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Ann Thorac Surg 1996;62:495-500
© 1996 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Postoperative Management of Patients With Hemopump Support After Coronary Artery Bypass Grafting

Bengt Peterzén, MD, Urban Lönn, MD, Ankica Babic, PhD, Hans Granfeldt, MD, Henrik Casimir-Ahn, MD, PhD, Hans Rutberg, MD, PhD

Linköping Heart Center and Department of Medical Informatics, University of Linköping, Linköping, Sweden

Accepted for publication March 15, 1996.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. In this study, we describe postoperative monitoring, pharmacologic therapy, and hemodynamic responses in patients receiving Hemopump support after postcardiotomy heart failure.

Methods. The Hemopump was used in 24 patients with severe left ventricular dysfunction after coronary artery bypass grafting.

Results. Fourteen patients (58%) were weaned from the Hemopump. Low to moderate doses of a combination of catecholamines, phosphodiesterase inhibitors, vasodilators, and vasoconstrictors were required to optimize Hemopump function and left ventricular unloading. Mean arterial blood pressure, mixed venous oxygen saturation, and urinary output were the most important therapy guidelines.

Conclusions. Together with our clinical protocol, the Hemopump effectively unloaded the failing ventricle while maintaining vital-organ perfusion. Doses of vasoactive drugs could be kept low. This approach to treatment provides good conditions for recovery of the stunned myocardium.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
See also page 500.

The Hemopump (DLP/Medtronic, Inc, Grand Rapids, MI) is a left ventricular assist device that delivers a maximal blood flow of about 5.0 L/min and enables effective unloading of the failing left ventricle (Fig 1Go) [1–5]. The rationale for using a left ventricular assist device in the postcardiotomy failing heart is to unload and decompress the stunned myocardium. The reasons for myocardial stunning are several and include ischemia, energy depletion, and reperfusion injury [6–8]. It is considered a reversible process if treated properly.



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  		Fig 1. . The Hemopump was inserted into the left ventricle (LV) through a graft anastomosed at the ascending aorta.

 
Treatment involves temporary reinstitution of cardiopulmonary bypass (CPB) and pharmacologic therapy using both inotropic agents and vasodilators. Energy substrates such as glucose-insulin-potassium and the amino acids glutamate and aspartate have been reported to shorten the period of myocardial stunning [9, 10]. If, despite these steps, the patient cannot be weaned from CPB, an intraaortic balloon pump is usually used. In our department, the Hemopump has been chosen more often in this situation than the intraaortic balloon pump [11].

This report describes the clinical protocol for monitoring, pharmacologic therapy and metabolic treatment we use in combination with Hemopump support to provide optimal unloading of the failing left ventricle with preserved vital-organ function.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Between September 1991 and November 1994, we used the Hemopump in 24 patients. During this period, 2,603 open heart surgical procedures were carried out in our department. The demographic data of the 24 patients are shown in Table 1Go. During the same period, the intraaortic balloon pump was used in 20 patients. As no other mechanical assist devices were used, the frequency of mechanical assist device during this time was 1.7%.


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  		Table 1. . Demographic Data for the 24 Patients Treated with the Hemopump
 
Indications for Hemopump Treatment
All patients had severe left ventricular failure, isolated or in combination with ischemia, right ventricular failure, or both. They all had shown an insufficient or adverse response to pharmacologic therapy. When a patient could not be weaned from CPB at the first attempt, an additional 30-minute reperfusion period on full bypass was employed. A complete check of the grafts and anastomoses was performed. The Hemopump was inserted when weaning could not be accomplished on the second attempt or if the heart failed after termination of CPB despite pharmacologic and metabolic therapy. Contraindications included severe aortic stenosis or insufficiency, the presence of a mechanical aortic valve prosthesis, aortic wall disease, left ventricular thrombus, and blood dyscrasia.

Perioperative Management
After premedication, anesthesia was induced using either high-dose fentanyl or our standard technique including fentanyl, midazolam hydrochloride or diazepam, and isoflurane. Muscle relaxation was achieved with intermittent doses of either pancuronium bromide or vecuronium bromide, and the patients were mechanically ventilated (Servo 9000; Siemens-Elema, Solna, Sweden).

During the operation, we used regular CPB equipment including a membrane oxygenator with the patient fully heparinized. Myocardial protection was achieved with crystalloid cardioplegic solution (Plegisol; Abbott Laboratories, North Chicago, IL) given in an antegrade or retrograde manner. Moderate general hypothermia (30° to 32°C) was used.

