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Ann Thorac Surg 2004;77:48-52
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

High systemic vascular resistance and sudden cardiovascular collapse in recovering norwood patients

Gail E. Wright, MDa, Dennis C. Crowley, MDa, John R. Charpie, MD, PhDa, Richard G. Ohye, MDb, Edward L. Bove, MDb, Thomas J. Kulik, MDa*

a Division of Pediatric Cardiology, Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Michigan, USA
b Section of Cardiac Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA

Accepted for publication July 1, 2003.

* Address reprint requests to Dr Kulik, C.S. Mott Children's Hospital, University of Michigan Medical Center, Womens L1242, Box 02024, 1500 East Medical Center Dr, Ann Arbor, MI 48109-0204, USA.
e-mail: tkulik{at}med.umich.edu


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Sudden death, remote from surgery, in patients with hypoplastic left heart syndrome (HLHS) after Norwood palliation is an important problem. The episodic nature of this syndrome has made its cause(s) difficult to ascertain. Observations made in hospitalized Norwood patients may afford insight into the pathophysiology of sudden death among these patients.

METHODS: We conducted a retrospective chart review.

RESULTS: Five patients with HLHS experiencing unremarkable recoveries from Norwood palliation, still hospitalized but extubated (only 1 in intensive care), had unexpected, acute decompensation 8 to 15 days postoperatively. All had acutely decreased peripheral perfusion; severe metabolic acidosis (mean HCO3 = 9 mEq/L, range 6 to 11 mEq/L; mean arterial lactate = 16 mmol/L, range 10 to 20 mmol/L, normal less than 2 mmol/L); relatively high arterial pO2, especially considering their low systemic perfusion (mean = 57 mm Hg, range 50 to 66 mm Hg on fraction of inspired oxygen (FiO2) less than 0.3 in 4 of 5 patients); and relatively high systolic blood pressure (mean systolic blood pressure = 91 mm Hg, range 78 to 116 mm Hg). During the preceding 24 hours, all had had systolic blood pressures of more than 85 mm Hg at multiple times. All were resuscitated with mechanical ventilation and administration of HCO3 and intravenous inotropic agents or vasodilators (1 also required extracorporeal membrane oxygenation), with rapid resolution of their acidosis. After decompensating, all were treated with oral antihypertensive agents; 1 had an early hemi-Fontan. All survived to discharge.

CONCLUSIONS: Increased systemic vascular resistance may be especially pernicious in Norwood patients—even remote from operation—as the condition increases myocardial work and O2 consumption while diminishing systemic perfusion. Chronic and acutely increased systemic vascular resistance may account for some cases of sudden unexpected death in Norwood patients.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Sudden unexpected death, remote from surgery, is an important problem in patients with hypoplastic left heart syndrome (HLHS) undergoing palliation by the Norwood procedure [1–10]. From 1997 to 1999 at our institution, 12% of patients with HLHS after Norwood palliation died suddenly and unexpectedly 3 days or more after surgery but before hospital discharge. Mahle and colleagues found a 4% incidence of unexpected death in a recent case-control study of 536 patients discharged home after Norwood palliation for HLHS [3]. The episodic nature of these occurrences makes determining their cause(s) difficult. To gain insight into the pathophysiology of these events, we reviewed the course of 5 selected patients with HLHS who had an unexpected sudden cardiovascular collapse while still hospitalized after the Norwood procedure.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
We retrospectively reviewed charts of 5 selected patients with HLHS after Norwood procedure who were successfully resuscitated from an in-hospital unexpected acute cardiovascular collapse more than 3 days after surgery. The patients underwent the Norwood procedure between March 1999 and April 2001 at the University of Michigan Congenital Heart Center. During this time, 107 patients with HLHS underwent the Norwood procedure at this institution with hospital survival of 78%. Data extraction included demographics, cardiac anatomy, echocardiographic findings, medications immediately before the event through discharge, heart rate, respiratory rate, blood pressure, pulse oximetry, laboratory studies, intake and output, feeding schedule, and reports from surgeries, cardiac catheterizations, and autopsies. This retrospective review was approved by the Institutional Review Board of the University of Michigan on March 14, 2002.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Five neonates with HLHS (4 mitral atresia/aortic atresia and 1 mitral hypoplasia/aortic hypoplasia) underwent Norwood operation at age 5 to 7 days (Table 1). All were full term with birthweights of 2.5 to 4.0 kg. Four had been diagnosed prenatally, and none presented in shock. None had associated chromosomal disorders. Two patients had restrictive atrial septal defects and underwent preoperative balloon atrial septostomy (patients 3 and 4). None had anomalous aortic arch vessels. The median ascending aorta diameter was 2.0 mm (range 1.5 to 3.2 mm). Cardiopulmonary bypass and deep hypothermic circulatory arrest times were similar to other Norwood patients at our institution with median times of 72 minutes (range 65 to 120 minutes) and 43 minutes (range 38 to 50 minutes), respectively [11]. Two patients had 3.5 mm right modified Blalock-Taussig shunts, and 2 patients had 4.0-mm right modified Blalock-Taussig shunts, compared 55% and 21% of the total Norwood population. Patient 1 initially had a 3.5-mm innominate-to-pulmonary artery shunt but underwent intraoperative upsizing of the shunt twice because of hypoxia, first to a 3.5-mm central shunt then to a 4-mm central shunt. Central shunts of this size were placed in 9% of the total HLHS population.


