Ann Thorac Surg 1995;60:978-984
© 1995 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Right-to-Left Veno-Arterial Shunting for Right-Sided Circulatory Failure
James P. Slater, MD,
Daniel J. Goldstein, MD,
Robert C. Ashton, Jr, MD,
Howard R. Levin, MD,
Henry M. Spotnitz, MD,
Mehmet C. Oz, MD
Division of Cardiothoracic Surgery, Department of Surgery, and Division of Circulatory Physiology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York
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Abstract
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Background. Right-sided circulatory failure, a complication of heart transplantation and left ventricular assist device use, results in decreased cardiac output due to diminished flow across the pulmonary circuit. We hypothesized that creation of a controlled right-to-left shunt would result in decompression of the right ventricle and improved systemic cardiac output at tolerable oxygen saturations. We also hypothesized that a peripheral veno-arterial shunt is physiologically superior to a central shunt.
Methods. Right atrial--femoral artery and right atrial--left atrial shunts were created in a large animal model (calf). Right-sided circulatory failure was induced by banding the pulmonary artery. Hemodynamic measures and blood gas determinations were obtained during nonshunted and shunted states.
Results. Peripheral and central shunts resulted in decreased right-sided pressures and increased cardiac output. Arterial oxygen saturation remained greater than 90% during shunting. The peripheral shunt had the added advantage of decreasing left ventricular end-diastolic pressure and left ventricular stroke work.
Conclusions. A controlled right-to-left shunt improved hemodynamics and cardiac output in a large animal model with right-sided circulatory failure. This strategy may be useful in the management of transplant and left ventricular assist device recipients with perioperative right-sided circulatory failure. Our studies also indicate that creation of a peripheral shunt has both physiologic and technical advantages over a central shunt.
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Introduction
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See also page 985.
Recently we described the use of a nonoxygenated, controlled, right-to-left veno-arterial shunt for the treatment of right-sided circulatory failure (RSCF) in 2 patients after cardiac replacement therapy [1]. The first patient, after numerous failed attempts, was successfully weaned from cardiopulmonary bypass after creation of a right-to-left shunt after cardiac transplantation. The second patient remained in cardiogenic shock despite left ventricular assist device support and maximal inotropic therapy due to RSCF. Creation of a right-to-left shunt resulted in decompression of the right ventricle, improved systemic hemodynamics, and eventual weaning and removal of left ventricular assist device and inotropic support.
Right-sided circulatory failure is a multifactorial entity in which the final common pathway is diminished blood flow across the pulmonary circuit resulting in a lower systemic cardiac output. Right-sided circulatory flow is the primary cause of death in 10% to 20% of early mortality (<30 days) after cardiac transplantation [2, 3], usually due to increased pulmonary vascular resistance in the recipient, or donor organ dysfunction [4]. Perioperative RSCF is also a complication in 20% to 40% of the increasing number of patients receiving left ventricular assist devices and is the leading cause of perioperative death [5, 6]. Causes in this population include altered ventricular interdependence and acute increased pulmonary vascular resistance in coagulopathic patients after prolonged cardiopulmonary bypass [5, 7, 8].
Pharmacologic therapy for RSCF includes pulmonary vasodilators and inotropic support for the right ventricle. Right ventricular assist devices can provide mechanical assistance for RSCF refractory to drug therapy. Right ventricular assist devices are capable of maintaining adequate cardiac output in most patients, but may fail when pulmonary vascular resistance is extremely elevated and increased flow to the pulmonary artery results in right ventricular distention and a leftward shift of the ventricular septum, which limits left ventricular filling [9]. In addition, right ventricular assist devices must be placed and removed in the operating room under general anesthesia.
In an effort to study a new and complementary approach to treating RSCF, we studied right-to-left veno-arterial shunting in a large animal model with induced RSCF. We hypothesized that this shunt would decompress the right ventricle and improve systemic hemodynamic stability, with tolerable levels of arterial desaturation. To determine the most advantageous shunt circuit we compared shunts to both the central and peripheral left-sided circulation.
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Material and Methods
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All animals received humane care in compliance with the ``Principles of Laboratory Animal Care'' formulated by the Institute of Laboratory Animal Resources and the ``Guide for the Care and Use of Laboratory Animals'' prepared by the National Institutes of Health (NIH publication 85-23, revised 1985).
Holstein calves (n = 6) weighing between 80 and 100 kg were premedicated with intramuscular midazolam (0.1 mg/kg) and ketamine (10 mg/kg). Anesthesia was induced with thiamylal (7 to 10 mg/kg intravenously); after intubation anesthesia was maintained using inhaled isoflurane (1.5% to 1.75% in 2 to 3 L O2).
