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1 Cardiovascular and respiratory disorders

 PFO results from intact primum and intact secundum septal
Central venous cannulae can pose a potential thromboembolic
risk in patients with a Fontan type circulation, and pulmonary fusion failure, and remains patent or probe-patent in an esti-
mated 30% of adults.163,164
artery catheterization may be riskier and measurements mislead-
ing with significant cardiac lesions and the presence of a shunt.161  Secundum ASD represents an omission of a portion of the
Transesophageal echocardiography is a useful real-time assess- septum secundum and is typically located at the midportion
ment tool for preload, ventricular function, and intracardiac of the interatrial septum.
 Primum ASD represents an omission of a portion of the septum
shunt assessment.
primum and is also associated with a cleft anterior mitral valve
leaflet with resultant mitral valve regurgitation. Primum ASD
Congenital heart disease shunt lesions
increases risk for LV dilatation and systolic dysfunction, LA
Traditionally, CHD shunt lesions have been characterized as enlargement, atrial fibrillation, pulmonary hypertension, and
either acyanotic or cyanotic (see Table 1.10). This differentiation RV dysfunction.
attempts to classify shunt lesions according to excessive pulmon-  Sinus venosus ASD represents an omission of the portion of the
ary blood flow (left-to-right shunt), or inadequate pulmonary septum secundum proximal to the superior vena cava (SVC). It
blood flow (right-to-left shunt). Many diseases that start as acya- causes PAPVR into the right atrium (RA) instead of the LA.
notic lesions may progress to cyanotic lesions as they approach  Unroofed coronary sinus ASD represents an absence of a parti-
an end-stage. The dynamic nature and complexities of the tion between the LA and the coronary sinus. This leads to
lesions, as well as the consequences of surgical repairs, further oxygenated LA blood communicating with deoxygenated RA
complicate the classification of CHD. (see Table 1.10). Generally, blood via the coronary sinus conduit.
pregnant women with congenital shunt lesions have favorable Isolated ASD lesions originate as predominately left-to-right
outcomes provided they have minimal functional impairment shunts. The amount of interatrial flow is dependent on the defect
and good myocardial function.162 size, the relative RA to LA pressure gradient, the presence or
absence of atrial contraction, and relative LV and RV compliances
during diastole when the atrioventricular valves are open.
Atrial septal defects
Chronic atrial level shunting results in RA and RV volume over-
There are five different subtypes of atrial septal defect (ASD). load with subsequent RA enlargement and atrial dysrhythmias,
These include patent foramen ovale (PFO), secundum ASD (80% as well as RV dilatation and RV systolic dysfunction. The pulmon-
of ASD), primum ASD, sinus venosus ASD with partial anomalous ary overcirculation will eventually culminate in pulmonary hyp-
pulmonary venous return (PAPVR), and unroofed coronary sinus. ertension, RV hypertrophy, and both RV diastolic and systolic
dysfunction. Ultimately, Eisenmenger syndrome can develop as
defined by reversal of shunt flow direction (due to fixed pulmonary
vascular obstructive changes). Progressive hypoxemia, polycythe-
Table 1.10 Classification of congenital heart disease
mia, and right-sided heart failure (jugular venous distension, liver
Atrial septal defects a
Acyanotic shunt lesions congestion, ascites, protein-losing enteropathies) may eventually
Ventricular septal defects a
Left-to-right shunts develop.
Patent ductus arterioses (PDA) a
Cyanotic shunt lesions Tetralogy of Fallot (TOF)
Management principles
Right-to-left shunts Ebstein™s anomaly
Post bidirectional Glenn or preFontan The management of the parturient with ASD depends upon the
procedure underlying lesion and its clinical consequences. In the absence of
Post fenestrated Fontan procedure with clinical evidence of RV dysfunction or pulmonary hypertension,
ASD is well tolerated during pregnancy.162,165 If there is cyanosis,
elevated pulmonary artery pressure
Truncus arteriosus RV dysfunction, or pulmonary hypertension, then invasive moni-
Total anomalous pulmonary venous return tors and real-time echocardiographic monitoring may be
Tricuspid atresia required. Removal of air from all venous lines is essential in
Hypoplastic left heart syndrome order to avoid systemic air emboli (particularly coronary and
D-transposition of the great arteries cerebral emboli).
Nonshunt lesions Coarctation of the aorta Hemodynamic goals:
 Maintain RA contraction. Normal sinus rhythm preser-
Valvular heart lesions
Cardiomyopathies vation is critical, especially in the setting of RV diastolic
Fully corrected shunt lesions (ASD, VSD, dysfunction from pulmonary hypertension-induced RV hyper-
PDA, TOF) trophy. Both atrial fibrillation and flutter lead to loss of normal
Post nonfenestrated Fontan procedure atrial contribution to ventricular preload. Rapid atrioventricu-
L-transposition of the great arteries lar conduction will further exacerbate the deleterious effects
of these dysrhythmias by causing insufficient ventricular filling
time. Antidysrhythmic agents or direct-current synchronized

