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Cardiac disease in pregnancy

Cardiac disease in pregnancy

Complicates about 1% of all pregnancy

Marked haemodynamic changes stimulated

by pregnancy has profound effect on
underlying HD.
Cardiovascular physiology during
Cardiac output increases by 50%
Almost 50% of the increase occur by 8/52
Changes more profound in multiple gestation
Cardiovascular physiology of preg.
Because significant hemodynamic alterations
are apparent early in pregnancy,
Women with severe cardiac dysfunction may
experience worsening of heart failure before
mid pregnancy.
Majority of HF also develops peripartum and
during the puerperium.
Diagnosis of Heart Failure
Many of the physiological adaptations of normal
pregnancy alter physical findings.
This makes diagnosis more difficult normal pregnancy:
Functional systolic murmurs are common
Respiratory effort may be accentuated as dyspnoea
Oedema of the leg is common after mid-pregnancy.

Important not to diagnose HF when non exist

and not to miss the diagnosis when it does exist.
Most symptoms related to
weight gain,
enlarging gravid uterus with pressure effects as well as
physiological anaemia of pregnancy.
Syncopal episodes or lightheadedness occur as a result of
mechanical compression of the gravid uterus on the IVC
leading to poor venous return to the heart and supine
hypotension syndrome.
Esp in the 3rd trimester.
Hyperventilation and orthopnea from mechanical pressure
of enlarged uterus on the diaphragm
Hyperventilation also due to effect of progesterone on the
respiratory centre
Palpitation from hyperdynamic circulation of pregnancy.
Clinical indicators of heart disease
during pregnancy.
Progressive dypsnoea
Paroxysmal nocturnal dyspsnoea- nocturnal cough
Chest pains
Easy fatigability
Fainting, dizziness, collapse
Leg swelling
Clubbing of fingers
Persistent neck vein distention raised JVP
Systolic murmur > grade 3
Persistent splitting 2nd heart sound
Diastolic murmur
Criteria for pulmonary hypertension
Pedal oedema
Coarse crepitations
Peripheral pulses abnormal characteristics
diastolic murmur heard during preg. requires
further investigation with echo and Doppler usg.
Physical signs
Bilateral basilar crackles common in normal
Due to atelectasis from basal compression of the
lungs by enlarged uterus
Peripheral pulses often collapsing and can be
confused with aortic regurgitation
Bilateral pedal edema
due to fall in oncotic pressure of plasma with
increased femoral venous pressure due to poor
venous return
Physical signs
Loud S1 suggest mitral stenosis
Low intensity S1 indicates--- 1st degree Heart block
Widely split S2 indicates----- atrial septal defect

Innocent murmur common in pregnancy due to

hyperdynamic or hyperkinetic circulation
Continous benign murmur- cervical venous hum and
mammary souffle due to haemodynamic changes
Venous hum- best heard over the right supraclavicular
Mammary souffle- best heard over the breast
Diagnostic studies of cardiovascular
disease in pregnancy.
Most are non invasive can be performed
safely during pregnancy.
Doppler echocardiography
Chest radiography
Radionuclide studies-Radio-labelled Tc albumin
or red cells to evaluate ventricular function
Thallium 201 used to evaluate regional coronary
Right sided heart catheterisation to measure
hemodynamic function and monitoring
Normal cardiac exam findings during
Jugular vein distension with prominent
Right ventricular impulse
Increased S1
Splitting S2
Systolic murmur
Venous Hum- continuous
Mammary souffle- systolic/ continuous
Diaphragm elevated in advanced pregnancy.
Heart size
15 degrees left axis deviation in pregnancy.
Atrial and ventricular premature contractions are

Sinus tachycardia

Allows non- invasive evaluation of structural and
functional cardiac factors
Chest radiography
Best done in the antero-posterior and lateral
Used with lead apron shield to minimize fetal exposure
to radiations
A- airway/ aortic notch
B- bones
D- diaphragm
F- fluid/ Kelly lines in CCF
G-gas bubble
H- hilar lymph nodes

i- impression- horizontal position of the heart with

increased lung markings
Xray rarely requreested in pgnancy
Clinical classifications of heart disease
New York Heart Association-NYHA
NYHA- 1st published in 1928
Class 1-
No limitation to physical activity
No symptoms of cardiac insufficiency or angina pain

