CARDIAC DISEASES IN PREGNANCY

MODERATOR: Dr. MUNIKRISHNAPRESENTED BY: Dr SUNANDA

HEART DISEASE IN PREGNANCY The overall incidence of heart disease

complicating pregnancy is approximately 1%.

During the last few decades, the etiology of heart disease in developed countries has changed from primarily rheumatic to predominantly congenital

(JAMES HIGH RISK 4th ed)

INCIDENCE IN INDIA According to an Indian study- incidence of

heart disease in pregnancy -1.3% RHD was the commonest(78%) – of which

MS commonest 71.54% Congenital heart disease(18.7)- 2nd most

common in pregnancy

PHYSIOLOGYHAEMODYNAMICS OF PREGNANCYANATOMICAL CHANGES Due to elevation of diaphragm consequent

to the enlarged uterus, the heart is pushed upwards & outwards with slight rotation to left.

PHYSIOLOGICAL CARDIOVASCULAR CHANGES IN PREGNANCY Increase in plasma volume by 40 to 50% Increase in cardiac output by 30 to 40% Increase in heart rate 10 to 15 BPM Decrease in blood pressure by 10 mmHg. Increase in red cell volume 15-20%These changes are normal in pregnancy

BLOOD VOLUME

Starts to increase from about 6th week, reaches maximum 40-50% above the non pregnant level at 30-32 weeks.

The level remains almost static till term

PLASMA VOLUME

Starts to increase by 6wks & it plateaus at 30 wks of gestation.

maximum is reached to the extent of 50% 91.25 litres

The increase is greater in multigravida, multiple pregnancy & with large baby.

RBC & HAEMOGLOBIN

RBC mass in increases to the extent of 20-30%

Total increase in volume is about 350ml RBC mass begins to increase at about 10

weeks & continues till term without plateauing.

Iron supplementation increases the RBC mass by 30%

Reticulocyte count increases by 2% Erythropoietin level is raised disproportionate increase in plasma & RBC

volume -haemodilution (fall in haematocrit)

CARDIAC OUTPUT

increases from 5th week, reaches its peak(30-40%) at about 30-34 week remains static till term.

CO increases further during labour(+50%) & immediately following delivery(+70%) over the prelabour values

BLOOD PRESSURE Systemic vascular resistance decreases(-

21%) due to smooth muscle relaxing effect of progesterone, NO, prostaglandins or ANP.

There is overall decrease in DBP & MAP by 5 to 10mm Hg.

The decrease in maternal BP parallels that of SVR

VENTRICULAR FUNCTION IN PREGNANCY ventricular volumes increase to accommodate

pregnancy induced hypervolemia This is reflected by increasing end systolic &

end diastolic dimensions. However - no change in septal thickness or in

ejection fraction. because these changes are accompanied by

substantive ventricular remodeling- plasticity – which is characterized by eccentric expansion of left ventricular mass that averages 30 to 35% near term.

return to prepregnancy values within a few months postpartum

CHANGES IN THE POSTPARTUM PERIOD The blood volume decreases by 10% within

the first 3 days hemoglobin level and the hematocrit

increase progressively for the first 2 wks Within 2 weeks systemic vascular

resistance increases by 30%

After the initial tachycardia associated with labour a bradycardia often develops in the early puerperium. The heart rate slowly returns to baseline levels over the next 2 weeks.

There is an immediate increase in cardiac output after delivery (within the first hour) by as much as 80%. After this there is a decrease over the next 4 weeks.

( GABBE 5th ed.)

THE CLINICAL FEATURES IN A NORMAL PREGNANCY WHICH CAN MIMIC A CARDIAC DISEASE ARE

 

Dyspnea - due to hyperventilation, elevated diaphragm.

Pedal Edema Cardiac impulse- Diffused and shifted laterally

2.5 cm outside MCL from elevated diaphragm. Jugular veins may be distended and JVP raised.   

