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Ann Thorac Surg 2000;69:1188-1191
© 2000 The Society of Thoracic Surgeons


ORIGINAL ARTICLES: CARDIOVASCULAR

Hemodynamic changes and right heart support during vertical displacement of the beating heart

Eyal Porat, MDa, Ram Sharony, MDa, Simon Ivry, MDa, Shigeyuki Ozaki, MDb, Bart P. Meyns, MD, PhDb, Willem J. Flameng, MD, PhDb, Gideon Uretzky, MDa

a Department of Cardiothoracic Surgery, Carmel Medical Center, Technion IIT, Haifa, Israel
b Center for Experimental Surgery and Anesthesiology, Katholieke Universiteit, Leuven, Belgium

Address reprint requests to Dr Porat, Department of Cardiothoracic Surgery, Carmel Medical Center, 7, Michal St. Haifa, 34362 Israel
e-mail: docporat{at}internet-zahav.net


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Hemodynamic instability during heart displacement in off-pump multivessel coronary artery bypass grafting might be related to right heart dysfunction. The Enabler (HemoDynamics Systems Ltd, Upper Yoqneam, Israel) is a cannula pump that expels blood from the right atrium into the pulmonary artery. We studied the hemodynamic changes and the role of the enabler during heart displacement.

Methods. Nine anesthetized sheep were assessed for hemodynamic changes during 90-degree heart displacement with or without Enabler support. Hemodynamic parameters included cardiac output, systemic arterial blood pressures, and left and right heart filling pressures.

Results. Heart displacement caused a significant decrease in cardiac output and systemic blood pressure (46% ± 5%, p = 0.001; and 20% ± 5%, p = 0.009, respectively), with a concomitant 137% ± 24% (p = 0.003) increase in central venous pressure. No significant change in left atrial pressure was observed. Activation of the Enabler caused a significant increase in cardiac output and systemic blood pressure (67% ± 15%, p = 0.01; and 17% ± 7%, p = 0.04, respectively), as well as a decrease in central venous pressure by 49% ± 8% (p = 0.0001).

Conclusions. Heart displacement causes hemodynamic instability mainly by right heart dysfunction. The Enabler significantly stabilized circulation during vertical displacement of the beating heart.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Coronary artery bypass grafting (CABG) without cardiopulmonary bypass was first introduced by Kolessov in 1967 [1]. This modality has regained its recognition as a result of awareness of the damaging effect of CPB [2, 3] and recent improvements in surgical equipment and techniques [4]. Most procedures address the left anterior descending coronary artery (LAD), without the need to displace the heart. However, revascularization of circumflex artery branches requires vertical displacement of the heart. When this maneuver is done on the beating heart it causes significant hemodynamic instability, manifested as reduction in stroke volume and arterial blood pressure [5]. Although biventricular failure has been proposed as the main cause of this phenomenon, the precise mechanism is still unknown.

To provide hemodynamic support during off pump CABG (OPCABG), several cardiac-assist devices have been proposed [4]. These devices support the left ventricle and provide flow and pressure to permit pharmacologically induced bradycardia. However, none of these devices addresses the problem of heart displacement that is required for multivessel OPCABG. The Enabler (HemoDynamics Systems Ltd, Upper Yoqneam, Israel) is a catheter pump designed to expel blood from the right atrium into the pulmonary artery in a pulsatile flow pattern. This support system unloads the right heart. We hypothesized that the main mechanism of hemodynamic instability during heart displacement involves right heart dysfunction. The aims of our study were to evaluate the hemodynamic changes during displacement of the beating heart and to determine the role of right heart assistance during this maneuver.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Nine sheep weighing 45 to 60 kg, were used in this study. All animals received humane care in compliance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).

Anesthesia
After 24 to 36 hours of food fasting, all animals received premedication with intramuscular atropine (0.2 mg/kg of body weight). General anesthesia was induced using 0.2 mg/kg intramuscular xylazine, and 10 mg/kg intramuscular ketamine. To facilitate endotracheal intubation, a nondepolarizing muscle relaxant, intravenous atracurium 0.5 mg/kg, was used. Positive pressure ventilation (Harvard apparatus) was started (oxygen:room air mixture 1:1; halothane 0.5% to 1.0%). Anesthesia was maintained with intravenous administration of fentanyl (0.02 mg/kg) and atracurium (0.5 mg/kg). Continuous external electrocardiogram was used for heart rate and rhythm recording.

Operative procedure and experimental protocol
After median sternotomy was done, the pericardium was opened and suspended. To prevent ventricular arrhythmia during manipulation of the heart, 100 mg of lidocaine hydrochloride was given intravenously with the opening of the pericardial sac. A continuous infusion at a dose of 1 mg/kg per hour was started thereafter. Baseline activated clotting time (ACT) was recorded, and heparin at a dose of 300 IU/kg was administrated intravenously. The ACT was maintained above 480 seconds throughout the procedure. Fluid manometer lines were inserted into the right atrium, right ventricle, pulmonary artery, left atrium, left ventricle, and right femoral artery for hemodynamic measurements. Simultaneous monitoring was done using an eight-channel recorder (Kipp & Zonen, Delft, The Netherlands). Continuous cardiac output monitoring was done using an ultrasonic flow probe (Transonic Systems, Ithaca, NY) placed around the aorta.

