Cardiodynamic effects of experimental right bundle branch block in canine hearts with normal and hypertrophied right ventricles

“Olwne

109

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Digoxin

26. Raabe DS Jr: Combined therapy with digoxin and nitroprusside in heart failure complicating acute myocardial infarction. Am J Cardiol 43:990, 1979. 27. Forrester JS, Diamond GA: Hemodynamic subsets in acute

in acute myocardial

infarction

infarction: A basis for prognosis and therapy. In Corday E, Swan HJC, editors: Clinical strategies in ischemic heart disease. Baltimore, 1979, The Williams & Wilkins Co, p 483.

Cardiodynamic effects of experimental right bundle branch block in canine hearts with normal and hypertrophied right ventricles Cardiodynamic effects of acute experimental right bundle branch block (RBBB) were studied in canine hearts: group A included 15 normal hearts; group B-l had seven hearts with mild right ventricular hypertrophy (RVH), and group B-2 had 11 hearts with marked RVH. The main sequential changes following RBBB were marked prolongation of the Q upstroke interval of the right ventricle and striking shortening of right ventricular systolic time that affected right and left ventricular interaction, particularly in the hearts with RVH. Hemodynamic changes were: the right ventricular end-diastolic pressure was elevated markedly (4.4 +- 2.2 - 9.8 f 2.6 mm Hg, p < 0.001) in group B-2, moderately (p < 0.01) in group B-l, and not at all in group A. The right ventricular positive peak dp/dt decreased remarkably (1036 + 151 - 827 + 152 mm Hg/sec, p < 0.001) in group B-2 and negligibly in the other groups. A significant correlation existed between the percentage of decrease in right ventricular peak dp/dt and the QRS duration of RBBB in each group (p < 0.01). The left ventricular peak negative dp/dt decreased distinctly (2570 + 326 - + 2055 f 362 mm Hg/sec, p < 0.01) in group B-2 and not at all in the other groups. The stroke volume showed 12% decrease in group B-2 (p < O.OOl), 8% decrease in group B-1 (NS), and no decrease in group A. In the presence of RVH, acute RBBB causes significant impairment of right and left ventricular function. The magnitude of the impairment invariably depends upon both the prior degree of RVH and the width of the QRS complex. (AM HEART J 109:69, 1985.)

Hisataka Yasui, M.D., Mochikazu Yoshitoshi, M.D., Masataka Komori, Ryuji Tominaga, M.D., Yoshito Kawachi, M.D., Yasutaka Ueno, M.D., Hiroshi Sunagawa, M.D., and Kouichi Tokunaga, M.D. Fukuoka, Japan

Right bundle branch block (RBBB) is one of the most frequent postoperative complications in the closure of a ventricular septal defect (VSD). Its

From the Divisions Children’s Hospital Kyushu University Received accepted

of Cardiovascular Surgery and Medical Center, and the Division School of Medicine.

for publication July 2, 1984.

Reprint requests: Hisataka gery, Fukuoka Children’s Fukuoka 810, Japan.

February Yasui, Hospital

1, 1984;

revision

M.D., Division Medical Center,

Pediatrics, of Cardiac received

June

of Cardiovascular 2-5-l. Tojin,

Fukuoka Surgery, 4, 1984; SurChuoku,

M.D.,

incidence has been reported to be as high as 40% to 70% .le4 However, surprisingly, there has been no systematic investigation as to how acute RBBB in such cases affects subsequent cardiac performance. There have been a number of articles concerning the effect of RBBB on cardiac performance in the nonhypertrophied (normal) heart. The effect of RBBB appears to be minimal and it does not influence the subsequent clinical course.5-10 In patients with a large VSD, right ventricular hypertrophy (RVH) is present and an abnormal contour of the chamber can be seen.l’ Therefore, it might be 69

January,

Yasui et al.

70

American

fGHT BUNDLE

Heart

1985 Journal

BRANCH

1. A, Experimental preparations. RV = right ventricle; LV = left ventricle. B, Method of producing RBBB. Bloodlessand easy production of RBBB can be accomplishedwithin 1 to 2 minutes. Fig.

