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Eur J Cardiothorac Surg 2001;19:179-184
© 2001 Elsevier Science NL

Right ventricular support for off-pump coronary artery bypass grafting studied with bi-ventricular pressure–volume loops in sheep

André L. Dekker, Gijs G. Geskes, Audrey A. Cramers, Willem R. Dassen, Jos G. Maessen, Kees B. Prenger, Frederik H. van der Veen

Department of Cardiothoracic Surgery, Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht, P. Debyelaan 25, 6229HX, Maastricht, The Netherlands

Received 8 August 2000; received in revised form 16 November 2000; accepted 18 November 2000.

Corresponding author. Tel.: +31-43-3876380; fax: +31-43-3875075
e-mail: fvv{at}scpc.azm.nl


   Abstract
Top
 Abstract
1. Introduction
 2. Animals and methods
 3. Results
 4. Discussion
 References
 
Objectives: Tilting the heart during off-pump coronary artery bypass grafting (OPCABG) causes a strong decrease in cardiac output. It is hypothesized that this decrease is caused by reduced right ventricular filling and that right ventricular support is thus the best way to restore cardiac output. Simultaneous left and right ventricular pressure–volume loops were used to test this hypothesis. Methods: In seven sheep, the heart was tilted with the use of an Octopus device. After unsupported tilting, a novel right ventricular support, the Enabler, was activated at a pulsatile flow of 1.6 l/min. Pressure–volume loops of both ventricles were obtained using conductance catheters, and cardiac output was monitored with an aortic flow probe. Results: Tilting reduced cardiac output by 31% (4.4–3.1 l/min, P=0.001) and right ventricular end-diastolic volume by 44% (86–51 ml, P=0.005), while right ventricular end-diastolic pressure did not decrease. Left ventricular systolic pressure was not significantly reduced upon tilting and even increased in two animals. During Enabler right ventricular support, the cardiac output remained 23% lower than pre-tilting values (3.4 vs. 4.4 l/min, P=0.001). Conclusions: Restricted right ventricular filling is the primary cause of the strong decrease in cardiac output during tilting. The Enabler right ventricular support can currently not restore cardiac output to pre-tilting values, mainly caused by its limited output and a decrease in right ventricular output upon Enabler activation. Constant monitoring of cardiac output is crucial during (unsupported or supported) tilting as blood pressure alone may not reflect the extent of the reduction in cardiac function.

Key Words: Minimal invasive surgery • Assist device • Hemodynamics • Cardiac output • Cardiac volume


   1. Introduction
Top
 Abstract
 1. Introduction
2. Animals and methods
 3. Results
 4. Discussion
 References
 
Left ventricular pressure–volume loops measured by a conductance catheter are now commonly used to measure the effect of disease, new drugs, left heart assist and cardiomyoplasty on left ventricular function [1–5]. Right ventricular pressure–volume loops are less often used [6,7], but also show good correlation with other techniques [8].

Simultaneous left and right ventricular pressure–volume loops are necessary for an in-depth investigation of cardiac function, especially when studying interventions that affect both ventricles. One such intervention is cardiac tilting for multivessel off-pump coronary artery bypass grafting (OPCABG) [9,10].

OPCABG eliminates the use of the extracorporeal circulation with its well-known complications [11]. In this procedure, the Octopus device (Medtronic Inc., Minneapolis, MI) is often used to stabilize the site of the anastomosis, but can also be used to lift and rotate the heart, thereby allowing multivessel OPCABG [12]. However, this so-called cardiac tilting is not without hemodynamic consequences; tilting the heart is reported to cause a 44% decrease in stroke volume in healthy pigs and to reduce systemic blood pressures with a concomitant higher right atrial pressure, suggesting right ventricular dysfunction [9,10]. The hemodynamic consequences of cardiac tilting limit the use of OPCABG in patients with poor cardiac function.

The Enabler (Hemodynamics Systems Ltd., Yoqneam, Israel) was developed to support the right ventricle during cardiac tilting, thereby making multivessel OPCABG possible in all patients. It consists of a 24F catheter that is placed via surgical preparation of the femoral vein or via the right atrium and creates a pulsatile flow, 1:1 triggered to the ECG [13,14].

