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Ann Thorac Surg 1995;59:443-447
© 1995 The Society of Thoracic Surgeons

Direct Mechanical Assistance of the Right Ventricle With the Hemopump in a Porcine Model

Graham J. Cooper, FRCS(Ed), Daniel Y. Loisance, MD, Masatoshi Miyama, MD, Yoshinobu Abe, MD, Philippe H. Deleuze, MD

CNRS UA 1431, Centre de Recherches Chirurgicales Henri Mondor, and Association Claude Bernard, Créteil, France

Accepted for publication October 8, 1994.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
In 6 pigs, a 14F Hemopump was placed through the pulmonary artery into the right ventricle. The pulmonary artery was banded proximal to the outflow port of the Hemopump, and tightening the band increased right ventricular peak systolic pressure by 50%. There were significant falls in right ventricular stroke volume (from 43 ± 7.3 mL [± the standard deviation] to 27 ± 8.0 mL; p < 0.001) and cardiac output (from 4.94 ± 0.76 L/min to 3.70 ± 0.95 L/min; p < 0.01) and increases in right ventricular peak systolic pressure (from 28 ± 9.7 mm Hg to 42 ± 17.1 mm Hg; p < 0.01) and end-diastolic pressure (from 2 ± 0.8 mm Hg to 12 ± 6.4 mm Hg; p < 0.02). Mean aortic pressure fell (from 65 ± 29.9 mm Hg to 61 ± 9.6 mm Hg; p < 0.01), but systemic vascular resistance was unchanged, thus indicating a fall in left ventricular output reflected by a decrease in mixed venous oxygen saturation (from 60% ± 8.9% to 47% ± 7.6%; p < 0.01). After 15 minutes with the Hemopump at maximum speed, these variables returned to control levels (stroke volume, 38 ± 4.5 mL; cardiac output, 4.50 ± 0.63 L/min; right ventricular peak systolic pressure, 29 ± 8.3 mm Hg; right ventricular end-diastolic pressure, 4 ± 2.0 mm Hg; mean aortic pressure, 72 ± 10.4 mm Hg; mixed venous oxygen saturation, 56% ± 4.6% [all, p = not significant versus controls]). The Hemopump restored right ventricular perfusion pressure (64 ± 10.0 mm Hg to 41 ± 8.8 mm Hg with banding [p < 0.001] to 56 ± 6.2 mm Hg with the Hemopump [p = not significant versus control]) and pressure-rate product (3,199 ± 1,252 mm Hg • min to 5,962 ± 2,796 mm Hg • min with banding [p < 0.01] to 3,368 ± 767 mm Hg • min with the Hemopump [p = not significant versus control]). With acute partial pulmonary artery obstruction, a right ventricular Hemopump restores right ventricular output, reverses associated changes in left ventricular output, and offloads the right ventricle.


   Introduction
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 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Right ventricular failure is a risk factor for death after orthotopic cardiac transplantation [1, 2], occurs in around 20% of patients receiving mechanical left ventricular assistance as a bridge to transplantation [3], and may complicate left ventricular assistance for postcardiotomy cardiogenic shock [4]. Of patients receiving mechanical circulatory assistance after an open heart operation, 30% require biventricular assistance and 23%, right ventricular assistance alone [5].

The Hemopump is an axial-flow pump traditionally used as a transfemoral left ventricular support device [6]. We have investigated the ability of a Hemopump placed from the pulmonary artery into the right ventricle to maintain the circulation in a porcine model of acute partial pulmonary artery obstruction.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Six mongrel pigs (mean weight, 64 kg; range, 58 to 70 kg) were anesthetized with intravenous sodium pentobarbital (30 mg/kg), mechanically ventilated through an endotracheal tube, and maintained with 1% to 2% halothane and 50% oxygen. 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).

Technique
A pulmonary artery thermodilution catheter was introduced through the right internal jugular vein, and a fluid-filled pressure catheter was placed into the aorta through the carotid artery. After sternotomy, pericardiotomy, and bilateral pleurotomy, a pursestring suture was placed in the pulmonary artery just proximal to its bifurcation. A tape was placed around the artery distal to the pulmonary valve but proximal to the pursestring suture. The animal was heparinized (3 mg/kg of sodium heparin), and a 14F Hemopump (Johnson & Johnson Interventional Systems Co, Rancho Cordova, CA) was placed through the pursestring suture so that its inflow port lay in the right ventricle and its outflow port, in the pulmonary artery beyond the tape (Fig 1Go). Immediately after insertion, the device was set to run at minimum speed (17,500 rpm).



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  		Fig 1. . Position of Hemopump and pulmonary artery band.