Chapter 1

cardioversion should be considered in this patient population, will cause a sympathetically mediated decrease in SVR and
only after LA thrombosis formation has been ruled out by hence a relative hypovolemia. Obstetric anesthesiologists need to
echocardiography. Antidysrhythmics and rate-controlling anticipate any accompanying loss of SVR with appropriate volume
medications may be required (e.g. amiodarone, calcium replacement and the judicious use of vasoconstrictors. To mini-
channel blockade, beta-blockade, digoxin). Prior to their mize hemodynamic disturbances, slow titration of epidural or
administration, cardiologists and obstetric care providers intrathecal medication is preferable to a single-shot spinal tech-
should be consulted so that any adverse effects on the parturi- nique. For maintenance of labor analgesia, a continuous infusion
ent and fetus (e.g. thyroid dysfunction from amiodarone) can of the lowest possible concentration of local anesthetic is prefer-
be monitored (see Chapter 2). able, avoiding, if possible, a large intermittent bolus administra-
 Maintain high to normal heart rates. This augments RV CO in tion. Saline should be used to determine loss of resistance when
the setting of impaired RV preload (diastolic dysfunction) and locating the epidural space, so as to avoid accidental i.v. injection
RV SV (systolic dysfunction). High to normal heart rates are of air and paradoxical systemic air embolism. Neuraxial opioids
essential in the setting of primum ASD where the added chrono- have minimal hemodynamic side effects compared to local anes-
tropy will help reduce the overall mitral valve regurgitation thetics. They can augment the analgesic effects of neuraxial local
fraction by reducing mitral valve annular diastolic distention. anesthetics, therefore allowing the use of lower concentrations of
 Maintain RV preload. A dilated RV with tricuspid regurgitation local anesthetic with less potential for vasodilation and hypoten-
will require a large RV preload to ensure an adequate SV is sion. Assisted vaginal delivery to minimize the cardiovascular
available to maintain adequate forward CO and to compensate stress associated with delivery is useful. Analgesic augmentation
for the regurgitant back flow. In addition, the restraining effects may be necessary to facilitate assisted delivery.
of a noncompliant RV will cause a fixed upper-limit preload on Since regional anesthesia for C/S has advantages for the mother
the RV. Ensuring the RV is maximally filled during diastole is and fetus, GA is reserved for parturients who require C/S but
important; otherwise SV, and hence overall pulmonary CO, will have contraindications to neuraxial techniques (e.g. coagu-
be impaired. Proper positioning to avoid aortocaval compres- lopathies, emergency C/S, patients who have severe orthopnea,
sion and anticipation of blood loss during delivery will help to or patients in cardiopulmonary extremis). Patients with RV
maximize RV preload. failure may have edematous laryngeal tissue due to poor central
 Contractility will need to be augmented in patients with RV venous drainage, and this may predispose to difficult intubation
systolic dysfunction in order to maintain pulmonary blood flow conditions. Other drawbacks to GA include loss of endogenous
(PBF). This intervention is particularly important in the pri- catecholamine balance, which may unmask a failing ventricle
mum ASD parturient where concomitant LV systolic dysfunc- and positive-pressure ventilation induced loss of venous return.
tion may coexist. Patients with primum ASD will also benefit Advantages of GA include (1) the ability to manipulate oxygena-
from the systolically augmented RV pushing more blood tion, ventilation, and anesthetic depth, which are central to the
through the pulmonary circuit to the dilated LV. Adequate LV management of patients with severe pulmonary hypertension; (2)
preload is necessary to offset the fractional loss of forward SV the ability to administer the inhaled pulmonary vasodilator nitric
to the backward mitral regurgitation jet during systole. oxide; and (3) the ability to use TEE for immediate assessment of
 Prevent increases in pulmonary vascular resistance (PVR) (see cardiopulmonary function.
Table 1.9). The choice between regional and GA should be individualized
 Maintain SVR to allow adequate right coronary artery perfu- and based on the clinical impact of the ASD. The anesthetic
sion pressure to the hypertrophied RV. technique should allow the anesthesiologist the best chance of
controlling hemodynamic parameters. The risk/benefit ratio of
any anesthetic technique must involve an understanding of the
Anesthetic options
pathophysiology of the cardiac lesion.166
For parturients with ASD undergoing a trial of labor, it is import-
ant to provide good analgesia and to minimize the cardio-
Ventricular septal defects
vascular stress of labor and delivery.1 Epidural (continuous or
patient controlled), CSE, or continuous spinal analgesia (CSA) Ventricular septal defects (VSDs) are the most common structural
heart defect, (approximately 20“35% of all CHD lesions).161,163,166
are all acceptable neuraxial analgesic techniques. However, if
the patient exhibits any coexisting coagulation abnormalities There are four major anatomical subtypes of VSD (see Table 1.11).
or is taking anticoagulants, then neuraxial regional anesthesia These include perimembranous (PM), muscular, outlet supra-
should be approached with appropriate caution according to cristal subarterial (SCSA), and inlet atrioventricular (AV) canal
established guidelines (see Table 1.7). Neuraxial anesthetic tech- (see Table 1.11). A VSD is often part of a more complex cardiac
niques, type of analgesics, dosages, and combination of agents anomaly (e.g. Tetralogy of Fallot).
should all be selected with consideration of their therapeutic
benefit (pain reduction, positive hemodynamic goal attainment)
Management principles
versus potential deleterious side effects (e.g. hypotension).
Techniques that provide effective analgesia with minimal, slow- The management of a parturient with a VSD is very similar to that
onset hemodynamic changes are ideal. Neuraxial local anesthetics of a patient with ASD with two major exceptions. Firstly, patients