The Hemopump (Medtronic Inc., Minneapolis, MI) is also used in beating heart CABG, but only to support the left ventricle during CABG of single or easily accessible vessels [15,16]. One study compared right and left heart bypass with the Biomedicus device and concluded that only right heart bypass could restore cardiac function during OPCABG [17].

It is hypothesized that (a) cardiac tilting reduces right ventricular filling which results in a decreased cardiac output and that (b) right ventricular support is thus the best way to counteract this effect. Because tilting and right ventricular support are interventions that affect both ventricles, simultaneous left and right ventricular pressure–volume loops were used to test these hypotheses.


   2. Animals and methods
Top
 Abstract
 1. Introduction
 2. Animals and methods
3. Results
 4. Discussion
 References
 
2.1. Animals and medication
All animals received humane care in compliance with the Guide for the Care and Use of Laboratory Animals (NIH publication 86-23, revised 1985) and the study was approved by our institution's animal ethics committee.

Seven female Texelaar sheep with an average weight of 68 kg (range 61–76 kg) were premedicated with atropine (s.c. 0.2 mg/kg). Anesthesia was induced with sodium thiopental (i.v.-bolus 15 mg/kg) and maintained with halothane (2%). After administration of muscle relaxant suxamethonium (i.v.-bolus 0.1 mg/kg) and analgetic buprenorfine (i.v.-bolus 0.01 mg/kg), a midsternotomy was performed, the pericardial sac was opened and lidocaine (i.v.-bolus 100 mg and i.v.-infusion 1 mg/kg per h) was given to prevent arrhythmia during heart manipulation. Heparin (i.v.-bolus 100 IU/kg) was administered and the activated clotting time was measured and kept above 400 s during the experiment. The animals were killed with an overdose of pentobarbital (i.v.-bolus 200 mg/kg).

2.2. Instrumentation
A Doppler aortic flow probe (Transonic, Ithaca, NY) was placed on the descending aorta and compared to thermodilution-derived cardiac output to include flow to the coronary arteries and the upper body, which was assumed to be a fixed percentage for the remainder of the experiment. Two conductance catheters (ANP-223N, Sentron, Roden, The Netherlands) were placed under fluoroscopy in the left and right ventricles via the femoral artery and jugular vein, respectively, (Fig. 1) and connected to two Leycom Sigma-5DF systems (Cardiodynamics, Leiden, The Netherlands).



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  		Fig. 1. Cartoon showing the Enabler catheter positioned in the right heart. Conductance catheters are placed in both ventricles with their pigtail in the ventricular apex.

 
The Enabler catheter was placed via the jugular vein (right atrium in one sheep) through the right ventricle into the pulmonary artery, so that the catheter's inlet valve was positioned in the right atrium and the outlet valve was positioned in the pulmonary artery (Fig. 1).

2.3. Measurements
The measurement protocol started with cardiac tilting by the Octopus device to expose the inferior wall, as described elsewhere [12]. After 5 min of unsupported tilting, the right ventricular support was activated at its maximum flow of 1.6 l/min for 10 min. In one sheep a posterior wall tilting procedure was performed [12]. The recorded hemodynamic signals included ECG, right and left ventricular pressure and volume, cardiac output and pump flow settings. Measurements were done at baseline, 5 min of cardiac tilting and 10 min of right ventricular support.

2.4. Conductance calibration
Parallel conductance was determined by the method described elsewhere [5]. Absolute volumes were determined by comparing conductance-derived stroke volume with the stroke volume measured by the aortic flow probe. Because the aortic flow probe measures the sum of both right ventricular support and right ventricular output, the right ventricular slope factor during activation of the right ventricular support was assumed to be the average of the slope factor before and after the activation.

2.5. Data analysis
All conductance measurements were analyzed with the Circlab 99 software package (Paul Steendijk, Leiden, The Netherlands). A non-parametric Friedman test with {alpha}=0.01 was used to select those variables in which at least one stage (baseline, tilt or right ventricular support) was different from the other stages. In these selected variables, statistically significant differences between the baseline, tilted and right ventricular support stages were tested using a paired t-test with Bonferroni correction for three multiple measures. Significance was assumed if the corrected P value was less than 0.05.


