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Ann Thorac Surg 1998;66:664-667
© 1998 The Society of Thoracic Surgeons

Supplement

The physiology of the bidirectional cavopulmonary connection

Robert M. Freedom, MDa, David Nykanen, MDa, Lee N. Benson, MDa

a Division of Cardiology, Department of Paediatrics, The Hospital for Sick Children and University of Toronto Faculty of Medicine, Toronto, Ontario, Canada

Address reprint requests to Dr Freedom, The Hospital for Sick Children, Rm 1503C, 555 University Ave, Toronto, ON, Canada M5G 1X8

Presented at the Workshop on "One and One-Half Ventricle Repairs," Gubbio, Italy, Dec 6–7, 1996.

Abstract

This article reviews the indications for the bidirectional cavopulmonary connection and demonstrates its efficacy in reducing mortality for the Fontan procedure. The indications for adding an additional source of pulmonary blood flow to the bidirectional cavopulmonary connection are discussed, but this issue remains controversial. Also unclear is whether the bidirectional cavopulmonary connection promotes symmetric growth of the pulmonary arteries, or whether growth of the left pulmonary artery is disadvantaged. Finally, systemic venous collateralization is a well-recognized sequel after cavopulmonary connection. The clinical implications of this collateralization are reviewed.

The classic Glenn shunt performed now for nearly 40 years has provided excellent and long-term palliation of complex cardiac malformations associated with low pulmonary blood flow, low pulmonary arterial pressures, and low pulmonary vascular resistance [1–7]. This particular shunt enhances systemic arterial oxygen saturation by increasing the effective pulmonary blood flow without increasing total pulmonary blood flow and without volume loading the ventricle. However, this procedure was largely abandoned by the mid-1970s because of the introduction of the classic Fontan operation as initially applied to patients with tricuspid atresia and then extended to patients with a wide range of congenitally malformed hearts not amenable to a biventricular repair [3, 7, 8]. In addition, in patients who had undergone the classic unilateral cavopulmonary connection, there was redistribution of blood flow to the dependent and thus basilar lobes of the lung [9]. Even more concerning were the increasing reports of acquired pulmonary arteriovenous malformations in the lung ipsilateral to the Glenn shunt as well as other complications including difficulties at subsequent repair [10]. These particular malformations were particularly egregious and not amenable to surgical or catheter-based intervention [11].

The bidirectional cavopulmonary connection

In the strategies employed to improve the outcome of the Fontan operation, many now advocate staging with a bidirectional cavopulmonary connection, the so-called hemi-Fontan procedure [12–16]. Most centers have adopted this strategy, including our own.

The bidirectional cavopulmonary shunt, like the classic Glenn anastomosis, by virtue of increasing the effective pulmonary flow improves the systemic arterial oxygen saturation, volume unloads the ventricle, and also alters the ventricular geometry, whether the ventricle is of right or left ventricular morphology [12–16]. Seliem and colleagues [17] have documented the changes in right ventricular end-diastolic volume and geometry early after the hemi-Fontan procedure in 35 patients with the hypoplastic left heart syndrome who had earlier undergone the first-stage Norwood procedure. After the hemi-Fontan procedure the right ventricular end-diastolic volume decreased by 33%. The right ventricular anterior wall increased in thickness by only 13%, and the wall mass/end-diastolic volume ratio increased by 111%.

There is certainly not unanimity as to what are the desirable criteria to perform a bidirectional cavopulmonary connection [13–16, 18–20]. Most authors would suggest that the mean pulmonary artery pressure should be less than 18 mm Hg, or ideally less than 15 mm Hg, with a calculated pulmonary vascular resistance less than 2.0 units/m2. Although there are some general guidelines as to the caliber of the pulmonary arteries that are acceptable for a bidirectional cavopulmonary connection, it is acknowledged that these measurements do not take into consideration the compliance of the vascular bed, the so-called maturity of the pulmonary vascular bed, or the very peripheral and intraparenchymal pulmonary arteries. The Nakata index of the 50 patients reported by Pridjian and colleagues [21] in their analysis of the outcome of the bidirectional cavopulmonary connection ranged from 80 to 821 mm2/m2 with a mean of 318 mm2/m2.

