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Ann Thorac Surg 1996;61:305-310
© 1996 The Society of Thoracic Surgeons


Experience With Generally Available Devices

Experience With Right Ventricular Assist Devices for Perioperative Right-Sided Circulatory Failure

Jonathan M. Chen, MD, Howard R. Levin, MD, Eric A. Rose, MD, Linda J. Addonizio, MD, Donald W. Landry, MD, Joseph J. Sistino, Ccp, Robert E. Michler, MD, Mehmet C. Oz, MD

Departments of Surgery, Medicine, and Pediatrics, Columbia-Presbyterian Medical Center, Columbia University College of Physicians & Surgeons, New York, New York

Abstract

Background. Right-sided circulatory failure remains a significant source of morbidity and mortality for both cardiac transplant and left ventricular assist device recipients.

Methods. We reviewed our experience with 11 patients who required a right ventricular assist device (RVAD) after either orthotopic heart transplantation or left ventricular assist device implantation. Variables analyzed included total time of RVAD support, hemodynamic and hematologic parameters, and parameters of end-organ perfusion. These were assessed at five time points: (1) at least 2 weeks before RVAD implantation, (2) intraoperatively just before RVAD insertion, (3) while on RVAD support, and, for those who survived, (4) just before RVAD explantation, and (5) off RVAD support. Survival was assessed as the ability to be weaned successfully from RVAD support. Urine output and serum transaminase levels were recorded throughout the period of RVAD support.

Results. Five patients received an ABIOMED 5000 BVS RVAD, and 6 received a Bio-Medicus centrifugal pump. Nine patients in the study underwent orthotopic heart transplantation and had development of right-sided circulatory failure from 0 to 96 hours after donor organ insertion, and 2 patients underwent left ventricular assist device implantation 12 to 48 hours before RVAD support. The mean time of RVAD support for survivors was 133.6 ± 33.6 hours (range, 107 to 190 hours). Six patients were successfully separated from RVAD support, and 5 patients died while on RVAD support. Causes of death included sepsis (2), biventricular failure (2), and coagulopathy (1). Continuous arteriovenous hemodialysis was employed in 3 of 6 survivors and 1 of 5 nonsurvivors.

Conclusions. Right ventricular assist devices work most effectively if implanted early enough to avoid significant, potentially irreversible end-organ injury. We liberally employ continuous arteriovenous hemodialysis, minimize the use of heparin immediately postoperatively, keep patients sedated, and continue RVAD support until the patient displays signs of hemodynamic and end-organ recovery as heralded by (1) a decrease in central venous pressure and, more importantly, a decrease in pulmonary artery diastolic pressure, (2) an increase in urine output, and (3) a decrease in serum transaminase levels.

Despite advances in perioperative management, right-sided circulatory failure (RSCF) refractory to medical management remains a significant source of morbidity and mortality for both cardiac transplant and left ventricular assist device (LVAD) recipients. In addition, the growing demand for donor organs has necessitated a broadening of the criteria by which donors are accepted, with more donor hearts of inferior quality currently being accepted when compared with previous years. As a result, a greater prevalence of intraoperative and early postoperative complications related to donor organ dysfunction is now being reported by transplant centers worldwide.

Moreover, the increasing use of LVADs has disclosed an associated 20% to 40% incidence of associated RSCF [1]. Numerous etiologic factors may be responsible for the RSCF that develops after mechanical left ventricular assistance, including altered ventricular interdependence, increased pulmonary vascular resistance, and changes in right ventricular loading [1, 2]. Currently, however, the limited understanding of this phenomenon has yielded no specific preoperative predictors. Thus, RSCF remains a major source of morbidity after LVAD insertion.

Although mechanical devices are increasingly being used for left heart assistance, reports documenting the use of right ventricular assist devices (RVADs) after heart transplantation have demonstrated disappointing results [35]. In addition, reports in the literature describing the temporary use of RVADs for RSCF that develops in the setting of mechanical left ventricular support have described contrasting findings [1].