   3. Results
Top
 Abstract
 1. Introduction
 2. Animals and methods
 3. Results
4. Discussion
 References
 
3.1. Cardiac tilting
In Table 1, hemodynamic data from the conductance measurements are summarized. They show that tilting caused a strong and significant reduction in cardiac output of 31%. This reduction was accompanied by a decrease in right ventricular end-diastolic volume of 44%, while end-diastolic pressure rose slightly but not significantly. These effects are also seen in the examples of pressure–volume loops given in Fig. 2. Left ventricular pressure did not significantly decrease and even increased in two animals upon tilting.


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  		Table 1. Hemodynamic changes during tilting and subsequent right ventricular supporta

 


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  		Fig. 2. Representative left and right ventricular pressure–volume loops before and after tilting with the Octopus device. Upon tilting the stroke volume, left ventricular end-systolic pressure and right ventricular end-diastolic volume decrease, but right ventricular end-diastolic pressure increases.

 
The ventricles reacted differently to cardiac tilting. This was best seen at the end of the tilting procedure; when the heart was placed back into its normal position, it was observed that the right ventricle immediately responded to the new situation while it took a number of beats for the left ventricle to adjust (Fig. 3).



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  		Fig. 3. Changes in left and right ventricular volume upon repositioning of the heart from a tilt into its normal position. The repositioning occurs between t=3 s and t=4 s. The slow variation in volume, especially seen in the left ventricle, is caused by ventilation. The right ventricle immediately responds to the new situation by an increase in end-diastolic volume within two to three beats. In contrast, the left ventricle slowly accommodates to the new situation in about ten beats.

 
3.2. Right ventricular support
The Enabler right ventricular support system mildly increased cardiac output and left ventricular end-diastolic volume, but not significantly, and cardiac output remained 23% lower than the pre-tilting value (Table 1). Upon right ventricular support activation, the right ventricular output was decreased by more than 0.5 l/min in five out of seven experiments.

These effects are seen in the examples of pressure–volume loops given in Fig. 4 and a similar result was obtained with the right ventricular support in the untilted heart as shown in Fig. 5; right ventricular stroke volume was strongly decreased when the right ventricular support was switched on, while left ventricular stroke volume only mildly increased.



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  		Fig. 4. Representative left and right ventricular pressure–volume loops before and after Enabler right ventricular support with the Enabler in the tilted heart. The left ventricular stroke volume and end-systolic pressure are increased upon right ventricular support. In contrast, the right ventricular stroke volume is decreased when the right ventricular support is switched on; the difference in stroke volume between left and right ventricles is caused by the right ventricular support.

 


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  		Fig. 5. Enabler right ventricular support with the heart in its anatomical position. The Enabler is switched on at t=3 s up to maximum flow (2.0 l/min) at t=5 s and then slowly turned back to zero flow at t=13 s. The left ventricular stroke volume and end-diastolic volume are slightly increased upon right ventricular support. The right ventricular stroke volume and end-diastolic volume decrease strongly when the Enabler is switched on. This unloading limits the Enabler's positive effect on left ventricular stroke volume.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Animals and methods
 3. Results
 4. Discussion
References
 
The results of this study demonstrate that simultaneous left and right ventricular pressure–volume loops measured by conductance catheters are useful to examine changes in cardiac function during cardiac tilting and subsequent right ventricular support by the Enabler. The conductance technique has been used successfully earlier in the assisted heart [3,4], but the heart was never placed in a non-anatomical position and both ventricles were never simultaneously studied during or after an intervention. This study not only shows that this is feasible, but also that it is necessary in a complicated intervention in order to know which ventricle causes a change in cardiac function, and which ventricle merely responds to the other.

4.1. The effect of tilting on cardiac function
Cardiac tilting causes a strong decrease in cardiac output. In the present study, this decrease was on average 31%, which is somewhat less than found by others in healthy pigs [9,10,17] and sheep [14]. Interestingly, cardiac output was much more decreased than left ventricular systolic pressure, as was observed previously [14]. Even more importantly, left ventricular systolic pressure was increased upon tilting in two out of seven sheep. This shows that blood pressure alone is most likely not a sensitive measure to estimate the extent of the hemodynamic worsening during cardiac tilting in the individual patient.

The observed decrease in cardiac output can be caused by (a) an increase in afterload, (b) a valvular defect, (c) a decrease in contractility or (d) a decrease in preload in either ventricle.