The bidirectional cavopulmonary anastomosis has been performed in ever younger patients [14, 19–22]. Reddy and colleagues [22] have reported the results of primary bidirectional superior cavopulmonary shunt in 9 infants between 1 and 4 months of age, with a mean age of 77 days and a median of 56 days. The mean preoperative mean pulmonary artery pressure was 12.8 mm Hg, the mean pulmonary vascular resistance 1.4 Wood units, and the mean ventricular end-diastolic pressure 6.8 mm Hg. The mean Nakata index was 109.64, with a range of 80.21 to 308.

One of the mechanisms by which the bidirectional cavopulmonary connection improves the systemic arterial oxygen saturation is to increase the so-called effective pulmonary blood flow [12, 13, 15]. With improvement in oxygenation, one would anticipate a reduction in the patient’s hemoglobin level and hematocrit. If the viscosity were significantly increased before the bidirectional cavopulmonary connection, a reduction of the blood viscosity would increase pulmonary flow. In this regard, Salim and colleagues [17] have studied the pulmonary/systemic blood flow ratio about 1.2 years after the bidirectional cavopulmonary connection was carried out in 29 patients. The pulmonary/systemic blood flow ratio calculated for all 29 patients was 0.58 ± 0.09. Because pulmonary venous desaturation was excluded, the calculated pulmonary/systemic blood flow ratio included that portion of pulmonary blood flow that became oxygenated, ie, the effective pulmonary blood flow.

The role of age in the consideration of a bidirectional cavopulmonary connection

Substantial clinical data have accumulated that the bidirectional cavopulmonary connection provides excellent early and midterm palliation, with a relatively low incidence of reoperation [12–22]. Gross and colleagues [23] have studied those maturational and hemodynamic factors predictive of increased hypoxemia after the bidirectional cavopulmonary connection. Their data indicated that patients who underwent the bidirectional cavopulmonary connection at greater than 3.9 years of age or with a body surface area greater than 0.65 m2 were at significantly increased risk for worrisome hypoxemia, which they defined as a systemic oxygen saturation of 75% or less. This should not be surprising considering the maturational decrease in the apportionment of systemic blood flow to the upper versus the lower body segment. Forbes and colleagues [24] have also studied the influence of age on the effect of the bidirectional cavopulmonary connection on left ventricular volume, mass, and ejection fraction. Their data indicated that the bidirectional cavopulmonary connection facilitated ventricular volume unloading and regression of ventricular mass in younger children (<3 years of age), and that the beneficial effect of this operation on ventricular end-diastolic volume and mass was clearly age-dependent. Furthermore their data showed that the older patient benefited less in terms of enhancing the systemic oxygen saturation from the bidirectional cavopulmonary connection.

The role of accessory pulmonary blood flow

The role of accessory pulmonary blood flow in the setting of a bidirectional cavopulmonary connection remains contentious. Mainwaring and colleagues [25] contend that there is a trend toward improved survival in those patients in whom accessory pulmonary blood flow is eliminated. Furthermore, they indicate that accessory pulmonary blood flow increases the likelihood of developing effusions and prolonging hospital stay. We wonder whether these inferences would be true in the older patient with a body surface area greater than 0.7 m2 when the upper segment-to-lower-segment ratio is disadvantageous. Frommelt and colleagues [26] have also addressed the issue of outcome in those patients with an additional source of pulmonary blood flow after a bidirectional cavopulmonary connection. Twenty-one of the 43 patients who had undergone a bidirectional cavopulmonary connection had an additional source of pulmonary blood flow. Although this group had higher postoperative oxygen saturations, they also had higher central venous pressures and were at risk for the late development of chylothorax. Another concern about forward flow from the ventricle to the pulmonary artery after construction of a bidirectional cavopulmonary connection is the anastomotic aneurysm [27].