Thus, in an effort to identify more precisely criteria governing the successful use of RVADs for acute RSCF, we reviewed the experience at the Columbia-Presbyterian Medical Center with 11 patients who required right ventricular assistance after either orthotopic heart transplantation or LVAD implantation.

Material and Methods

We reviewed the records of all patients undergoing open heart operations at the Columbia-Presbyterian Medical Center since 1990, and selected those patients who underwent right ventricular support with an RVAD for more than 1 hour.

Variables analyzed included total time of RVAD support, hemodynamic parameters (mean, systolic, and diastolic pulmonary artery pressures; central venous pressure; pulmonary capillary wedge pressure; cardiac output; heart rate; right ventricular stroke work; pulmonary vascular resistance; and transpulmonary gradient), hematologic parameters (hematocrit, total platelet count, protime, and prothrombin time), and parameters of end-organ perfusion (levels of serum glutamic-oxaloacetic transaminase, serum glutamate pyruvate transaminase, total and direct bilirubin, serum blood urea nitrogen, and serum creatinine). These variables were assessed at five time points: (1) at least two weeks before RVAD implantation, (2) intraoperatively just before RVAD insertion, (3) while on RVAD support, and, for those who survived, (4) just before RVAD explantation, and (5) off RVAD support. Survival was assessed as the ability to be weaned successfully from RVAD support. Urine output and serum transaminase levels were recorded throughout the period of RVAD support.

The LVAD used, the TCI Heartmate 1000 IP (Thermo Cardiosystem, Inc, Woburn, MA), is a pneumatic device of pusher-plate design that uses pulses of air to pump blood with a maximum stroke volume of 85 mL. The device is implanted through a median sternotomy incision using apical cannulation to maximize left ventricular unloading. The outflow graft is anastomosed to the right lateral aspect of the ascending aorta.

Operative Implantation of the RVADs
Early in our experience, we used a Bio-Medicus circuit (Eden Prairie, MN) for RVAD support; our most recent 5 patients were managed with an ABIOMED (Danvers, MA) device. The Bio-Medicus circuit consists of a vortex centrifugal pump model BP-80 with 3/8-inch internal diameter arterial and venous tubing. Cannula selection varied, although several fundamental aspects were constant. The venous cannula was placed through the tip of the right atrial appendage to allow placement of several circumferential sutures around the cannula and appendage tissue as well as to reduce the possibility of hemorrhage. The pulmonary arterial cannula was secured with two pursestring sutures. This connection tended to bleed due to the thin nature of the pulmonary artery and the extremely high pulmonary arterial pressures usually encountered; this aspect of the circuit was a major limitation.

In contrast, the ABIOMED BVS 5000 provides a coated Dacron graft that is anastomosed to an oblique incision in the pulmonary artery and rarely bleeds. Although reestablishment of cardiopulmonary bypass is required to place this outflow cannula, we found that the benefits provided during the several-day support period made this effort worthwhile. The venous L-shaped cannula is inserted as described above and angled toward, but not inside, the inferior vena cava. As is true for the Bio-Medicus circuit, the cannula and tubing must be deaired before the institution of support. The system uses a microprocessor-based drive console to supply pneumatic power to a two-chambered blood pump. Beat rates and systolic intervals are determined automatically by sensing driveline air flow at the console.

The cannulas can be brought out through intercostal spaces or more commonly in a subxiphoid position, allowing chest closure as desired. We have not closed the sternum in these patients to avoid needle hole bleeding, to preserve the sternum for later closure after the removal of RVAD support, to allow rapid reexploration in the event of hemorrhage, and to avoid compression of the heart in these hemodynamically unstable patients. Heparin was generally administered 12 to 24 hours after support was instituted; however, the activated clotting time was maintained less than 180 to 200 seconds and heparin administration was stopped immediately if bleeding occurred during the support period.

The patients were kept sedated during the support period. Pharmacologic support of the surviving patients became progressively easier as blood flow across the lungs into the left atrium increased. Once the decision to remove the device was made, full inotropic support and heparinization were reinstituted. The device flows were reduced at 1-L increments over a 15-minute period, ensuring that the central venous and systemic blood pressures were maintained at stable levels. If these maneuvers were tolerated, the patient was taken to the operation room and the device was removed. The pulmonary artery outflow graft was clamped at the anastomosis and oversewn, leaving a cuff attached to the pulmonary artery. The sternum could be closed primarily in these patients. Despite concerns over the possibility of later sternal wound infection, none occurred in our series.