Class 11
Slight limitation to physical activity
Comfortable at rest
Discomfort results in the form of excessive fatigue,
palpitation, dyspnoea with ordinary physical activity
Clinical classification-NYHA
Class 111
Marked limitation of physical activity
Comfortable at rest, but less than ordinary activity causes

Class 1V
Severely compromised
Inability to perform any physical activity
Symptoms of cardiac insufficiency and or angina pain at

SIU &co -2001, expanded on the NYHA classification

and devised a scoring system for predicting cardiac
complications during pregnancy
predictors of cardiac complications
Prior heart failure,
transient ischaemic attack
NYHA >111 or cyanosis
Left sided heart obstruction - Defined by Echo
Ejection fraction < 4o%

The risk of
pulmonary oedema, stroke, sustained arrythmmias,
cardiac arrest, cardiac death was substantially
increased with even one of these factors
Preconceptional counselling
Beneficial to women with pre-existing cardiac
Life- threatened cardiac disease can be
reversed by corrective surgery and subsequent
pregnancy less dangerous
Maternal mortality varies directly with
functional classification at preg. onset.
Special group with mechanical valves needing
warfarin prophylaxis.
Risk of maternal mortality caused by
various types of Heart disease- 3grps
Group 1
Minimum risk- 0.1%
NYHA 1&11+-Mitral stenosis,
Corrected bioprosthetic valve
Corrected TOF
Pulm/Tricuspid dx

Group 2
Moderate risk- 5-15%
Mitral stenosis + NYHA 111,1V OR atrial fibrillation
Aortic stenosis
Fallot tetralogy- uncorrected
Aortic coarctation without valvular involvement
Previous MI
Marfan syndrome with normal aorta
Artificial valve
Risk of maternal mortality caused by
various types of Heart disease
Group 3
Major risk- 25-50%
Pulmonary hypertension
Aortic coarctation + valvular involvement
Marfan syndome with aortic involvement
Eissenmengar synd.
Congenital heart dx
Genetic predisposition- 3-4%

Marfan syndome
Aortic stenosis
Pulmonary stenosis
Ventricular septal defects
Atrial septal defect
Persistent ductus arteriosus
Coartation of the aorta
Tetralogy of fallot
General management of cardiac
disease in pregnancy
Team approach- obstetrician, neonatologist,
cardiologist, anaesthesiologist

4 changes that affect mgt are emphasized by

ACOG- 1992
50% increase in cardiac output and blood volume
Further fluctuation of CO and BV peripartum
Decline in systemic vascular resistance
pregnancy induced hypercoagulability
Management of class1 & 11
Rare exception- most advance through preg without
CCF of gradual onset.
1st/ warning sign- basal rales and nocturnal cough

Attention directed toward prevention and early

detection of heart failure.
Prevent infection sepsis may precipitate cardiac
Pneumococcal and influenza vaccine recommended
Life style modifications- Smoking prohibited
Management of class 1 & 11
Labour and delivery
In general vaginal delivery preferred unless obstetrical
indication for C/S
Induction of labour is generally safe
Pulmonary artery catheterisation for continous
hemodynamic monitoring
Pain relief- epidural recommended or iv analgesic
Problem with spinal is maternal hypotension
esp clients with pulm. HPTN and aortic stenosis.
Narcotic conduction analgesics or GA may be preferred.
Semi- recumbent position with lateral tilt
Vitals checked frequently in b/n contraction.
PR> 100 and RR > 24 may suggest and impending ventricular
2nd stage may be shortened with forceps or vacuum extract.
Client who have shown little or no evidence of
cardiac dx during preg., labour, delivery may
still decompensate postpartum
Close monitoring
Active management of the 3rd stage to prevent
Correct anaemia and prevent infection and
thrombo- embolism
Management of class111 & 1V
Uncommon in modern obstetric practice

If woman chooses to get pregnant

Made to understand the risk involved
Must cooperate fully with planned care
If seen early should be offered pregnancy interruption
If woman insists on carrying the preg. then prolonged
hospitalisation with bed rest recommended
Epidural analgesics for labour and delivery
Vaginal delivery preferred
C/S limited to obstetrical indication as they tend to
tolerate surgical procedures poorly.
Surgically corrected heart disease
Majority of clinically significant heart lesions are
repaired during childhood.

