Pulmonary artery balloon counterpulsation in the management of right heart failure during left heart bypass

J

THoRAc CARDIOVASC SURG

89:264-268, 1985

Pulmonary artery balloon counterpulsation in the management of right heart failure during left heart bypass Pulmonary artery ballooncounterpulsation was imtituted in 10 pigs whenright ventricularfailure limited cardiac output. Global myocardial depression was produced by inflfiion of propranolol, and the left ventricle was fully supported by left heart bypass. A stable model of failure was achieved in six pigs. FoUowing application of pulmonaryartery balloon counterpulsation right atrial pressure decreased from 18.2 ± 2.1 to 15.9 ± 2.5 rnm Hg (p < 0.05). Cardiac output increased from 416 ± 94 to 758 ± 127 m1/min (p < 0.001). Right ventricular stroke work increased from 0.29 ± 0.07 to 0.65 ± 0.12 gm . m, (p < 0.05).There was no cardiac output beforeor after imtitution of ballooncounterpulsation in four pigs studied during ventricular fibriUation or asystole. We conclude that pulmonary artery balloon counterpulsationimproved cardiac output and right ventricularstroke work in a modelof right ventricular failure where the pulmonarycirculationwas unalteredand the left ventricle supportedby left heart bypass. Balloon counterpulsation was not effective during ventricular fibriUation or asystole. Pulmonary artery balloon counterpulsationshould be considered when right ventricularfailure limits cardiac output during left heart bypass.

Paul A. Spence, M.D., Richard D. Weisel, M.D., Jane Easdown, M.D., Karim A. Jabr, P.M.T., C.P., and Tomas A. Salerno, M.D., Toronto, Ontario, Canada

Bmonary artery balloon counterpulsation is effective in improving cardiac function in right ventricular failure caused by severe pulmonary hypertension.':' Right ventricular failure caused by ischemia may also occur despite normal pulmonary vascular resistance. The primary problem is myocardial dysfunction rather than increased right ventricular afterload. Patients who develop right ventricular failure with an acute myocardial infarction-the right ventricular infarction syndromeexemplify this situation.' Ischemic right ventricular failure is a frequent complication during left heart bypass for shock after cardiopulmonary bypass.' In this From the Divisionsof Cardiovascular Surgery, St. Michael's Hospital. Toronto General Hospital and the University of Toronto, Toronto, Ontario, Canada Supported by the Medical Research Council of Canada and the Dean's Fund of the University of Toronto, Toronto, Ontario, Canada. Received for publication Jan. 20, 1984. Accepted for publication March 20, 1984. Address for reprints: T. Salerno, M.D., St. Michael's Hospital, 30 Bond St., Toronto, Ontario, Canada M5B IW8.

264

situation right ventricular failure is unmasked when the left ventricle is unloaded. If overall cardiac output is inadequate despite full support of the left ventricle by left heart bypass a second pump must be employed to assist the right heart circulation. The present study was undertaken to assess the efficacy of pulmonary artery balloon counterpulsation in supporting the failing right ventricle during left heart bypass in animals whose pulmonary circulation was not altered.

Materials and methods Ten pigs weighing 40 to 45 kg were premedicated with pentobarbital (Nembutal) (10 rug/kg) intraperitoneally and anesthetized with thiopental (Pentothal) (30 rug/kg) intravenously. After tracheostomy, the animals' lungs were ventilated with 50% oxygen with a volume respirator. A catheter was inserted into the left carotid artery for arterial pressure measurement. A Swan-Ganz catheter was floated into the pulmonary artery via the right internal jugular vein. A median sternotomy was then performed and catheters were inserted for pressure

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Pulmonary artery balloon counterpulsation

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Fig. 1. Setup for left heart bypass andpulmonary artery balloon counterpulsation. Note theposition oftheballoon in thepulmonary artery above the pulmonary valve. Atrioventricular (A V) sequential pacing was used to maintain the heart rate at 100 beats/min.