In the intensive care unit (ICU), the patients were sedated with a combination of morphine and midazolam, and mechanical ventilation was continued until termination of Hemopump treatment. Blood gas analyses were performed using an ABL 4 (Radiometer, Copenhagen, Denmark) or a BGE (ILS Laboratories, Milano, Italy). Measurements of oxygen saturation were performed using an OSM 3 (Radiometer).

Monitoring of Hemodynamics
The patients were monitored using a Hewlett-Packard five-lead electrocardiogram, which allows ST-T segment analyses. A radial artery cannula was placed before induction of anesthesia. During Hemopump support, arterial pressure was preferably obtained through the femoral artery. Hemodynamic data from the start of the operation were incomplete because only 9 of the 24 patients had a Swan-Ganz catheter inserted at that time. All patients transferred to the ICU had complete hemodynamic monitoring. A Swan-Ganz catheter with a rapid-response thermistor allowing real-time measurements of mixed venous oxygen saturation (SvO2) (Baxter Healthcare, Irvine, CA) was used in 11 of the 24 patients.

Hemodynamic measurements were performed five times: before or after induction of anesthesia but before operation (baseline); prior to Hemopump insertion; in a hemodynamically stable situation in the ICU while on Hemopump support; just before weaning from the Hemopump; and after removal of the Hemopump. All measurements during Hemopump treatment were performed with the pump at its maximal speed of 25,000 rpm.

Pharmacologic Therapy
The aim of pharmacologic therapy was to maintain right ventricular function and to achieve low pulmonary and systemic vascular resistances. Metabolic support was used in an attempt to further minimize the negative effect of myocardial stunning. Pharmacologic therapy prior to insertion of the Hemopump, during stay in the ICU, and after weaning from the Hemopump included a combination of catecholamines, phosphodiesterase III inhibitors, vasodilators, and vasoconstrictors. Energy substrates such as glucose-insulin-potassium as well as the amino acids glutamate and aspartate were frequently given.

Statistical Analyses
Basic descriptive statistics were performed to describe data. Paired and unpaired Student t tests were used to determine the significance of hemodynamic measurements. Recordings just prior to insertion of the Hemopump were compared with measurements obtained during and after Hemopump treatment. A p value of less than 0.05 was considered significant.


   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
Clinical Course
The candidates for Hemopump treatment all had postcardiotomy heart failure but none of the specified contraindications. No additional selection criteria were applied.

Fourteen patients (58%) survived, and 10 died. Eight of the nonsurvivors had severe biventricular failure, and the right ventricle was unable to deliver sufficient blood to the left ventricle. Two patients died of left ventricular failure despite adequate Hemopump support and pharmacologic therapy. Seven of the nonsurvivors died in the operating theater and 3, in the ICU. All patients weaned from the Hemopump were discharged from the hospital. For the 20 patients treated with an intraaortic balloon pump, the survival rate was 50%.

Pharmacology
The various inotropic agents and vasodilators used and their individual dosages are presented in Table 2Go. Dobutamine hydrochloride and epinephrine were used in low to moderate doses. Norepinephrine was used as a combined inotropic and vasoconstrictor drug. Both amrinone lactate and milrinone were used in low doses and in combination with catecholamines.


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  		Table 2. . Use of Catecholamines and Phosphodiesterase III Inhibitorsa,b
 
The vasodilators and the vasoconstrictors used are shown in Table 3Go. Nitroglycerin was used in low doses in an attempt to reveal ischemia and in combination with phosphodiesterase III inhibitors for dilation of the pulmonary vessels. If the systemic vascular resistance index (SVRI) and mean arterial blood pressure (MAP) tended to increase, sodium nitroprusside in low doses was used.


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  		Table 3. . Use of Vasodilators and Vasoconstrictorsa,b
 
Angiotensin II was used to keep MAP within acceptable limits. Prior to Hemopump insertion, high doses were sometimes required to maintain an acceptable MAP, and even during the early phase of Hemopump support, angiotensin infusion was maintained at a high level because of a very low SVRI. The SVRI, however, was deliberately allowed to remain in the lower range of normal to optimize flow delivery of the Hemopump.

Metabolic Support
All patients except 1 received metabolic support with glucose-insulin-potassium. Eight patients received a combination of glucose-insulin-potassium and glutamate. Two patients received a combination of glucose-insulin-potassium, glutamate, and aspartate, and 1 patient had glutamate only.

Hemodynamic Response
From the complete hemodynamic profile, the following variables were found useful: cardiac index, SvO2, SVRI, MAP, mean pulmonary artery blood pressure, pulmonary capillary wedge pressure, right ventricular ejection fraction, and pulmonary vascular resistance index.

