Right ventricular dysfunction following cold potassium cardioplegia

J

THORAC CARDIOVASC SURG

90:243-250, 1985

Right ventricular dysfunction following cold potassium cardioplegia Right coronary artery stenoses limit cardioplegic delivery to the right ventricle and may contribute to postoperative right ventricular dysfunction. Right ventricular function was evaluated in 39 patients with right coronary artery stenoses following elective coronary bypass operations. Hemodynamic and nuclear ventriculograpbic measurements, made between 3 and 6 hours postoperatively, revealed a progressive increase in pulmonary arterial pressure, pulse rate, and right ventricular ejection fraction (p < 0.05). Right ventricular end-diastolic volume index (calculated from the thermodilution stroke index divided by the nuclear ejection fraction) decreased, but right atrial pressure increased (suggesting a decrease in compliance~ The response to the infusion of 2 units of plasma (volume loading) was evaluated 3 hours postoperatively (EARLY) and again 5 hours postoperatively (LATE) in 21 patients. Right ventricular performance (the relation between cardiac index or right ventricular stroke work index and right ventricular end-diastolic volume index) and right ventricular systolic function (therelationbetween systolic pulmonary arterial pressure and right ventricular end-systolic volume index) weredepressed EARLY and improved LATE (p < 0.01 in analysisof covariance). Left ventricular performance (the relation between cardiacindexor left ventricular stroke workindexand left ventricular end-diastolic volume index) and left ventricular systolic function (the relation between systolic blood pressure and left ventricular end-systolic volume index) weresimilarEARLYand LATE. Right ventricular diastolic function (the relationbetween rightatrial pressure and right ventricular end-diastolic volume index) and left ventricular diastolic function (therelation between left atrial pressureand left ventricular end-diastolic volume index) weresignificantly greater LATE than EARLY. Right, but not left, ventricular performance and systolic function were transiently depressed, and right and left ventricular diastolic stiffness were transiently decreased in the EARLY postoperative period. In patients with right coronary artery stenoses, current methods of cardioplegia may inadequately protect the right ventricle, but further studiesare required to establishthe relation between intraoperative protection and postoperative function.

George T. Christakis, M.D., Stephen E. Fremes, M.D., Richard D. Weisel, M.D., Joan Ivanov, R.N., M. Mindy Madonik, B.Sc., Susan J. Seawright, R.T.(N.M.), and Peter R. McLaughlin, M.D., Toronto, Ontario, Canada

h e effects of cardioplegic protection during coronary bypass grafting on right ventricular (RV) function have not been extensively studied.' Right coronary artery lesions may limit the delivery of cardioplegic solutions to the right ventricle," 3 and inadequate protection may From the Divisions of Cardiovascular Surgery and Nuclear Cardiology, the Toronto General Hospital and the University of Toronto, Toronto, Ontario, Canada. Supported by the Canadian and Ontario Heart Foundations and the Medical Research Council of Canada. Received for publication Aug. 3, 1984. Accepted for publication Oct. 19, 1984. Address for reprints: Richard D. Weisel, M.D., Division ofCardiovascular Surgery, Toronto General Hospital, 200 Elizabeth St., Eaton North 13-224, Toronto, Ontario. Canada M5G I L7.

depress RV function postoperatively despite normal left ventricular (LV) function.' This study was designed to evaluate RV function after elective coronary artery bypass grafting in patients with right coronary artery stenoses. Hemodynamic and nuclear ventriculographic measurements were employed to evaluate R V function and to account for differences in RV loading conditions.

Methods Thirty-nine consecutive patients (35 men and four women) with right coronary artery stenoses greater than 75% scheduled for elective coronary bypass agreed to participate in an evaluation of postoperative ventricular function and signed a consent form approved by the 243

The Journal of Thoracic and Cardiovascular Surgery

2 4 4 Christakis et al.

