- Wiley Online Library

Pediatric Anesthesia ISSN 1155-5645
REVIEW ARTICLE
Anesthetic considerations for neonates undergoing
modified Blalock-Taussig shunt and variations
Helen M. Holtby
Division of Cardiac Anaesthesia, Department of Anaesthesia and Pain Medicine, Hospital for Sick Children, University of Toronto, Toronto, ON,
Canada
Keywords
anesthesia; neonates; congenital heart
disease; cardiac surgery; Blalock-Taussig
shunt
Correspondence
Helen M. Holtby, Department of
Anaesthesia and Pain Medicine, 555
University Ave, Toronto, ON M5G 1X8,
Canada
Email: [email protected]
Section Editor: Andy Wolf
Accepted 2 October 2013
doi:10.1111/pan.12295
Summary
The first Blalock-Taussig (BT) shunt was reported in 1944, and during the
last 70 years, the procedure has evolved with the development of new materials and devices, and surgical approaches. It has, however, remained central to
the palliation of neonates with complex congenital heart disease. The indications have expanded from the original aim of alleviating cyanosis and the
pathophysiological results of chronic hypoxemia. They now include lesions
with single ventricles, and rehabilitation of small pulmonary arteries. The
physiology and hemodynamics of BT shunt circulations are very complex,
and adverse hemodynamic events can be difficult to recognize. The consequences of shunt failure can be fatal, and the mortality (3–15%) and morbidity remain distressingly high even in the current era. Neonates undergoing BT
shunt procedures or undergoing noncardiac surgery with this anatomy are
challenging for the anesthesiologists to manage. There is a significant incidence of periprocedural cardiac arrest, often related to myocardial ischemia.
A clear understanding of the anatomy and physiology is important. Any discussion of BT shunt in the current era has to include consideration of hypoplastic left heart syndrome and ‘single ventricle’ physiology.
Introduction
It is never ‘Just a B-T shunt…’
The original Blalock-Taussig (BT) shunt was performed at Johns Hopkins Hospital in 1944 on a cyanotic
19-month-old girl, given ether in oxygen for general
anesthesia (1) by Dr Merel Harmel. An end-to-side
anastomosis of the proximal left subclavian artery into
the left pulmonary artery (PA) was performed. Alfred
Blalock and Vivian Thomas had been working on models of patent ductus arteriosus (PDA). Dr Helen Taussig
believed that babies with right ventricular outflow tract
obstruction were blue because of inadequate pulmonary
blood flow (Qp). This was not the prevailing wisdom at
the time. They hypothesized that if a ductus arteriosus
could be created it would increase blood flow to the
lungs and ‘blue babies’ would benefit. The procedure
gained widespread acceptance, and for more than three
decades, the treatment of tetralogy of Fallot (TOF) was
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staged with BTS in infancy and subsequent takedown
and full repair in childhood. Those who enjoy film are
referred to ‘Something the Lord Made’(2).
The BT shunt was subsequently modified (mBTS)
from an end-to-side direct vascular anastomosis to the
current side-to-side tube graft maintaining subclavian
artery continuity. It is most commonly performed on
the right side (3). The surgery can be performed via thoracotomy or sternotomy. It does not require the support
of cardiopulmonary bypass (which was not in existence
for the original procedure), although it is used
frequently in some centers (4).
In the modern era, the indications for this palliative
procedure have expanded far beyond the original concept, and other therapeutic options now exist, such as
ductal stents that achieve the same physiologic result.
In 1973 in Toronto, Peter Olley and Flavio Coceani
described the effect of prostaglandin E (PGE1) on the
maintenance of ductal patency, and reported its use in
neonates (5). This meant improved survival with less
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H. M. Holtby
hypoxic injury for the babies and more and better sleep
for surgeons and anesthesiologists. Long-term PGE1
infusions have been used to palliate infants listed for
heart transplantation or to defer surgery to allow for
growth. There are significant side effects including gastric outlet obstruction, pseudo Bartter’s syndrome and
hyperostosis, particularly of digital bones (6).
