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Ann Thorac Surg 2006;81:1429-1434
© 2006 The Society of Thoracic Surgeons

Original article: Cardiovascular

Inhaled Nitric Oxide Use in Bidirectional Glenn Anastomosis for Elevated Glenn Pressures

Hemant S. Agarwal, MBBSa,*, Kevin B. Churchwell, MD, FAAPa, Thomas P. Doyle, MDb, Karla G. Christian, MDc, Davis C. Drinkwater, Jr, MDc, Daniel W. Byrne, MSd, Mary B. Taylor, MDa

a Department of Pediatrics, Division of Pediatric Critical Care, Vanderbilt University School of Medicine, Nashville, Tennessee
b Department of Pediatrics, Division of Pediatric Cardiology, Vanderbilt University School of Medicine, Nashville, Tennessee
c Department of Pediatric Cardiothoracic Surgery, Vanderbilt University School of Medicine, Nashville, Tennessee
d Department of Biostatistics, Vanderbilt University School of Medicine, Nashville, Tennessee

Accepted for publication November 3, 2005.

* Address correspondence to Dr Agarwal, Pediatric Critical Care, Vanderbilt Children’s Hospital, 2200 Children’s Way, 5121 B Doctors’ Office Tower, Nashville, TN 37232-9075 (Email: hemant.agarwal{at}vanderbilt.edu).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Children frequently undergo bidirectional Glenn anastomosis in the staged surgical management of single ventricle physiology. The purpose of our study was to investigate the role of inhaled nitric oxide therapy in children with marked elevations in Glenn pressures after this surgery.

Methods: A retrospective study over a 30-month period was performed. The effect of inhaled nitric oxide therapy was analyzed in children with marked elevations of Glenn pressures resulting in decreased systemic perfusion. Effects on Glenn pressures, respiratory indices, and systemic perfusion were evaluated after initiation of nitric oxide therapy and compared with baseline parameters.

Results: Sixteen patients were placed on nitric oxide therapy for marked elevations of Glenn pressures (22.4 ± 3.9 mm Hg). In the 11 responsive patients, there were significant reductions in Glenn pressures (from 22.4 mm Hg to 17.1 mm Hg, p < 0.001) and significant improvement in partial pressure of oxygen to fraction of inspired oxygen ratio (from 49 to 74.3, p = 0.001) and oxygenation index (from 17 to 12, p = 0.005). There was simultaneous significant reduction in inotrope score (from 14.9 to 11.4, p < 0.001) and fluid volume support (from 11.4 mL/kg to 2.3 mL/kg, p < 0.001) in the responsive patients. Five patients that failed to show any response were found, subsequently, to have an anatomic lesion.

Conclusions: Inhaled nitric oxide produces significant reduction in Glenn pressures and improvement in systemic perfusion and pulmonary gas exchange in patients with marked elevations of Glenn pressures after bidirectional Glenn anastomosis. Patients who fail to respond should be investigated for an anatomic lesion.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The bidirectional Glenn anastomosis (BDG) is an operation that diverts systemic venous blood from the superior vena cava to both lungs, thereby providing effective pulmonary blood flow in children with single ventricle physiology. This procedure, based on initial experimental work of Carlon and colleagues [1] and subsequently performed for the first time by Haller and colleagues [2] in 1966, has become a well-defined procedure in the staged surgical management of children with single ventricle physiology. However, some of these children demonstrate postoperative complications, including elevated Glenn pressures, superior vena cava syndrome [3], and low systemic oxygen saturations [4], despite preoperative evaluations including cardiac catheterization. Inhaled nitric oxide (iNO), a selective pulmonary vasodilator, may have a therapeutic role in the immediate postoperative period in these patients. Evidence for use of iNO postoperatively in children undergoing BDG is limited with equivocal results [5–8]. The aim of the present study was to review our experience of iNO therapy in children undergoing BDG with marked elevations in Glenn pressures.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
A retrospective study was conducted in the pediatric cardiac intensive care unit of the Monroe Carell Jr. Children’s Hospital at Vanderbilt. Institutional Review Board approval was obtained on May 5, 2002 and patient consent was waived for the study. Chart review of all patients who had undergone BDG over a period of two and half years from August 2000 to January 2003 was undertaken. Demographic characteristics such as age, weight, and sex, preoperative cardiac defect, and baseline oxygen saturations were noted. Preoperative cardiac catheterization results were examined for pulmonary artery pressure and pulmonary vascular resistance. Operative records were reviewed for cardiopulmonary bypass time, aortic cross-clamp time, and surgical procedures. Postoperative transesophageal echocardiography was reviewed for pressure gradient or stenosis across the Glenn shunt.

