Download Congenital Heart Disease - Singapore General Hospital

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Dr Masitah binte Ibrahim
Associate Consultant
Department of Neonatal &
Developmental Medicine
The Infant with
Congenital Heart Disease
Congenital heart defects (CHD) constitute the commonest birth defect
in the newborn with a reported prevalence of 8.12 per thousand live
births (National Birth Defect Registry, Singapore, 1994 to 2000).
Diagnosis may be made through routine fetal ultrasonography in
mid-trimester, especially in serious life-threatening CHD. Oftentimes,
diagnosis of CHD is not made till screening at birth. In other cases,
diagnosis is made only days to weeks after discharge. It is thus
imperative that diagnosis of CHD be considered in a symptomatic baby
even if previous clinical examination was normal.
The baby with CHD may present in various ways. History-taking may
reveal cardiac failure such as poor feeding, breathlessness, excessive
sweating, recurrent chest infections, and failure to thrive, while
syncope may suggest the presence of arrhythmias. An older child
with coarctation of aorta may have headache caused by the resulting
hypertension. A family history of CHD must be sought for, since the
risk of CHD then increases (Mother with CHD: 6% risk, Father with
CHD: 3% risk, 2 siblings with CHD: 4% risk, Previous sibling with
CHD: 2% risk). A few infants are at increased risk of CHD from
maternal uncontrolled insulin-dependent diabetes, systemic lupus
erythematosus or alcoholism (causing the fetal alcohol syndrome).
Others may be affected by maternal medications, like carbamazepine,
phenytoin or lithium (Ebstein anomaly).
Although the infant with CHD may be asymptomatic, dysmorphic
features consistent with Down syndrome or VACTERL association may
be the only clues to an underlying CHD. Central cyanosis (detected
from tongue color) implies an oxygen saturation of less than 85%.
Pulse oximetry is a useful supplementary method of screening for
mild cyanosis. There may be signs of cardiac failure, such as faltering
growth, excessive forehead perspiration, tachycardia, abnormal
pulses, poor peripheral perfusion (cold hands and feet), respiratory
distress (tachypnea, retractions), lung crepitation or rhonchi, and
hepatomegaly. Heart failure within the first week of life implies
presence of a duct-dependent lesion and constitutes an emergency.
Unlike in adults, raised jugular venous pressure cannot be assessed
in children under 4 years old. Clubbing may be visible only after 6
months old in the thumbs or toes, and is best assessed by holding the
thumbs back to back, to demonstrate loss of normal nail bed curvature.
After corrective surgery, clubbing disappears.
The commonest cardiac murmur is the innocent murmur, otherwise
known as functional or physiological murmur. Such a murmur is
generated by turbulent flow associated with anemia or inter-current
infections. Understandably, innocent murmurs generate a lot of parental
anxiety. A guide to the innocent murmur is to remember the 5 “S”s Soft (no thrill), Systolic, Short (never pansystolic), aSymptomatic and
situated at the left Sternal edge. Innocent murmurs may change with
posture, are not associated with abnormal or added heart sounds, and
antibiotic prophylaxis is not required. Note that diastolic murmurs are
never innocent. Table 1 provides a quick guide to cardiac murmurs.
CHDs may be classified into acyanotic and cyanotic. Tables 2 to 6
summarize the clinical features, CXR and ECG of some commoner
CHDs. Definitive diagnosis is usually made following referral to a
pediatric cardiologist.
Table 4. Clinical features, CXR, and ECG of CHD with mixed shunts.
Types
Clinical features
CXR
ECG
Mixed shunt (Blue and breathless)
• Present antenatally or at 2 to 3 weeks old with mild cyanosis and heart failure
• Includes most complex CHD
at birth;
Superior axis;
Complete atrio-ventric- No murmur at birth, may develop in first few weeks Normal
pulmonary vascular
Bi-ventricular hypertrophy
ular septal defects
May present with heart failure at 1 to 2 months Increased
markings and cardiomegaly at 1 month at 2 mth; RVH
Cyanosed when duct closes;
Superior axis;
Decreased or increased pulmonary
Tricuspid atresia
Usually no murmur
Absent RV voltages;
vascular
markings
Can be very well at birth
Large P-wave
Ejection systolic (ESM)
Pansystolic (PSM)
Continuous
Diastolic
Location
Upper right sternal edge (carotid thrill)
Upper left sternal edge (no carotid thrill)
Mid/lower left sternal edge
Long harsh systolic murmur + cyanosis
Left lower sternal edge (± cyanosis)
Apex (much less common)
Rare at left lower sternal edge
Left infraclavicular (± collapsing pulse)
Infraclavicular (+ cyanosis + lateral thoracotomy)
Any site (lungs, shoulder, head, hind-quarter)
Left sternal edge/apex (± carotid thrill or VSD)
Median sternotomy (± pulmonary stenosis murmur)
Apical (± VSD)
Diagnosis
Aortic stenosis
Pulmonary stenosis or atrial septal defect (ASD)
Innocent murmur
Tetralogy of Fallot
Ventricular septal defect (VSD)
Mitral regurgitation
Tricuspid regurg (Ebstein anomaly)
Patent ductus arteriosus
BT shunt
Arteriovenous fistula
Aortic regurgitation
Tetralogy of Fallot (ToF), repaired
Mitral flow (rarely stenosis)
Table 2. Clinical features, CXR, and ECG of CHD with Left –to-Right shunts.