With successful repair, many women attempt


Other cardiac lesion may advance into adulthood

without notice
Use of prosthesis to replace severely damaged mitral
or aortic valve:overall maternal mortality 3-4%
Pregnancy carefully considered
Those on mechanical valve prosthesis must be
anticoagulated throughout pregnanacy

Maternal complications
Thromboembolism, maternal death, CCF, PPH
TBE from prosthesis and PPH from anticoagulants

Fetal outcome
Generally poor
Stillbirth, NND, spont. abortions, IUGR, preterm delivery
with prematurity syndrome, embryopathy-
heparin Vs warfarin
. heparin is less effective than warfarin in preventing thromboembolic

Better maternal outcome is achieved with the use of warfarin

throughout pregnancy

Poor fetal outcome achieved with warfarin used throughout preg.

Embryopathy rate 6.4%

Embryopathy eliminated when heparin is used between 6-12

weeks but risk of TBE increased

Risk of complication higher when daily dose of warfarin > 5mg.

Low dose unfractionated heparin is inadequate in preg. With prior

valvular replacement
LMW heparin in preg. with prosthetic heart valve
should be discouraged.

Alternative for further evaluation

Antiplatelet therapy with Dipyrindamole, aspirin
Thrombolytic agent

Porcine xenograft
Bioprosthesis with less thrombogenic effect
Anticoagulation not required
Less durable and may be replaced after 10 years
Mechanical heart valve
ACOG recommend full anticoagulation throughout
preg. (2000)
Unfractionated heparin SC , BD
Starting dose 35,000iu. Monitor twice a week
warfarin 2.5- 5mg daily
INR target 2-3
Substitute with unfractionated heparin b/n 6-12 weeks
and again 36week till delivery
Heparin stopped just before delivery
If delivery supervenes while anticoagulation is still
effective and bleeding is encounted
Protamine sulphate iv is used.
Mechanical heart valve
Anticoagulant therapy with heparin or warfarin may be
restarted after 6hours of vaginal delivery.

Following C/S full anticoagulation withheld for at least


Warfarin can safely be given to breast feeding mothers

because transfer to milk is minimal.

combined OCP relatively contraindicated in women with
prosthetic valve
Increase the chance of thromboembolic event
Sterilization offered without compromise
Valve replacement during preg.
Uncommon. Usually postponed until after delivery
But may be life-saving
Associated with increase maternal mortality &
morbidity as well as perinatal mortality

Surgical procedures
Surgical ( mitral) valvotomy- less preferred
Percutaneous transcatheter balloon dilatation of mitral
valve. Largely replaced valvotomy in preg.
Open mitral commissurotomy
Balloon valvuloplasty- treatment of choice in refractory
CCF in preg. Women.
Heart transplantation
Major problem in the past was vasculopathy and
rejection of the allograft.
Recent studies shows high success rate due to
availability of efficacious drugs to prevent this.
The 1st successful pregnancy in a heart transplant
recipient reported in 1988
Available data shows transplanted heart
responds normally to pregnancy induced changes
Associated complications
Developing PIH(50%)
Preterm delivery( 50%)
Valvular Heart Disease(VHD)
mitral stenosis
Chief cause of VHD is Rheumatic fever/

Dilated LA, increase LAP, pulmonary HPTN dev.
Management of mitral stenosis
Limited physical activity recommended
Dietary Na+ restriction
Diuretic therapy
Sinus tachycardia- Rx B- blockers
Acute atrial fibrillation-
iv verapamil ( 5-10mg)
Or electro- cardioversion performed
Chronic fibrillation-
Digoxin or B- blockers or ca2+ channel blocker
Anticoagulation with heparin indicated
Management of mitral stenosis
Labour and delivery
Epidural to relief stress , pain, anxiety of labour
Care taken to avoid fluid overload
Vaginal delivery preferred
Intrapartum endocaditis prophylaxis may be given
Pulmonary artery catheter insertion may be useful in