In the right lateral decubitus position a left thoracotomy was performed with excision of the fifth rib. The inferior pulmonary ligament was divided and the lung retracted dorsally. The pericardium was incised longitudinally. The aorta was dissected free to the ductus arteriosus, dividing the azygos vein. The ductus was clamped to eliminate the possibility of a naturally occurring left-to-right shunt. The pulmonary artery was isolated proximal to its bifurcation.
A multidirectional shunt circuit was created using cannulas placed in the right atrium (32-mm Bard cannula; Bard Co, Billerica, MA), the left atrium (30-mm Bard cannula), and the right femoral artery (18-mm Bard femoral cannula) (Fig 1
). Blood drawn through the right atrial cannula by a centrifugal pump (Biomedicus Inc, Eden Prarie, MN) was returned via a Y-shaped arterial line to either the left atrium or the left femoral artery. Flow direction was controlled by clamping one limb of the circuit. An in-line OxySAT 2000 (Baxter Health Care Corp, Irvine, CA) oxygen saturation meter was placed in the venous return line and used to estimate mixed venous oxygen saturation.
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Fig 1. . Calf model and instrumentation. Cannulas are in the right atrium, left atrium, and femoral artery. Pressure transducers are in the right ventricle, pulmonary artery, and left ventricle. Flow probe catheters are in the carotid artery, superior vena cava, femoral artery, inferior vena cava, and pulmonary artery (PA). The PA is banded. (O2 sat = oxygen saturation; R. = right.)
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Ultrasonic flow probes (Transonic Systems Inc, Ithaca, NY) were placed around the pulmonary artery, descending aorta, and left carotid artery. Micromanometer pressure transducers (Millar Instruments Inc, Houston, TX) were placed in the right ventricle, pulmonary artery, and left ventricle after calibration with a water column. A Swan-Ganz catheter in the pulmonary artery, and catheters in the superior and inferior venae cavae and carotid and femoral arteries allowed measurement of blood pH and oxygen saturation.
An umbilical tape, placed around the pulmonary artery, was fastened to a ratcheted snare and used to band the pulmonary artery in an incremental fashion.
The optimal shunt flow rate (Qmax) was defined as the maximal flow with a mixed venous oxygen saturation greater than 60% determined by the in-line saturation monitor. This resulted in an arterial oxygen saturation greater than 90%. Once Qmax was determined, it was used consistently for that animal throughout the remainder of the experiment. As shown in our previous studies Qmax typically approached 50% of cardiac output just before shunting [1].
The experimental protocol required right heart failure to be established, after which right-to-left shunting was initiated to improve hemodynamic stability. A time line representation of the protocol is depicted in Figure 2. After baseline data were obtained, the pulmonary artery was banded to produce right ventricular failure. The animal was allowed to stabilize for 4 minutes before all measures were repeated. Veno-arterial shunt flow was then instituted at Qmax through one limb of the shunt circuit. Four minutes later, measurements were repeated. Shunt flow at Qmax was then redirected to the other limb of the circuit. A 4-minute stabilization period was followed by repeated measurements. Shunt flow was then stopped and the pulmonary artery band removed. The animal was allowed to stabilize before the pulmonary artery band was reapplied and the above protocol repeated. Shunt order was alternated between experiments, and analysis showed that order had no impact on the final results.
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Fig 2. . Time line representation of experimental protocol. Order of peripheral and central shunt is interchangeable. (PA = pulmonary artery.)
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Data were digitized in real time at speed of 200 Hz by an analog--digital converter (MacLab/8 model Mac Lab MkIII; ADInstruments, Pty Ltd, Australia), filtered with a 50 Hz low-pass filter, and recorded by a Macintosh computer (Macintosh IIcx; Apple Computers Inc, CA). Blood gas determinations were performed using a Nova Stat 3 Profile (Nova Biomedical Inc, Waltham, MA).
Hemodynamic variables including right ventricular end-diastolic pressure, right ventricular peak systolic pressure, pulmonary artery pressure, left ventricular end-diastolic pressure, pulmonary artery flow, descending aortic flow (AoF), and carotid flow were measured for each experimental condition. For the peripheral shunt aortic flow was calculated as measured flow plus shunted flow (AoF(p) = AoF + Qmax) to account for left sided circulation not captured by the aortic flow probe. Oxygen saturation was obtained at the same time points from the carotid, femoral, and pulmonary arteries and the inferior and superior venae cavae. Finally, pH determinations were performed at the carotid artery and femoral vein.
