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CARDIAC DISEASES
IN PREGNANCY
ANCY CHACKO
GOVT. CON
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Cardiac Output
• rises significantly as early as the first trimester of
pregnancy.
• It continues to rise and reaches a plateau
between 28 and 34 weeks of gestation.
• It rises in response to the plasma volume
increase, hormonal influences, and autonomic
nervous system (ANS) influences.
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Blood Volume
• Blood volume increases by plasma volume
expansion and red blood cell multiplication. The
mean plasma volume increase is 50% over the
prepregnant volume, and red cell multiplication
is in proportion to volume expansion if nutritional
requirements are met.
• Increased volume maintains a dilated systemic
vasculature.
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Hormonal Influences
• Increased oestrogen leads to systemic
vasodilation. Vasodilation increases cardiac
output because of lowered peripheral resistance.
Prolactin increases myocardial contractility
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Autonomic Nervous System
• when the ANS is activated or blocked, dramatic
changes in the maternal blood pressure can
result.
• The cardiovascular system is hyper filled from
increased blood volume and hyper dynamic
because of the predominance of the ANS.
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Venous Pressure
• Increased venous pressure, especially in the
lower extremities, occurs in pregnancy. This can
lead to a normal finding of an accentuated
jugular pulse.
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Heart
• A slightly enlarged heart sometimes occurs in
pregnancy because of the upward and leftward
anatomic displacement of the heart. Benign
dysrhythmias can occur, presumably because of
the normal influences on myocardial contractility.
NORMAL CARDIAC PHYSIOLOGY
Antepartum
Inferior Venacava
• When the weight of the gravid uterus lies against
the inferior vena cava, partial or total occlusion
reduces return volume to the heart and
subsequent output.
NORMAL CARDIAC PHYSIOLOGY
Intrapartum
• Uterine contractions normally increase cardiac
output 20% to 30% and stroke volume because
of increased intravascular volume, which leads
to an increase in the workload of the heart.
• During the contraction, an additional 300-500 ml
of blood is forced out of the uterus into the
maternal circulation
• The workload can be relieved by positioning the
patient laterally and by administering pain relief,
especially with epidural anaesthesia
NORMAL CARDIAC PHYSIOLOGY
Postpartum
• In the immediate postpartum period, there is a
high risk for fluid volume overload caused by
remobilization of fluid into vascular
compartments.
PHYSIOLOGICAL CHANGES IN
PREGNANCY
• Increase in cardiac output by 40%
• Increase in stroke volume by 10%
• Increase in heart rate by 10% or 15bpm
• Increase in blood volume by 40%
• Decrease in peripheral resistance and diastolic
blood pressure
Additional factors responsible for
deterioration of function of the
damaged heart
• Advancing age
• Left ventricular hypertrophy
• Appearance of risk factors such as infection,
anaemia, preeclampsia, excessive weight gain
and multiple pregnancies, which further increase
the cardiac load
• History of previous heart failure
• Inadequate supervision
New York Heart Associations’
Functional Classification of Heart
Disease
Class I No limitation of activities; no symptoms
from ordinary activities.
Class II Slight, mild limitation of activity;
comfortable with rest or with mild exertion. More
than ordinary physical activity results in fatigue,
palpitation, dyspnea, or anginal pain
New York Heart Associations’
Functional Classification of Heart
Disease
Class III Marked limitation of activity;
comfortable only at rest. Less than ordinary
physical activity causes fatigue, palpitation,
dyspnea, or anginal pain.
Class IV Confined to bed or chair; any
physical activity brings on discomfort and
symptoms occur at rest. If any physical activity is
undertaken, discomfort is increased
INCIDENCE
• 1% of pregnancies.
Etiology
• Rheumatic heart (75%): mitral valve affection is
the commonest followed by aortic valve then
both or others.
• Congenital heart diseases (10%):
Acyanotic (left to right shunt): more common, includes
septal defects and patent ductus arteriosus.