The Enabler support system consists of a pulsatile pump and a disposable cannula-valve unit that expels blood from the right atrium into the pulmonary artery (Fig 1). The device consists of an electrohydraulically driven piston that forces fluid into the disposable head, triggered by the electrocardiogram [6]. The fluid displaces a polyurethane membrane, enabling pulsatile blood flow through the cannula using a valve mechanism (Fig 2). During the unloading phase, the blood is pumped from the side holes of the catheter located in the right atrium, through a one-way valve. At this phase, the tip holes in the pulmonary artery are kept closed by another opposite one-way valve. In the expelling phase, the side holes are kept closed, permitting expelling of blood only from the tip holes. Each stroke displaces a maximal blood volume of 72 mL, in a frequency ranging from 40 to 180 strokes per minute.



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Fig 1. Mode of insertion of the Enabler cardiac support system. The device expels blood from the right atrium into the main pulmonary artery.

 


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Fig 2. Schematic cross section of the Enabler cardiac support system. Left, unloading phase; right, expelling phase. The Enabler consists of a pulsatile pump, a disposable head, and a cannula-valve unit. The pump comprises an electrohydraulically driven piston that forces fluid into and out of the head against a polyurethane membrane. This electrocardiogram (ECG)-triggered process generates a pulsatile blood flow through the cannula using a unique valve mechanism. (PA = pulmonary artery; RA = right atrium.)

 
After surgical preparation of the right jugular vein, the Enabler was inserted and the tip of the cannula was advanced to the main pulmonary artery. Tip positioning was verified by pressure measurement. The heart was displaced vertically to gain access to the Cx artery branches by using the Octopus system (Octopus Tissue Stabilizer; Medtronic Inc, Minneapolis, MN, USA). Hemodynamic parameters were recorded before Enabler activation, 3 minutes after heart displacement, and 15 minutes after Enabler activation.

Statistical analysis
Results are presented as mean ± standard deviation for absolute values and as mean ± standard error of the mean for relative results. For comparisons between different stages of the trial (baseline, displaced, and assisted displaced heart), repeated-measures analysis of variance was done. The repeated-measures analysis of variance test criteria for the hypothesis of stage effect were used to test overall change in a variable during the trial. For comparisons we used contrasts between the nth level (displaced and assisted displaced heart) and baseline condition for all variables. The analysis was done with SAS 6.12 software (SAS Institute, Cary, NC) using the generalized linear models (GLM) procedure using repeated-measures analysis of variance with profile contrast option. A p value of less than 0.05 was considered significant.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
The hemodynamic condition of all animals was stable during the baseline phase. All animals survived the study protocol. No inotropic support was given, nor was defibrillation needed during the entire procedure. Blood loss was minimal without need for blood transfusions. Table 1 summarizes the hemodynamic values recorded during the study.


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Table 1. Hemodynamic Changes During Heart Anterior Displacement and Enabler Activationa

 
During anterior displacement of the heart, cardiac output decreased by 46% ± 5% (p = 0.001). We found a significant reduction in systolic, diastolic, and mean arterial blood pressure of 20% ± 5% (p = 0.009), 25% ± 6% (p = 0.005), and 23% ± 6% (p = 0.005), respectively. Right ventricular end-diastolic pressure as well as central venous pressure increased by 350% ± 64% (p = 0.005) and 137% ± 24% (p = 0.003), respectively. In contrast, no significant changes were noted in either mean pulmonary artery pressure, which increased by 25% (p > 0.05), left atrial pressure, or left ventricular end-diastolic pressure (8% ± 0.2% [p > 0.05], and 31% ± 20%, [p > 0.05] respectively) during anterior displacement of the heart.

During Enabler activation for 15 minutes, the cardiac output increased by 67% ± 15% (p = 0.01). Systolic, diastolic, and mean systemic blood pressures increased by 17% ± 7%, 21% ± 9%, and 18% ± 8%, respectively (p = 0.04, p = 0.03, p = 0.04, respectively). Central venous pressure decreased by 49% ± 8% (p = 0.0001), while no significant changes were observed in left atrial pressure, left ventricular end-diastolic pressure, and heart rate.


    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
This study shows the hemodynamic changes that occur during vertical displacement of the beating heart and the improvement obtained with right side assist by the Enabler.

Performing CABG on the beating heart has numerous advantages [7] but still poses several problems. Adequate exposure and stabilization of the target vessels must be obtained to permit high quality anastomosis while maintaining a stable hemodynamic condition. To provide adequate myocardial protection during beating heart coronary artery operations, pharmacologic intervention, preconditioning, and mechanical unloading devices have been suggested [4, 8]. When OPCABG to posterior wall vessels is done, vertical displacement of the heart is necessary, but it causes marked hemodynamic instability.