The baseline cardiac index was low (Fig 2AGo). The Hemopump was inserted in most patients when they were still on CPB. Therefore, the cardiac index was relatively high during this period. During Hemopump treatment, there was an increase in cardiac index, with further improvement after Hemopump removal. Compared with the measurements obtained before Hemopump insertion, there were no significant differences. The SvO2 at baseline was higher than that measured before insertion of the Hemopump. During Hemopump treatment, SvO2 showed a significant increase to normal levels (see Fig 2AGo).



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  		Fig 2. . Values for (A) cardiac index (CI) and mixed venous oxygen saturation (SvO2) and for (B) mean arterial blood pressure (MAP) and systemic vascular resistance index (SVRI) before, during, and after Hemopump (HP) support. Data are shown as the mean ± the standard deviation. (ICU = intensive care unit; * = p < 0.05.

 
Both MAP and SVRI values showed a fall from baseline to the measurement before Hemopump insertion (Fig 2BGo). During Hemopump treatment, the MAP increased except for the measurement in the ICU. Low SVRI levels were noticed before, during, and after Hemopump support.

The pulmonary capillary wedge pressure and mean pulmonary artery pressure measurements showed high baseline values (Fig 3AGo). During Hemopump treatment, the pulmonary capillary wedge pressures fell to within normal limits. The mean pulmonary artery pressure increased during and after Hemopump treatment.



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  		Fig 3. . Values for (A) pulmonary capillary wedge pressure (PCWP) and mean pulmonary artery blood pressure (PAPm) and for (B) right ventricular ejection fraction (RVEF) and pulmonary vascular resistance index (PVRI) before, during, and after Hemopump (HP) support. Data are shown as the mean ± the standard deviation. (ICU = intensive care unit.)

 
There was a nonsignificant increase in right ventricular ejection fraction throughout the whole period but without complete normalization (Fig 3BGo). The pulmonary vascular resistance index decreased from baseline to the measurement made prior to Hemopump support. During and after Hemopump treatment, the values were almost normal.


   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
The Hemopump is an axial-flow pump that gives a continuous blood flow of approximately 5.0 L/min. In combination with proper right ventricular function, it can maintain adequate perfusion of vital organs.

During the first 12 to 24 hours after Hemopump insertion and with optimal pharmacologic therapy, an entirely nonpulsatile arterial blood pressure curve was observed, and during this period, echocardiography showed that the aortic valves were closed around the Hemopump cannula. The relatively low filling pressures during Hemopump treatment suggested proper unloading of the left ventricle. Echocardiography in this situation showed a small, decompressed left ventricle [13]. Under this condition, there is a reduction in the pressure and radius of the left ventricle, and it is unloaded in a similar way as the empty beating heart on full CPB. The decrease in wall tension is followed by a concomitant decrease in myocardial oxygen demand, which should favor recovery of the stunned myocardium [14, 15]. There are also experimental data [16] suggesting a relative increase in myocardial blood flow during Hemopump support.

The MAP during this time was low with average values of 50 to 70 mm Hg. Even lower levels were noticed but were accepted as long as diuresis and SvO2 were within normal limits.

The Hemopump performs better when peripheral resistance is low because an axial-flow pump is afterload sensitive [3, 17, 18]. It is not possible to calculate blood flow from the pump speed or to measure it on the console. Therefore, the thermodilution technique was applied to estimate the cardiac output and index. Immediately after Hemopump insertion, the continuous flow from the device seems to cause vasodilation. We administered angiotensin II through a left atrial catheter to achieve SVRI levels just below normal [19]. There are reports [20, 21] of the beneficial effect of administering vasoconstrictors through a left atrial catheter. We used angiotensin II frequently and found it easy to titrate. Clinically, no negative effects from the splanchnic circulation were observed.

The increase in right ventricular ejection fraction throughout the period might have been due to immediate and aggressive treatment of increased pulmonary vascular resistance. A low pulmonary vascular resistance is probably the most important factor for efficient right ventricular function [22, 23]. This was achieved with conventional therapy such as nitroglycerin or nitroprusside in combination with phosphodiesterase III inhibitors. During Hemopump treatment, inotropic support was used to maintain good right ventricular function and indirectly, good Hemopump function. Doses were kept as low as possible in an attempt not to increase the myocardial oxygen consumption too much and to avoid negative side effects. High inotropic stimulation should be kept as a backup in case malfunctioning of the left ventricular assist device occurs.