1 Cardiovascular and respiratory disorders

Table 1.11 Classification of ventricular septal defects (VSD)

VSD subtype Incidence Description

Perimembranous Most common subtype Located in the membranous portion of the interventricular septum (IVS), which stretches
(80% of VSD) between the conal-trigone and muscular septa.
Muscular 10% of VSD Situated within the muscular-trabecular region of the IVS. Often consists of multiple holes
(˜˜Swiss-cheese-like™™ in appearance).
Supracristal 4% of VSD Located distal to the crystal supraventricularis and proximal to the semilunar valves. Usually
associated with aortic valve insufficiency as the right Æ noncoronary aortic valve leaflets
tend to prolapse via a VSD-generated Venturi jetstream effect during diastole.
Inlet atrioventricular 6% of VSD Located in the posterior IVS juxta-tricuspid valve area. Often associated with complete AV
canal canal defects.

with unrestricted shunt flow (i.e. no pressure gradient between condition and the desired hemodynamic goals. (See various anes-
the LV and the RV) are predisposed to both accelerated congestive thetic options described under ASD.)
heart failure (CHF) and pulmonary hypertension from the pul-
monic overcirculation. Secondly, left-to-right VSD shunt flow
Cyanotic congenital heart lesions
can be attenuated by SVR reduction, unlike left-to-right ASD
shunt flow, which is uncoupled to SVR. Congenital heart disease with right-to-left shunt is associated
with recirculation of poorly saturated blood. Peripheral cyanosis
occurs when >5 g/dl of unsaturated hemoglobin is present.
Anesthetic options
Cyanosis varies directly with hematocrit. It is important to
Neuraxial or GA can be used provided the onset of analgesia or remember that an anemic parturient with poor oxygen saturation
anesthetic is initiated in a slow, controlled manner with appro- may not manifest cyanosis, whereas with polycythemia, cyanosis
appears at higher oxygen saturations.167 Cyanotic lesions are
priate hemodynamic monitoring. (See various anesthetic options
described under ASD.) more likely associated with congestive heart failure, worsening
of functional status, fetal loss, preterm labor, and IUGR.15 Fetal,
not maternal factors are usually responsible for intolerance of the
Patent ductus arteriosus
pregnancy and labor.168
Patent ductus arteriosus (PDA) represents 8“15% of CHD A physiologic response to hypoxemia in women with cyanotic
lesions.161 Patent ductus arteriosus consists of a retained vascular lesions is polycythemia, which is a useful compensation up to a
communication between the left pulmonary artery and the prox- hematocrit of 60%. An increase in blood viscosity beyond this level
imal descending thoracic aorta distal to the left subclavian artery. offsets any advantages that an increase in hematocrit brings in
A large PDA mimics an unrestricted VSD in that it can lead to terms of oxygen delivery. Symptoms of hyperviscosity include
pulmonic overcirculation with resultant CHF and pulmonary headache, sluggish mentation, disorientation, double-vision, fati-
gue, muscle weakness, myalgias, and paresthesias.169 Polycythemia
hypertension. As pulmonary hypertension develops, the left-to-
right shunting will diminish and ultimately reverse, resulting in contributes to tissue ischemia in low flow states because of the
Eisenmenger syndrome. increase in blood viscosity and can lead to thrombosis in situ.