Several approaches have been suggested to stabilize hemodynamics during heart displacement. The Trendelenburg maneuver increases right side preload, thus improving cardiac output and systemic arterial blood pressures [5, 9]. This maneuver emphasizes the role of adequate right ventricular output. Although it is possible to maintain stable hemodynamic conditions with this maneuver, it was not found to be an optimal solution in conditions such as reduced left ventricular function or acute ischemia. Others reported the use of left ventricular assist devices for providing hemodynamic support during OPCABG using centrifugal [10, 11] or axial flow pumps [12, 13]. Our finding that left heart filling pressures did not change significantly during heart displacement, as well as the reported importance of right ventricular preload on cardiac output [5], caused us to concentrate on right ventricular function and seek a method to bypass the distorted right ventricle and augment pulmonary blood flow.

The previous observation that left atrial pressure did not change significantly despite a reduction in stroke volume has led to the concept of left ventricular dysfunction during heart displacement [5]. We suggest that a reduction in pulmonary blood flow prevents an increase in left atrial pressure during heart displacement.

The increase in central venous pressure and right ventricular end-diastolic pressure during heart displacement is consistent with the results of Grüdeman and colleagues [5] and indicate right ventricular inflow obstruction and mechanical dysfunction of the right heart, respectively. Activation of the Enabler caused further decrease in right ventricular end-diastolic pressure representing right ventricular bypass, with concomitant increase in left ventricular cardiac output. The increase in pulmonary blood flow and subsequently the flow to the left atrium caused an increase in cardiac output, which prevented the increase in left atrial pressure.

Our data demonstrate the hemodynamic changes and the supportive effect of right heart assist with the Enabler during vertical displacement of the beating heart. This study was conducted on normal hearts. The hemodynamic deterioration that occurs during displacement of a compromised left ventricle is expected to be even more profound. We believe that our conclusions will be applicable with ischemic myocardium and impaired left ventricular function.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Kolessov V.L. Mammary artery-coronary artery anastomosis as method of treatment for angina pectoris. J Thorac Cardiovasc Surg 1967;54:535-544.[Medline]
  2. Kirklin J.K., Westaby S., Blackstone E.H., Kirklin J.W., Chenoweth D.E., Pacifico A.D. Complement and the damaging effects of cardiopulmonary bypass. J Thorac Cardiovasc Surg 1983;86:845-857.[Abstract]
  3. Westaby S. Organ dysfunction after cardiopulmonary bypass. A systemic inflammatory reaction initiated by the extracorporeal circuit. Intensive Care Med 1987;13:85-95.[Medline]
  4. Westaby S., Benetti F.J. Less invasive coronary surgery. Ann Thorac Surg 1996;62:924-931.[Free Full Text]
  5. Grüdeman P.F., Borst C., van Herwaarden J.A., Mansvelt Beck H.G., Jansen E.W.L. Hemodynamic changes during displacement of the beating heart by the Utrecht Octopus method. Ann Thorac Surg 1997;63:S88-S92.
  6. Rottenberg D., Sondak E., Rahat S., Borman J.B., Dviri E., Uretzky G. Early experience with a true pulsatile pump for heart surgery. Perfusion 1995;10:171-175.[Free Full Text]
  7. Benetti F.J., Naselli G., Wood M., Geffner L. Direct myocardial revascularization without extracorporeal circulation. Experience in 700 patients. Chest 1991;100:312-316.[Abstract/Free Full Text]
  8. Flameng W.J. Role of myocardial protection for coronary artery bypass grafting on the beating heart. Ann Thorac Surg 1997;63:S18-S22.
  9. Grüdeman P.F., Borst C., van Herwaarden J.A., Verlaan C.W.J., Jansen E.W.L. Vertical displacement of the beating heart by the Octopus tissue stabilizer. Ann Thorac Surg 1998;65:1348-1352.[Abstract/Free Full Text]
  10. Waldenberger F.R., Haisjackl M., Holinski S., Lengsfeld M., Konertz W. Centrifugal pumps as left ventricular assist for coronary revascularization on a beating heart. Artif Organs 1998;22:698-702.[Medline]
  11. Waldenberger F.R., Hotz H., Haisjackl M., Konertz W. Surgical coronary revascularization of the beating heart. Z Kardiol 1996;85(Suppl 4):35-41.
  12. DeRose J.J., Jr, Umana J.P., Madigan J.D., et al. Mechanical unloading with a miniature in-line axial flow pump as an alternative to cardiopulmonary bypass. ASAIO J 1997;43:M421-M426.[Medline]
  13. Lönn U., Peterzén B., Granfeldt H., Casimir-Ann H. Coronary artery operation with support of the hemopump cardiac assist system. Ann Thorac Surg 1994;58:519-523.[Abstract/Free Full Text]
Accepted for publication October 19, 1999.




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