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Ann Thorac Surg 1997;63:835-837
© 1997 The Society of Thoracic Surgeons

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Case Reports

Monitoring Systemic Venous Oxygen Saturations in the Hypoplastic Left Heart Syndrome

Divisions of Thoracic and Cardiovascular Surgery and Pediatric Cardiology, University of Louisville School of Medicine, Louisville, Kentucky

Accepted for publication October 9, 1996.

	Abstract

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
Although progress has been made in treating hypoplastic left heart syndrome, improvements in perioperative care may further decrease mortality. We present a case in which continuous monitoring of systemic venous oxygen saturation allowed stabilization and successful management of a critically ill infant. Systemic venous oxygen saturation may provide a more accurate representation of a child's clinical status, allowing more rapid intervention and better outcomes.

	Introduction

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
Although much progress has been made in the treatment of infants with the hypoplastic left heart syndrome, overall survival remains low [1]. Improvements in the perioperative care of these infants may substantially decrease mortality. Studies we performed in an animal model of the univentricular circulation suggest that systemic venous oxygen saturations (SvO₂s) can provide a useful guide for therapy [2]. We present a case in which monitoring SvO₂s was instrumental in the successful management of a child with hypoplastic left heart syndrome.

A 2-day-old female neonate was referred for treatment. She was the 3.4-kg product of an uneventful pregnancy and normal spontaneous vaginal delivery. Apgar scores were 8 and 9 at 1 and 5 minutes, and she was stable for the first 12 hours of life. Feeding intolerance then developed, accompanied by progressive tachypnea, tachycardia, groaning, and increasing cyanosis, and she was transferred emergently to our institution.

On admission, the child had a respiratory rate of 72/min, a heart rate of 156 beats/min, temperature of 38.2°C, and blood pressure of 63/43 mm Hg. She was dusky and had petechiae over the head and neck. Distal pulses were weak and capillary refill was delayed at 3 seconds. No cardiac murmurs were appreciated. The initial arterial blood gas measurement is seen in Table 1 (measurement 1). Emergency intubation was performed, and a repeat arterial blood gas measurement was performed on ventilator settings of inspired oxygen concentration of 0.30, IMV 5, and positive inspiratory pressure/positive end-expiratory pressure of 18/4 mm Hg (measurement 2). Intravenous prostaglandin E₁ (0.1 µg·kg^-1·min^-1) administration was started. Early on the morning of the first hospital day the patient's blood pressure decreased to 37/31 mm Hg, and a dopamine infusion was started at 10 µg·kg^-1·min^-1. Due to persistent hypotension, the dopamine dose was soon increased to 20 µg·kg^-1·min^-1, and dobutamine (20 µg·kg^-1·min^-1) administration was started. Arterial blood gas measurements were obtained after the hypotensive episode (measurement 3).

Over the 3 days following admission, the patient had recurrent hemodynamic and respiratory instability, including a sudden respiratory decompensation on the second hospital day. At this time her heart rate decreased to 45 beats/min, her arterial oxygen saturation fell to 23%, and her systolic blood pressure was 40 mm Hg. Her hemodynamics and saturations slowly improved, and Carbair (21% O₂, 5% CO₂) was introduced into the ventilator circuit at a rate of 1 L/min. On hospital day 3 the patient had another respiratory decompensation, requiring hand ventilation, during which she was poorly responsive and showed signs of compromised perfusion. Throughout this period the patient required doses of dopamine and dobutamine of 20 µg·kg^-1·min^-1.

In an attempt to improve the management of the patient's hemodynamic status, on hospital day 4 we placed a 4F oximetric catheter (Abbott Biomedical, North Chicago, IL) via the umbilical vein and positioned its tip in the midportion of the inferior vena cava. Continuous monitoring of SvO₂s was started. Before catheter placement, arterial saturation was 71%, and an arterial blood gas measurement was taken (measurement 4). Venous oxygen saturation at this point was only 37% (measurement 5).

A number of interventions were then performed with the aim of increasing SvO₂. The rate of Carbair administration was first increased to 3 L/min, and the dopamine infusion was decreased to 14 µg·kg^-1·min^-1. Dobutamine administration was decreased to 16 µg·kg^-1·min^-1. Each intervention had the effect of increasing SvO₂ incrementally, and after supplemental N₂ was added to lower the inspired oxygen fraction to 0.17 on hospital day 5, SvO₂ finally increased to 59%. Measurement of arterial blood gases showed no base deficit (measurement 6). Systolic blood pressure ranged from 65 to 86 mm Hg.

With the patient hemodynamically more stable, a repeat echocardiogram showed substantial improvement in tricuspid valvular function, with only mild (1⁺) regurgitation. Accordingly, the decision was made to proceed with operative intervention. Before the operation, the patient was able to be weaned to continuous positive airway pressure and then extubated, with a systemic arterial oxygen saturation (SaO₂) of 84% and SvO₂ of 70% on room air. Just before the operation, the patient had her dose of dopamine decreased to 11 µg·kg^-1·min^-1 and her dose of dobutamine decreased to 14 µg·kg^-1·min^-1.

The patient underwent first-stage palliation (Norwood procedure). A 3.5-mm polytetrafluoroethylene modified Blalock-Taussig shunt was placed. Pulmonary homograft tissue was used to augment the aortic arch. Intraoperative epicardial echocardiography showed mild (1⁺) tricuspid regurgitation off bypass.