Right and left ventricular stroke work calculations were performed for all experimental states (stroke work = stroke volume x mean ventricular pressure). Right ventricular stroke volume was calculated by dividing pulmonary artery flow by heart rate. Left ventricular stroke volume during central shunt was calculated as (AoF + carotid flow)/heart rate. Left ventricular stroke volume during peripheral shunt was calculated as (AoF(p) + carotid flow)/heart rate.
An unpaired Student's t test was used to compare mean values during baseline and right circulatory failure conditions. A paired analysis of variance using the Bonferroni multiple comparisons test was used to compare both shunt states with the right circulatory failure condition and each other.
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Results
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A representative example of the effects of pulmonary artery banding, peripheral shunting, and central shunting is presented in Figure 3. Pulmonary artery banding caused an increase in right-sided and a decrease in left-sided pressures. Flows through the pulmonary artery, aorta, and carotid artery were also decreased. Shunting resulted in decreased right-sided pressures and improved flow through both pulmonary and systemic circulations.
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Fig 3. . Representative data from 1 animal, showing baseline and then right-sided circulatory failure under the three shunt conditions. (AOF = aortic flow; CF = carotid flow; LVP = left ventricular pressure; PAF = pulmonary artery flow; PAP = pulmonary artery pressure; RVP = right ventricular pressure.)
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Mean hemodynamic effects of banding the pulmonary artery are presented in Figure 4. Right ventricular end-diastolic pressure and right ventricular peak systolic pressure were increased markedly after placement of the pulmonary artery band (p < 0.05), and left ventricular end-diastolic pressure decreased (p < 0.05). Pulmonary artery, aortic, and carotid artery flows decreased (p < 0.05). Mixed venous oxygen saturation decreased from 77.3% ± 6.0% to 42.3% ± 5.6% (p < 0.05 versus baseline).
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Fig 4. . (Top) Mean (± standard error of the mean) right ventricular peak systolic pressure (RVPSP), right ventricular end-diastolic pressure (RVEDP), pulmonary artery pressure (PAP), and left ventricular end-diastolic pressure (LVEDP) at baseline and after placement of pulmonary artery (PA) band. (Bottom) Mean (± standard error of the mean) pulmonary artery flow (PAF), aortic flow (AOF), and carotid flow at baseline and after placement of PA band.
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Mean effects of central and peripheral shunts on pulmonary and systemic hemodynamic parameters, oxygen saturation and blood pH are presented in Table 1 and Figures 5--9. Right ventricular pressures decreased with both shunts (p < 0.01) (see Figs 5, 6). Pulmonary artery pressure also decreased (p < 0.01, peripheral; p < 0.05, central) (see Fig 5). Left ventricular end-diastolic pressure decreased during the peripheral shunt (p < 0.05), but not the central shunt (see Fig 6). Pulmonary artery flow increased during the peripheral shunt (p = 0.07), but was not affected by the central shunt (see Fig 7). Aortic and carotid flows were improved by both shunts (see Fig 7). Right ventricular stroke work was unchanged by shunting (see Fig 8). Left ventricular stroke work was decreased during the peripheral shunt when compared with both the nonshunted state (p < 0.05) and the central shunt (p < 0.001) (see Fig 8).
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Table 1. . Comparison of Pressure, Flow, Stroke Work, Oxygen Saturation, and pH Values With Pulmonary Artery Banded During No Shunt, Peripheral Shunt, and Central Shunt
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Fig 5. . Mean (± standard error of the mean) right ventricular peak systolic pressure (RVPSP) and pulmonary artery pressure (PAP) during right-sided circulatory failure in each experimental condition. (ANOVA = analysis of variance.)
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Fig 6. . Mean (± standard error of the mean) right ventricular end-diastolic pressure (RVEDP) and left ventricular end-diastolic pressure (LVEDP) during right-sided circulatory failure in each experimental condition. (ANOVA = analysis of variance.)
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Fig 7. . Mean (± standard error of the mean) pulmonary artery (PA), aortic, and carotid artery flows during right-sided circulatory failure in each experimental condition. (ANOVA = analysis of variance.)
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Fig 8. . Mean (± standard error of the mean) right ventricular (RV) and left ventricular (LV) stroke work during right-sided circulatory failure in each experimental condition. (ANOVA = analysis of variance.)