 
Fluid-filled catheters were inserted in the left and right atria and ventricles for pressure measurements (Hewlett-Packard model 7758B chart recorder). Heart rate was recorded from the electrocardiogram. Right ventricular output was measured by thermodilution as the mean of three readings. Cold saline solution was injected into the right atrium with the thermistor lying in the pulmonary artery before its bifurcation but beyond the outflow port of the Hemopump; measurements therefore represent the output of the native ventricle and the Hemopump. Pulmonary artery pressures were recorded before insertion of the Hemopump, as interference caused by catheter vibration prevented meaningful measurement with the Hemopump running. All other control measurements were made with the Hemopump running at minimum speed.

The tape around the pulmonary artery was tightened to produce a 50% increase in right ventricular systolic pressure, and 5 minutes later, measurements were repeated. The Hemopump was then switched to maximum speed (44,000 rpm), and measurements were repeated after 1 minute and 15 minutes of assistance. After this, with the pulmonary artery still banded, the Hemopump was returned to minimum speed, and 5 minutes later, the final set of measurements was made.

Calculations
Right ventricular stroke volume was calculated as CO/HR, where CO = right ventricular cardiac output plus the Hemopump output and HR = heart rate. Systemic vascular resistance was calculated as (MAP - RAP)/CO x 80, where MAP = mean arterial pressure, RAP = mean right atrial pressure, and CO = right ventricular cardiac output plus the Hemopump output, the assumption being that this equaled left ventricular output. Right ventricular perfusion pressure was calculated as DAP - RVEDP, where DAP = diastolic aortic pressure and RVEDP = right ventricular end-diastolic pressure. Right ventricular pressure–rate product was calculated as RVPSP x HR, where RVPSP = right ventricular peak systolic pressure and HR = heart rate. Pulmonary vascular resistance was calculated as (MPAP - LAP)/CO x 80, where MPAP = mean pulmonary artery pressure, LAP = mean left atrial pressure, and CO = cardiac output.

Statistical Analysis
Results are given as the mean ± the standard deviation. Serial measurements were compared with repeated-measures analysis of variance. When indicated, paired t tests with the Bonferroni correction were used to compare individual time points. A probability of less than 0.05 is considered significant.


   Results
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 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
The in vitro flow of the Hemopump with porcine blood was 250 mL/min at minimum speed and 1,500 mL/min at maximum speed. Before introduction of the Hemopump, mean pulmonary artery pressure was 16 ± 2.9 mm Hg and pulmonary vascular resistance, 158 ± 8.7 dynes • s • cm-5.

Hemodynamic data are given in Table 1Go, and percent changes are shown in Figure 2Go. With banding of the pulmonary artery, right ventricular stroke volume and cardiac output fell, and heart rate increased. There were significant increases in right ventricular peak systolic, end-diastolic, and mean right atrial pressures. Mean aortic and left ventricular peak systolic pressures decreased, but there were no significant changes in left ventricular end-diastolic and mean left atrial pressures or systemic vascular resistance. Mixed venous oxygen saturation decreased significantly from 60% ± 8.9% to 47% ± 7.6% (p < 0.01). There was a significant fall in right ventricular perfusion pressure and a significant increase in right ventricular pressure–rate product.


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  		Table 1. . Hemodynamic Data With Partial Pulmonary Artery Banding and Hemopump Assistancea
 


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  		Fig 2. . Percent changes in hemodynamic variables with partial pulmonary artery banding alone and after 15 minutes of Hemopump assistance. Values are shown as the mean with the standard deviation for six experiments. (CO = cardiac output; HR = heart rate; MAP = mean aortic pressure; MVO2 = mixed venous oxygen saturation; NS = not significant; RVPP = right ventricular perfusion pressure; RVPRP = right ventricular pressure–rate product; RVPSP = right ventricular peak systolic pressure; SV = stroke volume.)

 
After 15 minutes of Hemopump assistance, although left ventricular peak systolic and end-diastolic pressures increased, these changes were not significantly different from the values with banding alone. Systemic vascular resistance remained unchanged. All other hemodynamic variables improved significantly compared with banding alone. Apart from the value for left ventricular peak systolic pressure, measurements were not significantly different from controls. Mixed venous oxygen saturation rose from 47% ± 7.6% to 56% ± 4.6% (p < 0.01), which was similar to the control value.

Although there was a trend for all measurements to gradually improve during the 15 minutes of Hemopump assistance, only the changes in right ventricular end-diastolic pressure (p < 0.05), perfusion pressure (p < 0.05), and heart rate (p < 0.01) were significant.