Table Il, Intramyocardial temperature measurements

Table I. Clinical information No. of patients Preoperative NYHA Class; I/II/III/IV Preoperative left ventricular ejection fraction No. of diseased vessels: 1/2/3 No. with right coronary artery stenosis No. with left anterior descending stenosis No. with circumflex artery stenosis Patients with previous myocardial infarction Cardiopulmonary bypass time (min) Aortic cross-clamp time (min) Highest postoperative SGOT (U/L) Highest postoperative CK-MB (U/L)

39 1/7/20/11 60% ± 15% 0/5/34 39 39 34 16 (42%) 105 ± 27 53 ± 22 71 ± 51 26 ± 15

Coronary artery distributions Right Initial temp. (0C) Lowest temp. (0C) Mean temp. (0C)

16.5 ± 3.8 11.4 ± 3.0 13.8 ± 3.0

Circumflex

14.6±5.1* 10.0 ± 3.5 12.1 ± 3.5*

12.5 ± 3.9t 7.9±2.1t 9.3 ± 3.0t

Legend: LAD, Left anterior descending coronary artery. 'p < 0.05, different from right coronaryartery. tp < 0.01, different from right coronaryartery.

university human experimentation committee. Patients requiring urgent revascularization, those who had had a myocardial infarction within I month of the operation, and those with a preoperative LV ejection fraction less than 40% were excluded. Additional preoperative, intraoperative, and postoperative information is summarized in Table I. All cardiac medications were continued until the morning of operation. Anesthesia was induced and maintained with fentanyl (75 J,Lg/kg), and muscle relaxation was achieved with pancuronium (lOO J,Lg/kg). Patients were ventilated with 100% oxygen, and anesthesia was supplemented with isoflurane as required. Cardiopulmonary bypass was instituted with a single, two-stage right atrial cannula and an ascending aortic cannula. Moderate hemodilution (hematocrit value 20% to 25%) and systemic hypothermia (25 C) were maintained during cardiopulmonary bypass. Multidose cold crystalloid cardioplegia was employed for myocardial protection. The cardioplegic solution was infused into the aortic root initially and into the aortic root and each completed vein graft after each distal anastomosis. Intramyocardial temperatures were measured with needle thermistor probes* from the anatomic regions perfused by each of the three major coronary arteries (right, left anterior descending, and circumflex) after each cardioplegic infusion. The initial, lowest, and mean temperatures were recorded for each region. The condition of the patients was stabilized in the intensive care unit before hemodynamic and scintigraphic measurements were made. All patients received 5 mg of morphine sulfate and 5 mg of diazepam intravenously before and as necessary between studies to ensure adequate sedation. Fluids were infused to maintain the left atrial pressure between 5 and 10 mm Hg. Measurements made during treatment for hypertension (mean

arterial pressure> 95 mm Hg) were excluded.' Measurements were made hourly between 3 and 6 hours after cross-clamp removal (time 0). Volume loading (the infusion of 1 or 2 units of plasma)"? was performed in 21 patients 3 hours after cross-clamp removal (EARLY) and again 5 hours postoperatively (LATE) to assess ventricular function. The following catheters were inserted intraoperatively: radial arterial, left atrial, and pulmonary arterial thermodilution. Hemodynamic measurements included pulse rate, systolic and mean radial arterial and pulmonary arterial blood pressures, right and left atrial pressures, and thermodilution cardiac output. Derived hemodynamic measurements included cardiac index, stroke index, RV and LV ventricular stroke work indices, and systemic and pulmonary vascular resistance indices by standard formulas.t? Arterial blood gases were also measured. Equilibrium gated nuclear ventriculograms were performed after in vivo red cell labeling with stannous pyrophosphate followed 25 minutes later by 25 J,LCi of technetium 99m pertechnetate.'" A Technicar Sigma 420 portable gamma camera with a general-purpose, parallel-hole collimator was placed in a 45 degree left anterior oblique postion with a 10 degree caudal tilt and was adjusted to maximize LV and RV separation and to minimize atrial overlap. A Medical Data Systems N computer was interfaced with the gamma camera, and scintigraphic data were acquired over a 3 minute period using 20 frames per R-R interval. RV and LV ejection fractions were calculated by commercially available software using a semi-automated edge detection program. * RV ejection fraction was determined from the RV region of interest by a modification of the technique described by Maddahi, Berman, and Matsuoka." The pulmonary artery was separated from the RV outflow tract, and the right atrium was separated from the right ventricle as much as possible. RV and LV end-diastolic volume indices (RVEDVI and LVEDVI) and end-

*Shiley Inc., Irvine, Calif

*Medical Data Systems. Ann Arbor, Mich.

Legend: NYHA. New York Heart Association. SGOT, Serum glutamic

oxaloacctic transaminase. CK-MB. Creatine kinase MB isoenzyme.