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Effects of shunting on oxygen saturation are illustrated in Figure 9. Carotid artery oxygen saturation decreased significantly during the central shunt (p < 0.05), but not during the peripheral shunt. Superior vena caval saturation was also lowered by the central shunt (p < 0.05). Femoral artery and inferior vena caval oxygen saturation were markedly decreased during peripheral shunting (p < 0.01), but not significantly affected by central shunting. Mixed venous saturation trended lower during peripheral shunting; this was not statistically significant.
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Fig 9. . Mean (± standard error of the mean) carotid artery (CA), femoral artery (FA), inferior vena cava (IVC), superior vena cava (SVC), and mixed venous (MV) oxygen saturations during right-sided circulatory failure in each experimental condition. (ANOVA = analysis of variance.)
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Carotid artery pH decreased during both central (p < 0.05) and peripheral (p < 0.01) shunting. Femoral vein pH also decreased during both shunts (p < 0.01) (see Table 1
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Comment
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Pulmonary artery banding in calves reproducibly results in RSCF detectable as an increase in right ventricular and mean pulmonary artery pressures and a decrease in left ventricular end-diastolic pressure. Flows through the pulmonary artery, aorta, and carotid artery are decreased. The effect of decreased systemic flow was detectable as a drop in the mixed venous oxygen saturation. This constellation of changes was useful for testing hemodynamic effects of central and peripheral shunts. We have previously demonstrated that a veno-arterial shunt approaching 50% of cardiac output results in mixed venous oxygen saturation of 60% [10]. This suggests that an animal without pulmonary disease is capable of maintaining adequate oxygenation when only half of the cardiac output is flowing through the pulmonary circulation.
Instituting flow across a right-to-left shunt decreased right-sided and pulmonary artery pressures, and increased flow in the aorta and carotid artery. This was true for both central and peripheral shunts. Direct comparison of the central and peripheral shunts revealed minimally lower blood flow through the carotid artery during peripheral shunting. However, left ventricular end-diastolic pressure was decreased and pulmonary artery flow was increased during peripheral shunting only. Lowering the end-diastolic pressure has the theoretical benefit of decreasing the work of the left ventricle by lowering filling pressures. The decrease in left ventricular end-diastolic pressure may decrease right ventricular afterload and permit increased pulmonary artery blood flow. Augmenting pulmonary artery blood flow leads to a proportional increase in oxygenated blood, which helps to offset the shunt and, perhaps more significantly, contributes to further decompression of the right ventricle. Although statistical significance was not reached, both right ventricular end-diastolic and systolic pressures tended to decrease to a greater degree during the peripheral shunt.
Ventricular stroke work is a load-dependent measure of contractility. Shunting up to 50% of venous return did not alter the work of the right ventricle, suggesting that the fixed obstruction in the pulmonary artery was limiting and that improving right heart pump function would not have improved systemic cardiac output. The peripheral shunt simultaneously resulted in decreased left ventricular stroke work and increased aortic flow. This represents a significant hemodynamic advantage to the left ventricle.
The physiologic cost of a right-to-left shunt is decreased systemic blood oxygen saturation. Oxygen saturation was most affected at the level of admixture between deoxygenated and oxygenated blood. Venous desaturation paralleled arterial desaturation. Mixed venous oxygen saturation, a rough index of mean tissue oxygen levels [11], was not significantly decreased during either shunt. The central shunt resulted in a small decrease in oxygen saturation in the head vessels. Femoral artery and inferior vena cava oxygen saturations were markedly decreased with peripheral shunting, but blood flowing to the head remained fully oxygenated. Arterial blood gas determinations at the carotid artery and femoral vein revealed statistically significant, but not clinically significant changes in pH (>7.3 and >7.2, respectively). This suggests no profound systemic or local acidosis as a result of shunting.
These initial studies indicate that a veno-arterial shunt may be useful in the treatment of perioperative right circulatory failure. One major limitation of the present study is short duration of observed shunt flow. Effects of shunting on arterial oxygen saturation and blood pH may not fully manifest during the time course studied. However, in our early clinical experience with this technique we have successfully shunted a perioperative heart transplant patient for 36 hours with no significant change in arterial saturation or systemic pH and no detectable ischemic changes in the lower extremity. A second limitation is the use of pulmonary artery banding as a model of pulmonary hypertension. We recognize that increasing right ventricular afterload by creating a fixed obstruction is not completely analogous to pulmonary hypertension, but this over-simplistic model does induce similar pathophysiologic responses in the right ventricle and systemic circulation and is reproducible enough to support its use.