CCF, arrythmias, IUGR, atrial fibrillation predisposing
to mural thrombus formation- cerebrovascular
embolism- stroke
Mitral insufficiency/ regurgitation
Causes of chronic mitral regurgitation
Rheumatic fever,
mitral valve prolapse
Dilated cardiomyopathy
Calcified mitral annulus
Antiphospholipid syndrome and SLE

Causes - Acute mitral insufficiency

Rupture chorda tendinae
Infarction of the papillary muscle of leaflet.
Mitral regurgitation
LV dilatation & eccentric LV hypertophy

Well tolerated in pregnancy

due to decrease systemic vascular resistance
resulting in less regurgitation
CCF rarely develops in preg.

Intrapartum prophylaxis against bacterial

Aortic stenosis
Most common stenotic valve is bicuspid valve
Disease of aging
If occurs < 30 years- congenital lesion
Less common due to decline in the incidence
of Rheumatic Disease
Aortic stenosis

Valve replacement indicated for symptomatic

Life expectancy averages only 5years
Severe AS is dangerous in pregnancy. MMR 8%

Patient s with valve gradient > 100mmhg

greatest risk
Management in pregnancy
Asymptomatic no treatment. Close observation
Symptomatic patients
Limitation of activity
Prompt treatment of infection
Persistent symptoms despite bed rest
Valve replacement or valvotomy using
cardiopulmonary bypass
Pulmonary artery catheter during labour due to the
narrow margin b/n fluid overload and hypovolaemia
Avoid diuretics
Aortic insufficiency/ regurgitation
Common causes
Rheumatic fever
Connective tissue abnormality
Congenital- marfan syndrome
Acute insufficiency
Bacterial endocarditis
Aortic dissection

Generally well tolerated in pregnancy

Bed rest & sodium restriction& diuretics
Epidural during labour and delivery
Bacterial endocarditis prophylaxis
Pulmonary stenosis
Less common
Caused by rheumatic fever
Usually congenital and associated with
fallot tetralogy and Noonan syndrome

Surgical correction before, during preg. If

symptoms progress.
Congenital heart disease
85% survive to adulthood

Atrial septal Defect-ASD

2nd most common cardiac lesion after bicuspid aortic valve
Most asymptomatic until 3rd and 4th decade
Secundum type defect forms 70% and usually associated
with mitral valve prolapse
Repair if discovered
Rare complication is Pulm. HPTN
Otherwise preg. Well tolerated
Prophylaxis against bacterial endocardits not
Ventricular septal defect- VSD
Defect spontaneously close in 90% of patient during
Paramembranous type constitute 75%
Physiological derangement is related to the size of the
Symptoms arise when defect size> aortic valve orifice.
Most children undergo surgical repair during childhood
before Pulm HPTN, CCF develops
When pulm. Artery pressure exceeds systemic pressure,
there is reversal or bidirectional blood flow or
Pregnancy is contraindicated and therapeutic termination
advise if contraception fails
Genetic predisposition- incidence of inheritance 10-15%
Persistent / patent ductus
Like other shunts, physiological consequence
related to its size

Most significant lesion repaired in childhood

Incidence of inheritance 4%

Unrepaired cases
Bacterial endocarditis prophylaxis
Cyanotic Heart Disease in pregnancy
Shunting of blood from right to left
Commonly encountered in pregnancy is tetralogy
of fallot.
Characterised by
Large VSD
Pulmonary stenosis
Overriding aorta receiving blood from both ventricles
Repair improves prognosis during pregnancy
Others- Ebsteins anomaly of tricuspid valve & RVF
Effects of cyanotic hear dx in preg.
Generally poor outcome
Unrepaired TOF leads to 10% maternal mortality

Chronic hypoxaemia- polycythaemia- fetal loss

Preg. Following repair improves outcome

Mustard repair for transposition of great artery

Fontan repair for congenital single functional ventricle

Labour and delivery
Vaginal delivery preferred unless obstetrical
indication for C/S.
Pulmonary artery catheterisation has limitation due
to bizzare anatomy
Epidural opiates well tolerated
Avoid sudden blood loss or hypotension

Secondary pulm. HPTN from cardiac lesion
PVR> SVR leading to right to left shunt- cyanosis
Commoner in ASD, VSD, PDA
Tend to tolerate hypotension poorly
Pulmonary hypertension
May be due to cardiac or pulmonary dx
Commonest cause is persistent or prolonged L-R shunt with
dev. of Eissenmenger syndrome.