0

Volume 90 Number 2

Right ventricular dysfunction

August, 1985

* p < 0.05 * * p < 0.01 Different than 6 hrs

systolic volume indices (R VESVI and LVESVI) were calculated from the thermodilution stroke index (SI) by the following formulas: N

RVEDVI = SI + RVEF RVESVI = RVEDVI - SI LVEDVI = SI + LVEF LVESVI = LVEDVI - SI

RV performance, the relation between cardiac index or RV stroke work index and RVend-diastolic volume index, was evaluated for each volume-loading episode. Differences between EARLY and LATE were assessed by an analysis of covariance. RV systolic function, the relation between the systolic pulmonary arterial pressure and RVend-systolic volume index, was evaluated for each volume-loading episode as an index of RV function, which was independent of preload and incorporated afterload. Differences between EARLY and LATE were assessed by an analysis of covariance. RV diastolic function was assessed by evaluating the relation between right atrial pressure and RV end-diastolic volume index for each volume-loading episode. Since both RV9 and LVIO diastolic pressure-volume relations are believed to be monoexponential in general configuration, the natural logarithm of the filling pressure was plotted against the diastolic volume. Differences between EARLY and LATE were assessed by an analysis of covariance. LV performance and systolic and diastolic function were analyzed by an analysis of covariance as previously described." Statistical analysis was performed by the Statistical Analysis System programs. * Serial hemodynamic and scintigraphic parameters were tested with respect to time by a repeated measures, analysis of variance, and differences were specified by Duncan's multiple range test I 1 when the analysis of variance was significant (p < 0.05). The hemodynamic and scintigraphic measurements before and after volume loading (EARLY and LATE) were compared by paired and unpaired t tests. Myocardial performance, systolic function, and diastolic compliance were compared between the EARLY and LATE periods by analysis of covariance, employing the general linear models procedure." The mean and standard error of the mean is depicted in the figures, and the mean and standard deviation is presented in the tables and text.

Results There were no perioperative deaths, and one patient developed a new Q wave, suggestive of aperioperative 'SAS Institute lnc., Cary, N. C.

245

E

E 2.6 E

::J

U

Ol

j-j

2.8

2.4

2.2

Ol

t-{

E 12 E

~ 10 0:

N

22

E

::J

I

~ 20

~ ~

E;

18

V)

~

95

90

80

ui

> 75

16

0:

70

45

K 95 Cll

8

E 85

100

.0

14

I

cf. 40

90

LJ.-

85

0:

~ 35

30

80

N

1"

75

E 65

~

~ 3.0

w

(/)

>

0:

>

2.5

0:

3

4

5

6

t

j/+-r *

t

55 45

~

3

Time Post Crossclamp

4

5

6

hours

Fig. 1. Right ventricular hemodynamic and scintigraphic measurements between 3 and 6 hours after cross-clamp removal. The differences from 6 hoursare specified (when the analysis of variance was significant, p < 0.05). C/. Cardiac index. PAPM. Mean pulmonary arterial pressure. RVSW/. Right ventricular stroke work index. RAP, Right atrial pressure. RVEDV/, Right ventricular end-diastolic volume index. RVEF, Right ventricular ejection fraction. RVESV/, Right ventricular end-systolic volume index. myocardial infarction, 2 days postoperatively. Two patients had nonspecific electrocardiographic changes, suggestive of perioperative ischemia. The maximal postoperative cardiac enzymes are presented in Table I. The initial, lowest, and mean intramyocardial temperatures for each anatomic region are presented in Table II. Temperatures measured in the region supplied by the right coronary artery were warmer than temper-

. The Journal of

2 4 6 Christakis et al.

Thoracic and Cardiovascular Surgery

or ;( r 6---• • Late

'*p < 0.05

2.8

:sE 2.6 E

::J i3

2.4 2.2 2.0

N

E 3.0

E

i» 2.5

~

en

1i:

2.0

2.8

N

--t, ,,

,

r

E ~ 2.6 E ::J 2.4

~ 25 E E

~

C/)

* 20

45

2.0

J-

,,

f-J

*

1

E

E

i:» ~ 30

en ~

Ol

J:

[J) C/)

20

I

50

65

75

85

60

70

LVEDVI mLlm 2

II.