The use of short-term veno-arterial shunting as a treatment for both right and left ventricular failure has previously been proposed by several authors. Connolly and associates [12–14] advocated its use based on animal experiments performed in the 1950s and 1960s in which experimentally induced heart failure was relieved by veno-arterial shunting. In these experiments veno-arterial shunting increased aortic root pressure, resulting in improved coronary blood flow and a subsequent improvement in ventricular function as measured by cardiac output [15]. This work culminated in a 1974 report in which 6 clinical cases were presented where veno-arterial shunting was used as short-term therapy for perioperative heart failure [16]. At that time Connolly's group advocated veno-arterial shunting over the then-emerging technology of intraaortic balloon counterpulsation as a better method of increasing coronary blood flow.
In the current era of cardiac replacement therapy we believe that there is a role for veno-arterial shunting as a short-term therapy for perioperative RSCF. Use of this modality presupposes a reversible condition such as transient pulmonary hypertension after cardiopulmonary bypass [17] or right ventricular stunning related to myocardial preservation or air emboli [18–20]. The common clinical manifestation in these scenarios is diminished cardiac output and systemic hypotension resulting in a decrease in mixed venous oxygen saturation. Use of inotropic drugs to augment arterial pressure vasoconstricts pulmonary and peripheral vascular beds and increases afterload, which further limits cardiac output and oxygen delivery to peripheral tissues. Intraaortic balloon pumps support left-sided circulation but do little to assist right ventricular function. On the other hand, right-to-left shunting augments cardiac output, directly resulting in increased systemic blood flow. We believe that the increase in effective cardiac output decreases the need for alpha-agonists and ultimately results in improved native cardiac output due to less pulmonary and peripheral vasoconstriction. The right ventricle is simultaneously decompressed with no appreciable decline in flow through the pulmonary artery. The resulting decrease in septal shift improves left ventricular filling, further improving native cardiac output. Veno-arterial shunting provides a limited window of support, during which time reversible conditions may improve and allow for weaning and discontinuation of the shunt.
Clinical use of a veno-arterial shunt for the treatment of RSCF is not novel. Shunt physiology is the mainstay of therapy for many patients with certain congenital cardiac anomalies and has been used sporadically for patients with end-stage primary pulmonary hypertension [21–25]. In these instances shunt physiology analogous to our central shunt is attained by creation of an atrial septal defect. Use of an atrial septal defect in the proposed situation would be less advantageous as the ability to control flow through the shunt would be limited and the ability to wean shunt flow would be lost. In addition, patients with atrial septal defects may require anticoagulation to decrease the risk of paradoxical emboli.
The present study suggests that shunting to the peripheral circulation may be preferable to a central shunt. Our experiments demonstrate shunting to the peripheral circulation results in better decompression of the right ventricle, improved pulmonary artery flow, and decreased left ventricular work with increased systemic flow. Physiologically, desaturated blood is shunted distal to vital organs, thereby decreasing the risk of the shunt. Systemic pH determinations and mixed venous oxygen saturation indicate that the shunt will be clinically well tolerated. However, the possibility of ischemia in the lower extremities eventually causing systemic acidosis requires further study.
Technical considerations also favor the peripheral shunt for clinical use. Venous inflow can accessed from the femoral vein and delivered to the femoral artery using small cannulas and a centrifugal pump. A femoral-femoral configuration allows chest closure and reduces the risks of infection and bleeding due to the shunt. This circuit may be established either in the operating room or in the cardiothoracic intensive care unit should the patient's condition warrant it postoperatively. Removal of the system may also be performed at the bedside with primary repair of the vessels as necessary. In addition, use of a heparin-bonded circuit makes systemic anticoagulation unnecessary.
This study demonstrates that a veno-arterial shunt has a beneficial effect on the hemodynamic profile of a large animal with induced right circulatory failure. These effects can be obtained at flow rates that do not result in significant oxygen desaturation. These effects are observed when shunting from the right atrium to either the left atrium or femoral artery, but are more pronounced with the peripherally directed shunt. This result may lead to an improved short-term treatment strategy for transplant and left ventricular assist device recipients in whom right circulatory failure develops in the perioperative period.
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Acknowledgments
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Doctor Oz is an Irving Research Scholar.
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Footnotes
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Presented at the Thirty-first Annual Meeting of The Society of Thoracic Surgeons, Palm Springs, CA, Jan 30--Feb 1, 1995.
Address reprint requests to Dr Oz, Department of Cardiothoracic Surgery, Columbia-Presbyterian Medical Center MHB-735, 177 Fort Washington Ave, New York, NY 10032.
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References
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Related Article
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Discussion
Ann. Thorac. Surg. 1995 60: 985.
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Abstract
Introduction