Statistics
Paired t tests were used for statistical analysis in this study.

Results

Patient Selection
Nine of 11 RVAD implantations were in heart transplant recipients selected from a total of 310 patients who received transplants between May 1990 and February 1994 at Columbia-Presbyterian Medical Center. One patient received an RVAD both after the placement of an LVAD as well as after his ultimate orthotopic heart transplantation 5 months later, and was considered two different patients for the purpose of analysis. An additional patient received an RVAD for RSCF that developed in the setting of LVAD implantation.

The RVAD cohort consisted of 1 woman and 10 men, with a mean age of 52.1 ± 13.0 years (range, 18 to 63 years) and a median age of 57 years. Nine patients in the study underwent orthotopic heart transplantation and had development of RSCF from 0 to 96 hours after donor organ insertion. Two patients underwent LVAD implantation 12 to 48 hours before RVAD support. Five patients received an ABIOMED BVS 5000 RVAD, and 6 received a Bio-Medicus centrifugal pump. The mean time of RVAD support for survivors was 133.6 ± 33.6 hours (range, 107 to 190 hours). Details of the demographic profiles of these patients are represented in Table 1Go.


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Table 1. . Demographic Profile
 
Six patients were successfully separated from RVAD support, and 5 patients died while on RVAD support. Causes of death included sepsis (2), biventricular failure (2), and coagulopathy (1). Continuous arteriovenous hemofiltration or hemodialysis was employed in 3 of 6 survivors and 1 of 5 nonsurvivors. The method for the placement of hemofiltration across the RVAD circuit has been described previously both by our group [6] and by others [7]. Early institution of continuous arteriovenous hemodialysis facilitated fluid management and reduced excess preload to an already distended right heart.

Hemodynamic Parameters
Hemodynamic parameters as measured at five different time points throughout RVAD support are compiled in Table 2Go. There were no significant differences between survivors and nonsurvivors with respect to preoperative pulmonary vascular resistance, transpulmonary gradient, or right ventricular stroke work.


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Table 2. . Hemodynamic Parameters
 
Changes in the pulmonary artery diastolic pressure and central venous pressure are represented for survivors and nonsurvivors in Figures 1 and 2GoGo. As seen in Table 2Go and Figure 1Go, for the survivors, pulmonary artery diastolic pressure decreased from a mean of 27 mm Hg intraoperatively to a mean of 23 mm Hg on RVAD support and a mean of 13 mm Hg after RVAD support (p < 0.01). Central venous pressure similarly decreased from a mean of 22 mm Hg intraoperatively to a mean of 11 mm Hg on RVAD support (p < 0.01) and a mean of 5 mm Hg after RVAD support (p < 0.01). This progressive decrease in right-sided pressures was not displayed by nonsurvivors (see Fig 2Go), in whom pulmonary artery diastolic pressure increased on RVAD support to a mean of 28 mm Hg from a mean of 23 mm Hg just before implantation.



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Fig 1. . Changes in the pulmonary artery diastolic pressure (PAD) and central venous pressure (CVP) are represented for survivors. Pulmonary artery diastolic pressure decreased from a mean of 27 mm Hg intraoperatively to a mean of 23 mm Hg on right ventricular assist device (RVAD) support, and a mean of 13 mm Hg after RVAD support (p < 0.01). Central venous pressure similarly decreased from a mean of 22 mm Hg intraoperatively to a mean of 11 mm Hg on RVAD support (p < 0.01) and a mean of 5 mm Hg after RVAD support (p < 0.01).

 


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Fig 2. . Changes in the pulmonary artery diastolic pressure (PAD) and central venous pressure (CVP) are represented for nonsurvivors. The progressive decrease in right-sided pressures was not displayed by nonsurvivors, in whom pulmonary artery diastolic pressure increased on right ventricular assist device (RVAD) support to a mean of 28 mm Hg from a mean of 23 mm Hg just before implantation.