The oximetric catheter was left in place for initial postoperative management. The patient had a steady recovery. Cardiac catheterization before discharge revealed good ventricular function, an unobstructed aortic arch, and mild (1⁺) tricuspid valve regurgitation.

	Comment

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
The hemodynamic instability that characterizes many infants with the hypoplastic left heart syndrome contributes to the continued high mortality associated with the defect. The unique parallel arrangement of the resistances in the systemic and pulmonary circulations is the primary factor contributing to this instability, with small perturbations in flows leading to potentially large derangements in the balance between the two circulations.

Diligent attempts to "balance" the pulmonary and systemic circulations appear to be met with some improvement in survival [3]. Unfortunately, there are few easily obtainable measurements to indicate when this balance has been achieved. Some of the more easily obtained bedside measurements, such as SaO₂, may not reflect an "unbalanced" flow ratio until the infant is extremely unstable. Rossi and associates [4] recently described a number of instances in which patients having an adequate SaO₂ progressed to rapid decompensation and even death. These patients likely had an excessively high pulmonary-to-systemic flow ratio (Q_P/Q_S ratio), which maintained adequate pulmonary flow, as reflected in an elevated SaO₂, but produced inadequate systemic flow to sustain end-organ function.

Although it has been suggested that obtaining "ideal" blood gas levels, defined as a pH of about 7.4, carbon dioxide tension of 35 to 40 mm Hg, and oxygen tension of about 40 mm Hg, reflects a balanced Q_P/Q_S ratio [5], it is possible to have optimal arterial blood gas levels and still have unbalanced flows. The present case demonstrates this with our patient having an arterial pH of 7.42, carbon dioxide tension of 36 mm Hg, and oxygen tension of 34 mm Hg and still having an SvO₂ of only 37%, implying that there was an excessively high Q_P/Q_S ratio. Conversely, arterial blood gases with an arterial oxygen tension greater than 40 mm Hg do not necessarily imply excessive pulmonary flow.

Accordingly, we have recently used both a computer model and an animal model of the univentricular circulation to try to find measurements that would more accurately reflect the patient's clinical status and the balance of flows in the systemic and pulmonary circulations [6]. This research suggested that SvO₂ is a good marker for both the Q_P/Q_S ratio and oxygen delivery. When SvO₂ is maximized, a Q_P/Q_S ratio that produces optimal oxygen delivery has been reached.

Prompted by these results, we have been following SvO₂ via placement of an oximetric catheter in our patients with the hypoplastic left heart syndrome. We have found the data that the catheters provide are extremely useful, as is clearly demonstrated in the present case. Persistent decreased SvO₂s, even in the face of adequate SaO₂ and arterial blood gases, alert us to situations in which an excessive Q_P/Q_S ratio may be leading to clinical instability but has not yet affected the SaO₂, thus allowing for earlier intervention. Continuous monitoring gives us immediate feedback regarding the effectiveness of interventions. By choosing therapeutic maneuvers aimed at increasing SvO₂, we have been able to ameliorate the clinical status of a number of unstable infants, the most dramatic instance being the case reported here. It is our hope that wider application of this approach may lead to improved outcomes for children born with these difficult defects.

	Acknowledgments

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
This study was supported in part by a grant from the Alliant Community Trust Fund. Doctor Riordan is a Cardiothoracic Research Fellow, Funded by Alliant Community Trust Fund.

	Footnotes

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
Address reprint requests to Dr Austin, Division of Thoracic and Cardiovascular Surgery, University of Louisville School of Medicine, 201 Abraham Flexner Way, Suite 1200, Louisville, KY 40292.

	References

Top Footnotes Abstract Introduction Comment Acknowledgments References

 

1. Weldner PW, Meyers JC, Gleason MM, et al. The Norwood operation and subsequent Fontan operation in infants with complex congenital heart disease. J Thorac Cardiovasc Surg 1995;109:654–62.[Abstract/Free Full Text]
2. Riordan CJ, Randsbaek F, Storey JH, Montgomery WD, Santamore WP, Austin EH. Balancing pulmonary and systemic arterial flows in parallel circulations: the usefulness of monitoring systemic venous oxygen saturations. Cardiol Young (in press).
3. Murdison KA, Baffa JM, Farrell PE, Chang AC, Barber G, Norwood WI Jr. Hypoplastic left heart syndrome: outcome after initial reconstruction and before modified Fontan procedure. Circulation 1990;(Suppl 4):199–207.
4. Rossi AF, Sommer RJ, Lotvin A, et al. Usefulness of intermittent monitoring of mixed venous oxygen saturation after stage I palliation for hypoplastic left heart syndrome. Am J Cardiol 1994;73:1118–23.[Medline]
5. Pigott JD, Murphy JD, Barber G, Norwood WI Jr. Palliative reconstructive surgery for hypoplastic left heart syndrome. Ann Thorac Surg 1988;45:122–8.[Abstract]
6. Barnea O, Austin EH, Richman B, Santamore WP. Balancing the circulation: theoretic optimization of pulmonary/systemic flow ratio in hypoplastic left heart syndrome. J Am Coll Cardiol 1994;24:1376–81.[Abstract]

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christopher J. Riordan Erle H. Austin, III Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Riordan, C. J. Articles by Austin, E. H. Search for Related Content PubMed PubMed Citation Articles by Riordan, C. J. Articles by Austin, E. H., III