Table

I. Morphometry and basal hemodynamicsof three groups GFOU~ A Normal heart (n = 1.5)

RVSP (mmHg) RVSP/LVSP RVwtlLVwt RVEDVILVEDV

20.6

k 2.7

0.18 0.71

+ 0.07 5 0.21

1.10

k 0.14

GFOU~ B-l RVSPILVSP < 0.5 (n = 71 50.4

t

6.1

0.39

zk 0.07

1.33 1.32

* 0.13 + 0.10

Values are mean + SD. Abbreviations: RVSP = right ventricular systolic pressure; RVSPiLVSP = the ratio pressure; RVwt/LVwt = the ratio of right ventricular muscle weight to left ventricular end-diastolic volume to left ventricular end-diastolic volume. *Difference between three groups. tDifference between groups A and B-l. fDifference between groups B-l and B-2.

expected that in a VSD the effects of RBBB on cardiac performance will be entirely different one from those observed in the normal heart. In 1977, we reported the unique finding that there was a significant detrimental effect from iatrogenic complete RBBB, not only upon the early postoperative course but also upon the long-term follow-up results following closure of high-resistance VSD.‘* Based on those results, we inferred that complete RBBB would have a serious, deleterious effect upon right and left ventricular performance in patients with high-resistance VSD.12 To test this hypothesis, the effect of RBBB on right and left ventricular function was studied in canine hearts with normal and hypertrophied right ventricles. The purpose of this article is to report the magnitude of the hemodynamic alterations on right and left ventricular function produced by acute experimental RBBB in dogs with and without RVH.

GFOU~

B-2

R VSPJL VSP > 0.5 (n = 11) L 10.4

p < 0.001*

0.74 1.62

-r k

0.11 0.24

p < 0.05*

1.46

+

0.29

p < O.O5t,

89.5

of right muscle

Statistics

ventricular systolic weight; RVEDV/LVEDV

p < 0.001*

pressure

to left = the ratio

ventricular of right

NSb

systolic ventricular

METHODS Preparation. Experiments were performed on 33 young mongrel dogs of both sexes, weighing 8.5 to 16.0 kg. Fifteen dogs had normal hearts. In 18 dogs RVH was produced by pulmonary artery banding 7 to 9 months prior to this study. In brief, anesthetized puppies, weighing 2 to 4 kg, underwent left thoracotomy. Chronic pressureoverload was imposedon the right ventricle by constricting the main pulmonary artery with a Teflon band (5 mm in width, 18 to 22 mm in length). After the operation, congestive heart failure was occasionally encountered and those dogswere not used in this study. The pulmonary artery band remained in place during the entire experiment. Procedure and instrumentation. The dogs were anesthetized with intravenous sodium pentobarbital (25 mg/kg). Following insertion of a cuffed endotracheal tube, ventilation wasmaintained by a positive pressurerespirator (Harvard Apparatus 607). Blood pH and Pao2 were maintained within the physiologic range. Body temperature was kept constant at 37’ C by a water blanket. The