Cyanotic (right to left shunt): e.g. Fallot’s tetralogy and
Eisenmenger’s syndrome which is more dangerous
carries a maternal mortality rate exceeding 25%.
• Others (5%): e.g. ischaemic heart disease,
arrhythmias and cardiomyopathy.
TYPES OF HEART DISEASE
CONGENITAL HEART DISEASE
• Atrial septal defect
• Ventricular septal defect
• Patent ductus arteriosus
• Tetralogy of fallot
• Eisenmengers complex
• Coarctation of aorta
TYPES OF HEART DISEASE
RHEUMATIC HEART DISEASE
• Mitral stenosis
• Mitral regurgitation
• Double mitral disease
• Aortic stenosis
• Aortic regurgitation
TYPES OF HEART DISEASE
OTHER RARER FORMS
• Cardiomyopathy
• Hypertensive heart disease
• Myocardial ischemia or coronary artery disease
ACYANOTIC CONGENITAL HEART
DISEASE
ASD
• After bicuspid aortic valve (which is much
commoner in males), secundum ASD is the
commonest congenital cardiac defect in adults.
Arrhythmias do not usually develop until middle
age.
ACYANOTIC CONGENITAL HEART
DISEASE
ASD
• No problems are anticipated during pregnancy
but acute blood loss is poorly tolerated. It can
cause massive increase in left-to-right shunting
and a precipitous fall in left ventricular output,
blood pressure, coronary blood flow and even
cardiac arrest.
ACYANOTIC CONGENITAL HEART
DISEASE
ATRIOVENTRICULAR DEFECTS
ACYANOTIC CONGENITAL HEART
DISEASE
ATRIOVENTRICULAR DEFECTS
• Atrioventricular defects are usually associated
with regurgitation through the atrioventricular
valves. They frequently cause heart failure in
infancy and require early surgery.
• pulmonary hypertension is more frequent if there
is significant mitral regurgitation.
• Residual mitral regurgitation or paced cardiac
rhythm may follow previous surgical treatment.
ACYANOTIC CONGENITAL HEART
DISEASE
VENTRICULAR SEPTAL DEFECT AND PATENT ARTERIAL DUCT
ACYANOTIC CONGENITAL HEART
DISEASE
VENTRICULAR SEPTAL DEFECT AND PATENT
ARTERIAL DUCT
• these defects which increase the volume load of
the left ventricle, are well tolerated in pregnancy
unless the defects are large and complicated by
pulmonary vascular disease
ACYANOTIC CONGENITAL HEART
DISEASE
PULMONARY STENOSIS
does not usually give rise to symptoms during pregnancy.
ACYANOTIC CONGENITAL HEART
DISEASE
AORTIC STENOSIS
ACYANOTIC CONGENITAL HEART
DISEASE
AORTIC STENOSIS
• cause problems during pregnancy
• Least uncommon is aortic valve stenosis..
• If symptoms are absent, the ECG is normal
(apart from voltage changes of left ventricular
hypertrophy) and an exercise test is well
performed, pregnancy will usually be
accomplished without trouble.
ACYANOTIC CONGENITAL HEART
DISEASE
AORTIC STENOSIS
• Achievement of the target heart rate with a
normal rise of blood pressure without the
development of ST- or T-wave changes can be
taken as an indication that pregnancy will be
safe. It should if possible be carried out before
advising about pregnancy
• Echocardiography (echo) will show good left
ventricular function.
• The Doppler transaortic valve velocity will rise
during pregnancy if the stroke volume increases
in abnormal fashion.
ACYANOTIC CONGENITAL HEART
DISEASE
AORTIC STENOSIS
• Any patient who develops angina, dyspnoea or
resting tachycardia should be admitted to hospital
for rest. Administration of a beta adrenergic
blocking drug will increase diastolic coronary flow
time and left ventricular filling with resultant
improvement in angina and left ventricular
function.