Types
Clinical features
CXR
Left to right shunt (Pink ± breathless)
• No signs or symptoms on day 1 because of high pulmonary vascular resistance
• Can develop signs of heart failure later, at 1 week
Secundum ASD (80% of ASDs)
ASD (atrial septal
Increased pulmonary vascular
Soft ESM at upper left sternal edge
defect)
markings
Fixed split S2
Partial R bundle branch
block; RVH
VSD (ventricular septal
defect)
Normal
Normal
Usually normal;
Large PDA may cause increased
pulmonary markings
Usually normal;
Large PDA may cause LV
volume loading
PDA
80-90% asymptomatic; quiet P2
loud pan-systolic murmur with thrill at lower left
sternal edge (the louder, the smaller the defect)
Asymptomatic or heart failure
Continuous or systolic murmur at left infraclavicular area
ECG
Table 3. Clinical features, CXR, and ECG of CHD with Right-to-Left Shunts.
Types
Clinical features
CXR
Right to left shunt (Cyanosed): Those that present on day 1 to 3 are usually duct-dependent
Usually asymptomatic
Usually normal;
Rarely severe cyanosis at birth
Tetralogy of Fallot
‘Boot-shaped’ heart, reduced
Loud harsh ESM at upper sternal edge
vascular markings if older
Usually do not develop heart failure
Transposition of great
‘Egg-on-side’ appearance;
arteries
Increased pulmonary vascular markings
Cyanosed when duct closes
Usually no murmur
Normal at birth;
Very sick, unless antenatally diagnosed
Pulmonary atresia
‘Boot-shaped’ heart when much older;
Decreased pulmonary vascular markings
Cyanosed at birth
Massive cardiomegaly;
Ebstein anomaly
Loud PSM, lower left sternal edge
Reduced pulmonary vascular markings
Very sick
ECG
Normal at birth;
RVH when older
Normal
May have superior axis
A Quarterly Jan - Apr 2013
Table 5. Clinical features, CXR, and ECG of CHD with obstruction in a WELL child
Types
Clinical features
CXR
Obstruction in the well child (Neither blue nor breathless) – Asymptomatic murmur
Aortic stenosis
ESM at upper sternal edge + carotid thrill
Normal
May have thrill at upper left sternal edge
Pulmonary stenosis
ESM at upper sternal edge from day 1 ± thrill
Normal
Quiet P2
Vascular rings and
Stridor
Lobar emphysema due to bronchial
slings
May have asymptomatic
compression
ECG
LVH
RVH
Vertical Version
Different Variations
Normal
Table 6. Clinical features, CXR, and ECG of CHD with obstruction in a SICK newborn
Types
Clinical features
CXR
Obstruction in the sick newborn : diagnosed when the PDA closes, or antenatal presentation
Absent femoral pulses;
Normal or cardiomegaly from Normal
Coarctation of aorta
No murmur; Right heart failure
heart failure
Breathless and severely acidotic
Hypoplastic left heart
syndrome
Critical aortic stenosis
Table 1. Differential diagnosis of cardiac murmurs
Nature
MICA (P) 101/05/2013
Total anomalous
pulmonary venous
connection
Often antenatally diagnosed
Absent femoral and brachial pulses
No murmur; Right heart failure
Breathless and severely acidotic
Rare, usually antenatally diagnosed
Absent femoral and brachial pulses
No murmur; Right heart failure
Breathless and severely acidotic
Poor prognosis
Cyanosis and collapse on day 1- 7
No murmur
Hepatomegaly, low cardiac output
May be breathless and severely acidotic
May present later if unobstructed, with murmur or
heart failure
ECG
Normal or cardiomegaly with
heart failure
Absent left ventricular forces
Normal or cardiomegaly with
heart failure
LVH
Normal/small heart;
Snowman in a snowstorm’
appearance
Normal in neonate;
RVH in older child
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Pulmonary
Artery
Heart Disease in
Pregnancy
Pulmonary
Vein
Right
Atrium
Left
Atrium
Mitral
Valve
Left
Ventricle
Pulmonary
Valve
Aortic
Valve
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Ventricle
Tricuspid
Valve
Inferior Vena Cava
Management of Labour
in Women with
cardiac disease
The Infant with
Congenital Heart
Disease
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Dr Chow Weien, Associate Consultant
Dr Tan Ju Le, Senior Consultant
National Heart Centre Singapore
Adult Congenital
Heart Disease in Pregnancy
Congenital Heart Disease (CHD) is the most common birth defect, affecting close to 0.8% of all live births. Patients
with congenital heart disease are now detected and diagnosed much earlier. In addition the advancement in
medical and surgical care has improved the survival outcomes of patients with CHD. This has resulted in a
significant number of women reaching childbearing age. However they are at a higher risk of maternal, fetal
and neonatal complications. Therefore it is important that women with CHD receive appropriate pre-pregnancy
counseling and management during their pregnancy.