(a) Afterload is not increased during cardiac tilting, as the end-systolic pressure in both left and right ventricles does not increase. Therefore, kinking of the aorta or the pulmonary artery does not seem to occur.

(b) The introduction of a valvular defect by tilting was discarded earlier by echocardiography observations in two previous studies [9,17].

(c) An acute decrease in contractility upon tilting is unlikely. No signs of tilting-induced ischemia were reported by other investigators [10] and hypoxia, which may occur due to low blood pressure during tilting, is more likely a consequence than a cause of the low cardiac output. One of the most reliable measures of contractility is the slope of the end-systolic pressure–volume relationship. Although this slope can be measured with a conductance catheter, this was not done as it requires caval vein occlusion, which would have interfered too much with the hemodynamic state of these animals during tilting.

(d) A decrease in preload, defined as end-diastolic volume, occurs in both ventricles upon tilting. The right ventricle can be argued to be the most likely cause of the decrease in cardiac output for two reasons. First, the right ventricle immediately reacts to the end of the tilt by increasing its end-diastolic volume and stroke volume, while the left ventricle slowly reacts to the increased filling by the Frank–Starling mechanism (Fig. 3). If the left ventricle was the problem during tilting, then it would have been the first to react to the end of the tilt. Second, a resistance to left ventricular filling would have increased pulmonary pressure and thus right ventricular afterload, which was not observed. In conclusion, reduced right ventricular filling is the major cause of the decrease in cardiac output during cardiac tilting.

The reduced right ventricular filling is not accompanied by a decrease in right ventricular end-diastolic pressure. This contradiction was observed before [9,10,17], and may be caused by a mechanical inhibition of right ventricular filling, for instance a compression of the ventricular wall by the tilting procedure. This is supported by a recent echocardiographic study which reported that right ventricular geometry changes during tilting [17]. Another explanation is that the ventricle is filled against gravitation because the apex is pointed upwards during tilting.

It has been shown that an extreme 20° Trendelenburg maneuver can partially restore cardiac function during a tilt via increased right heart filling pressure and thus increased preload [9,10]. This is in agreement with our finding that right ventricular filling is the problem during cardiac tilting. However, it should be noted that the reported acute two-fold increase in right atrial pressure caused by the Trendelenburg maneuver has the inherent risk of atrial fibrillation [18], and should therefore be avoided if possible.

4.2. Right ventricular support with the Enabler
The Enabler right ventricular support is not able to fully recover cardiac output to pre-tilting values. Our results correspond well with the recently published results with the Biomedicus device and the Enabler as a right heart bypass, which were also shown to only partially restore cardiac function [14,17]. Another support system, the Hemopump, has also been used in OPCABG [15,16], but this is a left ventricular assist device and might not be suitable, as it is the right ventricle that needs support.

There are two explanations why the Enabler did not fully restore cardiac output. First, activation of the Enabler further decreases right ventricular output. Likely mechanisms are a reduction in right ventricular filling because the Enabler sucks blood from the right atrium, or an increase in right ventricular afterload caused by simultaneous ejection of the Enabler and the right ventricle. Second, the forward flow of the Enabler, the difference between right and left ventricular output (see Table 1), is only 0.9 l/min. Possible explanations are (a) the right ventricular output is overestimated because the conductance slope factor can not be measured (see Section 2), and (b) the Enabler causes regurgitation across the pulmonary valve, which would mean that part of the Enabler output is used to fill the right ventricle rather than flowing towards the lungs.

In conclusion, current right ventricular support systems can not fully restore cardiac function during tilting. Furthermore, the output of a right ventricular support should not be assumed to be a net extra output, and monitoring of the end result, cardiac output, is therefore crucial.

4.3. Limitations of the study
In this study, the animals had low blood pressure, cardiac output, ventricular volumes and poor ventricles compared to humans. It can be expected that tilting will be better tolerated by the human heart.


   Acknowledgments
 
This study was financially supported by Hemodynamics Systems Ltd., Yoqneam, Israel. We gratefully acknowledge the biotechnical assistance provided by Jo Habets and Theo van der Nagel, the study support by Veronica Elias-Weissmann, and the comments on the manuscript by David Shoshani.


   References
Top
 Abstract
 1. Introduction
 2. Animals and methods
 3. Results
 4. Discussion
 References
 

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