momtonng in the right atrium, right ventricle, left atrium, and left ventricle. Connections were made to Statham transducersand a Gould multichannel recorder. After administration of heparin (3 mg/kg) a No. 20 Bardex cannula was advanced into the right internal carotid artery and used for arterial blood flow return. A purse-string suture was placed around the left atrial appendage and a No. 28 armoured cannula was inserted into the left atrium. The cannula was drained into a reservoir placed 60 em below heart level. A 22 cc balloon (modified from the Datascope intra-aortic balloon [Datascope Corp., Paramus N. Lj) was introduced into the pulmonary artery via the free wall of the right ventricle and directed into the left or right pulmonary trunk. The balloon and electrocardiographic monitoring leads were connected to a Datascope System 82 Console, in which helium was used for counterpulsation (Fig. 1). Left heart bypass was then instituted from the left atrium to the right internal carotid artery by means of a calibrated nonpulsatile Sarns roller pump. Baseline measurements were taken in all 10 animals. Heart failure was induced by infusion of propranolol in increments of I to 3 mg. The total dose administered ranged from 10 to 74 mg. In all animals atrioventricular sequential pacingwas used to maintain the heart rate at 100 beats/min. Lactated Ringer's solution was infused to increase the right atrial pressure above 15 mm Hg. Heart failure was characterized by a decrease in right ventricular output and a large increase in right atrial pressure relative to a small increasein pulmonary artery

pressure. During this period, blood gas levels and pH were monitored and sodium bicarbonate was administered to maintain pH values within normal limits. The left atrial pressurewas kept below 2 mm Hg and the left ventricular pressure was kept below aortic pressure so that no ejection occurred from the left ventricle. A stable model (6 pigs) resulted when cardiac output remained constant and depressed despite elevated and constant right atrial pressure for 5 minutes. Hemodynamic measurements were then made and pulmonary artery balloon counterpulsation was initiated. Counterpulsation was timed from the electrocardiograph on a one-to-one basis. Inflation and deflation points were adjusted to produce maximal cardiac output. After counterpulsation was adjusted, hemodynamic measurements were repeated following a 5 minute period to ensure equilibration. Counterpulsation was then terminated and a return to initial hemodynamic parameters was confirmed. In four pigs ventricular fibrillation or asystole occurred without a stable model of failure. Hemodynamic measurements were made before and after balloon counterpulsation in these animals also. The hemodynamic measurements taken included right atrial pressure, right ventricular pressure, pulmonary artery pressure, left atrial pressure, left ventricular pressure, and heart rate. Cardiac output was measured as the flow in the calibrated left heart bypass circuit. Because ejection did not occur from the left ventricle, the entire pulmonary venous return, and thus the right

The Journal of

2 6 6 Spence et al.

Thoracic and Cardiovascular Surgery

+

200

+

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<,

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6

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6

10

14

18

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RAP(mmHg)

Fig. 2. Cardiac output (CO) and right ventricular stroke work (RVSW) are plotted against right atrial pressure (RAP) for baseline during left heart bypass (LHBP). right ventricular (RV) failure, and right ventricular failure with balloon counterpulsation. Note the severity of the shock model. Cardiac output and right ventricular stroke work were increased and right atrial pressure was decreased by balloon counterpulsation.

Table I. Hemodynamic parameters* PVR (mm HgjLjmin)

Baseline on LHBP (n

SEM RV failure (n

SEM RV failure

= 10)

= 6)

+ PABe

(n

= 6)

SEM

3.4 0.53 18.2t 2.10 15.9 t§

9.1 0.61

87.0:1: 34.3 35.5

. 2.5

8.7

Legend: RAP, Right atrial pressure. RVS/RVD, Right ventricular systolic/diastolic pressures. PAP. Pulmonary artery pressure. Ao, Aortic pressure. CO. Cardiac output. RVSW, Right ventricular stroke work. PVR, Pulmonary vascular resistance. SEM, Standard error of the mean. °Note the improvement in cardiac output, right ventricular stroke work, and right atrial pressure with balloon counterpulsation.

tDifference from baseline p

< 0.01.