Postoperatively, Glenn pressures were recorded in all patients. The Glenn pressures were measured in the patients on the ventilator as they were placed on low positive end expiratory pressure (PEEP) of 0–2 cm of water (H2O). Marked elevation of Glenn pressures was defined as elevated Glenn pressures (~ 20 mm Hg) in association with decreased systemic perfusion and hemodynamic instability. Patients with marked elevation of Glenn pressures were placed on iNO therapy. The iNO was delivered to the patient as a continuous flow into the inspiratory limb of the ventilatory circuit (INOVENT; GE Healthcare, UK). A microprocessor-controlled system allowed 1 to 80 parts per million (ppm) NO delivery and a chemiluminescence method (Pulmonox system; Messer Griesheim, Vienna, Austria) continuously measured NO and nitrogen dioxide in the circuit. Patients were initially placed on 20 ppm of iNO and increased to 40 ppm if they failed to respond, as evidenced by no significant reduction in Glenn pressures. Patients were labeled as nonresponders if no response was seen at 40 ppm. Further evaluation, including echocardiography and cardiac catheterization, was undertaken in nonresponders to rule out anatomic lesions. Patients were labeled as responders to iNO if they demonstrated a reduction in Glenn pressures and an improvement in systemic perfusion. The iNO was weaned in the responsive patients as per institutional weaning protocol after 1 hour of stabilization. All patients were mechanically ventilated using synchronized intermittent mandatory ventilation with pressure control and pressure support mode of ventilation on Servo 300A ventilators (Siemens-Elema AB, Solna, Sweden). Patients were initially placed on low PEEP (0–2 cm H2O) and 8–10 mL/kg tidal volume breaths. Mechanical ventilation and oxygen therapy were based on maintenance of oxygen saturation between 80% and 85% and normal partial pressure of carbon dioxide (PaCO 2). Sedation was used very judiciously in our patient population and pressure support ventilation was encouraged. Patients were rapidly weaned and extubated after their initial stabilization and improvement in systemic perfusion to encourage spontaneous ventilation. Continuous infusions of dopamine, dobutamine, epinephrine, and milrinone for inotrope support and crystalloid solutions for fluid volume resuscitation were administered, respectively, when necessary. Indication for inotrope usage and fluid volume support were at the discretion of the bedside physician to maintain adequate systemic perfusion based on blood pressure, heart rate, PaO 2 levels, and base deficit.

To analyze systemic perfusion, the heart rate, systemic blood pressure, inotrope score [9], fluid volume resuscitation, and base deficit of all patients receiving iNO therapy was studied. To analyze the effect of iNO therapy on pulmonary gas exchange, ventilator parameters such as PEEP, peak inspiratory pressure (PIP), inspiratory time, respiratory rate, and fraction of inspired oxygen (FiO 2) were noted. Arterial blood gas samples were analyzed for partial pressure of oxygen (PaO 2), PaCO 2, oxygen saturation, and base deficit. Partial pressure of oxygen to fraction of inspired oxygen ratio (PaO 2/FIO 2) and oxygenation index (OI) (OI = mean arterial pressure x FiO 2/PaO 2) were calculated based on the above parameters. The effect of iNO therapy in all patients with elevated Glenn pressures were evaluated 1 hour and 3 hours after initiation of iNO therapy.

The results were analyzed using the statistical software SPSS (SPSS Inc, Chicago, IL) and R (www.r-project.org). All continuous results are expressed as mean ± standard deviation. A {chi}2 or Fisher’s exact test were used for categorical comparisons. The response to iNO therapy was studied at 1 hour and 3 hours after initiation of iNO therapy in comparison with baseline values before starting iNO therapy by means of the 2-tailed paired t test or the Wilcoxon signed rank test.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
A bidirectional Glenn anastomosis was performed in 44 infants over a period of 30 months (Table 1). Sixteen patients received iNO therapy in the immediate postoperative period for marked elevations in Glenn pressures (22.4 ± 3.9 mm Hg). The iNO was initiated within 3 hours of surgery in the operative room coming off cardiopulmonary bypass or in the intensive care unit in all 16 patients. Patients with marked elevation of Glenn pressures had significant elevation of preoperative pulmonary artery pressure (p = 0.001) and pulmonary vascular resistance (p = 0.006). No significant difference in the demographic characteristics, preoperative baseline oxygen saturation, and preoperative cardiac lesions was seen in these patients (Table 1). No significant difference was observed in the operative details of patients requiring iNO therapy for elevated Glenn pressures. Fourteen of 16 patients requiring iNO therapy underwent additional cardiac surgery: 5 patients underwent pulmonary artery reconstruction, 2 patients had a Damus-Kaye-Stansel procedure, 2 patients had a bilateral bidirectional Glenn procedure, 2 patients had ligation of the left superior vena cava, 1 patient had left atrial reduction, 1 patient had partial anomalous pulmonary venous return correction, and 1 patient had a pulmonary valvectomy. A Blalock-Taussig shunt was preserved in 3 patients to improve oxygenation. A longer cardiopulmonary bypass time was seen in the group of 16 patients receiving iNO although it did not reach statistical significance (p = 0.062) (Table 1).


