Cardiac diseases complicating pregnancy

82
CARDIAC DISEASES IN PREGNANCY ANCY CHACKO GOVT. CON

Transcript of Cardiac diseases complicating pregnancy

Page 1: Cardiac diseases complicating pregnancy

CARDIAC DISEASES

IN PREGNANCY

ANCY CHACKO

GOVT. CON

Page 2: Cardiac diseases complicating pregnancy

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.

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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.

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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

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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.

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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.

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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.

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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.

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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

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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.

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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

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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

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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

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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

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INCIDENCE

• 1% of pregnancies.

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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.

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TYPES OF HEART DISEASE

CONGENITAL HEART DISEASE

• Atrial septal defect

• Ventricular septal defect

• Patent ductus arteriosus

• Tetralogy of fallot

• Eisenmengers complex

• Coarctation of aorta

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TYPES OF HEART DISEASE

RHEUMATIC HEART DISEASE

• Mitral stenosis

• Mitral regurgitation

• Double mitral disease

• Aortic stenosis

• Aortic regurgitation

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TYPES OF HEART DISEASE

OTHER RARER FORMS

• Cardiomyopathy

• Hypertensive heart disease

• Myocardial ischemia or coronary artery disease

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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.

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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.

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ACYANOTIC CONGENITAL HEART

DISEASE

ATRIOVENTRICULAR DEFECTS

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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.

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ACYANOTIC CONGENITAL HEART

DISEASE

VENTRICULAR SEPTAL DEFECT AND PATENT ARTERIAL DUCT

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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

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ACYANOTIC CONGENITAL HEART

DISEASE

PULMONARY STENOSIS

does not usually give rise to symptoms during pregnancy.

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ACYANOTIC CONGENITAL HEART

DISEASE

AORTIC STENOSIS

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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.

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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.

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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

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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.

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ACYANOTIC CONGENITAL HEART

DISEASE

COARCTATION OF THE AORTA

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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

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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.

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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.

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ACYANOTIC CONGENITAL HEART

DISEASE

EBSTEIN’S ANOMALY

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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.

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CYANOTIC CONGENITAL HEART

DISEASE

TETRALOGY OF FALLOT

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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

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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

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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

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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.

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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.

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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

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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

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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.

Page 47: Cardiac diseases complicating pregnancy

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.

Page 48: Cardiac diseases complicating pregnancy

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.

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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.

Page 50: Cardiac diseases complicating pregnancy

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

Page 51: Cardiac diseases complicating pregnancy

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.

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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.

Page 53: Cardiac diseases complicating 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.

Page 54: Cardiac diseases complicating pregnancy

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.

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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.

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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

Page 57: Cardiac diseases complicating pregnancy

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 .

Page 58: Cardiac diseases complicating pregnancy

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.

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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.

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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.

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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.

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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.

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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

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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

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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.

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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

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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.

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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

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MATERNAL EFFECTS

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FETAL AND NEONATAL

EFFECTS

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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.

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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

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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

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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

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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

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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

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MANAGEMENT OF NYHA

CLASS I AND II DISEASE

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MANAGEMENT OF NYHA

CLASS III AND IV DISEASE

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USUAL MEDICAL MANAGEMENT AND

PROTOCOLS FOR NURSE PRACTITIONERS

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Drug Therapy

• Heparin

• Furosemide

• Digitalis

• Tocolytics

• Beta-Blockers

• Quinidine

• Disopyramide Phosphate

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NURSING MANAGEMENT

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