AATS: American Association for Thoracic Surgery.
Watch the AATS Leadership Video
 
Wednesday Morning, April 16, 1975
Back to Annual Meeting Program

WEDNESDAY MORNING, APRIL 16, 1975

8:30 A.M. Scientific Session

Imperial Ballroom

MYOCARDIAL PRESERVATION

(Open Discussion)

Chairman - W. G. Bigelow

Metabolism (Abstract 23) David C. MacGregor

Biochemistry (Abstract 24) R. W. Busuttil

Retrograde Coronary Perfusion (Abstract 25) Robert A. Poirier

Low Output Syndrome (Abstract 26) Gerald Buckberg

Subendocardial Flow (Abstract 27) Charles F. Reuben

Local Deep Hypothermia (Abstract 28) Randall B. Griepp

Intra-Aortic Balloon Pumping (Abstract 29) David Bregman

Intra-Aortic Balloon Pumping (By Invitation) Donald B. Effler

INTERMISSION - VISIT EXHIBITS (Albert Hall)

Coronary Perfusion (By Invitation) Dwight C. McGoon

Anoxic Arrest (By Invitation) Denton A. Cooley

Ventricular Fibrillation (By Invitation) Ronald J. Baird

Open Discussion (Seventy Minutes)

Summary and Perspective (By Invitation) James V. Maloney, Jr.


23. Ischemic Contracture of the Left Ventricle: Production and Prevention

DAVID C. MacGREGOR*, GREGORY J. WILSON*, SHIGEO TANAKA*,

DONALD E. HOLNESS*, WOLFGANG LIXFELD*,

MALCOLM D. SILVER* and LORRAINE J. RUBIS*, Toronto, Ontario, Canada

Sponsored by W. G. Bigelow, Toronto, Canada

Ischemic contractive of the left ventricle ("stone heart") is a recognized complication of prolonged periods of interruption of the coronary circulation during open-heart surgery. We have examined the effects of moderate hypothermia (28°C) and preoperative beta-adrenergic blockade (propranolol, 0.5 mg/kg; 1.0 mg/kg) on contracture development during ischemic arrest of the heart.

Four groups of 8 dogs each were placed on total cardiopulmonary bypass and ischemic arrest of the heart was produced by cross-clamping the ascending aorta and venting the left ventricle. Intramyocardial carbon dioxide tension was continuously monitored by mass spectrometry. When anaerobic energy production ceased, as indicated by a final plateau in the intramyocardial carbon dioxide accumulation curve, the ischemic arrest was terminated and the contractile state of the heart observed. These results are tabulated below:

Group

Temperature

Propranolol

Termination of Arrest

Ischemic

Contracture

Time

PCO2

I

38°C

none

*54.4±4.2 mm

474±29 mm Hg

yes

II

38°C

0.5 mg/kg

79.6±5.1 min

527±38 mm Hg

yes

III

38°C

1.0 mg/kg

76.6±4.9 min

455±42 mm Hg

yes

IV

28°C

none

120.4±5.5 min

341±26mmHg

no

*Mean ± SEM; 8 dogs in each group

We conclude that beta-adrenergic blockade delays, but does not prevent, the onset of ischemic contracture of the left ventricle under normothermic conditions. Moderate hypothermia appears to completely prevent this complication.

*By invitation


24. Protective Effect of Methylprednisolone on the Heart During Ischemic Arrest

R. W. BUSUTTIL*, W. J. GEORGE* and R. L. HEWITT,

New Orleans, Louisiana

Although corticosteriods have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure, and the few reports regarding use of steroids in myocardial ischemia have been conflicting. This study was undertaken to determine if a pharmacological dose of the glucocorticord, methylprednisolone, (MP) would protect the heart during ischemic cardiac arrest.

A randomized double-blind study was performed in 25 dogs. Biochemical and hemodynamic parameters were assessed during and after cardiopulmonary bypass and 30 minutes of ischemic cardiac arrest. Group I (11 animals) received MP 30 mg/Kg I.V. at 18 hours and 1 hour prior to surgery. Group If (13 animals) served as controls and received MP vehicle at the same time periods. Blood pH, gases, and electrolytes were measured; aortic, left aerial, and left ventricular pressures were monitored; the first derivative of the left ventricular pressure (dp/dt max) was also determined. Arterial and coronary sinus blood samples were assayed for iactate levels and activity of the lysosomal enzyme, β-glucuronidase. Left ventricular muscle was assayed for the nucleotides, cyclic AMP and cyclic GMP.

Following restoration of coronary flow, mean aortic and left ventricular systolic pressures and left ventricular contractility as determined by dp/dt max and dp/dt max/IP were depressed in both groups as expected but were significantly higher in Group I than in Group II (p <0.05). An increase in levels of both cyclic nucleotides occurred in each group during ischemia, but this increase in cyclic GMP was significantly greater in Group II (p <0.05). ^3-glucuronidase activity and myocardial potassium loss as determined in coronary sinus blood were both significantly greater in Group II than in Group I (p <.05).