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  		Table 1 Preoperative and Operative Data of Patients Undergoing BDG
 
Eleven patients (69%) had a positive response to iNO therapy as seen by a significant reduction in the Glenn pressures (p = 0.006 at 1 hour and p < 0.001 at 3 hours post therapy). Patients with marked elevation of Glenn pressures had a higher inotrope score (p < 0.001), required greater fluid volume support to maintain their systemic perfusion (p < 0.001), and had a higher negative base deficit (p = 0.019) (Table 2). After initiation of iNO therapy there was a significant reduction in inotrope score (p < 0.001 at 1 and 3 hours), the need for fluid volume resuscitation (p = 0.003 at 1 hour and p = 0.001 at 3 hours), and an improvement in the base deficit (p = 0.002 at 1 hour and p = 0.006 at 3 hours) (Table 3). On evaluation of the respiratory indices, there was a significant improvement in the PaO 2/FIO 2 ratio (p = 0.002 at 1 hour and p = 0.001 at 3 hours) and a significant reduction of OI (p = 0.003 at 1 hour and p = 0.005 at 3 hours) after initiation of iNO therapy in the 11 responsive patients (Table 4). No significant reduction of PaCO 2 was observed at 3 hours of therapy (p = 0.35).


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  		Table 2 Immediate Postoperative (Prior to iNO Therapy) Data of Patients
 

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  		Table 3 Effect of iNO Therapy on Glenn Pressures and Systemic Perfusion
 

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  		Table 4 Effect of iNO Therapy on Respiratory Indices
 
Five patients failed to show a therapeutic response to iNO therapy as evidenced by no reduction of their elevated Glenn pressures. All 5 patients had elevated preoperative pulmonary vascular resistance and one patient had Blalock-Taussig shunt. All of these patients were subsequently found to have a hemodynamically significant anatomic lesion (Table 5). All 5 patients required a second operative procedure with 4 patients surviving.


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  		Table 5 Failure of iNO Therapy
 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
In our study iNO therapy produced a statistically significant reduction in Glenn pressures, correlating with an improvement in systemic perfusion postoperatively in children undergoing BDG. Glenn pressures fell from 22.4 mm Hg to 19.1 mm Hg at 1 hour and 17.1 mm Hg at 3 hours, respectively, in 69% of patients after iNO initiation. In the remaining 31% of patients, an anatomic lesion explained the persistence of elevated Glenn pressures and decreased systemic perfusion.

Patients with elevated Glenn pressures had a statistically significant elevation of preoperative pulmonary artery pressures (17.5 ± 4.0 mm Hg) and pulmonary vascular resistance (2.6 ± 1.1 Woods units x meter2) in our study. The reason for this elevation is unclear but it is well known that continuous release of endogenous nitric oxide from the pulmonary endothelium plays an important role in maintaining basal pulmonary vasorelaxation and low pulmonary artery pressures. Potentially, these patients could have poor baseline endogenous nitric oxide synthesis and/or release presenting as elevated baseline pulmonary vascular resistance. Furthermore, endothelial dysfunction after cardiopulmonary bypass [10] produces additional impairment of endogenous nitric oxide release. These two factors most likely contributed to the marked elevation of Glenn pressures observed. Response to iNO therapy in our study population is in contrast to previous studies that failed to show a beneficial effect of iNO in BDG patients [6, 8]. The postoperative Glenn pressures (17 ± 2 mm Hg and 17 ± 3 mm Hg) in their studies [6, 8] were lower than our patient population (22.4 ± 3.9 mm Hg). In our study, we failed to observe any further reduction in Glenn pressures 3 hours post-iNO therapy when pressures reached 17.1 ± 3.4 mm Hg. The iNO causes vasodilatation and reduction in pulmonary vascular resistance in the presence of pulmonary vasoconstriction. It has very little effect on pulmonary vascular resistance if the pulmonary vascular tone is not elevated [11] as observed in studies by Adatia and colleagues [6, 8].