Physiological Changes that occur during Pregnancy
In order to meet the increased metabolic demands of the mother and the fetus, pregnancy
induces major changes in the cardiovascular system. Around the 24th week of gestation,
the plasma volume reaches its maximum of approximately 40% above baseline. Cardiac
output increases by 30-50% during pregnancy. The increase in cardiac output aggravates
the haemodynamic burden in obstructive lesions such as valvular stenosis as well as
pulmonary vascular disease. During labour, uterine contractions, pain, anxiety, exertion,
bleeding, anaesthesia, and infection may contribute to significant rises in blood pressure
and cardiac output. During the postpartum period, return of blood to the maternal
circulation associated with uterine involution and resorption of leg oedema can also cause
a pronounced increase in cardiac preload and cardiac output. It usually takes several
weeks before pregnancy-induced hemodynamic changes return back to normal.
Maternal Cardiovascular Risk Assessment
Based on the European Society of Cardiology Guidelines on the management of
cardiovascular diseases during pregnancy published in 2011, women with CHD should
first be counseled on the risk of pregnancy before they decide to become pregnant. The
Modified World Health Organization (WHO) Classification4 further provides a form of risk
assessment for various congenital heart conditions as outlined in Table 1 and Table 2.
Both ventricular septal defects (VSD) and atrial septal defects (ASD) are common
congenital defects seen in pregnant women. Most patients with ASD and VSD may be
asymptomatic before pregnancy.
Ventricular Septal Defect
Atrial Septal Defect
Risk Risk of pregnancy by medical
class condition
No detectable increased risk of maternal
I
mortality and no/mild increase in
morbidity.
Small increased risk of maternal mortality
II
or moderate increase in morbidity.
Significantly increased risk of maternal
mortality or severe morbidity. Expect
counselling required. If pregnancy is
III decided upon, intensive specialist cardiac
and obstetric monitoring needed
throughout pregnancy, childbirth, and the
puerperium.
Extremely high risk of maternal
mortality or severe morbidity; pregnancy
IV contraindicated. If pregnancy occurs
termination should be discussed. If
pregnancy continues, care as for class III.
Table 1. Modified WHO Classification of Maternal
Cardiovascular Risk Principles
Patent Ductus Arteriosus
Defect
Defect
Management of Labour
Conditions in which pregnancy risk is WHO I
•Uncomplicated, small or mild
-pulmonary stenosis
-patent ductus arteriosus
-mitral valve prolapse
•Successfully repaired simple lesions (atrial or ventricular
septal defect, patent ductus arteriosus, anomalous pulmonary venous drainage).
Patent Ductus Arteriosus (PDA)
•Unoperated atrial or ventricular septal defect
WHO II-III (depending on individual)
•Mild left ventricular impairment
•Hypertrophic cardiomyopathy
•Native or tissue valvular heart disease not considered
WHO I or IV
Bicuspid Aortic Valve
•Systemic right ventricle
•Fontan circulation
Pulmonary Valve Stenosis
•Marfan syndrome without aortic dilatation
•Aorta <45mm in aortic disease associated with bicuspid
aortic valve
•Repaired coarctation
WHO III
•Mechanical valve
•Cyanotic heart disease (unrepaired)
•Other complex congenital heart disease
•Aortic dilatation 40-45 mm in Marfan syndrome
•Aortic dilatation 45-50 mm in aortic disease associated
with bicuspid aortic valve
•Previous peripartum cardiomyopathy with any residual
impairment of left ventricular function
Aortic
valve
A small and uncomplicated patent ductus arteriosus (PDA) shunts blood from
the aorta to the pulmonary artery but is unlikely to cause significant complications
during pregnancy. The risk of complications during pregnancy becomes higher if
a large PDA has resulted in left ventricular dilatation or pulmonary hypertension.