Results of this study demonstrate that pretreatment with a pharmacologic dose of MP significantly enhances cardiac recovery after ischemia. Lysosomal membrane stability and modulation of cyclic GMP levels may be critical determinants in the mechanism of cardiac ischemia.

*By invitation


25. Drip Retrograde Coronary Sinus Perfusion (RCSP) for Myocardial Protection

ROBERT A. POIRIER*, ROBERT A. GUYTON*, and

CHARLES L. McINTOSH*, Bethesda, Maryland

Sponsored by A. G. Morrow, Bethesda, Maryland

Moderate hypothermia is frequently utilized as a sole method of myocardial protection when the aortic root is cross-clamped but not opened. This leaves the myocardium anoxic since at 27°C, oxygen utilization has been shown to only be reduced 50%. A combination of low pressure (15-20 mmHg), low flow (1cc/kg/ mm) RCSP with oxygenated blood and moderate hypothermia (29°C) was demonstrated to yield significantly better (P< 0.001) protection to LV function in dogs than moderate hypothermia alone. The only apparatus was an ordinary intravenous bottle and tubing periodically filled by the bypass pump, and perfusion was by gravity drip into a balloon catheter inserted blindly into the coronary sinus through a stab wound in the right atrial wall. Left ventricular function studies were recorded prior to and following 1 hour of aortic cross-clamping at identical preloads (LVEDP) and heart rates (atrial pacing). Aortic pressure (after-load) was returned to a level as close to baseline as possible by constriction of the descending thoracic aorta. Changes in ventricular function after one hr. of aortic cross-clamping are noted below.

Cardiac Output

LV Stroke Work

Peak Dp/Dt

I RCSP at normothermia (8 dogs)

↓40%

↓42%

↓23%

II Moderate hypothermia (8 dogs)

↓62%

↓75%

↓44%

III RCSP and moderate hypothermia (8 dogs)

↓6%

↓9%

↓5%

Fifteen of sixteen hearts in Groups I and HI continued to beat, and remained pink for the entire hour of cross-clamping (one fibrillated at 20 minutes) while all those in Group II fibrillated (average of 17 min.). Following 1 hr. of aortic cross-clamping, the average aortic pressure in Group III was returned to within 4% of baseline (1 with complete, 6 with partial and 1 without aortic constriction), while Group II could only be returned to a level which was 37% lower than baseline (despite complete aortic constriction in all animals). The advantages of RCSP combined with moderate hypothermia are (1) an additional mode of protection when the aortic root is clamped but not opened, (2) a supply of oxygen to what is otherwise an anoxic myocardium, (3) a technique and apparatus which are simple and require a minimum of attention. With reference to possible intra-aortic surgery, this low flow retrograde perfusion does not produce serious intra-aortic visual obstruction. The above results, combined with the simplicity of the modality, suggests that RCSP may be indicated when moderate hypothermia is otherwise chosen to be the sole source of myocardial protection.

*By invitation


26. Depressed Postoperative Myocardial Performance: A Preventable Complication of Open Heart Surgery

GERALD BUCKBERG, GORDON OLINGER*, DONALD MULDER,

JAMES V. MALONEY, JR., Los Angeles, California

Depressed postoperative myocardial performance ("low output syndrome") requiring inotropic or mechanical circulatory support is due to subendocardial necrosis and is the major cause of death after open heart surgery (Taber, Najafi, Buckberg). Before July 1972, we, as others, used ischemic arrest, profound topical hypothermia, and ventricular fibrillation and needed inotropic drugs in approximately one-third of patients undergoing aortic valve replacement or coronary revascularization and in one-half of patients undergoing mitral valve replacement. Reported mortalities (mitral valve replacement and high risk coronary revascularizations) ranged from 10-40%. Our experimental studies show this morbidity and mortality is caused by ischemic injury to the heart resulting from inadequate myocardial protection during bypass.

Based on these experimental studies, we have, since July 1972, employed the following principles clinically: 1) maintain beating empty heart whenever possible, 2) avoid ventricular fibrillation, 3) avoid prolonged profound topical hypothermic arrest, 4) avoid severe hemodilution, 5) maintain adequate coronary perfusion pressure (at least 80 mm Hg), 6) limit ischemic periods to less than 12 minutes, 7) prolong total bypass as necessary to repay myocardial oxygen debt, 8) optimize DPTI/TTI (supply/demand ratio) pre and postoperatively.

In 189 consecutive operations using these principles, postoperative inotropic support was required in a) one (5%) of 22 mitral valve replacement patients (one death), b) one (2%) of 46 aortic valve replacements (two deaths), c) 10 (7%) of 121 coronary revascularization patients (three deaths), including 56 high risk patients. Of the 12 patients requiring inotropic support, the above principles were violated in four and five others were high risk coronary revascularizations.

We conclude that postoperative depressed myocardial performance requiring pharmacologic or mechanical circulatory support can be virtually avoided by adhering to principles of adequate cardiac protection during open heart surgery.