Primary pulm. Hypertension is rare

Usually idiopathic/ occurs in the absence of cardiac dx

Suspected risk factors include

HIV, HPV 8, SCDx, pulm. Embolism, thyrotoxicosis, antiphospholipid
antibodies, interstitial and restrictive lung dx

Criteria for diagnosis

Mean PAP >25mmhg at rest using cardiac catheterisation
or >30mmhg with exertion in the absence of heart dx
Chronic Thromboembolic dx underlying a pulmonary dx
Management of pulmonary
Preconceptional counselling is imperative
Preg. Contraindicated in severe cases
Treatment with nifedipine and prostacycline
for at least 1 year before preg.
Prognosis is poor and mean survival is 2years
Long term treatment with prostacycline
(iv epoprostenol) and trepostinil (sc),
analoque significantly reduces PVR.
Maternal mortality is 30-65% with primary dx
For symptomatic patients
Limitation of activity
Cardiac position
Diuretics and supplemental O2
Nifedipine and prostacyclin therapy
Adequate analgesia in labour.
Morphine administered intra-thecally
Intubation + inhaled NO during labour
Forceps and vacuum delivery
Use of pulmonary artery catheterisation to avert
Mitral valve prolapse
May involve the valve leaflet, annulus, or chordae
Incidence 2.3% among women of reproductive
Most asymptomatic incidental findings at echo
Preg women with MVP rarely have any cardiac
Pregnancy well tolerated.
Preg. Induced hypervolaemia may improve
valvular alignment
Small risk- infective endocarditis, ischaemic
stroke and cerebral embolism.
Peripartum cardiomyopathy
Diagnosis of exclusion
Similar to idiopathic dilated cardiomyopathy in
the non-pregnant woman
It describes women with peripartum HPTN
with no apparent etiology.
Its doubtful if there is pregnancy induced
Endomyocardial biopsy performed on non-
preg women with unexplained
cardiomyopathy revealed 50% had myocarditis
Diagnostic criteria- 2000
Cardiac failure in the last month of pregnancy
>36weeks or within 5-months postpartum.

Absence of identifiable cause for the heart failure

Absence of recognizable heart dx prior to the last

month of pregnancy. Eg PIH, preeclampsia, eclampsia.

Left ventricular dysfunction demonstrated by Echo.

Depressed shortening or ejection fraction.
Occurs in 1:1500 to 1: 15,000

Nb- r/o other causes of acute ventri. Dysfxn.

Idiopathic cardiomyopathy in preg.
Prolonged use of beta- mimetic tocolysis with
terbutaline has been implicated
Studies have demonstrated 50% of such cases
as myocarditis at biopsy
Presentation- signs and symptoms of HF
Hallmark finding is massive cardiomegaly/ CXR
ejection fraction < 45% or fractional shortening <
30% or both
And end- diastolic dimension > 2.7cm/m2
Management of idiopathic
cardiomyopathy. in pregnancy.
Treatment for CCF- Bed rest with limited activity
Prop in cardiac position + supplemental O2
Na+ restriction
Diuretics given to reduce preload
Hydrallazine or vasodilator given to reduce afterload
ACE inhibitor avoided antepartum due to fetal effect
but useful postpartum
Prophylactic heparin recommended due to the
associated risk of thromboembolism.
Causes of maternal death- end stage HF,PE, stroke
Subsequent preg. inadvisable
Infective endocarditis
Infection of the cardiac endothelium that
produces vegetations that usually deposit on
the valves.
Can involve a native or a prosthetic valve
Associated with iv drug abuse
Greatest risk is corrective surgery for CHD
50% of cases have identifiable pre-existing
cardiac lesion.
Subacute bacterial endocarditis
Caused by low virulence bacterial infection
superimposed on an underlying cardiac lesion
Common organisms- viridans group A
streptococcus., Enterococcus spp.,
staphylococcus aureus
Staph. aureus predominant among iv drug
Staph. epidermidis commonly cause prosthetic
valve infection
Strep. pneumoniae and Neisseria gonorrhea may
cause acute or fulminant disease.
Clinical presentation
Varies and develops insidiously
Murmur- 80-85%
Anorexia, fatique, flu-like symptoms, Anaemia, and
Petechia , focal neurological manifestation, chest and
abdominal pains
Symptoms and signs of CCF