Bicuspid aortic valve rarely causes significant problems during pregnancy
unless it is associated with severe and symptomatic aortic stenosis. Pregnant
women with severe aortic stenosis are at high risk for complications. They are
more likely to develop heart failure and premature labour during their pregnancy,
and are at greater risk for complications even after pregnancy. These patients
with severe aortic stenosis may need to have their valve replaced before they
become pregnant. The bicuspid aortic valve may also close incompletely giving
rise to aortic regurgitation. If the aortic regurgitation is severe, it will lead to left
ventricular dilatation and increase the risk of complications during pregnancy. In
women of childbearing age, bio-prosthetic aortic valve is preferred because no
anticoagulation is required.
•Severe mitral stenosis, severe symptomatic aortic stenosis
Pulmonary
valve
ASD can result in chronic left-to-right shunting of blood, which can cause
overload of the right ventricle especially during pregnancy.
•Most arrhythmias
WHO II (if otherwise well and uncomplicated)
•Severe systemic ventricular dysfunction (LVEF <30%,
NYHA III-IV)
Stenotic Aortic Valve
Atrial Septal Defect (ASD)
•Repaired tetralogy of Fallot
Conditions in which pregnancy risk is WHO II or III
•Pulmonary arterial hypertension of any cause
Stenotic Pulmonary Valve
A large VSD can lead to significant overload of the left ventricle and heart failure
early in life and large VSDs are generally repaired in childhood. As a result most
unrepaired VSDs encountered in the adult population are small and pregnancy
is well tolerated.
Nonetheless women with isolated repaired VSD or ASD have a low risk for cardiac
complications of less than 1% during pregnancy. The risk of complications
however becomes higher when there is a reversal of shunt from right-to-left
through a large ASD or VSD with pulmonary hypertension. These patients need
to be counseled against pregnancy and are advised to practice safe and effective
forms of contraception. This is because Eisenmenger Syndrome poses a high
risk to both the mother and the fetus, with a reported high maternal death rate of
40% to 50% and a miscarriage rate of 30%.
•Atrial or ventricular ectopic beats, isolated
Conditions in which pregnancy risk is WHO IV
(pregnancy contraindicated)
Defect
Ventricular Septal Defect (VSD)
•Marfan syndrome with aorta dilated >45 mm
•Aortic dilatation >50 mm in aortic disease associated with
bicuspid aortic valve
•Native severe coarctation
Table 2. Modified WHO Risk Assessment for Congenital Heart
Conditions
There may be a slightly increased risk of miscarriage and pre-term birth in
women with severe pulmonary stenosis (PS). However unlike patients with
severe aortic stenosis, pregnancy is generally well tolerated even in patients with
moderate to severe PS and the condition is generally associated with a low risk
of complications during pregnancy.
Management of Patients with Congenital Heart Disease during
Pregnancy
Management of patients with congenital heart disease during pregnancy requires
an experienced team comprising the cardiologist, obstetrician and anaesthetist
in a specialized centre. Patients with preexisting congenital heart disease or other
high-risk cardiac conditions can be referred to a joint clinic such as the SGHNational Heart Centre Joint Cardiology-Obstetric Clinic for further management
and assessment using echocardiography or cardiac MRI. These patients will
require a detailed physical examination, closer monitoring and follow up.
The team will decide on the mode of delivery based on the underlying CHD
condition and risk assessment. Normal vaginal delivery for women with CHD
is still preferred except in high-risk patients while assisted vaginal delivery or
caesarean section may be recommended to avoid the hemodynamic changes that
occur during normal vaginal delivery and to minimize the overall cardiac risks.
Outcomes of Pregnancy in Women with CHD
Majority of patients with CHD can undergo normal pregnancy and delivery
without complications. However it is important that physicians should conduct
a thorough cardiac risk assessment and high-risk patients with CHD should be
managed by an experienced team.
Women with
cardiac disease
in
Dr Devendra Kanagalingam
Senior Consultant
Dept of Obstetrics & Gynaecology
Singapore General Hospital
Cardiac disease in pregnancy is increasingly common. This is, in
part, due to advances in medical care which have allowed infants
with congenital heart disease to be treated and to bear children.