With the pulmonary artery still banded, 5 minutes after the Hemopump was switched back to minimum speed, all variables returned to a level similar to that when the band was first tightened. Arterial oxygen saturation was unchanged at control (99% ± 0.9%), with banding (99% ± 0.7%), and after 15 minutes of Hemopump assistance (99% ± 0.7%). Hematocrit was similar at the beginning (30% ± 3.2%) and end (30% ± 3.9%) of the experiment. After the sacrifice of the animal at the end of each experiment, the right ventricle and pulmonary artery were opened to confirm correct placement of the band and the Hemopump across it.


   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
This study was designed to assess the ability of the Hemopump to transfer blood from the right ventricle to the pulmonary artery in the face of a mechanical barrier to right ventricular ejection. This model of acute partial pulmonary artery banding mimics clinical situations in which right ventricular failure is related to increased pulmonary vascular resistance as can occur after cardiopulmonary bypass or orthotopic cardiac transplantation [2]. In the clinical situation this increase in afterload can be imposed on underlying right ventricular dysfunction. The pulmonary artery band was tightened to produce about a 50% increase in right ventricular peak systolic pressure. This created visible dilatation of the right ventricle in all animals with increases in right ventricular and right atrial pressures and a 39% reduction in stroke volume. Right ventricular output was reduced by only 26% because of the increase in heart rate.

This alteration in right ventricular function reduced left ventricular output; mean aortic pressure fell, and as systemic vascular resistance remained constant, left ventricular output must have fallen. This is reflected by the decreased mixed venous oxygen saturation. Although there was no significant change in mean left atrial or left ventricular end-diastolic pressures, the reduction in left ventricular output is likely to have been a result of decreased left ventricular preload.

Increased right ventricular pressure does not directly impair left ventricular function. Indeed, for a given left ventricular end-diastolic volume, left ventricular work output is augmented by an increase in right ventricular pressure [7], and when preload is accounted for, neither right ventricular pressure overload nor combined pressure and volume overload impairs left ventricular systolic function [8, 9]. Despite this augmentation of left ventricular function, a reduction in preload is the primary effect of partial pulmonary artery occlusion [7]. In this experiment, the absence of change in left ventricular filling pressures is likely due to the reduction in left ventricular compliance [10] that accompanies increased right ventricular pressures as a result of altered left ventricular geometry [11] and reversed septal curvature [7, 10].

In animal studies, the conventionally placed 21F Hemopump, theoretically capable of producing a flow of 3.5 to 4.0 L/min [12], increases cardiac output by 0.6 [13] to 2 L/min [14], representing 36% [13] and 50% [14] of total cardiac output. In clinical use, similar increases in cardiac index are reported, ranging from 1 L • min-1 • m-2 or 36% of total cardiac index [12] to 1.3 L • min-1 • m-2 [15, 16], representing 38% [15] and 41% [16] of total cardiac index. When used to support high-risk angioplasty, the 14F Hemopump produces flows of about half those obtained with the 21F device (unpublished observations). In this experimental model, we found the 21F Hemopump too long to allow satisfactory placement and were constrained to use the 14F device.

In the right ventricle, with partial pulmonary artery banding, the 14F Hemopump returned right ventricular stroke volume and output to control levels. As heart rate returned to the control value, the increased output was due to the increased stroke volume. This increase in output was a mean of 800 mL/min, which is 50% of in vitro flow and 19% of total right ventricular output.

In this right ventricular configuration, although producing a similar proportion of its potential flow compared with the left ventricular configuration, the Hemopump produced a lower contribution to total output. Given that Hemopump flow is dependent on afterload [12] and that pulmonary artery pressure is lower than aortic pressure, it might be expected that in the right ventricle, the Hemopump would produce greater flows than in the left. We advance two explanations for this difference. First, although all animals had a normal pulmonary vascular resistance at the outset, we were not able to record changes with the Hemopump running, and this resistance may have increased. Second, Hemopump flow is also dependent on the position of the inflow port [12]. However, both inflow and outflow ports were lying free after the sacrifice of the animal, it is unlikely that this was the cause.

The improvements in right ventricular function and pressures were reflected in improved left ventricular indices. Mean aortic pressure was restored, and systemic vascular resistance remained constant, thereby indicating an increase in left ventricular output, which was reflected by the increased mixed venous oxygen saturation. Left atrial pressure increased significantly, indicating that an increase in preload was responsible for this improvement.

The gradual improvement in indices over 15 minutes of Hemopump assistance is possibly due to offloading of the right ventricle by the Hemopump. One obvious explanation, that the band loosened while the Hemopump was running at maximum speed, is disproved by the finding that hemodynamic values returned to equivalent levels when the Hemopump was switched back to minimum speed.