Maternal hematocrit >60%, SaO2 <80%, RV hypertension, and
syncopal episodes are all poor prognostic signs in pregnant
Management principles (see Atrial septal defects)
women with CHD.170 Cyanotic CHD may be associated with multi-
The focus of hemodynamic management is to assess the severity of ple coagulation factor deficiencies increasing the risk of peripartum
the lesion and to determine the degree of secondary pathophysiol-
ogy. If the parturient has a small PDA with no signs or symptoms of
pulmonary hypertension, RV failure, or hypoxemia, then labor or
Tetralogy of Fallot
C/S will likely be uneventful. If, however, there is associated pul-
monary hypertension, RV failure, or hypoxemia, then RV inotropic Tetralogy of Fallot (TOF) is the most common cyanotic CHD
lesion and accounts for 5“15% of CHD.73 Parturients with TOF
support (e.g. epinephrine, dopamine, milrinone, dobutamine),
PVR reduction, SVR maintenance and normovolemia are required. have an increased risk of adverse events including ventricular
Maintenance of SVR and volume status are also important. failure, dysrhythmias, embolic phenomena, increased fetal loss,
and congenital fetal abnormalities.171 Tetralogy of Fallot consists
of (1) nonrestrictive VSD; (2) over-riding aorta; (3) dynamic sub-
Anesthetic options
pulmonic right ventricular outflow tract (RVOT) obstruction; and
The choice between various neuraxial techniques for labor, and (4) RV hypertrophy. The worse the RVOT obstruction, the greater
between regional versus GA for C/S, should be based on patient the right-to-left shunt of blood through the VSD.

Chapter 1

Ebstein anomaly
Other possible secondary pathologies include RV systolic
and diastolic dysfunction, and end-organ visceral damage
Ebstein anomaly represents less than 1% of all CHD defects.
from chronic hypoxemia, polycythemic microvascular sludging
Although quite variable in its presentation, the basic pathophy-
and reduced CO. Most parturients with TOF have undergone
siologic features of Ebstein anomaly include:
surgical correction or palliation during childhood. Pregnancy-
(1) A downward displacement of both posterior and septal tricus-
induced cardiovascular changes can unmask residual symp-
pid valve leaflets into the RV such that the basal portion of the
toms of surgically corrected TOF. Patients with fully corrected
RV becomes ˜˜atrialized™™. This leads to diminished RV cavity size
TOF usually tolerate pregnancy well; however, dysrhythmias,
and results in decreased right ventricular stroke volume and CO.
thromboembolic events, and progressive failure may compli-
(2) A redundant anterior tricuspid valve leaflet that can cause an
cate pregnancy.171
obstruction to blood flow through the right side of the heart.
If the parturient has a history of corrective surgery during
(3) Tricuspid valve regurgitation with concomitant elevated RA
infancy or childhood, then severe pulmonic insufficiency may
pressures and RV systolic dysfunction.
arise secondary to trans-pulmonic valve annular patching. Right
(4) A PFO or secundum ASD with right-to-left shunting due to the
ventricular dilatation, RV systolic failure, and elevated RA pres-
high RA pressures.
sures may subsequently develop. Ventricular septal defect patch
(5) An increased incidence of supraventricular reentry tachydys-
or oversew leaks should be ruled out by echocardiography and by
checking baseline room air oxygen saturation.