• If despite these measures angina, pulmonary
congestion and left ventricular failure persist or
progress, balloon aortic valvotomy to be
considered
•
ACYANOTIC CONGENITAL HEART
DISEASE
• If surgery is needed, the foetus should be
delivered by caesarean section under general
anaesthetic before valve replacement. Delivery will
be followed by immediate improvement in the
mother and in operating conditions for the
surgeon.
• If aortic valve replacement is carried out during
pregnancy on account of the mother’s poor
condition the foetus is likely to die either during
induction or during cardiopulmonary bypass.
ACYANOTIC CONGENITAL HEART
DISEASE
COARCTATION OF THE AORTA
ACYANOTIC CONGENITAL HEART
DISEASE
COARCTATION OF THE AORTA
• Aortic coarctation may first be diagnosed during
pregnancy and should always be excluded when
raised blood pressure is recorded at booking.
• Although the blood pressure can be lowered
adequate control cannot be maintained during
exercise which brings the risk of cerebral
haemorrhage or aortic dissection
• The patient should therefore be advised to rest
and avoid exertion
ACYANOTIC CONGENITAL HEART
DISEASE
COARCTATION OF THE AORTA
• .Surgery can be carried out during pregnancy as
cross clamping of the aorta does not affect lower
segment blood flow but the risk of local
complications to the aorta is increased.
• The risk of dissection is increased in patients with
pre-existing aortic abnormality associated with
coarctation, Marfan syndrome or other inherited
disorders of connective tissue.
ACYANOTIC CONGENITAL HEART
DISEASE
COARCTATION OF THE AORTA
• Normal delivery with an accelerated second stage
should be planned unless anticipated obstetric
problems suggest that caesarean section would
be preferable.
• Foetal growth is normal and pre-eclamptic
toxaemia is rare.
ACYANOTIC CONGENITAL HEART
DISEASE
EBSTEIN’S ANOMALY
ACYANOTIC CONGENITAL HEART
DISEASE
EBSTEIN’S ANOMALY
• Patients with Ebstein’s anomaly of the tricuspid
valve have ventricular displacement of the septal
and/or posterior leaflets of the tricuspid valve
together with a sail-like anterior leaflet. There is
usually an associated atrial communication.
• Cyanosis may develop and lead to poor foetal
growth but if acyanotic; they usually do well in
pregnancy.
CYANOTIC CONGENITAL HEART
DISEASE
TETRALOGY OF FALLOT
CYANOTIC CONGENITAL HEART
DISEASE
TETRALOGY OF FALLOT
• The association of severe right ventricular outflow
tract obstruction with a large sub aortic ventricular
septal defect and over-riding aorta causes right
ventricular hypertrophy and right-to-left shunting
with cyanosis.
• Pregnancy is tolerated well but foetal growth is
poor with a high rate of miscarriage, prematurity
and small-for-dates babies.
• The haematocrit tends to rise during pregnancy in
cyanosed women
CYANOTIC CONGENITAL HEART
DISEASE
TETRALOGY OF FALLOT
• The arterial saturation falls markedly on effort so
rest is prescribed to optimize foetal growth but
subcutaneous heparin should be given to prevent
venous thrombosis and paradoxical embolism.
• Women who have had a previous surgical
correction of the tetralogy do well in pregnancy
CYANOTIC CONGENITAL HEART
DISEASEEISENMENGER SYNDROME
• Pregnancy in women with
pulmonary hypertension
associated with reversed
central shunt carries high risk.
• In women with ventricular
septal defect (Eisenmenger
complex) it may be as high as
50%.
• Sterilization should be advised
or abortion followed by
sterilization
CYANOTIC CONGENITAL HEART
DISEASE
EISENMENGER SYNDROME
• Women with pulmonary hypertension who still have
predominant left-to-right shunts are at lesser risk and may
do well during pregnancy.
• If a woman with Eisenmenger syndrome insists on
continuing her pregnancy, she should rest as much as
possible and be admitted to hospital by the end of the
second trimester or as soon as the resting arterial
saturation starts to fall.