Hematocrit was unchanged throughout the experiment, a finding showing that a reduction in blood viscosity was not responsible. However, banding reduced right ventricular perfusion pressure. It was gradually restored during the 15 minutes of Hemopump assistance. The initial fall, in association with the significant rise in the rate-pressure product, may have produced right ventricular ischemia. These changes were reversed by the Hemopump, possibly resulting in a progressive increase in the contribution of the right ventricle to the improvement in hemodynamic variables. The deleterious effects of pulmonary artery banding can be ameliorated by improving right coronary artery flow [17], and when used in the left ventricle, the Hemopump decreases left ventricular effective work [14] and myocardial oxygen consumption [13] and may increase coronary perfusion [16].

These findings suggest that in a model of acute partial pulmonary artery obstruction, a right ventricular Hemopump is able to restore right ventricular output, reverse the associated changes in left ventricular output, and offload the right ventricle.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Loisance, Centre de Recherches Chirurgicales Henri Mondor, Faculté de Médecine, CHU Henri Mondor, 8, rue du Général Sarrail, 94010 Créteil, France.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Griepp RB, Stinson EB, Clark DA, Shumway NE. Determinants of operative risk in human heart transplantation. Am J Surg 1971;21:192–7.
  2. Kirklin JW, Naftel DC, McGriffin DC, McVay RF, Blackstone EH, Karp RB. Analysis of morbid events and risk factors for death after cardiac transplantation. J Am Coll Cardiol 1988;11:917–24.[Abstract]
  3. Kormos RL, Borovetz HS, Gasior T, et al. Experience with univentricular support in mortally ill cardiac transplant candidates. Ann Thorac Surg 1990;49:261–72.[Abstract]
  4. Cooper GJ, Withington PS, Wood AJ, Magee PG, Lewis CT, Graham TR. Right ventricular failure in patients requiring left ventricular assistance. Int J Artif Organs 1993;16:405–10.
  5. Pennington DG, McBride LR, Swartz MT, et al. Use of the Pierce–Donachy ventricular assist device in patients with cardiogenic shock after cardiac operations. Ann Thorac Surg 1989;47:130–5.[Abstract]
  6. Wampler RK, Moise JC, Frazier OH, Olsen DB. In vivo evaluation of a peripheral access axial flow blood pump. ASAIO Trans 1988;34:450–4.[Medline]
  7. Feneley MP, Olsen CO, Glower DD, Rankin JS. Effect of acutely increased right ventricular afterload on work output from the left ventricle in conscious dogs. Circ Res 1989;65:135–45.[Abstract/Free Full Text]
  8. Kelley DT, Spotnitz HM, Beiser GD, Pierce JE, Epstein SE. Effects of chronic right ventricular volume and pressure loading on left ventricular performance. Circulation 1971;44:403–12.[Abstract/Free Full Text]
  9. Olsen CO, Tyson GS, Maier GW, Spratt JA, Davis JW, Rankin JS. Dynamic ventricular interaction in the conscious dog. Circ Res 1983;52:85–104.[Abstract/Free Full Text]
  10. Bemis CE, Serur JR, Borkenhagen D, Sonnenblick EH, Urschel CW. Influence of right ventricular filling pressure on left ventricular pressure and dimensions. Circ Res 1974;34:498–504.[Abstract/Free Full Text]
  11. Elzinga G, Van Grondelle R, Westerhof N, Van Den Bos GC. Ventricular interference. Am J Physiol 1974;276:941–7.
  12. Frazier OH, Wampler RK, Duncan JM, et al. First human use of the Hemopump, a catheter-mounted ventricular assist device. Ann Thorac Surg 1990;49:299–304.[Abstract]
  13. Scholz KH, Hering JP, Schröder T, et al. Protective effects of the Hemopump left ventricular assist device in experimental cardiogenic shock. Eur J Cardio-thorac Surg 1992;6:209–14.[Abstract]
  14. Shiiya N, Zelinsky R, Deleuze PH, Loisance DY. Changes in hemodynamics and coronary blood flow during left ventricular assistance with the Hemopump. Ann Thorac Surg 1992;53:1074–9.[Abstract]
  15. Wiebalck AC, Wouters PF, Waldenberger FR, et al. Left ventricular assist with an axial flow pump (Hemopump): clinical application. Ann Thorac Surg 1993;55:1141–6.[Abstract]
  16. Dubois-Randé JL, Deleuze P, Zelinsky R, et al. Coronary hemodynamics during Hemopump left intraventricular assistance. Int J Arti Organs 1992;15:234–8.
  17. Brooks H, Kirk ES, Vokonas PS, Urschel CW, Sonnenblick EH. Performance of the right ventricle under stress: relation to right coronary flow. J Clin Invest 1971;50:2176–83.



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