atures in the distribution of the left anterior descending or circumflex coronary arteries. Serial measurements. Fig. 1 depicts the principal hemodynamic and scintigraphic variables between 3 and 6 hours after cross-clamp removal (time 0). Mean pulmonary arterial pressure, pulse rate, and RV ejection fraction increased (p < 0.01), and RV end-systolic volume index decreased (p < 0.05). Right atrial pressure increased (NS*), and RV end-diastolic volume index decreased (p = 0.08), suggesting a decrease in diastolic compliance. LV hemodynamic and scintigraphic variables measured between 3 and 6 hours postoperatively are presented in Table III. Left atrial pressure increased (NS), and LV end-diastolic volume index decreased (p = 0.09), suggesting a decrease in LV diastolic compliance. Systemic vascular resistance index decreased (NS), and pulmonary vascular resistance index increased (p = 0.06). Arterial hypoxemia did not account for the rise in pulmonary arterial pressure. Pulmonary arterial temperature increased significantly (p < 0.01) from 35° ± 2° C (at 3 hours) to 37° ± 2° C (at 6 hours). Volume loading. Fig. 2 depicts RV and LV performance. RV performance was depressed EARLY and

95

2

-l~ ,-----r

c,

Fig. 2. Right and left ventricular performance are depicted. Right ventricular performance was depressed EARLY (3 hours postoperatively) and improved LATE (5 hours postoperatively). Abbreviations as described in Fig. I and Table

not significant.

1~f

E E 130

--.t,,,,...,,i 40

55

RVESVI mL/m

/

40 N

RVEDVI mLlm 2

=

* p < 0.01 Early different than Late

i3 2.2

70 80 90 100 110 120

*NS

l>---_Late

Early different than Late

3.0

3.0 N

0 _ 0 Early

30

0 - . . 0 Early

15

I

20

I

25

I

30

I

35

LVESVI mUm 2

Fig. 3. Right and left ventricular systolic function are depicted. Right ventricular systolic function was depressed EARLY (3 hours postoperatively) and improved LATE (5 hours postoperatively). SPA, Systolic pulmonary arterial index. SBP, Systolic blood pressure. LVESVI, Leftventricular end-systolic volume index.

improved LATE. The slopes of the cardiac index-RV end-diastolic volume index relations were similar, but the EARLY curve was shifted to the right. Both the slope and the position of the RV stroke work index-RV end-diastolic volume index relation were depressed EARLY because the pulmonary artery pressure was lower EARLY and did not increase with volume loading. LV performance was not different EARLY and LATE. Cardiac index and LV stroke work index were lower LATE because of a lower LV end-diastolic volume index. Fig. 3 depicts the RV and LV systolic pressurevolume relations. R V systolic function was depressed EARLY, and the pressure-volume curve was shifted down and to the right. Although the systolic blood pressure and LV end-systolic volume index were higher EARLY, the EARLY and LATE curves were not statistically different. Fig. 4 illustrates the RV and LV diastolic pressurevolume relations. Volume loading significantly (p < 0.01) increased both right and left atrial pressures and RV and LV end-diastolic volume indices both EARLY and LATE. Although right and left atrial pressures were not different, RVend-diastolic volume indices were significantly higher than LV end-diastolic volume indices both EARLY and LATE. The slopes of

Volume 90 Number 2 August, 1985

the diastolic pressure-volume relations were similar, but both the right and left ventricles were more compliant EARLY than LATE. Discussion Although LV function has been extensivelyevaluated after coronary bypass operations,'>" RV function has been infrequently assessed.' In this study, RV function was determined early postoperatively in patients with right coronary artery stenoses. The transient depression in performance and systolic function could have been due to incomplete cardioplegic protection of the right ventricle. Equilibrium gated nuclear ventriculography was employed to evaluate RV volumes and ejection fraction and to detect subtle changes in RV function. Equilibrium gated nuclear ventriculography provides an accurate and reproducible estimate of the RV ejection fraction," 16-18 which avoids assumptions about RV geometry. These studies reported an excellent correlation between equilibrium gated measurements and both contrast ventriculography and gated first-pass nuclear studies.v"" Slutsky and colleagues" found the reproducibility and interobserver variability for the equilibrium RV ejection fraction calculation to be less than 4%. However, there are limitations to the RV ejection fraction calculation by equilibrium nuclear ventriculography.":" The right atrium is located posterior and lateral to the right ventricle in the left anterior oblique view, and right atrial exclusion may be difficult in this projection. The pulmonary artery may be difficult to separate from the RV outflow tract. Inclusion of portions of the right atrium or the pulmonary artery in the RV region of interest results in an underestimation of the ejection fraction and overestimation of the RV volumes. In addition, a decrease in RV size can reduce right atrial overlap and increase RV ejection fraction. The increase in ejection fraction with time found in this study could partially be explained by a decrease in atrial overlap. Despite its limitations, nuclear ventriculography offers significant advantages over other techniques for assessing RV function. Echocardiography" and sonomicrometry" provide an estimate of RV size and function but cannot calculate RV volumes or ejection fraction. Postoperative septal wall motion abnormalities" further complicateRV assessment by these techniques. Nuclear ventriculography permits an assessment that is independent of RV geometry. Transient RV dysfunction. Rewarming (between 3 and 6 hours postoperatively) was associated with a decreasein mean arterial pressure and systemic vascular resistance index, but an increase in pulmonary arterial