Management principles
Management principles
The management of a parturient with Ebstein anomaly centers on
Hemodynamic goals for uncorrected TOF include:
the severity of the dysrhythmias and right heart failure. Reentry
 Maintain normal sinus rhythm to augment RV diastolic filling.
atrial tachydysrhythmias can be managed either medically or by
 Maintain adequate RV preload to relieve the dynamic RVOT
radiofrequency ablation techniques. Right ventricular systolic
dysfunction may require exogenous inotropic support, especially
 Reduce chronotropy to minimize RVOT muscular infundibular
as CO requirements increase during pregnancy and delivery.
Heart rates should be kept elevated to both minimize tricuspid
 Avoid increases in inotropy (e.g. catecholamine surges during
regurgitation and to maintain pulmonary arterial flow, since RV
labor), which may worsen the dynamic RVOT obstruction.
stroke volume is already impaired. Pulmonary vascular resistance
 Maintain SVR to keep the VSD shunt going left-to-right and to
reduction will help minimize regurgitation across the tricuspid
augment right coronary artery perfusion to the hypertrophied
valve and promote forward pulmonary CO.
If the parturient with TOF is post transpulmonic valve annular
patch repair with residual severe pulmonic insufficiency, then it is
Anesthetic options
important to:
General and regional anesthesia have been used successfully in
(1) Maintain RV preload to compensate for the RV dilatation.
patients with Ebstein anomaly for labor and C/S.173,174,175 The
Augment preload with i.v. fluids and avoid sudden decreases
choice between various neuraxial techniques for labor, and
in preload following neuraxial or GA.
between regional versus GA for C/S, should be based on the
(2) Maintain RV inotropy if RV systolic dysfunction is present
patient™s condition and the desired hemodynamic goals
with appropriate inotropes (e.g. epinephrine, dopamine, mil-
(see Atrial septal defects).
rinone, dobutamine).
(3) Maintain RV chronotropy to decrease the diastolic run-off of
pulmonary artery blood into the RV through the incompetent
Coarctation of the aorta
or absent pulmonic valve. Heart rates can be maintained with
Aortic coarctation comprises approximately 6“8% of the CHD
inotropes or anticholinergics as indicated.
population. Most coarctations are located distal to the left subclavian
(4) Decrease PVR to reduce regurgitant pulmonary artery blood
artery and juxta-opposite the remnant ductus arteriosus tissue (liga-
flow back into the lower resistant RV during diastole (see
mentum arteriosum). Patients with an uncorrected coarctation who
Table 1.9).
reach adulthood generally develop collateral blood flow through
nonductal arteriosus mechanisms to allow for viable postcoarctation
Anesthetic options
distal aortic perfusion. Clinically, patients with aortic coarctation
exhibit proximal hypertension, distal hypotension, systolic ejection
Various anesthetic and analgesic techniques have been used in
patients with TOF for vaginal birth and C/S.172 The choice murmurs, LV hypertrophy, and LV diastolic dysfunction. Pregnancy-
related changes (decreased SVR, increased blood volume, and
between various neuraxial techniques for labor, and between
increased CO) are poorly tolerated by patients with a coarctation.
regional versus GA for C/S, should be based on the patient™s
They are also at increased risk of ascending aortic arch complica-
condition and the desired hemodynamic goals (see Atrial septal
tions (dilatation, aneurysm, and rupture) and premature coronary