The left ventricular assist device and pharmacologic therapy were used in combination with metabolic support in all patients. The rationale behind metabolic intervention is to minimize the time and the negative effects of myocardial stunning and to reduce the size of potential myocardial infarction. Glucose-insulin-potassium treatment was used with high doses of insulin, 1 IU • kg-1 • h-1 or more, to achieve maximal metabolic effect. It was usually started immediately after removal of the aortic cross-clamp whenever problems in weaning from CPB were expected. Supraphysiologic doses of insulin cause a marked reduction in peripheral resistance, which can be beneficial for the failing myocardium and eventually Hemopump function [17, 18, 24]. If severely ischemic electrocardiographic recordings were noticed preoperatively or postoperatively, an infusion of glutamate or aspartate or both was started. These amino acids may possibly enhance glycolysis during ischemia. They can also serve as important substrates for the replenishment of Krebs cycle intermediates lost during ischemia [9, 10].

Recovery of the left ventricle was indicated by an increase in pulsatile activity on the arterial pressure recording. The majority of survivors started to show signs of recovery within 24 to 48 hours. When this was noticed, stepwise weaning from the Hemopump over 6 to 8 hours was performed. When the weaning procedure was completed, the pump speed was at a minimum [3, 13]. Stopping the pump completely causes major aortic insufficiency with retrograde flow through the pump house into the left ventricle (Wulff et al, unpublished results). One patient, who did not show signs of myocardial recovery, was accepted for heart transplantation. After 3 days of Hemopump support, the patient received a HeartMate left ventricular assist device and then underwent successful transplantation after 3 months.

An adverse effect of Hemopump treatment is destruction of blood elements, which has previously been reported by us [11] and others [3, 18]. There was a slight increase in plasma free hemoglobin and a reduction in platelets, but major negative effects of this nature were not noticed. We emphasize that initial complete reversal of heparin is very important. In the ICU, a heparin infusion aiming at an activated clotting time in the range of 150 to 200 seconds was used to avoid clotting in the pump. Pericardial effusion may be unmasked by decompression of the left ventricle. Blood around the left atrium with obstruction of blood flow into the left ventricle was seen in some patients. If the obstruction is severe, it is best indicated by poor Hemopump performance and a low SvO2. The diagnosis is confirmed by echocardiography.

We conclude that the Hemopump can effectively decompress the failing left ventricle, thereby providing good conditions for recovery of the stunned myocardium with preserved vital-organ perfusion. Low doses of inotropic drugs are required, and the principles of pharmacologic therapy are to optimize pulmonary and systemic vascular resistances. The SvO2, MAP, and diuresis are the most important clinical guidelines to evaluate the adequacy of therapy.


   Acknowledgments
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
This investigation was supported by grants from the Linköping Heart Center Fund, Linköping, Sweden.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Address reprint requests to Dr Peterzén, Linköping Heart Center, University Hospital, S-581 85 Linköping, Sweden.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Wampler RK, Moise JC, Frazier OH, Olsen DB. In vivo evaluation of a peripheral vascular access axial flow blood pump. ASAIO Trans 1988;34:450–4.[Medline]
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  4. Butler KC, Moise JC, Wampler RK. The Hemopump-a new cardiac prosthesis device. IEEE Trans Biomed Eng 1990;37:193–6.[Medline]
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  6. Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146–9.[Abstract/Free Full Text]
  7. Royster RL. Myocardial dysfunction following cardiopulmonary bypass: recovery patterns, predictors of inotropic need, theoretical concepts of inotropic administration. J Cardiothorac Vasc Anesth 1993;7:S19–25.
  8. Vinten-Johansen J, Nakanishi K. Postcardioplegia acute cardiac dysfunction and reperfusion injury. J Cardiothorac Vasc Anesth 1993;7:S6–18.
  9. Lazar HL, Buckberg GD, Manganaro AJ, Becker H, Maloney JV Jr. Reversal of ischemic damage with amino acid enhancement during reperfusion. Surgery 1980;88:702–9.[Medline]
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  11. Lönn U, Peterzén B, Granfeldt H, Babic A, Casimir-Ahn H. Hemopump treatment in patients with postcardiotomy heart failure. Ann Thorac Surg 1995;60:1067–71.[Abstract/Free Full Text]
  12. Higgins TL, Estafanous FG, Loop FD, et al. Stratification of morbidity and mortality outcome by preoperative risk factors in coronary artery bypass patients: a clinical severity score. JAMA 1992;267:2344–8.[Abstract/Free Full Text]
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  16. Scholz KH, Hering JP, Schröder T, et al. Protective effects of Hemopump left ventricular assist device in experimental cardiogenic shock. Eur J Cardiothorac Surg 1992;6:209–14.[Abstract]
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