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heart and great vesselswere exposed through a median sternotomy. Left and right ventricular pressures were monitored by catheter tip micromanometers(Miller PC360) inserted through the left carotid artery and the right femoral vein, respectively. A catheter tip micromanometer was carefully calibrated in the water at 37’ C in a dark place before and after an experiment to avoid errors by manometerdrift. Aortic flow wasmonitored by an electromagnetic flow meter (Statham SP-2201) placed around the ascendingaorta. The sinoatrial node wasmechanically crushed and the heart rate was kept constant by bipolar atria1 pacing at 150 bpm. Myocardial temperature was maintained by covering the heart with warm moist sponges.A schemaof the experiment is shownin Fig. 1, A. The ECG (lead II), full left and right ventricular pressures, the first derivatives of left and right ventricular pressures(Differentiator, Sanei 1309, Tokyo, Japan), and phasicaortic flow were recorded simultaneouslyat a paper speed of 50 cm/set (Polygraph: Sanei 142-8, Recorder: Sanei5:32ME). Following control measurement,cardiodynamic effects of a shamoperation and RBBB were studied in all experiments. Sham operation. To study the effect of the surgical approach itself in making RBBB on cardiac function, a shamoperation was performed. Following insertion of an electrocautery into the right ventricle through a purse string small stab incision at the anterior wall of the right ventricle and burning of the septum rather than the right bundle branch, recordings of the hemodynamic parameters were made prior to induction of RBBB. No ECG changeswere noticed in this procedure. Induction of RBBB (Fig. 1, iY). RBBB was induced within 1 to 2 minutes. The main right bundle branch was searched by pressing its probable running site of the septum, just inferior to the papillary muscleof the conus, with the tip of an electrocautery inserted through the sameincision as that of the sham operation. Light pressure on the right bundle branch made a new, deep, and wide S wave on continuously monitored lead II. Then one burst of burning was performed to make it permanent. RBBB wasconfirmed by taking all standard limb leadsof an ECG. We waited for 10 minutes after RBBB production to stabilize hemodynamics,then the samerecording as before RBBB was performed. Morphological studies. After experiments, the dogs were killed by a bolous injection of 20 ml of 20% KC1 solution. The heart wasexcised.No VSD wasfound. Right and left ventricular volumeswere measured.13 The weight of the ventricular muscle was determined according to Herrmann’@ method. Fifteen days after the heart was immersedin 10% formalin solution, the ventricular muscle masswas divided in the plane of the midseptal line, which wasan anatomic landmark formed by the intersection of the scroll musclelayers from the two ventricles. Data analysis. The ECG was studied for cardiac rate and QRS duration and was also used as a reference point for the onset of ventricular depolarization (Q wave). Timing of the various ventricular events was studied through the following intervals (Fig. 2): (1) Q upstroke

RBBB

and cardiac

function

71

Fig. 2. Experimental recordings of a dog in group B-l. Note the marked delay of the onset of right ventricular pressurerise and shortening of t-peak dp/dt after right bundle branch block (RBBB). A slow upslope at the beginning of right ventricular pressure before RBBB changedto the steep upslope after RBBB.

interval (electromechanical interval), (2) time to peak dp/dt (t-peak dp/dt), and (3) dp/dt interval (time interval between peak positive dp/dt and peak negative dpfdt). Changesin the contour of the right and left ventricular pressure curves were assessedby the following data: right and left ventricular systolic pressures(RVSP and LVSP), right and left ventricular end-diastolic pressures (RVEDP and LVEDP), and rates of development of right and left ventricular pressures(dp/dt). Stroke volume was calculated by tracing the phasic aortic flow with planimetry. All indices above were averaged from 20 consecutive beats. Statistical analysis. Values are expressed as mean ? standard deviation of the mean. Statistical significance of the difference between mean values was analyzed by Student’s t test with p < 0.05 taken as significant.

January.

72

Yasui et al.

Q mm0

American

upstroke 30

peak cp/dt 60

90

120

150

180

210

240

macrc

Fig. 3. The sequentialchangesof right and left ventricular contraction following RBBB. Note the wide time lag of pressure upstroke between right and left ventricles (shaded triangle) and marked decreasein the sum of t-peak dp/dt and dp/dt interval (d) following RBBB. a = Q upstroke interval; b = peak dp/dt, c = dp/dt interval; pre = before RBBB; = after RBBB; RVP = right ventricular pressure;L VP = left ventricular pressure.