1 Cardiovascular and respiratory disorders

artery disease. Coexisting congenitally malformed bicuspid aortic Patients with congenital valvular lesions (e.g. pulmonary ste-
valves may predispose these patients to accelerated AS. nosis and AS) may present during pregnancy. The management
and anesthetic options of congenital valvular lesions are similar
to those of aquired valvular lesions (see Valvular lesions).
Management principles
Percutaneous balloon valvuloplasty is the option of choice in
Management of parturients with coarctation of the aorta is simi- patients with severe symptomatic pulmonary valvular stenosis
during pregnancy.13 Labor and C/S in patients with pulmonary
lar to that of fixed supravalvular aortic stenosis (see Aortic steno-
sis). The only caveat is that proximal BP (brain, heart) must be stenosis have been successfully managed with epidural, CSE, and
continuous spinal anesthesia.68,187,191
measured in the right upper extremity while distal BP (utero-
placental, mesenteric) should be measured in the lower extremity. Due to the rarity and heterogenicity of many adult CHD lesions,
In addition, proximal hypertension secondary to a coarctation can good evidence-based literature to guide management and
masquerade as preeclampsia, therefore separate upper and lower anesthetic options is lacking. While case reports present useful
extremity BP measurements can help differentiate the two condi- information, they may be limited in their applicability to other
tions. Preeclampsia in a parturient with a coarctation would be a patients with a similar lesion. Slight differences between repor-
unique situation that requires aggressive treatment of the proximal ted cases can have significant hemodynamic consequences.
hypertension. Although rare, the major maternal risk from a coarc- Management guidelines from experts and consensus panels
tation is aortic dissection, so BP should be aggressively managed.6 may be valuable sources of information to help plan the manage-
ment of patients with adult CHD.159 The desired hemodynamic
The treatment of upper-limb BP may lead to excessive hypoten-
sion below the aorta, causing uteroplacental insufficiency and fetal goals, the choice between regional versus GA for C/S, and analge-
compromise.8 sic options for labor pain, must be individualized and should be
based on the woman™s specific lesion and pathophysiology.

Anesthetic options
Surgically corrected congenital heart disease
Anesthetic choices and considerations are similar to those for
patients with aortic stenosis (see Aortic stenosis). Epidural, CSE, Most significant CHD lesions, or lesions that are not compatible
and spinal block for labor analgesia and C/S have been used with longevity, are usually surgically repaired before pregnancy.
successfully in parturients with coarctation of the aorta.176,177,178 Asymptomatic patients with repaired CHD usually tolerate
Single-shot spinal anesthesia is a poor choice due to the potential pregnancy and delivery without complications. However,
for precipitous cardiovascular changes.172 If GA is undertaken, BP patients with repaired CHD may have residual defects and under-
increases during endotracheal intubation and surgical stimulation lying myocardial dysfunction. Delayed repair of CHD is more
should be minimized (see Aortic stenosis). likely to be associated with residual ventricular dysfunction.
Successful surgical repair of cyanotic CHD lesions prior to preg-
nancy results in a significant improvement in maternal and neo-
Other congenital heart disease lesions
natal outcomes.192
There are many CHD lesions beyond the scope of this chapter. There are many palliative and corrective surgical procedures
Brickner et al. have described various rare CHD lesions.179,180 for CHD (see Table 1.12). Each corrected CHD lesion must be
Many lesions are incompatible with life or longevity. Some individualized and its current pathophysiological function, as
lesions are very rare and therefore are unlikely to present during well as the original anatomical lesion, should be considered
pregnancy. when planning patient management. Case reports provide inter-
There are a number of reports of patients with transposition of esting, but patient-specific, management plans. Guidelines pro-
the great vessels during pregnancy. Neuraxial and GA have been duced by the European Society of Cardiology may help guide the
successfully performed for labor and C/S.181,182,183 Pregnancy is management of surgically repaired CHD lesions.159
usually well tolerated in the asymptomatic patient with corrected
transposition of the great vessels.184
Fontan repair
Truncus arteriosus is a rare congenital malformation with a
poor prognosis if left untreated. It occurs when only one artery The Fontan procedure is synonymous with total caval-pulmonary
arises from the heart to give rise to the systemic, pulmonary, and arterial direct continuity. The procedure is usually the final stage
coronary arteries. Pregnant patients will usually have surgically in a multisurgical approach to correct certain CHD lesions (tri-
corrected lesions and survival to the reproductive years is seen. cuspid atresia, hypoplastic left heart syndrome, double inlet ven-
Management and anesthetic options for C/S have been described tricle, and pulmonary atresia). All post-Fontan patients are
in women with truncus arteriosus.185,186 considered univentricular, meaning they have been converted
The management of pregnant women presenting with complex to single ventricular physiology, which is solely responsible for
congenital heart lesions must be individualized. Both general and supporting systemic CO. This ventricle can be either a morpho-
regional anesthetic options have been used to manage pregnant logic RV or a morphologic LV. If the systemic ventricle is a mor-
patients with complex congenital heart lesions in the obstetric phologic RV (as is the case with hypoplastic left heart syndrome),
setting.187,188,189,190 then one needs to have a heightened expectation of encountering

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