• She should then be kept in hospital with continuous pulse
oximetry, 60% oxygen by nasal cannulae and prophylactic
subcutaneous heparin.
CYANOTIC CONGENITAL HEART
DISEASE
EISENMENGER SYNDROME
• Foetal growth should be carefully monitored and the baby
delivered as soon as growth slows or stops.
• Caesarean section under general anaesthesia is preferred
in order to avoid the exertion of normal labour
• Epidural analgesia or anaesthesia cause systemic
vasodilatation and a fall in arterial saturation even with
maximal hydration
• Oximetry, subcutaneous heparin and passive
physiotherapy should be continued and mobilization should
proceed only slowly.
• Nebulized prostacycline can be used to try to prevent
pulmonary vasoconstriction.
CYANOTIC CONGENITAL HEART
DISEASE
EISENMENGER SYNDROME
• When sudden death occurs (usually in the postpartum
period) resuscitation is rarely successful and no additional
cause is found at autopsy.
• Death is usually preceded by vagal slowing, a fall in blood
pressure and oxygen saturation followed by ventricular
fibrillation
CYANOTIC CONGENITAL HEART
DISEASE
PRIMARY PULMONARY HYPERTENSION
• Causes great loss of cardio respiratory reserve. The right
ventricle may be unable to increase its stroke output and
tachycardia leads to right ventricular ischaemia and failure.
Dyspnoea may increase to a crippling level and the
pulmonary vascular disease may progress.
• PPH may occur in as many as 14% of women with SLE so
exclusion of this should be a routine part of the
assessment of fitness for pregnancy of such women.
• Pulmonary embolism may cause dyspnoea of recent onset
but in PPH an ECG will show right ventricular hypertrophy
and echocardiography is immediately diagnostic
CYANOTIC CONGENITAL HEART
DISEASEMITRAL STENOSIS
• remains most common potentially lethal
pre-existing heart condition in
pregnancy.
• Dyspnoea may have been absent or
unremarked on before the pregnancy
• It may be missed during routine
antenatal examination because the
murmur is diastolic and sub mammary.
• The first indication of trouble is sinus
tachycardia at rest. The anxiety caused
by the dyspnoea increases the
tachycardia and exacerbates the
problem.
CYANOTIC CONGENITAL HEART
DISEASE
MITRAL STENOSIS
• The mitral stenosis may previously not have been
recognized and should pulmonary congestion or oedema
develop in any pregnant woman chest radiograph and
echocardiography are mandatory.
• Patients with mitral stenosis complicated by pulmonary
hypertension are less vulnerable to the development of
pulmonary oedema but tend to develop congestive heart
failure.
• The ECG shows left atrial P waves and right axis deviation.
• The chest X-ray shows a small heart but with prominence
of the left atrial appendage and left atrium and pulmonary
congestion or oedema.
CYANOTIC CONGENITAL HEART
DISEASE
MITRAL STENOSIS
• Oxygen should be given and the heart rate slowed by relief
of anxiety with a sedative or opiate, 20 mg of intravenous
frusemide administered and metoprolol 50 or l00 mg as
necessary to secure and maintain a heart rate of under 90
beats/min.
• Most young women have mitral valves which are suitable
for balloon valvotomy and this should be carried out after
the patient’s condition has improved. If necessary she can
safely be moved to a hospital with major cardiac facilities. If
the mitral valve is unsuitable, a beta blocking drug can be
used throughout pregnancy.
CYANOTIC CONGENITAL HEART
DISEASE
MITRAL STENOSIS
• Digoxin should only be used if atrial fibrillation occurs as it
does not slow the heart in sinus rhythm.
• If an open operation on the mitral valve is going to be
required, this should be deferred until after delivery
• Epidural analgesia or anaesthesia is suitable for the patient
with mitral stenosis provided it is not complicated by severe
pulmonary hypertension and right ventricular failure.
CYANOTIC CONGENITAL HEART
DISEASE
MITRAL AND AORTIC VALVE DISEASE
• Individual assessment of the severity of mitral and/or aortic
valve obstruction determines the likely tolerance of
pregnancy.
