og_---

-*O_$&-;-TJ--.0 0 o w&r 0 ;:;;i l .*-.* a---__ .

(165%)

RVEDV

(0 200.

LAmax

Y

(135%)

?i

0

0

LVEDV(142%)

20

0

l

,I

9

l

:: r

. .0

8

0 ,/-a-;,

P

and those obtained by the Fick method in spite of assumed oxygen consumption values for the latter determinations (Table IV). The mean QL~/QR~ ratio was 1.59 f 0.09 compared with the Fick QP/QS of 1.97 f 0.16 (P = not significant). Unlike the contralateral left ventricle in atria1 septal defect, which demonstrated reduced output, the contralateral right ventricle in patent ductus arteriosus had an output that did not differ from the predicted normal value of 4.41 liters/min per m2. The end-diastolic volume/pressure ratios of the right ventricle were also analyzed and compared with those of the normal children. The mean “distensibility” index of the right ventricle was 10.41 f 0.65 cms/m2/mm Hg. This was lower than the normal value (12.7 f 0.8 cm3/m2 per mm Hg) but not significantly so. The mean distensibility index of the left ventricle of six children, in whom it could be determined, was 11.3 f 2.1 cm3/m2

;: 2

100 t

. --------AAY

RVEDV (101%)

LVEDV w/d

40

IO

2.0

30

QLV/QRV

QRV /QLV A 0

RV LA LV

l

. (142.6)

Left Ventricle

FIQURE 6. Summary of volume changes in the three cardiac chambers in atrial septal defect (left) and patent ductus arteriosus (right). Volumes were expressed as percent of the predicted normal (% PN), and were plotted against the angiographically derived pulmonary to systemic flow iatios (Q&QLV). Regression lines are shown; the numbers in parentheses represent mean values. LA = left atrium; LAmax = left atrial maximal volume; LV = left ventricle; LVEDV = left ventricular enddiastolic volume: RV = right ventricle; RVEDV = right ventricular enddiastolic VOlume.

Right Ventricle n= 21

n = 24

100

i r = 0.96

60

Y= 67.7

I BSA

2X-6.62 \

X -2.27 I

0.5

0

Y=82

t

10

I 0

05 BSA cm”)

Cm’)

Observed Value. Predicted Valueo ----

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FIGURE 7. Right (RVEDV) and left (LVEDV) ventricular end-diastolic volumes plotted against body surface area (@A) in patent ductus arteriosus. Corresponding predicted normal values, derived from equations in Table IV, are shown. The regression lines of the observed and normal values are also shown.

VENTRICULAR

per mm Hg. This was significantly higher than the normal (7.2 f 0.47 cm3/m2 per mm Hg, P <0.0025). The changes in the three chambers are also summarized in Figure 6 (right) and have been plotted against the angiographically derived pulmonarylsystemic flow ratios. As shown by the superimposed left ventricular and left atria1 regression lines, the degree of enlargement of both chambers relative to shunt flow was similar. The size of the contralateral right ventricle remained normal. Discussion The usefulness of a multivariable regression formula for predicting normal cardiac chamber size has been previously shown4s*gJ4 and is again demonstrated. In this approach, the age, body size and heart rate are taken into consideration in interpreting the relative magnitude of the calculated volumes. None of the children in our control group (used for deriving the predicting formulas) had any demonstrable cardiac abnormality. This rigid approach was adopted since we have observed abnormal chamber volumes even in small shunting defects or mild valvular insufficiency (data in preparation). For the same reason, children with surgically corrected cardiac defects were excluded from this group. This approach assumes that body size (height or weight, or both, relative to age) follows the same distribution curve as that of the normal (control) population. This is not necessarily true for patients with severe heart disease, in which case the predicted normal values may become spuriously high or low. None of the subjects in our two study groups had a body size outside the normal range. Normal Values Ventricular volumes: As in previous studies,sy7BJ4 the end-diastolic volumes of the right ventricle were greater than those of the corresponding left ventricle in the normal children. This difference may be related to the normally greater distensibility of the right than the left ventricle. Greater right atria1 than left atria1 volumes have also been observed in normal children and have been explained similarly.8 On the other hand, other studies,6 using different methods for right and left ventricular volume calculation, have shown similar end-diastolic volumes for both chambers. This discrepancy, although disturbing, is not critical provided that the observed values by any method have appropriate controls by that method, such as the predicted normal volumes derived from legitimate regression equations. Ventricular distensibility: The comparable “distensibility” of the right and left ventricles in the newborn period is consistent with the circulatory dynamics in utero. Thereafter, the diastolic volume/pressure relations of both ventricles increase, that of the right ventricle being significantly greater. The most rapid change occurs during the 1st year when a significant reduction in pulmonary vascular resistance is observed.