The development of coronary stents enables the same
physiological result as a BTS in the cardiac catheterization laboratory. Stents can be deployed in the PDA permitting the discontinuation of PGE1. This may avoid a
surgical incision, but there are anatomic variations in
the ductus in patients with CHD which can make it
impossible from a percutaneous approach (7). The
placement of ductal stents as part of hybrid palliation of
hypoplastic left heart syndrome (HLHS) is frequently
performed via sternotomy (8)
Recent publications on the outcomes of mBTS
patients report distressingly high mortality and morbidity in neonates. Exclusion of patients undergoing the
Norwood procedure or pulmonary arterioplasty (as surrogates for complexity) still reveals a significant incidence of adverse outcomes. In both single center and
multicenter investigations, the mortality in single ventricle patients is around 15%, and in patients with two
ventricles, it is 3–5% (4,9). This is higher than many
neonatal cardiac repairs.
McKenzie and colleagues (10) identified sternotomy,
anatomic site, use of cardiopulmonary bypass (CPB),
and Ebstein’s anomaly as risk factors for death. In the
multicenter analysis performed by Petrucci and others
(4), risk factors for death were weight <3 kg, preoperative ventilation, single ventricle palliation, and specifically, pulmonary atresia with intact ventricular
septum. One-third of deaths occurred in the first 24 h
postoperatively.
Indications for Blalock-Taussig shunt
There are fundamentally three reasons to perform a B-T
shunt or its equivalent (i.e., a ductal stent) on a neonate:
1 Blood flow to the lungs is provided via the PDA: The
baby will die of hypoxia if the duct closes.
2 Blood flow to the body is provided via PDA: The
baby will die of systemic shock or myocardial
ischemia if the duct closes.
3 The pulmonary arteries are small, and there is an
attempt to encourage growth by increasing flow.
Typical examples of the first situation include tricuspid atresia, pulmonary atresia, and TOF when there is a
contraindication to complete repair. Neonatal Ebstein’s
anomaly with functional pulmonary atresia is a rare
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Pediatric Anesthesia 24 (2014) 114–119
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indication. The current strategy of early primary repair
means that BT shunts are generally performed in complex situations, either anatomically (aberrant coronary
anatomy) or physiologically (prematurity, intracerebral
bleed, or other contraindication to CPB). It is also an
option if other anomalies require evaluation or repair.
Some centers choose to do BTS rather than neonatal
TOF repair in those patients who are very desaturated
when the duct closes.
Hypoplastic left heart syndrome (HLHS) constitutes
the second example. The Norwood operation is aortic
arch reconstruction, PDA ligation, and mBTS. In the
Norwood procedure, the mBTS provides the route for
pulmonary blood flow and is intended to be the
resistance component. In the ‘Hybrid procedure’, as an
alternative palliation, the arch is unrepaired, favoring
flow to the pulmonary arteries via the stented duct.
Bilateral pulmonary bands are therefore placed to limit
pulmonary blood flow, improving systemic perfusion.
The third example is pulmonary atresia, VSD with
aortopulmonary collaterals and inadequate pulmonary
arteries.
In any of the diagnoses presented, there are surgical
and pharmacological and catheter-based options, and
pediatric anesthesiologists will be involved at some or
several stages of the child’s care. There are different considerations depending on the surgical procedure and the
cardiac diagnosis.
Physiology of Blalock-Taussig shunts
The physiology of circulations incorporating mBTS is
complex. The complications depend on factors such as
ventricular size and morphology, the presence of more
than one source of pulmonary blood flow, the size and
position of the aortic arch, and the presence of antegrade flow through the aortic valve. Two ventricles are
generally better than one (and left better than right if
not). If there is more than one route for pulmonary perfusion, (such as pulmonary stenosis rather than atresia,
or aortopulmonary collaterals) the effects of shunt stenosis or thrombosis are attenuated. However, the possibility of shunt occlusion may be increased if there is
another route for PBF, and the possibility of too much
PBF may be increased. If there is pulmonary atresia
(either functional or anatomic), and no collaterals, shunt
occlusion results in sudden death from hypoxemia.