• Rheumatic aortic stenosis is always associated with mitral
stenosis and sometimes also with tricuspid valve
involvement.
• Atrial fibrillation may develop at a young age in patients
with multi valve disease and if this occurs during
pregnancy, DC cardio version should be carried out
CYANOTIC CONGENITAL HEART
DISEASE
MITRAL VALVE PROLAPSE
• Floppy mitral valve may be sporadic or inherited as a
dominant condition in some families with variants of Marfan
syndrome.
• Pregnancy is well tolerated.
CYANOTIC CONGENITAL HEART
DISEASE
MARFAN SYNDROME
• The treatment of women with Marfan syndrome who
already have aortic root widening but desire children
remains very difficult both with regard to the mother’s
safety and in relation to the dominant inheritance of the
condition.
• Most such patients should not undertake pregnancy until
after aortic root replacement with resuspension of the
aortic valve particularly if there is a family history of aortic
dissection or rupture.
• All patients with Marfan syndrome should be treated with a
beta blocking drug throughout pregnancy.
CYANOTIC CONGENITAL HEART
DISEASEMARFAN SYNDROME
• Despite this many women with the Marfan syndrome go through
pregnancy without complication.
• A benign family history together with echo evidence of a normal
aortic root is encouraging predictors of a successful outcome for
the Marfan woman.
CYANOTIC CONGENITAL HEART
DISEASE
INFECTIVE ENDOCARDITIS
• Infective endocarditis is rare in pregnancy but threatens the
life of both mother and child.
• Treatment is essentially the same as outside pregnancy
with emergency valve replacement if indicated.
• the baby should be delivered if viable before the maternal
operation.
• Antibiotic prophylaxis is discretionary for normal deliveries
in women with congenital or valve disease but should be
given in women with artificial heart valves or a history of
endocarditis.
CYANOTIC CONGENITAL HEART
DISEASE
Hypertrophic cardiomyopathy
• Hypertrophic cardiomyopathy (HCM) is an autosomal
dominant disease characterized by hypertrophy of the
undilated left and sometimes also the right ventricle
• HCM is not infrequently first diagnosed in pregnancy when
a systolic murmur leads to an ECG and echocardiography
study.
• Most patients are asymptomatic and do well.
• Patients with HCM respond well to pregnancy by a useful
increase in their normally reduced left ventricular cavity
size and stroke volume.
• In severe cases the left atrial pressure may rise particularly
if sinus tachycardia develops.
CYANOTIC CONGENITAL HEART
DISEASEHypertrophic cardiomyopathy
• Symptoms of shortness of breath, chest pain, dizziness or
syncope indicate the need for a blocking drug.
• Ventricular arrhythmias common in older patients are
uncommon in the young.
• Sudden death has only very rarely been reported during
pregnancy.
• It is most important in all patients to avoid vasodilatation
during labour and delivery or postpartum blood loss.
Caesarean section is required for the rare hemodynamically
compromised patient with a high left atrial pressure or for
obstetric reasons.
• It is most unusual to find hypertrophy in the infants of mothers
with HCM
CYANOTIC CONGENITAL HEART
DISEASEPERIPARTUM CARDIOMYOPATHY
• It is usually arbitrarily defined as heart failure occurring
within a month before or 6 months after child birth in women
who had not previously been known to have heart disease.
• It is alleged to cause 5% of the cardiac deaths that occur in
relation to pregnancy.
• Peripartum cardiomyopathy does not differ clinically from
dilated cardiomyopathy except in its temporal relationship to
pregnancy.
• If endomyocardial biopsy is carried out within a month of the
onset it usually shows changes of myocarditis and like acute
myocarditis occurring outside pregnancy, survivors of the
acute illness tend to improve .
CYANOTIC CONGENITAL HEART
DISEASEPERIPARTUM CARDIOMYOPATHY
• The severity varies from catastrophic to subclinical when it
may be discovered only fortuitously through
echocardiography.