:j:Difference from baseline p < 0.05. §Difference from right ventricular failure p

< 0.05.

'l[Difference from right ventricular failure p < 0.01.

ventricular output, was captured in the bypass circuit. This was confirmed by comparison of cardiac output determined by left heart bypass (CO LHBP) and cardiac output determined by thermodilution (COTD ) by means of the Swan-Ganz catheter in the pulmonary artery: CO L H BP = 1.01 CO TD

-

0.03 (r

= 0.98)

Right ventricular stroke work was calculated from mean pulmonary artery pressure (mPA) , mean right atrial pressure (RA), heart rate (HR), and cardiac output (CO) as follows: RVSW = (mPA - RA) X COl HR X 0.0136 (gm . m). Pulmonary vascular resistance (PVR) was also calculated with the mean left atrial pressure (LA) as PVR = (PA - LA)/CO (mm Hg/

Lzrnin). Statistical analysis was performed with the Statistical

Analysis System (SAS Institute, Cary, N. C.). The response to propranolol and pulmonary artery balloon counterpulsation was evaluated in a one-way analysis of variance, differences were specified by Duncan's multiple range test, and the response to balloon counterpulsation was also evaluated by Student's paired t test." Results are reported as the mean and the standard error of the mean. All animals were treated in accordance with the National Academy of Science Guidelines. Results Table I and Fig. 2 summarize the hemodynamic characteristics of all pigs. Propranolol and volume loading resulted in a stable model of right ventricular failure in six pigs, characterized by a significant increase in right atrial pressure, right ventricular systolic and

Volume 89 Number 2

Pulmonary artery balloon counterpulsation

February. 1985

50

267

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Fig. 3. Pulmonary artery (PA) diastolic augmentation is evident but right ventricle (RV) systolic pressure is unchanged by pulmonary artery balloon counterpulsation.

diastolic pressure, pulmonary artery pressure, and pulmonary vascular resistance. Significant decreases were observed in aortic pressure, cardiac output, and right ventricular stroke work. When pulmonary artery balloon counterpulsation was applied to six pigs in right ventricular failure, there was a significant reduction in right atrial pressure and right ventricular diastolic pressure and a significant increase in cardiac output and right ventricular stroke work. A typical trace of the right ventricular and pulmonary artery pressures before and after balloon counterpulsation is displayed in Fig. 3. Asystole or ventricular fibrillation occurred in four pigs. The right atrial, right ventricular, and pulmonary artery pressures equalized and there was no cardiac output. Pulmonary artery balloon counterpulsation resulted in pulsatile pulmonary artery tracings, but there was no measured cardiac output. Discussion When left heart bypass is used to treat shock after cardiopulmonary bypass, right ventricular performance often limits cardiac output. 5 If right ventricular failure is severe and does not respond to volume expansion and inotropes, a second pump must be applied to the right heart circulation. Since this is difficult, pulmonary artery balloon counterpulsation was proposed as an alternate treatment. A number of experiments have shown that pulmonary

artery balloon counterpulsation is effective in treating right ventricular failure caused by severe pulmonary hypertension. I·] Counterpulsation with a pulsatile assist device also improved cardiac output when a right atrium-pulmonary artery anastomosis was performed after exclusion of the right ventricle in dogs.' Although these experiments suggested that pulmonary artery counterpulsation may be useful, none accurately modelled the key features of right ventricular failure in left heart bypass where there is severe biventricular depression of myocardial function.' In addition, unloading of the left ventricle may accentuate the degree of right ventricular dysfunction." In our experiment, animals underwent left heart bypass and propranolol was infused to produce heart failure. Very large doses were given intravenously. Propranolol causes beta receptor blockade, but at these large doses it is unlikely that this was the mechanism responsible for the development of heart failure. At high doses propranolol has quinidine-like properties that cause depression of myocardial contractility."" Reports of massive intoxication with propranolol in man document a syndrome of extreme hypotension and bradycardia. I I This quinidine-like effect has been recently related to sodium channel blockade. 12 The results of these experiments showed that propranolol generated a model of severe heart failure. There was a large decrease in right ventricular output and right ventricular stroke work despite large increases in right ventricular diastolic pressure. The mean pulmo-