Bidirectional Glenn shunt physiology requires a pressure gradient to be maintained between the superior vena cava and the pulmonary vasculature. It is, however, a low pressure circuit and any elevation of pulmonary artery resistance in BDG can be overcome by only marginal increases in superior vena caval pressure. A greater fluid volume and inotrope support was required initially in our patients to overcome the elevated Glenn pressures and to maintain systemic perfusion. The drop in Glenn pressures after iNO therapy facilitated forward flow from the superior vena cava to the pulmonary circulation, improving the stroke volume of the single ventricle and systemic perfusion, correlating with a significant reduction in inotrope score and fluid volume support.

Serial evaluations of PaO 2/FIO 2 ratio and OI were incorporated in our study to assess pulmonary gas exchange. The PaO 2/FIO 2 ratio is a convenient and widely used index of oxygen gas exchange [12, 13]. Similarly, OI is an important index to monitor, serially, mechanical ventilation support and oxygenation as it takes PEEP, PIP, inspiratory time, and FIO2 into consideration. The specific accuracy of pulmonary indices in patients with single ventricle physiology can be questioned. Although we believe that besides the absolute number the trends over time are an accurate indicator of an increase or loss in pulmonary function in these patients. Initially, the respiratory indices were potentially maintained by sustaining the pulmonary perfusion with increased inotrope and fluid volume support. After iNO therapy, although there seemed to be no significant difference in PaO 2, evaluation of respiratory indices revealed a significant improvement in the PaO 2/FIO 2 ratio and a reduction in OI at 1 and 3 hours post-iNO in the responsive patients. The iNO probably produced this improvement in pulmonary gas exchange not only by a reduction in Glenn pressures but also by amplifying the local alveolar hypoxic response [14], resulting in redistribution of blood flow to lung regions with a better ventilation to perfusion ratio [15]. The intrapulmonary distribution of blood flow and ventilation (V/Q distribution) that determines pulmonary gas exchange is commonly impaired after a cardiopulmonary bypass procedure [16]. The patient population in our study had a longer cardiopulmonary bypass time as compared with patients without elevated Glenn pressures, although it did not reach statistical significance (p = 0.062).

The iNO therapy did not cause sustained reduction in PaCO 2 levels beyond 1 hour as appropriate ventilator changes were made to maintain PaCO 2 levels in the normal range. The cerebral and pulmonary circulations are connected in series in BDG leading to direct competition of cerebral and pulmonary autoregulatory mechanisms. Hypercarbia has been demonstrated to improve cerebral blood flow, thereby increasing pulmonary blood flow and oxygenation after BDG in patients with normal Glenn pressures [17–19]. We maintained PaCO 2 levels in the normal range as our patient population had markedly elevated Glenn pressures and hypercarbia is known to increase pulmonary vascular resistance.

Five patients in our study failed to show a significant response to iNO as demonstrated by no changes in Glenn pressures, inotrope score, fluid volume resuscitation, PaO 2/FIO 2 ratio, and OI. Anatomic lesions were found in all 5 patients, requiring a second operative procedure. A failure of significant response to iNO can be helpful to differentiate reversible elevated pulmonary vascular resistance from residual anatomic lesions [20].

Additionally, using logistic regression analysis our study demonstrates that all patients with preoperative pulmonary artery pressure 16 mm Hg or greater, followed by postoperative Glenn pressure 19 mm Hg or greater, required iNO in the immediate postoperative period. Several studies have identified preoperative pulmonary artery pressure less than 15 mm Hg as a desirable criterion to perform BDG [4, 21–24] and operations performed in patients with elevated pulmonary artery pressures have an increased risk of poor outcome [3, 25, 26].The iNO may be beneficial to manage BDG patients with elevated preoperative pulmonary artery pressures and pulmonary vascular resistance. Although our study had the limitations of no control group, cardiac output measurements, serum lactate levels, mixed venous oxygen saturations, or pulmonary function tests, we believe that a properly constructed randomized prospective study will be beneficial to validate our results.

We conclude that iNO therapy significantly reduces Glenn pressures and improves systemic perfusion and pulmonary gas exchange in a subset of patients with marked elevations in Glenn pressures after BDG. The iNO may have a therapeutic role in patients with elevated preoperative pulmonary artery pressures and pulmonary vascular resistance who undergo BDG. Patients who fail to respond to iNO should be evaluated for anatomic lesions.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
The authors express their gratitude to Frederick E. Barr, MD, for a critical review of the manuscript and his suggestions. This work has been supported in part by grant M01 RR-00095 from the National Center for Research Resources, National Institutes of Health.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

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