• In the worse scenario fulminating pulmonary oedema and
congestive failure develop with dyspnoea, orthopnoea,
tachycardia, hypotension and fluid overload.
• The patient has a third heart sound gallop and sometimes a
mitral regurgitant murmur.
• Systemic embolism from mural thrombus may herald the on
ventricular arrhythmias or precede the development of
clinical heart failure and pulmonary embolism may further
complicate the clinical picture.
CYANOTIC CONGENITAL HEART
DISEASEPERIPARTUM CARDIOMYOPATHY
• The ECG shows sinus tachycardia and sometimes
supraventricular and ventricular ectopic beats or sustained
tachycardia. The QRS complexes may be normal, low
voltage or show a conduction defect or the changes may be
focal and suggest myocardial infarction. The chest X-ray
shows an enlarged heart with pulmonary congestion or
oedema and often bilateral pleural effusions.
Echocardiography shows dilatation which usually involves
all four chambers
• A small pericardial effusion is often present. Doppler
ultrasound shows mitral, tricuspid and pulmonary
regurgitation through structurally normal valves.
CYANOTIC CONGENITAL HEART
DISEASEPERIPARTUM CARDIOMYOPATHY
• Peripartum cardiomyopathy is more frequent in women with
multiple pregnancies probably because of the greater
haemodynamic burden.
• It also seems to be more common in women with pre-
existing structural heart disease probably because of a
reduced cardiovascular reserve which allows what would
have been subclinical to become overt. This could also
explain an alleged association with pre-eclamptic toxaemia.
There is no convincing evidence that the disorder is more
common in socially deprived, multiparous, older or black
mothers. The basis for the disease seems to be
immunological. Evidence of an infective viral origin is rarely
found.
CYANOTIC CONGENITAL HEART
DISEASEPERIPARTUM CARDIOMYOPATHY
• Occasionally a family history of dilated cardiomyopathy is
obtained and it may be that pregnancy is a trigger for the
development of immunologically based myocarditis and
heart failure in a genetically predisposed individual at a
hemodynamically vulnerable time.
CORONARY ARTERY DISEASE
Coronary atheroma is rare in young women except in
association with familial hypercholesterolaemia but angina
occasionally develops in older women who have delayed
pregnancy especially in association with hypertension,
smoking and diabetes and it is always exacerbated during
pregnancy.
When myocardial infarction occurs in pregnancy it usually
develops without preceding angina because the underlying
cause is not usually atherosclerotic.
Spontaneous coronary artery dissection is the commonest
cause and sudden severe chest pain the usual
manifestation. Most occur during late pregnancy or
peripartum and myocardial infarction has been attributed to
the administration of oxytocic agents.
PULMONARY EMBOLISM• Untreated pulmonary embolism in pregnancy has a high
mortality.
• The diagnosis is frequently missed.
• It may occur unexpectedly during pregnancy but more often
postpartum and is particularly likely in women treated by
bed rest because of pre-eclampsia or following caesarean
delivery.
• The incidence continues to be higher for the 6 weeks after
delivery than during pregnancy.
• Inherited resistance to activated protein C is found in as
many as 20% of women who develop pulmonary embolism
in pregnancy or while taking oral contraceptives
PATHOPHYSIOLOGY OF HEART DISEASE
Stroke Volume
Stroke volume is the amount of blood ejected
with each contraction of the left ventricle. It is affected by
four interrelated factors:
• Diastolic filling pressure
• Distensibility of the ventricle
• Myocardial contractility
• Aortic pressure which is the
amount of pressure the
ventricle must overcome to
push blood into the aorta
PATHOPHYSIOLOGY OF HEART DISEASE
Contractility
• There is a direct relationship between diastolic volume and
the amount of blood pumped during systole.
• The greater the diastolic filling pressure, the more the fibres
of the left ventricle stretch during diastole and the harder
they contract during systole, increasing stroke volume and
cardiac output.