The most robust circulation is the original indication
(now least performed), where there is inadequate pulmonary blood flow and TOF. In this situation, both ventricles eject into great vessels, although there is right
ventricular outflow tract obstruction, and right to left
shunt in the ventricles. The primary issues are volume
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loading of the heart, coronary steal, and shunt thrombosis. Volume loading of the heart can cause A-V valve
regurgitation and is a particular problem in single ventricles. The potential for coronary steal exists (because
of blood flow diverted into the low-pressure pulmonary
vascular bed) causing myocardial ischemia, arrhythmias,
acute ventricular dysfunction, and sudden death. This
may be exacerbated by increased ventricular enddiastolic pressure. It may be preceded by low diastolic
blood pressure which is an indicator of high pulmonary
to systemic blood flow ratio (Qp:Qs). Diastolic blood
pressures of less than 30 mmHg are a cause for
concern and close observation. A useful initial strategy
is to employ maneuvers which increase PVR, such as
reducing minute ventilation, and higher PEEP levels.
In the longer term, there is a concern for the development of increased pulmonary vascular resistance (which
can be unilateral) or pulmonary hypertension.
In patients with small pulmonary arteries, the effectiveness of the mBTS in improving oxygen delivery may
be limited and under those circumstances hypoxia is a
major concern.
In HLHS and variants, the total cardiac output
emerges from the heart and diverts either into the pulmonary vascular bed or the systemic circulation. There
are multiple opportunities for circulatory collapse, and
for occult reductions in systemic oxygen delivery, myocardial ischemia, and inadequate systemic perfusion. In
the absence of flow from the left ventricle (aortic valve
or mitral valve atresia), blood exits the heart via the PA
and flows right to left via the duct, and then passes retrograde around the aortic arch The coronary arteries
are a very long way back from the perfusing (right) ventricle. Right-sided ventricles are more likely to dilate in
the context of volume loading (which is inherently
greater in single ventricle hearts). Tricuspid valve
regurgitation occurs frequently and causes further
inefficiency in oxygen delivery. Changes in systemic or
pulmonary vascular resistance cause changes in pulmonary and systemic blood flow (Qs). Reduction in Qs
because of increased Qp will tend to be self-perpetuating: vasoconstriction is a normal physiologic response to
hypotension, and this may become catastrophic. Barnea
and others have made mathematical models to try to
understand and predict the changes in oxygen delivery
(DO2) that occur with changes in Qp, Qs, and cardiac
output (CO) (10,11). Such models illustrate the dilemmas facing the clinician (12). It is difficult to diagnose
physiological derangements using currently available
monitors.
To summarize some of the originally observations
from the model for the Norwood circulation (i.e., ‘single
ventricle physiology’) described by Barnea:
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H. M. Holtby
1 Arterial saturation is an unreliable guide to oxygen
delivery. It is possible to have significant reduction in
oxygen delivery in association with no change or
modest increases in SaO2.
2 Decreases in pulmonary vein saturation cause major
errors in estimates of Qp/Qs. It will be underestimated. This is a common problem in the operative
period.
3 If there is high PBF, hence high Qp/Qs, there is only
limited compensation in DO2 with increasing CO.
These papers are important for the clinician because
they describe the multiple assumptions made using
routine monitors. They improve our understanding of
oxygen delivery, cardiac output, Qp/Qs in complex circulations. Even the models use assumptions, mixed
venous saturation is a theoretical construct in hearts
with shunts. In two ventricle hearts without a shunt, the
adequacy of cardiac output and oxygen delivery and
consumption can be ascertained using measured mixed
venous saturation, classically from the PA. There is no
such point in the body to make measurements in complex CHD. The use of near-infrared spectroscopy for
measurement of tissue oxygenation is used as additional
monitoring of infants with complex CHD (13), but not
everyone is convinced (14,15). Skepticism has also been
expressed about the benefits of pulse oximetry, but most
anesthetists would be extremely unhappy to practice
without it despite the limitations (see 1 above!) (16).
Measurement of oxygen consumption and calculation of
Qp and Qs have also improved our understanding of the
hemodynamics of single ventricles (17).
The clinician caring for the child with a BT shunt has
to ascertain whether indicators of adverse hemodynamics are real, significant and then diagnose the cause (18).
The desaturated, hypotensive neonate may have: hypovolemia and low hemoglobin, which will result in very
low venous saturations in combination with low CO;
shunt occlusion and hypoxic cardiac failure; or high pulmonary vascular resistance and low systemic vascular
resistance. They may also have respiratory disease and
low pulmonary vein saturation. On the other hand, the
child with high saturation and hypotension may have a
high cardiac output and vasodilation, or be vasoconstricted and minutes away from cardiac arrest.