The Journal of Thoracic and Cardiovascular Surgery

2 6 8 Spence et ai.

nary artery pressure increased only slightly despite a large increase in right atrial pressure. The calculated pulmonary vascular resistance increased as expected with the decrease in output from the right ventricle. When pulmonary artery balloon counterpulsation was applied there was a large increase in cardiac output and right ventricular stroke work, and filling pressures decreased. Right ventricular systolic pressure did not decrease. Pulmonary valve incompetence may account for this. Examination of the right ventricular outflow tract through the open right ventricle at autopsy in these animals revealed considerable lateral motion of the balloon catheter at the level of the pulmonary valve. The mean pulmonary artery pressure did not change. This may suggest that balloon counterpulsation in the pulmonary artery may act by a different mechanism when pulmonary hypertension is not present. With pulmonary hypertension improvement in right ventricle performance is associated with a reduction in the afterload to the right ventricle.' It is possible that volume displacement through the pulmonary arteries rather than afterload reduction is more important when pulmonary pressures are low. This model of right ventricular failure in which the left ventricle supported by a left heart bypass is directly analogous to the right ventricular failure that occurs after left ventricular assist devices are applied in cardiogenic shock. The results suggest that balloon counterpulsation in the pulmonary artery may be a simple and effective alternative when a second pump would be required to support the right ventricle. This model also simulates, to some degree, right ventricular failure occurring in other situations, when left ventricular function is impaired and the pulmonary circulation is not altered, such as in the right ventricular infarction syndrome. With these encouraging results, we are currently developing a percutaneous device for clinical trials.

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REFERENCES Kralios AC, Zwart HHJ, Moulopoulos SD, Collan R, Kwan-Gett CS, Kolff WJ: Intrapulmonary artery balloon pumping. Assistance of the right ventricle. J THORAC CARDIOVASC SURG 60:215-232, 1970 Spotnitz HM, Berman MA, Reis RL, Epstein SE: The effects of synchronized counterpulsation of the pulmonary artery on right ventricular hemodynamics. J THORAC CARDIOVASC SURG 61:167-174, 1971 Jett GK, SiwekLG, PiconeAL, ApplebaumRE, Jones M, Austen G: Pulmonary artery balloon counterpulsation for right ventricular failure. An experimental evaluation. J THORAC CARDIOVASC SURG 86:364-372, 1983 Cohn IN, Guiha NH, Broder MI, Limas CJ: Right ventricularinfarction. Clinicaland hemodynamic features. Am J Cardiol 33:209-214, 1974 Pierce WS, Parr GVS, Myers JL, Pal WE, Bull AP, Waldhausen JA: Ventricular-assist pumping in patients with cardiogenic shock after cardiac operations. N Engl J Med 305:1606-1616, 1981 Duncan DB: Multiple range and multiple F tests. Biometrics 2:2-42, 1955 de La Riveire AB, Haasler G, Maim JR, Bregman D: Mechanical assistance of the pulmonary circulation after right ventricular exclusion. J THoRAc CARDIOVASC SURG 85:809-814, 1983 Miyamoto AT, Tanaka S, Matloff JM: Right ventricular function during left heart bypass. J THORAC CARDIOVASC SURG 85:49-53, 1983 GibsonDG: Pharmacodynamicproperties of beta adrenergic receptor blocking drugs in man. Drugs 7:8-38, 1974 Nies AS, Shend DG: Clinical pharmacology of propranolol. Circulation 52:6-15, 1975 Frishman W, Jacob H, Eisenberg E, Ribner H: Clinical pharmacology of the new beta adrenergic blocking drugs. Part 8. Salt poisoning with beta adrenoreceptor blocking agents. Recognition and management. Am Heart J 97:797-807, 1979 Matthews JC, Baker JK: Effects of propranolol and a number of its analogues on sodium channels. Biochem PharmacoI31:1681-1685,1982