• However, if the muscle fibres are stretched beyond a certain
point, there is a loss of distensibility. This loss decreases the
force of contractions and therefore decreases cardiac
output.
PATHOPHYSIOLOGY OF HEART DISEASE
Preload
• Preload is the force responsible for stretching the ventricular
muscles. It is also called diastolic filling pressure.
• If the preload is low, the ventricular muscle will not stretch
enough for effective contractility. This leads to decreased
stroke volume.
• If preload is too high, the muscle fibres will be
overstretched. This also results in decreased contractility,
leading in turn to decreased stroke volume
PATHOPHYSIOLOGY OF HEART DISEASEAfterload
• Afterload is the amount of pressure resistance in the aorta
to the emptying of the left ventricle. It is the volume in the
ventricles at the end of diastole and is also called systemic
vascular resistance.
• Systemic vascular resistance (or afterload) is measured by
taking blood pressure readings.
• The higher the afterload, the greater the force required by
the left ventricle to overcome aortic pressure with systolic
pressure to force the aortic valve to open.
• A high afterload decreases stroke volume and cardiac
output if the pressure cannot be effectively overcome.
• Right heart failure may result from persisting high afterload.
SIGNS AND SYMPTOMS
• Dyspnoea severe enough to limit usual activity
• Progressive orthopnoea
• Paroxysmal nocturnal dyspnoea
• Syncope during or immediately following
exertion
• Chest pain associated with activity
MATERNAL EFFECTS
FETAL AND NEONATAL
EFFECTS
DIAGNOSTIC TESTING
• Diagnosis of cardiac disease is made by the
presentation of symptoms.
• An electrocardiogram (ECG), an
echocardiogram, a series of laboratory tests
including cardiac enzymes and electrolytes, and
a chest radiograph are the usual means, during
pregnancy, to define the lesion or assess current
status.
• When the pregnant woman is given
anticoagulant therapy, coagulation studies are
done. If the woman is taking digitalis, therapeutic
blood levels are measured.
MANAGEMENT OPTIONS
PRE PREGNANCY
• Obstetrician and cardiologist in collaboration
• Discussion of maternal and foetal risks
• Discussion of safe and effective contraception
• Evaluate current cardiac status
• Optimize medical and surgical management
• Advise against pregnancy with certain conditions
MANAGEMENT OPTIONS
PRENATAL
• Assess functional class of heart disease
• Termination is an option with some conditions
• Optimize medical management
• Avoid or minimize aggravating factors
• Anticoagulant for certain conditions, discuss the
risks and benefits of continued warfarin therapy
vs changing to subcutaneous heparin
MANAGEMENT OPTIONS
PRENATAL
• Anaesthesiology
• Antibiotics with certain conditions
• Foetal surveillance
• Growth and foetal surveillance
• Detailed foetal cardiac ultrasonography if the
patient has congenital heart disease
MANAGEMENT OPTIONS
PRENATAL
• Anaesthesiology
• Antibiotics with certain conditions
• Foetal surveillance
• Growth and foetal surveillance
• Detailed foetal cardiac ultrasonography if the
patient has congenital heart disease
LABOUR AND DELIVERY
• Prophylactic antibiotics with certain conditions
• Avoid mental and physical stress, consider
epidural
• Labour in the left lateral and upright positions
• Monitor electromagnetic more invasive
monitoring is needed with certain conditions
• Full resuscitation facilities should be available
• Provide continuous foetal heart rate monitoring
• Assisted second stage with certain conditions
• Avoid ergotamine for the third stage
MANAGEMENT OF NYHA
CLASS I AND II DISEASE
MANAGEMENT OF NYHA
CLASS III AND IV DISEASE
USUAL MEDICAL MANAGEMENT AND
PROTOCOLS FOR NURSE PRACTITIONERS
Drug Therapy
• Heparin
• Furosemide
• Digitalis
• Tocolytics
• Beta-Blockers
• Quinidine
• Disopyramide Phosphate
NURSING MANAGEMENT