Diagnosis- Dukes criteria

Positive blood culture for TYPICAL organisms
Evidence of endocardial involvement doppler ECHO
Negative ECHO study does not exclude endocarditis AS
lesions 3-4mm and those of tricuspid valve may be
Usually medical and timely surgical intervention
Knowledge of infecting organisms

Most viridans strep. Sensitive to iv penicillin and

gentamycin for 2/52

Those allergic to peniciliin are either desensitized or

substituted for iv ceftriaxone or vancomycin for 4/52

Staph. and enterococcus treated according to microbial

sensitivity for 4-6weeks

Prosthetic valve infection treated for 6-8weeks

Persistent native valve infection as well as infected

prosthetic valves may have to be replaced.
Endocarditis in pregnancy
Maternal mortality is 25-30%
Uncommon in pregnancy

American college of cardiology/ American Heart

association endorsed by ACOG -2003 recommend
antimicrobial prophylaxis to prevent bacterial
endocarditis based on risk stratification

Recommended for high risk

May recommend for moderate risk
Not recommended in low risk individuals
High risk- prophylaxis recommended
Prosthetic cardiac valve
Prior bacterial endocarditis
Complex cyanotic CHD
Surgically constructed systemic-pulm. Shunts

Moderate risk
Acquired valvular dysfunction- Rheum. HDx
Mitral valve prolapse + valvular regurgitation
Low risk
MVP without valvular regurgitation
Physiological, functional, or innocent murmur
Previous Kawasaki dx without valvular dxfn
Previous Rheumatic fever without valv. Dxfn
Cardiac pacemakers of implanted defibrillators
Prior coronary bypass- graft surgery should be
administered intrapartum

Recommended prophylaxis- ACOG/AHA

Iv/im ampicillin 2g + 1.5mg/kg gentamycin max 120mg
followed by oral ampicillin 1g or amoxycillin qid
If allergic to penicillin- iv vancomycin 1g over 1-2hours
Cardiac arrythmias are commonly encountered during
preg. labour , delivery, and puerperium

Perhaps the normal but mild hypokalaemia of preg.

induces arrythmias

Bradyarrythmias including complete heart block are

compatible with a succesful pregnancy outcome
Some with complete heart block may need temporary
cardiac pacing
Those with permanent artificial pacemakers tolerate preg.
Should prompt consideration of underlying cardiac dx
eg. Wolff- Parkinson White syndrome and parosxymal
supraventicular tachycardia

Medical- digoxin, adenosine of calcium channel blockers.
Adenosine effective as cardioversion in hemody. stable pxt
Electro cardioversion not contraindicated in preg.
But vigilance required to prevent uterine contractions and
fetal bradycardia

Atrial flutter and fibrillation- r/o thyrotoxicosis

Prophylatic heparin indicated in preg. To prevent stroke
Ventricular tachycardia
Uncommon without an underlying heart dx

May be precipitated or stimulated by

Physical exercise
Psychological stress
Anaesthesia provoked tachcardia- prolonged QT interval

Rx- B- blockers or defibrillation

QT interval prolongation on ECG

may predispose individual to a potentially fatal ventricular
Disease of the Aorta
Marfan syndrome and coarctation of the aorta (COA)
places the pregnant woman at increased risk of aortic
50% of cases of aortic dissection related to pregnancy
Other risk factors- bicuspid valve, Noonan syndrome,
Turner syndrome, Ehlers- Danlos
Aortic intimal tear-medial haemorrhage- rupture
Severe chest pains-ripping, tearing, stabbing in nature
Diminution or loss of peripheral pulses in recently acquired
murmur of aortic insufficiency
Differential diagnosis
Pulm. Embolism
Aortic valve rupture
Abruptio placenta and uterine rupture- added 1991

90% of cases have abnormal CXR

Gold standard for diag- aortic angiography
But used more frequently- CT, MRI, dop.USG
The urgency of the situation dictates best method