post

RESULTS Groups of dogs, morphometry, and basal hemodynamics. The dogs were divided into two groups

according to the existence of the previous pulmonary artery banding. Group A consisted of 15 dogs with no previous operation; thus they had normal hearts. Group B consisted of 18 dogs with previous pulmonary artery banding, and RVH was noted as described below. Group B was divided into two subgroups according to the ratio of RVSP to LVSP: subgroup B-l (seven dogs) had RVSP/LVSP < 0.5, and subgroup B-2 (11 dogs) had RVSP/LVSP >= 0.5. Mean values of RVSP, RVSP/LVSP, the ratio of right ventricular muscle weight to left ventricular muscle weight (RVwt/LVwt), and the ratio of right ventricular end-diastolic volume to left ventricular end-diastolic volume in each group are summarized in Table I. The mean values of RVSP of groups A, B-l, and B-2 were 21,50, and 90 mm Hg, respectively, in the differences between the three groups were statistically significant (p < 0.001). RVwt/LVwt increased in relation to the increase of RVSP (Table I). Sequential changes of right ventricular contraction by RBBB. Fig. 2 shows a typical tracing. After RBBB

the right ventricular pressure starts rising considerably later than normal. Changes of sequence of the various ventricular events from electrical excitation

Heart

1985 Journal

were calculated and summarized in Table II. With RBBB, the mean value of QRS duration in all three groups was significantly increased. The increase in QRS duration in the three groups was similar and no significant differences were found among them. The mean values of Q upstroke interval of groups A, B-l, and B-2 were markedly prolonged from 26.3 f 4.2, 25.0 f 2.5, and 26.4 -t 4.8 msec before RBBB to 60.8 & 9.7, 61.1 * 8.9, and 68.7 ? 9.0 msec following RBBB, respectively (p < 0.001 in all groups). After RBBB, t-peak dpldt in all three groups was dpldt significantly shortened. Following RBBB, interval in all three groups was markedly shortened. Thus, the mean value of the sum of t-peak dp/dt and dp/dt interval of all groups, which represented right ventricular systolic time, was markedly diminished to about 83% of the pre-RBBB value. Sequential changes of left ventricular contraction by RBBB. The timing of various left ventricular events

was not modified by RBBB in all groups as shown in Table II. The sequential changes of right and left ventricular contractions are illustrated in Fig. 3. Note that the first wide delay of upstroke of the right ventricular pressure (indicated by a shaded triangle) was progressively shortened and seemed to be compensated for during a cardiac cycle. Right ventricular

hemodynamic

changes

(Table

Ill).

After RBBB, the change of RVSP in all three groups was very small and insignificant. In group A, change of R VEDP after RBBB was minimal. In group B- 1, a small but significant increase in RVEDP was noted (p < O.Ol), and the marked elevation of RVEDP from 4.4 -t 2.2 before RBBB to 9.8 ? 2.6 mm Hg following RBBB was observed in group B-2 (p < 0.001). In groups A and B-l, the change of right ventricular peak dpldt after RBBB was insignificant, and in group B-2, significant diminution of peak dp/dt from 1036.1 f 151.8 mm Hg/sec to 827.4 ~fr 152.6 mm Hg/sec was noted after RBBB (p < 0.001). Left

ventricular

hemodynamic

changes

(Table

III).

Before RBBB, LVEDP of group B-2 was significantly higher than that of group A (p < 0.05). Peak negative dp/dt of left ventricular pressure (left ventricular peak negative dp/dt) of group B-2 was significantly smaller than those of groups A and B-l (p < 0.05). After RBBB, LVSP did not change in groups A and B-l and decreased slightly in group B-2. LVEDP did not change in all groups. Left ventricular peak dpldt did not change in groups A and B-l, and decreased slightly in group B-2. Left ventricular peak negative dpldt did not change in groups A and B-l, but in group B-2 it decreased significantly from 2561 +- 560 before RBBB to

Volume Number

109 1

RBBB and cardiac function

73

%change of RY

pak

dp/dt

% 40 -

n groupA

A 30 -

. A

group

0 group

1 so

70

(N=15) B-l

(N=7)

B-2

(N= 11)

P 110

100

120 msec QRS

duration

Fig. 4. Relationship betweenQRS duration of RBBB and percentageof changeof right ventricular (RV)

peak dpldt. A significant correlation between them was noted.