 
There were no significant differences between preoperative and post-RVAD hemodynamic parameters in the survivors.

Hematologic Parameters and Parameters of End-Organ Perfusion
No significant differences in hematologic parameters or parameters of end-organ perfusion were noted between survivors and nonsurvivors, or among the time points of RVAD support studied. Daily serum transaminase levels for survivors and nonsurvivors over the first 5 days of RVAD support are represented in Figure 3Go. As demonstrated, serum glutamic-oxaloacetic transaminase level tended to decrease in survivors throughout the period of RVAD support. A similar trend was present in nonsurvivors; however, the absolute values of the serum transaminase levels were nearly tenfold higher.



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Fig 3. . Daily serum transaminase levels for survivors and non-survivors over the first 5 days of right ventricular assist device (RVAD) support are represented. As demonstrated, serum glutamic-oxaloacetic transaminase (SGOT) level tended to decrease in survivors throughout the period of RVAD support. A similar trend was present in nonsurvivors; however, the absolute values of the serum transaminase levels were nearly tenfold higher.

 
Urine output was recorded for those RVAD recipients who did not receive continuous arteriovenous hemofiltration or dialysis. Total urine output notably improved throughout the period of RVAD support in the survivors, but did not in the nonsurvivors.

Comment

The development of RSCF after both cardiac transplantation and LVAD insertion remains a major source of morbidity and mortality for patients undergoing these two procedures. This complication has increased with both the expansion of the donor pool to include marginal donors and the increasing use of LVADs as a bridge to transplantation, unveiling a growing incidence of associated perioperative RSCF. Yet, although many preoperative parameters have been suggested as predictors of RSCF in these settings, none has emerged with precise prognostic value.

Mechanical right ventricular assistance has been used in a variety of conditions for which temporary support of the failing right ventricle is indicated. Reports in the literature regarding the use of RVADs after both cardiac transplantation and LVAD insertion, however, have generated conflicting results [15]. We undertook the current investigation to review the RVAD experience at Columbia-Presbyterian Medical Center in an effort both to evaluate lessons learned in the implementation of these devices, as well as to identify guidelines for their successful use.

Right-sided circulatory failure may be characterized by a constellation of findings on hemodynamic evaluation and physical examination. Hemodynamically, RSCF is reflected by right atrial pressures greater than 20 mm Hg, left atrial pressures less than 10 mm Hg, a cardiac index of less than 1.8 L•min-1•m-2, and decreasing cardiac output developing in the setting of high pulmonary arterial and central venous pressures. Tricuspid regurgitation may contribute to right ventricular inefficiency and thus worsen RSCF. Intraoperatively, the right ventricle appears distended, a finding that may be correlated with echocardiographic evidence of the interventricular septum extending into the left ventricle. On physical examination, a gallop may be present on auscultation postoperatively, and a liver edge may be palpable well below the costal margin, reflecting a significant degree of hepatic congestion.

Previous investigators have suggested hemodynamic parameters that may be useful in predicting posttransplantation RSCF, including pulmonary vascular resistance, pulmonary vascular resistance index, and the transpulmonary gradient [810]. However, in the present study, none of these parameters accurately distinguished survivors from nonsurvivors of RVAD support.

In part, there exists an inherent difficulty in predicting RSCF in these clinical settings, owing largely to its multifactorial etiology. In addition to right ventricular ischemia and altered interventricular mechanics, numerous other factors involved in the perioperative management of these patients also must be considered as potential contributors to RSCF. Extensive bleeding, requiring multiple blood product infusions, increases both the intravascular volume and the pulmonary vascular resistance. Similarly, the addition of vasopressors to these often hypotensive patients also increases pulmonary vasoreactivity, resulting in an increased right ventricular afterload from an increase in both pulmonary resistance and left atrial afterload. Moreover, the use of cardiopulmonary bypass itself may be associated with a concomitant increase in pulmonary vascular reactivity [11, 12].