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  		Table 1. Patient Characteristics

 
All patients were still hospitalized but were extubated and were considered to be recovering well, with only one still in the intensive care unit, when each had an unexpected acute cardiovascular decompensation 8 to 15 days after the Norwood procedure. The presenting signs were generally fussiness with markedly diminished peripheral perfusion. The events were clinically similar with the constellation of acutely decreased peripheral perfusion, severe metabolic acidosis, high arterial pO2 relative to their anatomy, and systolic blood pressure (SBP) at or above the upper limits of normal (Table 1). We found a profound metabolic acidosis with serum HCO3 ranging from 6 to 11 mEq/L (mean = 9 mEq/L) and arterial lactate 10 to 20 mmol/L (mean = 16 mmol/L, normal < 2 mmol/L). All patients exhibited relatively high arterial pO2, especially considering their low systemic perfusion, with arterial pO2 ranging from 50 to 66 mm Hg (mean = 57 mm Hg, on fraction of inspired oxygen (FiO2) < 0.30 in 4 of 5 patients). Systolic blood pressure ranged from 78 to 116 mm Hg (mean SBP = 91 mm Hg) preceding the event. In 3 patients, blood pressures were measured noninvasively; however, arterial line placement during resuscitation confirmed SBP elevations despite decreased peripheral perfusion. In the other 2 cases, all blood pressures were measured invasively. All had SBP higher than 85 mm Hg multiple times during the 24 hours preceding the decompensation despite being treated with afterload reduction. Three patients were given captopril (dose range 0.3 to 1.5 mg/kg/day), and 1 was given a milrinone infusion at 0.5 µg · kg-1 · min-1. In the fifth patient, a milrinone infusion had recently been discontinued with anticipated initiation of captopril, which had not yet been administered before the event.

In contrast to Mahle's findings, none of these patients had associated arrhythmias, clinically relevant residual cardiac lesions, or clinically apparent seizures at the time of the event [3]. Only 1 patient had a history of perioperative arrhythmia (supraventricular tachycardia in patient 2). The episodes were not temporally related to feedings. Median hematocrit before the event was 45% (range 41% to 48%), and median hematocrit at the time of the decompensation was 40% (range 33% to 46%). In addition to the afterload reducing medications noted above, the patients were being given 1 or more of the following medications preceding the event: furosemide, spironolactone, chlorothiazide, digoxin, aspirin, ranitidine, metoclopramide, cefazolin, theophylline, lorazepam, dexamethasone, and calcium gluconate.

All patients were initially resuscitated with intubation, mechanical ventilation, sodium bicarbonate, and packed red blood cells, with or without antibiotics. One patient required chest compressions and was placed on extracorporeal membrane oxygenation emergently. Four of the 5 neonates were placed on milrinone. Once aggressive support was reinstituted, the severe metabolic acidosis resolved within 12 hours. No data suggested infection as a cause of decompensation. Initial echocardiograms after the event were notable only for depressed right ventricular systolic function, which improved before discharge in all patients. Between initial resuscitation and stabilization on oral antihypertensive medications, intravenous nicardipine, nitroprusside, or enalaprilat were necessary to adequately control SBP in 3 of 5 patients. Chronic antihypertensive therapy consisted of captopril in all patients (0.6 to 3.2 mg/kg per day) and isradipine (0.6 to 0.7 mg/kg per day) in addition to captopril in 2 patients. Because of refractory hypertension, patient 2 had renal imaging and was found to have a left kidney infarction.

Patient 1 had a second episode of unexpected acute cardiovascular collapse with the same constellation of findings 13 days after initial collapse. She had recovered and was awaiting discharge studies. In retrospect, she had remained hypertensive despite treatment with captopril between the episodes. After resuscitation and stabilization again, she then underwent hemi-Fontan palliation at 5 weeks of age.