The possibility of myocardial ischemia, low cardiac
output, inadequate intravascular volume, primary pulmonary disease, shunt failure, iatrogenic causes and
changes in systemic or pulmonary vascular resistance,
and oxygen carrying capacity must be considered in all
situations. This is before contemplating the effects of
surgical manipulations. The reason to delineate these
possibilities is to point out that neither hemodynamics
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Pediatric Anesthesia 24 (2014) 114–119
H. M. Holtby
nor saturation are very good indicators of adequate systemic oxygen delivery.
Anesthetic management of the neonate
undergoing BTS
Odegard and colleagues reviewed their experience with
cardiac arrest in children undergoing cardiac surgery
over a 5-year period from 2000 to 2005 (19). The incidence of cardiac arrest during closed cardiac surgery
was highest in patients undergoing mBTS for pulmonary atresia, with a frequency of 3.6/100. This is higher
than the Norwood procedure (2.2/100). The majority of
anesthesia related arrests in children undergoing cardiac
surgery were attributed to myocardial ischemia.
Petrucci and colleagues analyzed the outcomes of neonatal mBTS using the Society for Thoracic Surgeons
(STS) Database (4). They assessed 1280 patients from 70
institutions. The mortality was 7.2%. One-third of the
deaths occurred in the first 24 h postoperatively. Preoperative acidosis, mechanical support (either ventilatory
or circulatory), renal impairment, diagnosis, and weight
were associated with the risk of death. Weight under
3 kg and preoperative shock were risk factors for morbidity (mechanical support, reoperation, low cardiac
output). Pulmonary atresia with intact ventricular
septum was the diagnosis of note. The use of cardiopulmonary bypass for mBTS appeared to have no impact
on mortality or morbidity. McKenzie and colleagues
reviewed the experience at Texas Children’s Hospital
over a 15-year period ending in 2011. A total of 712
patients had 730 mBTS procedures. The median age of
patients was 8 days. The hospital mortality was 3.4%
with two ventricles, and 15% with one. They identify
sternotomy as a risk factor for death.
The preoperative evaluation of a neonate presenting
for BTS should include the anatomic diagnosis and the
surgeon’s plan. Details such as aortic arch anatomy, and
the possibility of aberrant subclavian artery are important. The use of CPB, sternotomy, or thoracotomy
changes the anesthetic plan for the baby and the conversation with the parents. There are also all the usual
considerations of neonatal physiology and the possibility of other anomalies, as well as genetic syndromes to
consider.
The anesthetic considerations for hybrid palliation
are described by Naguib et al. (20). The authors comment on the differences between the Norwood operation
and this alternative. Sadly, the long-term outcomes are
not different (21).
The importance of preoperative shock on postoperative outcome makes the perinatal history important.
There are fetal screening programs for CHD, and there
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remains debate on the effectiveness of such interventions
(22). The timely administration of PGE1 avoids the possibility of duct-related cardiovascular collapse, which is
a good thing for the individual patient. The vast
majority of newborns have PGE1 infusions running on
presentation for surgery. The usual dose is 0.01–
0.1 mcgkg 1min.
The outcome data alone on these patients prescribe
invasive monitoring. We proceed as for a procedure with
cardiopulmonary bypass (arterial line, generally left
sided, i.e., not the shunt side, central line, NIRS). Particular attention should be paid to the baseline ECG trace
and the diastolic blood pressure. The ordinary anesthetic routines, such as the use of fiO2 of 1.0 for intubation, a tendency to hyperventilate if anxious, (the
practitioner, not the patient!), and anesthetic vapors all
tend to decrease PVR, increase Qp/Qs, and decrease
diastolic blood pressure with the resultant concerns for
myocardial ischemia and systemic perfusion. A balanced
anesthetic technique, combining narcotic and vapor supplemented with muscle relaxant is usually undertaken.
Desaturation is relatively frequent when the pulmonary
end of the anastomosis is being undertaken as the pulmonary artery is clamped. Paradoxically, this may be
less of an issue via thoracotomy, as clamping the PA will
reduce ventilation perfusion mismatch. It is our practice
generally to discontinue prostaglandin infusions when
the duct is ligated. Blood should be immediately available. If irradiated blood is not routinely provided for
neonates, the suspicion of 22q11 deletion should prompt
a specific request.