Table

II. Timing of right and left ventricular events before and after RBBB Group A (n = 15) RBBB

QRS

duration

Q upstroke

t-peak

dpldt

dp/dt

interval

interval

Before After Statistics* Before After Statistics* Before After Statistics* Before After Statistics*

Values are mean + SD. Abbreviations: RV = right ventricle; and negative peak dp/dt. *Difference between before and after fp < 0.05 differences between group tp < 0.01 differences between group

RV

26.3 60.8

p < 48.1 32.1

p < 154.3 138.0

p <

Group B-l (n = 7)

43.3 rf: 4.6 89.1 + 17.8 p < 0.001 + 4.2 22.0 f 2.0 + 9.7 24.0 + 2.6 0.001 NS f 5.5 54.7 f 3.1 k 5.6 53.7 f 5.0 0.001 NS * 10.0 150.3 + 9.5 f 7.5 151.3 * 12.0 0.01 NS

LV = left ventricle;

RV

LV

RBBB

25.0 61.1

p< 49.5 34.2

p < 157.2 133.7

p <

= right bundle branch

Group B-Z (n = 11) LV

RV

43.8 2 11.3 84.0 + 11.9 p < 0.001 f 2.5 21.7 + 2.0 k 8.9 20.1 f 1.2 0.001 NS f 3.3 54.8 f 3.6 + 3.3 58.2 + 5.8 0.001 NS 2 7.5 154.3 T!Z4.8 + 6.4 152.5 rfr 4.6 0.001 NS

block; dp/dt

interval

LV 47.8 rt 10.0 88.4 I!Z 13.4

p < 0.001 26.4 k 4.8 68.7 + 9.0 p < 0.001 47.3 k 7.8 33.8 k 8.9 p < 0.001 167.2 + 16.3t 142.8 rt 16.9 p < 0.01

= time interval

between

19.9 + 3.4 21.5 k 3.7 NS 52.0 + 3.2 52.8 + 6.5 NS 168.0 + 6.6$ 167.8 k 6.8f NS

positive

peak dp/dt

RBBB. B-2 and groups B-l and A. B-2 and groups B-l and A.

2183 + 576 mm Hg/sec after RBBB (p < 0.01). Total systemic vascular resistance (TSR) did not change significantly in all groups. In groups A and B-l, the change in stroke volume after RBBB was insignificant, but in group B-2, the stroke volume decreased significantly from 6.5 * 0.9 before RBBB to 5.8 + 0.7 ml after RBBB (p < 0.005). RBBB effects and QRS duration. The effects of RBBB on right ventricular peak dp/dt are expressed as a percentage of change, which was plotted against QRS duration of RBBB in Fig. 4. There was a

significant correlation between the percentage of change of right ventricular peak dp/dt and QRS duration in all three groups. The regression of each group is shown by the solid line. Left and right ventricular pressure loops. To clarify the effects of RBBB on right and left ventricular interaction, simultaneous left and right ventricular pressures were plotted every 5 msec with right ventricular pressure on the ordinate and left ventricular pressure on the abscissa. Typical left and right ventricular pressure loops before and after RBBB in

January,

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Yasui

Table

et al.

American

111.Hemodynamics

(mm Hg)

RVEDP

(mm

Hg)

RV peak dp/dt Hg/sec)

(mm

Stroke

volume

(ml)

LVSP

(mm

LVEDP

Hg)

(mm

Hg)

LV peak dpidt Hg/sec)

(mm

LV peak negative (mm Hg/sec)

TSR

(mm

Hg/L/min)

dpldt

1985 Journal

before and after RBBB RBBB

RVSP

Heart

Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics* Before After Sham operation Statistics*

Values are mean ? SD. Abbreviations: RVEDP = right ventricular end-diastolic pressure; end-diastolic pressure; TSR = total systemic vascular resistance *Difference between before and after RBBB. tp < 0.05 difference between groups B-2 and A. tp < 0.05 differences between group B-2 and gmups R-l and A.

groups A and B-2 are illustrated respectively.