Right ventricular dysfunction

Early

16 15 14 13 OJ 12 ro0 11 (/)

c

~

01

I

E E ~

::J (/)

(/)

~ c,

10 9 8 7

6 5

!

0--.1>---

Left Side Right Side

*

L

-i(

1

I

I

I

I

I

l I I

I

I

I

I

I

I

I

I

I

247

..Late

f-

• p < 0.01 Early different than Late

Fig. 4. Right and left ventricular diastolic compliance relations are depicted (employing a natural logarithmic scale for pressure). Both right and left ventricular diastolic compliance were increased EARLY and decreased LATE, Right ventricular measurements are right atrial pressure and right ventricular end-diastolic volume index. Left ventricular measurements are left atrial pressure and left ventricular end-diastolic volume index.

pressure and pulmonary vascular resistance index. Pulmonary vasoconstriction could have resulted from a decrease in functional residual capacity and pulmonary compliance which occurs during this period." Although extravascular lung water may accumulate postoperatively, arterial blood gas analysis (Table III) but did not reveal arterial hypoxemia. Despite an increase in pulmonary arterial pressure and pulse rate, RV ejection fraction increased postoperatively (without a change in LV ejection fraction), suggesting transient RV dysfunction. Rabinovitch and associates,' using gated first-pass nuclear ventriculography, also found isolated RV dysfunction 5 days postoperatively in three of 12 patients with right coronary artery disease. They reported that the postoperative RV ejection fraction was signifIcantly lower than the preoperative values without a decrease in LV ejection fractions. Although ejection fraction has been employed extensivelyas an index of RV function," 24 it is critically dependent on preload, afterload, and pulse rate. Therefore, the loading conditions must be carefully defined when changes in .ejection fraction are being interpreted." Brent and colleagues" found that the RV ejection fraction correlated poorly with more sensitive indices of RV function. Calculation of RV performance, systolic function,

The Journal of

2 4 8 Christakis et al.

Thoracic and Cardiovascular Surgery

Table ID. Left ventricular hemodynamic and pulmonary function measurements Hours postoperatively

3 MAP (mm Hg) LAP (mm Hg) LVSWI (gm . rn/rn") LVEF (%) LVEDVI (mljm') SVRI dyne. sec/ems /rn') PVRI (dyne. sec/em'/m') Arterial Po, (mm Hg)

98 9 33 48 60 3,538 234 234

± ± ± ± ± ± ± ±

5

4

20 4 9 12 15 2,232 123 101

95 ± 10 ± 31 ± 52 ± 52 ± 3,243 ± 275± 198 ±

12 6 II 15 12 1,146 196 79

92 ± 12 ± 30 ± 54 ± 53 ± 2,487 ± 250 ± 184 ±

6

13 4 8 14 12 809 120 58

93 II 33 54 56 2,516 286 178

± ± ± ± ± ± ± ±

18 5 13 12 14 934 150 36

Legend: MAP, Mean arterial pressure. LAP, Left atrial pressure. LVSWI, Left ventricular stoke work index. LVEF. Left ventricular ejection fraction. LVEDVI, Left ventricular end-diastolic volume index. SVRI, Systemic vascular resistance index. PVRI, Pulmonary vascular resistance index. Po" Oxygen tension.