Rx of aortic dissection- antihypertensives to lower BP

Proximal- needs resection + Valve replacement eg aort. aneurysm

Distal abdominal aneurysm- more complex. Conservative mgt

Marfan syndrome-MS
Inherited as autosomal dominant trait with high
degree of penetrance
Prenatal diagnosis possible using linkage analysis
Caused by abnormal fibrillin produced by FBN1
Fibrillin is a constituent of elastin making MS a
connective tissue dx
Pathology progressive aortic dilatation with
valvular insufficiency and aortic dissection/aneur.
Long term with B- blockers
Effects in pregnancy
High risk factors are aortic dilatation of > 40mm or mitral valve

Women with minimal or no dilatation with normal cardiac function

counselled about small but potentially dangerous complication of
aortic dissection

Preg. Safer MS with no CVS manifestation

Recommend B- blocker prophylaxis thr. Preg.

Aortic root dilatation > 40mm- dissection more likely. And elective
surgery considered before preg.

General recommendation is C/S for marfan syndrome with aortic

Aortic coarctaton (COA)
Rare lesion
Usually associated with other abnormalities
Bicuspid aortic valve, cerebral artery aneurysm
PDA, ASD,and turner syndrome
Collateral formation above the level of coarctation
HPTN in the upper limb but normal or reduced in the lower limb
MMR is 3%
Antihypertensive with B- blockers required

Aortic rupture more likely in late preg. Or early puerperium

Cerebral haemorrhage from circle of Willis aneurysm may

Effect in pregnancy (COA)
CCF may warrant termination of pregnancy to improve
cardiac function
Some recommend resection of the coarctation during
pregnancy to protect against dissecting aneurysm and
aortic rupture
Risk to the fetus due variable period of collateral clamping.
Some recommend C/S to prevent transient HPTN
accompanying labour which may lead to aortic rupture
and cerebral aneurysm
But available facts suggest C/S limited to obstetric
Intrapartum bacterial endocarditis prophylaxis
Ischaemic Heart disease
Classical incidence- 1: 10,000
Rare complication in pregnancy

Coronary artery dx leads to myocardial infarction.

Risk factors
Smoking, dyslipidaemia, obesity, previous MI, DM, HPTN.
Shock from PPH

Serum cardiac specific contractile protein, Troponin I
Levels not detectable during pregnancy, vaginal, C/S
Serum myeloperoxidase used to predict major cardiac
Pregnancy with prior IHD
( infarction remote from preg)
Advise on preg. After MI is unclear
IHD is a characteristically progressive, and its
association with HPTN, DM, not advisable
Major complication- angina and CCF
Pregnancy increases cardiac workload.
General consensus
Measure ventricular performance prior to conception.
Radionuclide studies
Coronary artery angiography
If there is no significant ventricular dysfxn, then
pregnancy well tolerated
Myocardial infarction during
Treatment similar to non preg. Women
Maternal mortality rate 30-35%
Recurrent infarction esp. in the 3rd trimester
Acute mgt.
Nitoglycerin + morphine + close BP monitoring
Lidocaine used to suppress malignant arrythmias
Ca channel blockers or beta- blockers if indicated
Tissue plasminogen activator may used in preg. remote
from term
Epidural indicated in labour
C/S reserved for obstetrical indication
Pulm artery catheterisation recommended with an
infaction within 6- months of delivery or presence of
ventricula dysfunction
Surgical/ invasive procedure for
unrelenting MI
Percutaneous transluminal coronary

Percutaneous balloon angioplasty

Transluminal intracoronary stenting

Hypertrophic cardiomyopathy
Affects 1: 500 adult
Commonly associated with phaeochromatosis,
Friedreich ataxia, turner syndrome, neurofibromatosis
Inheritance is autosomal dominant disorder-50%
Pathology- idiopathic LV myocardial hypertrophy
Diagnosis- confirmed by ECHO
Sudden death common
symptoms worsens with exercise
CCF occurs in 40% with preg.
Rx- ca2+ channel blockers and B- blockers
Route of delivery determined by obstetrical indication
Spinal anaeathesia contraindicated
Endocarditis prophylaxis

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