Group A (n = 1.5)

Group B- 1 (n = 7)

“0.6 + 2.7 20.5 IL 3.0 20.6 i 2.8 NS 2.6 i 0.9 2.5 rt 1.1 2.6 k 1.0 NS 408.9 2 52.0 405.7 + 71.0 410.0 f 52.0 NS 6.9 L 1.1 7.1 k 1.9 6.9 * 1.2 NS 121.5 + 7.6 117.2 i 14.0 121.8 i 7.8 NS 3.6 i 0.9 3.9 +_ 0.5 4.6 t 0.9 NS 2533 i 386 2516 +- 500 2536 k 390 NS 3417 i 526 3242 i 588 3425 + 531 NS 117.2 i 21.6 118.0 + 15.6 117.0 * 21.2 NS

50.4 2 6.1 51.9 ? 10.2 50.8 t 6.3 NS 2.1 k 1.1 3.8 _+ 1.6 2.3 + 1.1 p < 0.01 639.0 + 78.6 627.7 -r 1020 641.1 i 80.2 NS 6.5 i 1.9 6.0 i1.9 6.6 i 1.9 NS 131.9 i 10.4 131.0 + 12.1 132.0 i 10.8 NS 5.7 + 1.4 6.0 i 1.1 5.8 2 1.4 NS ‘L356 ?z 489 2350 rt 493 2358 + 491 NS 3233 i 353 3182 5 512 3238 i 355 NS 104.0 2 29.4 114.9 r 27.6 105.0 i 29.0 NS

RV peak dp/dt

in Figs. 5 and 6,

DISCUSSION Asynchronous contraction. RBBB impaired coordinated depolarization and mechanical activation of the entire myocardium (Table II, Fig. 3). Wennemark et al5 and others6mghave noted that prolonged Q upstroke interval of the right ventricle resulted in asynergy of both ventricles and shortening of right ventricular ejection time following RBBB and have suggested these may affect right ventricular function in the normal heart. It may also involve lack of

= peak dp/dt

of right ventricular

Group

B-2

(n = 111

pressure;

89.5 k 10.4 87.6 rt 9.1 90.5 * 10.8 NS 4.4 + 2.2 9.8 2 2.6 4.5 2 2.2 p < 0.001 1036.1 rt 151.8 827.4 i 152.6 1040.2 + 150.6 p < 0.001 6.5 + 0.9 5.8 t 0.7 6.6 + 0.9 p < 0.005 126.4 & 14.5 118.6 I 18.0 126.9 +_ 14.8 NS 7.7 + 2.9t 7.6 -t 1.0 7.6 + 3.0 NS 2535 +_ 466 2418 + 566 2537 t 470 NS 2561 of- 5601 2182 + 576 2565 +_ 556 p < 0.01 98.1 i 17.6 98.7 i 12.2 99.0 + 16.5 NS

LVEDP

= left ventricular

simultaneous contribution of all of the right ventricular myocardium. Gilmore et a1.14have suggested the importance of synchronous ventricular contraction on cardiac function by showing that the ventricle produces less external stroke work from any given end-diastolic pressure when direct electrical stimulation instead of a normally propagated impulse causes it to contract. Right ventricular hypertrophy. The effects of RBBB on right ventricular function in the normal heart have been reported to be minimal.5-8 The present experiment showed that the ill effects of RBBB on right and left ventricular function became greater as