and diastolic compliance provided an accurate assessment of ventricular function, which accounted for differences in preload and afterload." RV performance provides a more sensitive index of RV function than ejection fraction. The cardiac index-RVend-diastolic volume index relation accounted for differences in preload, and the RV stroke work index-RV enddiastolic volume index relation accounted for differences in both preload and afterload. The analysis of covariance permitted a comparison between the EARLY and LATE periods, which specified differences in both slope and position. RV performance was depressed EARLY, whereas LV performance was not changed EARLY. RV systolic function provided an index that was independent of preload and incorporated afterload.l'v'>" Both clinical" and experimental":" studies have suggested that RV systolic function can be employed as an index of RV contractility. Brent and associates" concluded that the R V systolic function was linear and comparable to LV systolic function," RV ejection fraction, performance, and systolic function were depressed EARLY and improved LATE. Since LV ejection fraction, performance, and systolic function did not change during this period, RV dysfunction may have resulted from inadequate RV protection. Severe right coronary artery stenoses limit cardioplegic delivery and may contribute to the warmer RV temperatures. Both noncoronary collateral and RV blood flow also contribute to the warmer temperatures. The ventral location of the right ventricle and its proximity to the operating room lights, as well as its inability to be submerged in topical hypothermic solutions, may also contribute to inadequate RV cooling. The temperature gradients between the left and right ventricles 2, 3o have been reported to result in persistent atrial' I, 32 and ventricular'<" activity during cardioplegic arrest and have been correlated with postoperative arrhythmias.":" Right coronary artery stenoses prevent

cardioplegic delivery,' result in warmer RV temperatures, and may induce RV dysfunction in the EARLY postoperative period. Incomplete myocardial protection could have induced biventricular ischemia, resulting in RV dysfunction. In previous studies, weS-7 found that lactate was released from the heart, and volume loading induced further ischemic anaerobic myocardial metabolism during the first 4 hours postoperatively (EARLY). Isolated RV dysfunction was found during a period when previous studies demonstrated ischemic myocardial metabolism. Four to 6 hours postoperatively (LATE), previous studies demonstrated normal myocardial metabolism' when both RV and LV function were normal. The pathophysiology of isolated R V dysfunction remains obscure. Patients with a previous inferior myocardial infarction are prone to develop isolated RV dysfunction in response to stress-induced ischemia. 17.23, 24 Postoperatively, abnormal septal function could result in isolated RV dysfunction. Studies employing both echocardiography and nuclear ventriculography after coronary bypass operations have found transient abnormalities of interventricular septal motion in the majority of patients." The abnormality may result from an augmented anterior motion of the heart or depressed septal contractility." Septal function is critical to RV performance, because animals with normal septal function have preserved RV performance, even when the RV free wall has been destroyed.":" During a period of incomplete myocardial metabolic recovery, RV but not LV dysfunction could have resulted from previous inferior myocardial infarctions, abnormal septal function, or from direct ischemic injury. Diastolic function. Both RV and LV diastolic stiffness were decreased EARLY and increased LATE. Studies by Mangano, Ellis, and Van Dyke 41, 42 in the operating room immediately following coronary bypass grafting and cold potassium cardioplegia demonstrated

Volume 90 Number 2

Right ventricular dysfunction

249

August. 1985

increased LV compliance. Their results, combined with ours, would suggest that LV stiffness was reduced after potassium cardioplegia and returned to normal 4 to 6 hours postoperatively.' RV stiffness followed a similar pattern. The stiffer ventricle did not result from ischemia because myocardial lactate metabolism was abnormal EARLY and normal LATE7 and R V function improved LATE. RV performance and systolic function were transientlydepressed following elective coronary bypass grafting. Inadequate cardioplegic protection of the right ventricle may have contributed to this transient dysfunction. However, further studies are required to determine whether better cooling of the right ventricle will improve postoperative RV function. We would like to extend our appreciation to Ms. Penelope J. Maton, B.Sc., for nuclear data acquisition and analysis, Ms. Barbara Brown, B.Sc., for biochemical testing, Mr. R. I. Fraser Baird and Mr. Ronald W. J. Baird, for assistance with hemodynamic and clinical data acquisition, and to Ms. Catherine Andrews for preparation of the manuscript. We also wish to extend our appreciation to the nurses and physicians of the cardiovascular operating rooms and intensive care unit for their assistance. REFERENCES Rabinovitch MA, Elstein J, Chiu RCJ, Rose CP, Artin A, Burgess J: Selective right ventricular dysfunction after coronary bypass grafting. J THORAC CARDIOVASC SURG 86:444-450, 1983 2 Chiu RCJ, Blundell PE, Scott HJ, Cain S: Importance of monitoring intramyocardial temperature during hypothermic myocardial protection. Ann Thorac Surg 28:317-322, 1979 3 Chiu RCJ, Mulder DS: Complications of cardioplegic preservation, A Textbook of Clinical Cardioplegia, MR Engelman, S Levitsky S, eds., Mount Kisco, N.Y., 1982, Futura Publishing Co., pp 391-404 4 Weisel RD, burns RJ, Baird RJ, Mickleborough LL, Burns RJ, Teasdale SJ, Ivanov J, Seawright SJ, Madonik MM, Mickle DAG, Scully HE, Goldman BS, McLaughlin PR: Effects of postoperative hypertension and its treatment. J THORAC CARDIOVASC SURG 86:47-56, 1983 5 Weisel RD, Burns RJ, Baird RJ, Hilton JD, Ivanov J, Mickle DAG, Teoh KH, Christakis GT, Evans PJ, Scully HE, Goldman BS, McLaughlin PR: Optimal postoperativevolume loading. J THORAC CARDIOVASC SURG 85:552563, 1983 6 Weisel RD, Burns RJ, Baird RJ, Hilton JD, Ivanov J, Mickle DAG, Teoh KH, Christakis GT, Evans PJ, Scully HE, Goldman BS, McLaughlin PR: A comparison of volume loading and atrial pacing following aortocoronary bypass. Ann Thorac Surg 36:332-344, 1983 7 Fremes SE, Weisel RD, Mickle DAG, Ivanov J, Madonik MM, Seawright SJ, Houle S, McLaughlin PR, Baird RJ:

Myocardial metabolism and ventricular function following cold potassium cardioplegia. J THORAC CARDIOVASC SURG 89:531-546,1985 8 Maddahi J, Berman DS, Matsuoka DT: A new technique for assessing right ventricular ejection fraction using rapid multiple-gated equilibrium cardiac blood pool scintigraphy. Circulation 60:581-589, 1979 9 Sibbald WJ, Driedger AA: Right ventricular function in acute disease states. Pathophysiologic considerations. Crit Care Med 11:339-345, 1983 10 Gaasch WH, Cole JS, Quinones MA, Alexander JK: Left ventricular compliance. Mechanisms and clinical implications. Am J Cardiol 38:645-653, 1976 11 Duncan DB: Multiple range and multiple F tests. Biometrics 11:2-42, 1955 12 Ray AA, Sail JP, Salter M: SAS User's Guide: Statistics, Cary, N.C., 1982, SAS Institute Inc. 13 Roberts AJ, Spies SM, Sanders JH, Moran JM, Wilkinson CJ, Lichtenthal PR, White RL, Michaelis LL: Serial assessment of left ventricular performance following coronary artery bypass grafting. J THORAC CARDIOVASC SURG 81:69-84, 1981 14 Reduto CA, Lawrie RM, Reid JW, Whissenand HH, Noon GP, Kanon D, DeBakey ME, Miller RR: Sequential postoperative assessment of left ventricular performance with gated cardiac blood pool imaging following aortocoronary bypass surgery. Am Heart J 101:59-66, 1981 15 Phillips HR, Carter JE, Okada RD, Levine FH, Boucher CA, Osbakken M, Lappas D, Buckley M, Pohost GM: Serial changes in left ventricular ejection fraction in the early hours after aortocoronary bypass grafting. Chest 83:28-34, 1983 16 Steele PP, Kirch D, LeFree M, Battock D: Measurements of right and left ventricular ejection fractions by radionuc1ide angiography in coronary artery disease. Chest 70:5156, 1976 17 Slutsky R, Hooper W, Gerber K, Battler A, Froelicher V, Ashburn W, Karliner J: Assessment of right ventricular function at rest and during exercise in patients with coronary artery disease. A new approach using equilibrium radionuclide angiography. Am J Cardiol 45:63-71, 1980 18 Dehmer G, Firth B, Lewis S, Willerson J, Hillis L: Direct measurement of cardiac output by gated equilibrium blood pool scintigraphy. Validation of scintigraphic volume measurements by a nongeometric technique. Am J Cardiol 47:1061-1067,1981 19 Bommer W, Weinert L, Neumann A, Neef J, Mason DT, DeMaria A: Determination of right atrial and right ventricular size by two-dimensional echocardiography. Circulation 60:91-100, 1979 20 Chitwood WR Jr, Hill RC, Sink JD, Kleinman LH, Sabiston DC Jr, Wechsler AS: Measurement of global ventricular function in patients during cardiac operations using sonomicrometry. J THORAC CARDIOVASC SURG 80:724-735, 1980 21 Righetti A, Crawford MH, O'Rourke RA, Shelbert H,

. The Journal of

2 5 0 Christakis et al.