Although not well illustrated by our overall averaged intraoperative data, pulmonary arterial pressures may be misleadingly low before RVAD implantation, a phenomenon more likely reflective of the poor output state of the patient than a true decrease in right-sided pressures. Lower than expected pulmonary arterial or central venous pressures may not always represent a contraindication to RVAD insertion, and thus the need for an RVAD may exist despite ``fictitiously'' low right-sided pressures. Indeed, these pressures may transiently increase as much as threefold during the initial period of RVAD support, as flow access across the lung beds is increased.

Neither the Bio-Medicus nor the ABIOMED system completely decompresses the right heart. Even when the same inflow cannula systems that provided complete decompression during cardiopulmonary bypass were used for RVAD support, a central venous pressure greater than 10 mm Hg was commonly encountered. More importantly, if the pulmonary arterial pressures were high enough, right ventricular distention occurred, presumably because no blood entering the chamber could be ejected across the pulmonary valve. Such distention can alter interventricular geometry, as evidenced by 1 patient in whom the septum impinged on the left ventricle sufficiently to compromise cardiac output; the benefit of sole RVAD therapy for such patients may be limited.

The RVAD improved elevated right-sided pressures in those who survived implantation and support. In particular, the central venous pressure of survivors decreased early after the institution of RVAD support, indicating the efficacy of the RVAD; the pulmonary artery diastolic pressure, in contrast, declined more slowly. As such, the gradual improvement in pulmonary artery diastolic pressure over time may in fact represent that component of the increased right ventricular afterload that is ``reversible'' in survivors. Whether the reduction in RSCF also reflects remodeling or recovery of stunned right ventricular myocardium remains unclear; however, for those who survived RVAD support, hemodynamics after removal of the RVAD were comparable with baseline values.

The RVAD appeared also to improve end-organ function in survivors, as indicated by an increase in urine output and a resolution of elevated serum transaminase levels, most likely by increasing both cardiac output and return to the left atrium and ventricle, as well as by relieving hepatic congestion. In contrast, neither right-sided pressures nor urine output improved in nonsurvivors. Serum transaminase levels in these patients, although qualitatively improved, remained elevated at tenfold normal levels.

The traditional indices of renal function (serum blood urea nitrogen and creatinine levels) did not improve as consistently throughout the period of RVAD support as did urine output. However, renal steady-state conditions were likely not reached during the relatively brief RVAD support period; thus, relative improvement in the glomerular filtration rate may have been masked. However, an increasing urine output presaged a subsequent decrease in serum blood urea nitrogen and creatinine levels after RVAD removal. Because urine output does not rely on a renal steady state to reflect renal perfusion, we believe that during the immediate postoperative period, urine output may better reflect changes in renal perfusion, and thus ultimately the glomerular filtration rate, than does either serum blood urea nitrogen or creatinine level.

Continuous arteriovenous hemofiltration and hemodialysis were employed in 4 RVAD recipients for both volume removal and correction of electrolyte imbalances. The period of RVAD support in many ways represents a temporary therapeutic window during which certain factors (eg, intravascular volume, electrolyte profile) can be optimized before explantation. We encourage the liberal employment of continuous arteriovenous hemofiltration in these patients with continuous intravenous fluid requirements and for whom hypervolemia may negatively contribute to an already elevated pulmonary vascular resistance.

In addition to isolated RSCF, the course of nonsurvivors was further complicated by biventricular failure, intractable coagulopathy, and sepsis. Although it is possible that there also may have been physical problems with device insertion, in general these complications represent conditions that were not amenable to improvement with isolated right ventricular mechanical assistance.

We prefer the use of the ABIOMED device over centrifugal pump RVADs for two reasons. First, its cannulas are easier to manage after implantation and are made for long-term use. As such, patients may be awakened postoperatively. Second, the ABIOMED closed-loop control system avoids the cost of continuous monitoring by perfusionists required by centrifugal devices. In our hospital, the estimated incremental labor and material cost of maintaining a patient on a centrifugal device is $1,000. If patients are managed for 5 days, as were on average our surviving patients, the cost of purchasing the dispensable ABIOMED pump is equaled.