All 5 patients survived to hospital discharge with lengths of stay ranging from 30 to 55 days (median 40 days). All survived to hemi-Fontan operation with no further decompensation episodes after discharge home. Hemodynamic data from their cardiac catheterizations before hemi-Fontan are presented in Table 2. Long-term outcome has been poor, however; all died by 27 months of age. Two died from right ventricular dysfunction after hemi-Fontan procedure; 1 from increased pulmonary vascular resistance after hemi-Fontan operation; 1 from complications of severe tricuspid insufficiency after hemi-Fontan; and 1 from hemorrhage on sternal entry at the hemi-Fontan operation. Autopsy results were available for 3 cases (patients 1, 2, and 5) but did not reveal any unexpected residual cardiac lesions or further elucidate the cause of death beyond the clinical findings. This group's outcomes are in marked contrast to the high survival rates after the hemi-Fontan procedure we have previously reported [12]. From 1995 to 1999, 8% of our total HLHS population died between the hemi-Fontan and Fontan or were not suitable for Fontan completion due to unfavorable hemodynamics.


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  		Table 2. Cardiac Catheterization Prior to Hemi-Fontan

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
Sudden death, remote from surgery, is a significant cause of mortality in patients with hypoplastic left heart syndrome following Norwood palliation [1–9]. Mahle and coworkers examined unexpected late deaths in 536 patients with HLHS who underwent Norwood palliation and survived to initial hospital discharge [3]. Unexpected death occurred in 4% of these patients, most commonly during the first few months of life. Documented perioperative arrhythmia and earlier year of Norwood procedure were associated with an increased risk of unexpected death in their multivariate analysis. Additionally, seizures or ventricular arrhythmias were noted in several patients before cardiac arrest, and residual cardiac lesions were identified on autopsy in 2 patients.

Very little is understood about the etiology of sudden death in these patients, and its episodic nature has made its cause(s) difficult to ascertain [10, 13, 14]. Thus, these observations made in hospitalized Norwood patients may afford unique and valuable insight into the pathophysiology of these events. Although the patients described here survived these episodes, their clinical status strongly suggested that had their abrupt decompensation not been fortuitously discovered, they would have succumbed quickly. Our patients manifested clinical findings of markedly diminished systemic blood flow (ie, they were cold and mottled with severe metabolic acidosis), with blood pressure at or above the upper limits of normal. This constellation would suggest, although not prove, that their systemic vascular resistance (SVR) was elevated.

High SVR may be especially pernicious in the Norwood patient, even remote from surgery (Fig 1). In these patients, elevated SVR increases both afterload and pulmonary blood flow, and thus increases myocardial work and oxygen consumption while diminishing systemic perfusion. Diminished systemic perfusion causes acidosis, which in turn further reduces myocardial function, initiating a "vicious cycle." Because myocardial perfusion may be decreased after the Norwood operation, the myocardium may be particularly prone to ischemia under these conditions, further compromising cardiac function [15]. Mathematical modeling of the "Norwood circulation" is consistent with this hypothesis: over a clinically relevant range of SVR, as SVR increases, arterial oxygen saturation rises but cardiac index and oxygen delivery fall [16]. There are also supportive data from the early postoperative period. Tweddell and associates noted decreased oxygen delivery with increased SVR in early postoperative Norwood patients [10, 17]. Subsequently, a strategy of control of SVR with alpha blockade in the first 48 hours after the Norwood operation has been associated with improved survival to hemi-Fontan at their institution [18].



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  		Fig 1. Effects of elevated systemic vascular resistance on Norwood pathophysiology. (PBF = pulmonary blood flow; SBF = systemic blood flow; SVR = systemic vascular resistance.)

 
The etiology of the increased SVR and SBP in these patients was not clear, except perhaps in 1 patient with a renal infarction. Perhaps altered baroreceptor function after extensive aortic arch dissection may predispose Norwood patients to episodic increases in SVR. Tweddell and colleagues demonstrated several such episodes of abrupt elevations of SVR in Norwood patients during the early postoperative period with deleterious effects on systemic oxygen delivery [10, 17]. Stressors, such as hunger or narcotic withdrawal, may precipitate a sympathetic surge, which is then poorly tolerated in patients with this pathophysiology [10, 16, 17]. Alternatively, it is possible that a subset of recovering Norwood patients experience a primary cardiac-related event, perhaps related to diminished coronary flow reserve, which results in angina and hypertension [15]. The fact that all of the patients described here died by age 3 years, despite successful resuscitation in the neonatal period, suggests they may be physiologically distinct from those who survive and do well.

This small descriptive study cannot determine predictors of sudden death. However, in our experience, elevated SBP, as noted in the patients described here, is not seen routinely in all recovering Norwood patients. Based on these observations and with concern about the deleterious effect of increased SVR in patients with "Norwood circulation," we have changed our late postoperative management and now treat "hypertension" much more aggressively.

Our observations suggest that chronic and acutely elevated SVR may account for some cases of sudden death in Norwood patients. Other causes, such as arrhythmias, shunt or coronary artery thromboses, or seizures, may account for other unexpected deaths in these patients.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
We thank Donna Wilkin for assistance with computer graphics.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

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