Hemodynamic instability can ensue when the shunt is
opened, due to blood loss or the changes in blood flow
that is, some of the systemic flow diverts to the PA. It is
common to see low saturations initially, and this can
probably be attributed to high PVR and pulmonary vein
desaturation secondary to lung collapse, hypoxic pulmonary vasoconstriction, and atelectasis. Transesophageal
echocardiography is undertaken to assess function and
shunt flow. Direct flow probes can also be used. NIRS
monitoring on the head and flank may also provide
guidance for management. An fiO2 of at least 30% is
preferable, and more oxygen may be required in the
short term. The intraoperative decisions are focused first
on technical issues: is the shunt the right size, not
kinked, and not narrowed. A shunt which is too short or
too large, in concert with a low pCO2 and high fiO2 will
have a high saturation and low diastolic blood pressure.
It is wise to check arterial blood gases at this point. If
there are no anatomic issues, a review of the physiologic
issues is performed: adequate preload, sinus rhythm,
good contractility (therefore by deduction reasonable
myocardial
perfusion),
reasonable
SVR,
and
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H. M. Holtby
appropriate PVR. Even though the shunt itself is a component of PVR, it is not the sole determining factor, so
changes in lung volume, alveolar oxygenation, pH, and
pCO2 will affect Qp (23). The use of inotropes may
improve hemodynamic parameters and oxygen delivery
but at the expense of increased consumption (24).
Postoperative pain is most commonly managed with
continuous narcotic infusion. While early extubation
has benefits for many patients following cardiac surgery,
the physiological vulnerability of neonates, particularly
those with CHD, is a risk. The changes in PVR, SVR,
and Qp which occur with lung re-expansion in combination with emergence from anesthesia, transition to
postoperative pain regimens, possible bleeding etc., all
contribute to the postoperative risk of cardiac arrest.
The incidence of failure to extubate neonates following
mBTS was investigated by Gupta and colleagues (25).
They found that 27% patients required either re-intubation or the instigation of noninvasive ventilation within
96 h. Decreased ventricular function was strongly
associated with failure. There was a 13% incidence of
diaphragmatic paralysis, all in the group that failed.
Postextubation hemodynamics also changed, with an
increase in heart rate and systemic blood pressure in
successful subjects.
Noncardiac surgery and mBTS
The child with palliated complex CHD who requires
surgery for other anomalies is at a higher risk of cardiac
arrest and death (26,27). This is multifactorial and
includes patient-related factors and there may be practitioner errors.
Many of the babies have feeding intolerance, and oral
aversion, and present for gastric tube insertion. There is
also a significant incidence of neurological injury
prompting requests for MRI scans.
Shunt thrombosis is a constant concern despite the
use of acetylsalicylic acid, clopidogrel, or low molecular
weight heparin. If shunt occlusion is suspected, urgent
echocardiography is indicated along with high inspired
oxygen, volume, and the use of systemic vasoconstricting drugs. Emergency cardiac catheterization is indicated if there are concerns about shunt patency or
pulmonary artery anatomy.
The use of NIRS can be helpful, and blood gas measurements can also be revealing. Consideration should
be given to intensive care unit admission postoperatively
for all patients, regardless of procedure.
When Helen Taussig challenged Alfred Blalock in
1943 and the subsequent surgery was undertaken, the
mortality of most CHD was 50–100%. Seventy years
later, that mortality is around 5%. It never was ‘Just a
BT shunt’, but in previous eras when operative mortality
for infants having open heart surgery was between 10
and 20%, the results of mBTS seemed much more
acceptable. A significant population of patients with
tetralogy of Fallot diluted the numbers of single ventricle and PA IVS patients, and HLHS was not even on
the agenda.
To quote Mckenzie and colleagues: ‘Despite the naive
stance, yet often stated, “It’s just a shunt,” the authors
maintain that construction of a proper mBTS in a neonate, via either sternotomy or thoracotomy, is an intellectually and technically challenging operation’. This is
equally true for the anesthesiologists managing the neonates in the operating room or in the critical care unit.
Ethical approval
There is no requirement for ethical approval or consent
for this article.
Funding
This research was carried out without funding.
Conflict of interest
No conflicts of interest declared.
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