Several lessons are apparent after reviewing our experience. First, RVADs work most effectively if implanted early enough to avoid significant, potentially irreversible end-organ injury. Second, we liberally employ continuous arteriovenous hemofiltration, as these patients often have ongoing continuous intravenous fluid requirements despite poor initial urine output. Third, we minimize the use of heparin immediately postoperatively in these often coagulopathic patients because of the potential for bleeding and the subsequent need for exogenous blood products that themselves carry an attendant risk of worsening RSCF by increasing pulmonary vascular resistance. The risk of potential microemboli to the pulmonary bed is unclear in this setting. Fourth, we keep patients sedated so as to decrease their oxygen consumption. Fifth, we continue RVAD support until the patient displays signs of hemodynamic and end-organ recovery as heralded by (1) a decrease in central venous pressure and, more importantly, a decrease in pulmonary artery diastolic pressure, (2) an increase in urine output, and (3) a decrease in serum transaminase levels.

Footnotes

Presented at The Third International Conference on Circulatory Support Devices for Severe Cardiac Failure, Pittsburgh, PA, Oct 28-30, 1994.

Address reprint requests to Dr Oz, Department of Surgery, Columbia-Presbyterian Medical Center, Presbyterian Hospital Box 295, 622 W 168th St, New York, NY 10032.

References

  1. Farrar DJ, Compton PG, Hershon JJ, Fonger JD, Hill JD. Right heart interaction with the mechanically assisted left heart. World J Surg 1985;9:89–102.[Medline]
  2. Farrar JD, Compton PG, Dajee H, Fonger JD, Hill JD. Right heart function during left heart assist and the effects of volume loading in a canine preparation. Circulation 1984;70:708–16.[Abstract/Free Full Text]
  3. Emery RW, Eales F, Joyce LD, et al. Mechanical circulatory assistance after heart transplantation. Ann Thorac Surg 1991;51:43–7.[Abstract]
  4. Nakatani T, Radovancevic B, Frazier OH. Right heart assist for acute right ventricular failure after orthotopic heart transplantation. ASAIO Trans 1987;33:695–8.[Medline]
  5. Fonger JD, Borkon AM, Baumgartner WA, Aschuff SC, Augustine S, Reitz BA. Acute right ventricular failure following heart transplantation: improvement with prostaglandin E1 and right ventricular assist. J Heart Transplant 1986;5: 317–21.[Medline]
  6. Chen JM, Levin HR, Catanese KA, et al. Use of a pulsatile right ventricular assist device and continuous arteriovenous hemodialysis in a 57 year old man with a pulsatile left ventricular assist device. J Heart Lung Transplant 1994;14:186–91.
  7. Macris MP, Barcenas CG, Parnis SM, Fuqua JM, Frazier OH. Simplified method of hemofiltration in ventricular assist device patients. ASAIO Trans 1988;34:708–11.[Medline]
  8. Bourge RC, Kirklin JK, Naftel DC, White C, Mason DA, Epstein AE. Analysis and predictors of pulmonary vascular resistance after cardiac transplantation. J Thorac Cardiovasc Surg 1991;101:432–45.[Abstract]
  9. Addonizio LJ, Gersony WM, Robbins RC. Elevated pulmonary vascular resistance and cardiac transplantation. Circulation 1987;76(Suppl 5):52–5.[Abstract/Free Full Text]
  10. Erickson KW, Constanzo-Nordin MR, O'Sullivan EJ, et al. Influence of pre-operative transpulmonary gradient on late mortality after orthotopic heart transplantation. J Heart Transplant 1990;9:526–37.[Medline]
  11. Smith WJ, Murphy MP, Appleyard RF, et al. Prevention of complement-induced pulmonary hypertension and improvement of right ventricular function by selective thromboxane receptor antagonism. J Thorac Cardiovasc Surg 1994;107:800–6.[Abstract/Free Full Text]
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D. Shum-Tim, B. W. Duncan, V. Hraska, I. Friehs, T. Shin'oka, and R. A. Jonas
Evaluation of a Pulsatile Pediatric Ventricular Assist Device in an Acute Right Heart Failure Model
Ann. Thorac. Surg., November 1, 1997; 64(5): 1374 - 1380.
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