Volume Number

RVP

109 1

RBBB and cardiac function

76

BEFORERBBB

50

LVP CONTRACTION

RVP

;;I

AFTER RBBB ,/,=,,,

100

oEi.I

50

100m9

t

AFTER RBBB

RELAXATION

LVP

Fig. 5. Left and right ventricular pressureloop of normal heart (group A) before and after RBBB. Time interval between points = 5 msec. CONTRACTION

right ventricular hypertrophy and outflow resistance progressed (Table III). Why is the detrimental effect of RBBB increased stepwise from group A to group B-2, despite the similar magnitude of asynchrony of the right ventricle of three groups as shown in Table II and Fig. 3? The ventricles are divided by the interventricular septum and are composed of successive layers of myocardium encircling the ventricular chambers.11B15 Thus, both ventricles interact in contraction and relaxation. To clarify the interaction of both ventricles, the left and right ventricular pressure loops are illustrated (Figs. 5 and 6). A complete synchronization of pressure upstroke and downstroke of both ventricles, which may be most efficient in pumping action, will make a straight line rather than a loop. In the normal heart a slight delay in right ventricular depolarization to that of the left ventricle made a very narrow loop (Fig. 5). In the heart with right ventricular hypertrophy, the loop was somewhat wide, reflecting some sequential delay in right ventricular contraction and relaxation due to marked pressure overload of the right ventricle (Fig. 6). Following RBBB, the loops became wider compared to those before RBBB,

50

100

mg

LVP

Fig. 6. Left and right ventricular pressureloop of the dog in group B-2 before and after RBBB. The loop superior to a solid line of 45 degreesindicates the negative interventricular pressuregradient between left and right ventricles.A = timing of peak negative dp/dt of left ventricular pressure &VP); B = timing of peak negative dp/dt of right ventricular pressure(RVP); C = onset of right ventricular pressure upstroke. Time interval between points = 5 msec.

to indicate that the delayed depolarization of the right ventricle would not affect the pressure interaction of both ventricles critically. It may be attributed to the fact that most of the right ventricular function depends on the left ventricular contraction in the normal heart.“,16 On the other hand, the width of the loop of the hypertrophied heart was very wide, because of the high pressure and less compliant right ventricle (Fig. 6). The concave curve at the contraction phase and the convex curve at the relaxation phase indicate much more serious asyn-

because of the asynchronous pressure process of

chrony of pressure upstroke and downstroke of both

both ventricles. The width of the loop of the normal heart, however, was still small, because of the low pressure and well compliant right ventricle (Fig. 5). The line of the loop in the contraction phase and relaxation phase was still nearly straight and seemed

ventricles than that of the normal suggest that the negative effect of ular coordination on cardiac increase with progression of right trophy. Indeed, right ventricular

heart. It seems to the loss of ventricfunction should ventricular hyperpeak dp/dt and

January,

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Yasui et al.

stroke volume following RBBB were significantly decreased despite the significant elevation of RVEDP in the hypertrophied heart group (Table III). Compliance and contractility. It seems unlikely that the compliance and the contractile state of the right ventricular myocardium itself are decreased by RBBB. Therefore, the rise in RVEDP after RBBB, theoretically, should induce the increase in right ventricular peak dp/dt. However, it actually did not change in group B-l and decreased significantly in group B-Z (Table III). It is conceivable that RBBB caused the asynergy of both ventricles as well as a less synchronous contraction of all of the right ventricular myocardium that in turn affected the pressure generation of the right ventricle, and resulted in a decrease in right ventricular peak dp/dt. The correlation between QRS duration and percentage of change of right ventricular peak dpldt, and the stepwise lowered regression from group A to group B-2 in Fig. 4 justifies this inferrence and may suggest that the wider the QRS complex of RBBB and the greater the hypertrophy of the right ventricle, the more deleterious the effect which might occur on right ventricular pressure generation. Additional mechanisms. Other probable causes of increased negative effects of RBBB include the following: (1) The lessened compensatory reserve of the heart with a hypertrophied right ventricle; the diminished contractile state of the right and left ventricles in the heart with RVH,“-” and the decrease in compliance of the hypertrophied ventriclez3 have been widely recognized. The unloaded right ventricle may simply dilate sufficiently to increase dp/dt and stroke volume without measurable change in RVEDP. The chronically overloaded, and thereby less complaint, right ventricle, however, may fail to increase RVEDV enough to raise dp/dt and stroke volume yet may still experience a measurable rise in RVEDP. Moreover, RVEDP after RBBB may be modified by left ventricular contraction since left ventricular contraction beginning at the end part of the diastolic phase of the right ventricle should increase stiffness of the ventricular septum and give some tension on the relaxation of the right ventricular free wall. The pressure curve change of RVEDP was minimal in group A, was gradual and mild in group B-l, and was steep and marked in group B-2. These findings may suggest that RVEDP after RBBB is affected by the preceding contraction of the left ventricle, and that its effect on RVEDP is greater as the compliance of right ventricular muscle is decreased. (2) The