Systolic ejection murmurs along the left sternal border occur in 96% of pregnant women and are believed to be caused by increased flow across the aortic and pulmonary valves & due to decreased blood viscosity

Continuous murmur at 2nd to 4th intercostal space-mammary souffle- due to increased blood flow through internal mammary vessels

Loud 1st heart sound with exaggerated splitting

Loud 2nd heart sound A 3Rd heart sound due to rapid diastolic

filling & rarely 4Th may be auscultated. Anemia Pulse rate is slightly raised often with

extrasystoles

CLINICAL INDICATORS OF HEART DISEASE DURING PREGNANCYSYMPTOMS progressive dyspnoea or orthopnoea Nocturnal cough Hemoptysis Syncope Chest pain

CLINICAL INDICATORS OF HEART DISEASE DURING PREGNANCYSIGNS Cyanosis Clubbing of fingers Persistent neck vein distension Systolic murmur grade 3/6 or greater Diastolic murmur Cardiomegaly Persistent arrhythmia Persistent split second sound Criteria for pulmonary hypertension

LEFT VENTRICULAR FAILURE OR

PULMONARY VENOUS HYPERTENSION

Easy fatigabilityShortness of breath

OrthopneaPulmonary congestion

RIGHT SIDED HEART FAILURE

Weight gainDependent oedema

HepatomegalyIncrease JVP

NYHA FUNCTIONAL CLASSIFICATION OF HEART DISEASESgrade symptomsGrade 1 Uncompromised - No

limitation of physical activity ordinary activity does not cause undue fatigue, palpitations, dyspnoes or angina

Grade 2 Slight limitation of physical activity. ordinary activity causes undue fatigue, palpitations, dyspnoes or angina

Grade 3 Marked limitation of physical activityComfortable at rest but less that ordinary activity causes symptoms

Grade 4 Severly compromisedInability to perform any physical activity without symptoms

PREDICTORS OF MATERNAL CARDIOVASCULAR EVENTS & RISK SCORE FROM THE CARPREG STUDY

1. Prior cardiac event( TIA, stroke, heart failure)

2. Baseline NYHA class > 2 or cyanosis3. Left heart obstruction( mitral valve area

<2 sqcm, aortic valve area< 1.5sqcm, peak LV outflow tract gradient> 30mm Hg by echocardiography)

4. Reduced systemic ventricular systolic function (ejection fraction <40%)

(Williams 23rd ed)

For each CARPREG predictor that is present a point is assigned

Risk estimation of cardiovascular maternal complications

0 point 5% 1 point 27% >1 point 75%

MODIFIED WHO CLASSIFICATION OF MATERNAL CARDIOVASCULAR RISKRISK CLASS RISK OF PREGNANCY BY

MEDICAL CONDITIONWHO 1 risk no higher than general

populationWHO 2 small increase in risk of

maternal mortality & morbidity

WHO3 significantly increased risk of maternal mortality or expert cardiac and obstetrical care required

WHO4 very high risk of maternal mortality or severe morbidity; pregnancy contraindicated & termination discussed

WHO RISK CLASS-1Uncomplicated, small or mild: Pulmonary stenosis VSD PDA Mitral valve prolapse with no more than

trivial mitral regurgitationSuccessfully repaired simple lesions Ostium secondum ASD VSD PDA Total anomalous pulmonary venous drainage

WHO RISK CLASS-2If otherwise uncomplicated: Unoperated ASD or VSD Repaired tetralogy of fallot Most arrhythmias

WHO RISK CLASS 2-3 (depending on individual) Mild LV impairment Hypertrophic cardiomyopathy Native or tissue valvular heart disease

not considered WHO4 Marfan syndrome without aortic dilation Heart transplantation

WHO RISK CLASS-3 Mechanical valve Systemic right ventricle Post fontan operation Cyanotic heart disease Other complex congenital heart disease

WHO RISK CLASS-4 Pulmonary arterial hypertension Severe systemic ventricular

dysfunction(NYHA 3-4 or LVEF <30%) Previous peripartum cardiomyopathy

with any residual impairment of left ventricular function

Severe left heart obstruction- MS or AS Marfan syndrome with aorta dilated >

40mm Aortic dilatation >50mm in aortic

disease associated with bicuspid aortic valve.