RESPONSE TO VOLUME OVERLOAD-MATHEW

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Our observations agree with the animal data of Romero et a1.,16 which have shown comparable pressure-volume relations of the fetal right and left ventricles, greater right than left ventricular distensibility after birth, and greater distensibility of the ventricles in the adult than in newborn subjects. The increase in ventricular and atria1 distensibility with age appears to be mostly a function of the increase in chamber volumes since no corresponding changes in filling pressures were observed in our subjects. The precise mechanism that promotes this age-related change in wall compliance is not known. It has been suggested that the relatively increased amounts of noncontractile cellular elements including surface membranes in the young heart may contribute to the latter’s reduced distensibility.16 Alterations in myocardial connective tissue concentration may also be responsible. Myocardial hydroxyproline concentrations have been shown to be greater in the right heart chambers than in the corresponding left chambers, and in the atria than in the ventricles.17 We have also observed, in studies on Wistar rats ranging in age from 1 day to 46 weeks (data in preparation), a progressive increase in left ventricular hydroxyproline concentration. It is thus possible that the increment in myocardial connective tissue concentration is a normal response of the heart to the increase in volume load accompanying body growth, and that similar changes occur in the volumeoverloaded right ventricle in atria1 septal defect or left ventricle in patent ductus arteriosus. This assumption remains to be proved. Other studies have also shown increased left ventricular distensibility in patients with mitral regurgitation.i8Jg Ventricular Overloading The right ventricular enlargement in atria1 septal defect and the left atria1 as well as left ventricular enlargement in patent ductus arteriosus are predictable changes. Previous studies have also demonstrated in-

. / / .. / l. . f

-2’ -4

0

.

;.

Y=O.56 X -0.01 r =0.91 p< 0.001 n=20

I +4

+8

I +I2

Peak “v” wove (mm Hg)

FIGURE 8. Relation of left to right atrial mean pressure gradient to peak V wave pressure

August 1878

gradient in secundum atrial septal defect.

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ATRIAL SEPTAL DEFECT Ostium Sacundum

PV PV

FIGURE 9. Schematic diagram of atrial shunting during ventricular systole while the atrioventricular valves are closed (left), and during diastole while the atrial and ventricular chambers are in free communication (right). Ao = aorta: IVC = inferior vena cava, LA = left atrium; LV = left ventricle; PV = pulmonary vein: RA = right atrium; RV = right ventricle; SVC = superior vena cava.

_

SYSTOLE

creased volumes of the right ventricle6y7 and right atrium12 in atria1 septal defect. The comparable enlargement of the left atrium and left ventricle in our subjects with patent ductus arteriosus reflects an identical response to the volume load. Left atria1 enlargement of atria1 septal defect: The pathogenesis of the left atria1 enlargement accompanied by reduced left ventricular size and systemic output in secundum atria1 septal defect is unclear. The atria1 enlargement suggests that the septal defect, although usually large, may still be somewhat functionally restrictive to transseptal flow. Analysis of the atria1 pressures in our patients recorded during catheter pullback from the left to the right atrium supports this view. The mean pressure gradients ranged from 0.5 to 6 mm Hg, and these correlated well with the peak V wave pressure differential between the two atria (Fig. 8), indicating inadequate pressure equilibration between the two atria1 chambers. Levin et a1.20 have also demonstrated consistent left to right atria1 pressure gradients during the latter half of ventricular systole, especially at the peak of the atria1 V wave and during atria1 contraction. Cineangiocardiographic analysis demonstrated major left to right shunting at these critical periods. Our hypothesis assumes that the left to right atria1 shunt during ventricular systole is not large enough to counterbalance the increased pulmonary venous return to the left atrium at this phase of the cardiac cycle. This would favor enlargement of the left atria1 chamber. The enlargement of the right atrium,12 even to a greater extent than that of the left, does not necessarily contradict this concept. Small left ventricle in atria1 septal defect: The tendency for the left ventricle to become small is likewise not paradoxical to this assumption. During ventricular diastole, the left atrium empties into the left

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ventricle as well as into the right atrium-right ventricle by way of the septal defect. Since the left ventricle is less distensible than the combined right heart chambers, preferential flow to the latter is favored, with consequent reduction in left ventricular filling. The diagrams in Figure 9 illustrate our hypothesis. The reduced left ventricular ejection fraction and low systemic output observed in this condition would be consistent with this concept of reduced left ventricular preload. Left ventricular dysfunction in atria1 septal defect: We have no data concerning the effects of increasing age upon the left heart changes in atrial septal defect since we did not perform serial hemodynamic studies. However, recent studies in adult patients with this disease have also demonstrated evidence for left ventricular dysfunction in the form of reduced enddiastolic volume, stroke volume and output.21 There is, therefore, sufficient evidence to suggest that the usual practice of delaying surgery for several years may not be the best policy in the management of this disease. The impaired cardiac output response to exercise of adult patients who have had total repair of atria1 septal defect22 could very well be a reflection of the left heart dysfunction already present before surgery. Right ventricle in patent ductus arteriosus: Unlike the left ventricle in atria1 septal defect, the right ventricle in patent ductus arteriosus is normal. This difference in response of the contralateral ventricles in the two entities may be related to the level of the shunt; in atria1 septal defect it is proximal to the contralateral ventricle, whereas in the latter it is distal to it. Left to right shunting occurs before and during ventricular filling in atrial septal defect, but after ventricular filling in patent ductus arteriosus. The systemic output and the right ventricular preload in the latter remain normal.

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VENTRICULAR RESPONSE TO VOLUME OVERLOAD-MATHEW

ET AL.

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August 1976

The American Journal of CARDIOLOGY

Volume 38

217