Pulmonary artery growth patterns after the bidirectional cavopulmonary connection

Data from Mendelsohn and colleagues [28] based on 30 patients undergoing the bidirectional cavopulmonary connection revealed a significant decrease in mean pulmonary artery pressure and a 32% decrease in indexed cross-sectional pulmonary artery area. Their data demonstrated a 13.5% decrease in the pulmonary artery contralateral to the bidirectional cavopulmonary connection without a significant change in the ipsilateral pulmonary artery diameter. They suggested that the cause of the decrease in size of the central pulmonary artery contralateral to the bidirectional cavopulmonary connection reflects diminished blood flow to that lung. If as their data suggested the bidirectional cavopulmonary connection does not promote pulmonary artery growth, and if pulmonary artery size is a risk factor for the Fontan operation, they ask whether the bidirectional cavopulmonary connection should be used as a staging maneuver. Reddy and colleagues [29], in a more recent publication, advocate the use of lower lobe pulmonary artery indices. They believe that a more appropriate measurement of pulmonary artery growth is the indexed cross-sectional area of the lower lobe branches of the right and left pulmonary arteries. Their data based on pulmonary artery indices, including the lower lobe index, did not change significantly after the bidirectional cavopulmonary connection and did not correlate with Fontan outcome. Although there is clearly an influence of pulmonary artery size on the postoperative hemodynamics of the Fontan procedure, the lower limits of indexed pulmonary artery dimension have not been fully resolved. Others have also shown relatively little growth of the left pulmonary artery after the bidirectional cavopulmonary connection [30]. Data show that a smaller pulmonary artery size is disadvantageous after the Fontan procedure, which is certainly not surprising [31].

The role of ventricular volume reduction in the genesis of systemic outflow tract obstruction in functionally one-ventricle hearts

The particular relationship between pulmonary artery banding and the development of subaortic obstruction in hearts with double-inlet left ventricle, rudimentary right ventricle, and discordant ventriculoarterial connections is complex [32–38]. Subaortic stenosis from a restrictive ventricular septal defect (VSD) occurs after pulmonary artery banding, and with both arterial outlets obstructed (the pulmonary artery by the pulmonary artery band and the systemic outlet from the restrictive VSD), myocardial hypertrophy is inevitable [33–41]. What remains contentious is the specific role of the pulmonary artery band in the genesis of the restrictive VSD. Rao [35] takes the position that it is the natural tendency for the moderate-sized VSD in these patients to become smaller that promotes the subaortic stenosis. Others take the position that reduction of left ventricular end-diastolic volume and remodeling of the left ventricle cause VSD restriction [36, 38]. We have taken the position for many years that pulmonary artery banding causes VSD restriction, subaortic stenosis, and then myocardial hypertrophy [32, 33, 39]. But it is likely that pulmonary artery banding by promoting both ventricular hypertrophy and some reduction of left ventricular end-diastolic volume accelerates the natural history of the moderate-sized muscular VSD to become smaller. Data published by Donofrio and colleagues [36] are interpreted to suggest that diminution in VSD size occurs early and is related to an acute alteration in ventricular geometry accompanying the reduction in left ventricular end-diastolic volume. Their own data indicated that this ventricular unloading was greater after a bidirectional cavopulmonary connection than after pulmonary artery banding. Furthermore, because systemic outflow tract obstruction has been documented after the Fontan operation, it is too simplistic to suggest that only one factor is responsible for the change in form and function of the VSD in these hearts [42].

Systemic venous collaterization and the bidirectional cavopulmonary connection

Gatzoulis and colleagues [43] have documented some of the causes of increasing cyanosis in 3 patients after the bidirectional cavopulmonary connection. They have shown that some "abnormal" venous pathways manifest themselves, dilate, and become hemodynamically important after surgical cavopulmonary anastomoses. Magee and associates [44] from the Toronto Hospital for Sick Children have also investigated systemic venous collateralization after the bidirectional cavopulmonary connection. Significant venous collateral formation was identified in 31% of our patients. Some of these connections have a systemic vein-to-pulmonary vein connection, thus promoting a right-to-left shunt.

Aortopulmonary collateral vessels after the bidirectional cavopulmonary connection

The development and recognition of aortopulmonary collateral vessels are well-known after bidirectional cavopulmonary connection [45–47], and as competitive flow, their presence has been implicated in the presence of increased incidence of pleural effusions and prolonged hospital stay after the Fontan operation [15, 25, 46, 47].

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