American

1985

Heart Journal

increased outflow resistance of the right ventricle; in the sudden impairment of pumping action due to RBBB, the severe outflow resistance will work as a heavier load to overcome than the mild one should. The important role of afterload on cardiac function has been documented in serial reports of afterload mismatch by Ross et alz4125 Left ventricular negative dp/dt and RVEDV. The mechanism of decrease in peak negative dp/dt after RBBB can be explained by the left and right ventricular pressure loop in Fig. 6. A convex curve of the loop before RBBB will result from the slower decrease of right ventricular pressure than left ventricular pressure, which may come from the isovolumic relation to the hypertrophied muscle of the right ventricle. The markedly increased RVEDV (RVEDV/LVEDV: 1.46 ? 0.29, Table I) may also play an important role in this phenomenon, as suggested by the findings of Taylor et al.“fi and Ludbrook et a1.,27in which left ventricular compliance was decreased by the probable displacement of the septum in the acutely induced volume overload of the right ventricle. By this phenomenon, right ventricular pressure became higher than left ventricular pressure as indicated by the loop superior to a solid line of 45 degrees in Fig. 6. It may cause leftward displacement of the septum, which would interfere with left ventricular relaxation. Tanaka et al.“R noted the paradoxic movement of the septum echocardiographically in patients with pulmonary hypertension. In fact, before RBBB, LVEDP and peak negative dp/dt of group B-2 were significantly higher and smaller than those of groups A and B-l, respectively (Table III). A similar phenomenon has been reported by Kelly et a1.29 in the heart with chronic right ventricular volume and pressure overload and this loop indicates the mechanism. After RBBB, the loop in group B-2 became much wider (Fig. 6). The delay of the relaxation of the powerful right ventricle caused a higher negative interventricular pressure gradient between the left and right ventricles in the isovolumetric relaxation phase than that before RBBB, by which leftward displacement of the septum (paradoxic motion) should be intensified. Moreover, it might not only increase stiffness of the septum but also induce some tension of the relaxing left ventricular free wall. Indeed, the significant decrease in peak negative dp/dt following RBBB, which had been generally accepted to indicate the relaxation disturbance of the left ventricle, was noted in group B-2 (Table III). Thus, it is likely that RBBB interferes with the relaxation of the left ventricle and changes left ventricular diastolic properties in the heart with a markedly hypertrophied

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and pressure overloaded right ventricle. Glantz et a1.3oand Spadaro et a1.31 reported that opening the pericardium increased ventricular diastolic compliance and reduced the correlation between right and left ventricular diastolic pressures. The results of the present experiment performed in the opened pericardium might be exaggerated if performed in the closed pericardium which is more physiologic. Conclusions. Based on the results in this experiment and our previous clinical data,12 we would state that RBBB is, indeed, an important complication affecting the postoperative course and morbidity by impairing right and left ventricular function in the surgical treatment of those congenital heart diseases particularly associated with right ventricular hypertrophy, such as high-resistance VSD, tetralogy of Fallot, and truncus arteriosus. However, the continuing elevation of right ventricular pressure in the present experimental model may play a considerable role in the cardiac dysfunction following RBBB. In view of these clinical implications, it remains necessary to do further study of the hypertrophied right ventricle with reduced outflow resistance. We thank Wilfred G. Bigelow, M.D., and William G. Williams, M.D., for their suggestions and review of this manuscript, and Chisa Inoue for her help in its preparation. REFERENCES

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