*By invitation


27. Dynamics of Subendocardial Flow During Cardiopul-monary Bypass

CHARLES F. REUBEN*, HARJEET SINGH*, ALFRED J. TECTOR*,

JOHN P. KAMPINE*, ROBERT J. FLEMMA and

DERWARD LEPLEY, Milwaukee, Wisconsin

Subendocardial flow was measured as temperature differential between the epicardial and subendocardium on cardiopulmonary bypass by a measured bolus of cold blood of known temperature injected into the aortic root. The probes with 0.1 millisecond time response were accurately placed in the subendocardium and epicardium, equidistant from the nearest coronary vessel. The temperature of the myocardium and blood in the aortic root were maintained constant by small variations from the heat exchanger. Flow ratios were obtained from areas under the thermal curves, integrating mean temperature change and time. D.C. operational amplifier offset the basal temperature. Subendocardial and epicardial flow ratios were recorded in 18 dogs: 1) at constant aortic root pressures during sinus rhythm and ventricular fibrillation; 2) at varying aortic root pressures during sinus rhythm; 3) at varying aortic root pressures during induced and spontaneous ventricular fibrillation.

In the non-working heart, the best flows to the subendocardium occurred consistently during sinus rhythm. Fibrillating heart at low aortic root pressure was the most disadvantageous to Subendocardial flow. High aortic root pressure during fibrillation improved Subendocardial flow. The determinants of subendocardial flow under various conditions of cardiopulmonary bypass help to explain the occurrence of Subendocardial necrosis on ischemic basis.

*By invitation


28. The Superiority of Aortic Crossclamping With Profound Local Hypothermia For Myocardial Protection During Aortocoronary Bypass Surgery

RANDALL B. GRIEPP*, EDWARD B. STINSON* and

NORMAN E. SHUMWAY, Stanford, California

Two hundred fourteen patients undergoing aortocoronary bypass grafting were allocated to two groups. In Group I (130 pts) distal anastomoses were carried out with the heart spontaneously fibrillating and the left ventricle vented. In Group II (84 pts) distal anastomoses were carried out with the aorta continuously crossclamped, and the myocardium protected by profound local hypothermia (cold saline immersion). The groups were equivalent with respect to age, sex, risk factors, and incidence of preoperative ventricular dysfunction. Postoperative LDH and SCOT were assayed, EKG's were reviewed for evidence of transmural myocardial infarction, and in a subset of each group postoperative hemodynamics were measured. Results:

Group I

Group II

P Value

# Deaths

2

0

.3

# Transmural infarcts

18

5

.1

Post op day 1 SCOT

102

66

.001

excluding transmural infarcts

90

62

.001

Post op day 1 LDH

359

298

.001

excluding transmural infarcts

334

295

.01

Left atrial pressure (mmHg)

13.3

13

.8

Cardiac index (L/min/M2)

2.5

2.4

.8

Cardiopulmonary bypass time (min/graft)

47

41

.001

These data indicate that in aortocoronary bypass surgery the use of aortic crossclamping and local hypothermia during performance of distal anastomoses: a) shortens operating time, b) reduces myocardial injury as assessed by serum enzyme levels, c) does not alter postoperative hemodynamics, d) possibly reduces the incidence of intraoperative myocardial infarction.

*By invitation


29. Intraoperative Unidirectional Intra-Aortic Balloon Pumping (IABP) in the Management of Left Ventricular Power Failure

DAVID BREGMAN*, EDUARDO N. PARODI*, RICHARD N. EDIE*,

FREDERICK O. BOWMAN, JR., KEITH REEMTSMA and JAMES R. MALM,

New York, New York

Left ventricular power failure and recurrent ventricular tachyarrhythmias following open heart surgery refractory to catecholamine therapy are associated with a mortality in excess of 90%. Unidirectional IABP was utilized in a group of intraoperative patients with the following criteria: (1) cardiac index < 2L/ min/M2, (2) left atrial pressure (LAP) ≥ 30 mmHg, (3) systolic BP ≤ 80 mmHg, (4) a requirement for nigh dose inotropic support, and (5) recurrent ventricular tachyarrhythmias.

Over a 24 month period, 25 patients were assisted following open heart surgery; 84% survived acutely and 64% were long-term survivors. All patients had a prompt fall in LAP (average -18 mmHg) in conjunction with hemodynamic stability, fewer arrhythmias, and a decreased requirement for pharmacologic support. Those patients who did not respond to IABP had myocardial infarction and/or subendocardial ischemia of 80% or more of the left ventricular myocardium.

Seven patients undergoing coronary revascularization (including 3 with associated left ventricular aneurysms) required intraoperative IABP, and 6 survived and were discharged. Intraoperative coronary graft flows were measured and they increased an average of 117% with IABP over baseline values. Coronary graft flows measured with and without IABP support demonstrated an average increase of 80% (range 50-100%, median 83%). An evaluation of simultaneous phasic coronary graft flow tracings, measurements of subendocardial blood flow, and other hemodynamic parameters have confirmed the beneficial clinical and experimental responses to unidirectional IABP.

*By invitation

We Model Excellence
Copyright © American Association for Thoracic Surgery. All rights reserved.
Read the Privacy Policy.
IMPORTANT REMINDER: The preceding information is intended only to provide
general guidance and not as a definitive basis for diagnosis or treatment in any particular case.
It is very important that you consult a doctor about any specific medical problem or question.