22

23

24

25

26

27 28

29

30

31

32

Daily PO, Ross J Jr: Interventricular septal motion and left ventricular function after coronary bypass surgery. Evaluation with echocardiography and radionuclide angiography. Am J Cardiol 39:372-377, 1977 Ali J, Weisel RD, Layug AB, Kirpke BJ, Hechtman HB: Consequences of postoperative alterations in respiratory mechanics. Am J Surg 128:376-382, 1974 Kaul S, Hopkins JM, Shah PM: Chronic effects of myocardial infarction on right ventricular function. A noninvasive assessment. J Am Coli Cardiol 2:607-615, 1983 Berger HJ, Johnstone DE, Sands JM, Gottschalk A, Zaret BL: Response of right ventricular ejection fraction to upright bicycle exercise in coronary artery disease. Circulation 60:1292-1300, 1979 Sagawa K: Editorial. The end-systolic pressure volume relation of the ventricle. Definitions, modifications and clinical use. Circulation 63: 1223-1227, 1981 Brent BN, Berger JH, Matthay RA, Mahler D, Pytlik L, Zaret BL: Physiologic correlates of right ventricular ejection fraction in chronic obstructive pulmonary disease. A combined radionuclide and hemodynamic study. Am J Cardiol 50:255-262, 1982 Sagawa K: The ventricular pressure-volume diagram revisited. Circ Res 43:677-683, 1978 Maughan WL, Skoukas AA, Sagawa K, Weisfeld ML: Instantaneous pressure-volume relationship of the canine right ventricle. Circ Res 44:209-315, 1979 Grossman W, Braunwald E, Mann T, McLaurin LP, Green LH: Contractile state of the left ventricle in man as evaluated from end-systolic pressure-volume relations. Circulation 56:845-852, 1977 Fisk RL, Ghaswalla D, Guilbeau EJ: Asymmetrical myocardial hypothermia during hypothermic cardioplegia. Ann Thorac Surg 34:318-322, 1982 Tchervenkov CI, Wynands JE, Symes JF, Malcolm 10, Dobell ARC, Morin JE: Persistent atrial activity during cardioplegic arrest. A possible factor in the etiology of postope:ative supraventricular tachyarrhythrnias. Ann Thorac Surg (in press) Novick RJ, Stefaniszyn JH, Morin JE, Tchervenkov CI,

Thoracic and Cardiovascular Surgery

33

34

35

36

37

38

39

40

41

42

Malcolm 10, Symes JF, Dobell ARC, Salerno TA: Atrial electrical activity and its suppression during cardioplegic arrest in pigs. J THORAC CARDIOVASC SURG 86:236-241, 1983 Brandt B III, Richardson JV, O'Bryan P, Ehrenhaft JL: Intramyocardial electrical and metabolic activity during hypothermia and potassium cardioplegia. Ann Thorac Surg 31:117-120,1981 Ferguson TB Jr, Smith PK, Buhrman WC, Lofland GK, Cox JL: Monitoring of the electrical status of the ventricle during cardioplegic arrest. Circulation 68:Suppl 2:27-33, 1983 Tchervenkov CI, Wynands JE, Symes JF, Malcolm 10, Dobell ARC, Morin JE: Electrical behavior of the heart following high-potassium cardioplegia. Ann Thorac Surg 36:314-319, 1983 Smith PK, Buhrman BS, Levett JM, Ferguson TB Jr, Holman WL, Cox JL: Supraventricular conduction abnormalities following cardiac operations. J THORAC CARDIOVASC SURG 85:105-115, 1983 Smith PK, Buhrman WC, Ferguson TB Jr, Levett JM, Cox JL: Conduction block after cardioplegic arrest. Prevention by augmented atrial hypothermia. Circulation 68:Suppl 2:41-48, 1983 Kagan A: Dynamic responsesof the right ventricle following extensive damage by cauterization. Circulation 5:816823, 1952 Guiha NH, Limas CJ, Cohn IN: Predominant right ventricular dysfunction after right ventricular destruction in the dog. Am J Cardiol 33:254-258, 1974 Sawatani S, Mandell C, Kusaba E: Ventricular performance following ablation and prosthetic replacement of right ventricular myocardium. Trans Am Soc Artif Intern Organs 20:629-636, 1974 Mangano DT, Van Dyke DC, Ellis RJ: The effect of increasing preload on ventricular output and ejection in man. Circulation 62:535-541, 1980 Ellis RJ, Mangano DT, Van Dyke DC: Ventricular distention reversal with furosemide following cardiopulmonary bypass. Surgery 88:137-147,1980