85% of infants with congenital heart disease now survive into
adulthood. Myocardial infarction and ischaemic heat disease
are also increasingly seen in pregnant women due to increasing
maternal age and increasing prevalence of obesity, diabetes,
hypertension and smoking. In developed countries such as the UK,
cardiac disease is now the most common cause of maternal deaths.
In making decisions about mode of delivery and the management
of labour in these women, it is important to consider the following:
undertake pregnancy against medical advice. These women as well
as those with significant cardiac failure or very poor ventricular
ejection fraction are usually advised delivery by caesarean section.
Other examples of cardiac conditions which may require caesarean
section for delivery are severe aortic stenosis and Marfan Syndrome
with aortic root dilatation. With aortic root dilatation, there is an
increased risk of aortic dissection during pregnancy. Decisions on
mode of delivery are ultimately made by a multi-disciplinary team
comprising the cardiologist or cardiothoracic surgeon, anaesthetist,
obstetrician and neonatologist after a discussion with the pregnant
woman.
1) The spectrum of cardiac conditions is diverse and must not be
considered as a single entity
If labour and vaginal delivery is deemed possible, an individualised
care plan is usually drawn up to highlight specific aspects
of labour which would be managed differently from low-risk
labours. Prophylactic antibiotics to prevent infective endocarditis
are a consideration for women with valvular heart diseases or
surgically-corrected congenital heart diseases in which turbulent
flow across these structures may predispose to bacterial seeding
and subsequent infection. Interestingly, current evidence-based
guidelines recommend that prophylactic antibiotics are not required
for women at risk of infective endocarditis in labour or delivery
regardless of the underlying cardiac condition. However, given
that infective endocarditis is a serious complication with potentially
devastating consequences, the decision for antibiotic prophylaxis is
usually individualised. Women who have prosthetic heart valves, for
instance, or high risk circumstances, such as prolonged rupture of
membranes are usually considered for antibiotic prophylaxis. The
long-standing practice of shortening the second stage by performing
a forceps or vacuum delivery once full dilatation is reached is now
thought to be unnecessary. Instead, these instruments are now
used only if the second stage is prolonged. This is because women
who are deemed fit for labour can usually tolerate the additional
cardiac stresses from bearing down in the second stage. In the
third stage of labour, oxytocin is usually used to ensure effective
uterine contractions and prevent postpartum haemorrhage instead
of syntometrine. This is because syntometrine can cause transient
maternal hypertension which may be detrimental to cardiac function.
2) Women who have very poor cardiovascular reserve and show
cardiovascular compromise prior to labour are often delivered
by caesarean section
3) Most women are deemed suitable for labour with a view to
vaginal birth but need to have an individualised care plan, again
specific to their cardiac status and condition.
Undeniably, there are increased demands to the cardiovascular
system in the course of a normal labour. Changes as a result of pain
and sympathetic response can be mitigated to a certain extent by
effective analgesia such as epidural analgesia. During the second
stage of labour, voluntary and involuntary expulsive efforts by the
mother result in an increase in cardiac output. These additional
demands on the heart are well-tolerated by healthy women and by
most women with cardiac disease who have been asymptomatic
antenatally. It is important to remember that 80% of the physiological
increase in cardiac output in pregnancy has already taken place by
12 weeks gestation and, if the woman with known cardiac disease
remains well, it is likely that she will tolerate the additional stresses
in labour without difficulty. It is for this reason that many women
can be planned for labour and vaginal delivery. A number of women
who are symptomatic during pregnancy and are deemed to be
at risk for further decompensation, may be advised delivery by
planned caesarean section. In general, these women would have
cardiac conditions which contraindicate pregnancy and would have
been advised to avoid pregnancy or have been offered a termination
of pregnancy. One example of this is Eisenmenger Syndrome, in
which an uncorrected ventricular septal defect (VSD) leads to
pulmonary hypertension and eventual reversal of the flow through
the VSD from a left-to-right shunt to a right-to-left shunt. The fall
in peripheral vascular resistance in pregnancy worsens the right-to
left shunt and the patient is cyanotic. Women with Eisenmenger’s
Syndrome have a 40% mortality during pregnancy and, therefore,
Cardiac disease in pregnancy is increasing in prevalence and is,
therefore, an important clinical problem. There is much reason
for optimism in that, when managed appropriately in a multidisciplinary setting, many women can achieve good outcomes
without significant morbidity or mortality.