EFFECTS OF MATERNAL CARDIAC DISEASE ON PREGNANCY

CRITICAL PERIODS when the danger of cardiac decompensation Is especially high:

Between 12-16 wks when haemodynamic changes of pregnancy begin

Between 28-32 wks when haemodynamic changes peak & cardiac demands are at a maximum

During labour & delivery : every uterine contraction injects 300-500

ml blood from uteroplacental circulation.

simultaneously during 2nd stage of labour maternal pushing decreases venous return to heart causing a decrease in CO

These sudden & frequent variations in CO during 2nd stage may turn to be critical for some women with underlying heart disease

soon after delivery of the baby & placenta sudden transfusion of blood from lower

extremities and the uteroplacental circulation to the systemic circulation - loss of obstructive effect of the uterus on the venous return

4-5 days after delivery. Decreased peripheral resistance with right

to left shunting & pulmonary embolization from silent ileofemoral thrombus are 2 of the problems hat may occur at this time

EFFECTS OF MATERNAL CARDIAC DISEASE ON THE FETUS Fetal morbidity - secondary to preterm

delivery & fetal growth restriction. relative inability to maintain an adequate

uteroplacental circulation. The frequency of these problems is related

to the severity of functional impairment of the heart & the severity of the chronic tissue hypoxia.

Another fetal risk is that of congenital heart diease

INDICATIONS FOR MTPABSOLUTE Eisemenger’s syndrome Primary pulmonary hypertension Single ventricle marfan’s syndrome with aortic root

diameter>7cm Peripartum cardiomyopathy Pulmonary veno occlusive disease

Relative Severe obstructive lesion Parous women with NYHA III&IV History of cardiac failure

When to do?Termination should be done using S&EBefore 12wks preferably 8wks

GENERAL MANAGEMENT PRINCIPLES counselled before pregnancy. Women with contraindications advised not

to conceive Those with valvular lesions should conceive

when they are in NYHA class I&II Those with severe disease eg severe MS

should undergo surgery before pregnancy

ANTENATAL CARE Should be seen regularly by cardiologist &

Senior obstetrician Educate about symptoms of worsening of

cardiac status Iron & vitamins including folic acid &

vitamin B complex & calcium should be prescribed to all cases

Ample rest should be ensued & exertion permitted only to a degree that falls just short of producing dyspnoea.

Cases in class 2 &3 should have 12 hrs in bed at night & if possible 2 hrs rest during the day

avoid infection Dental extraction under antibiotic cover

is safer than filling. Urine culture must be done in all cases

to exclude asymptomtic bacteriuria febrile illness - treated aggressively

Weight gain should not be allowed to exceed 0.6kg in any one week- diet & reduced salt intake

Careful vigilance for preeclamsia Fetal monitoring routine USG, fetal

ECHO, NST,BPP Anemia -diagnosed early and vigorously

treated - potential to precipitate & aggravate failure

Warfarin used in first trimester can cause foetal embryoparthy

Nasal hypoplasia-4.6% Hypertelorism Prominance of frontal bone Short stature Mental retardation-2.6% Stippling of epiphysis of long

bones(chondrodysplasia punctata)-4.6%

INDICATIONS FOR ADMISSION Women with class III&IV should be

admitted when diagnosed untill delivery or functional status improves

Class I&II admitted 2wks prior to expected date of delivery

Worsening of cardiac status Cardiac failure Appearnce of symptoms & sign like cough,

dysnea,basal lung crepitations

EVALUATION OF PATIENTCHEST RADIOGRAPHY Should generally be avoided but if required

an abdominal shield should be used. In pregnancy a chest xray often shows

straightening of left upper cardiac border, slight prominence of the pulmonary artery, an enlarged heart & prominent lung markings.

Small pleural effusions may be seen in the 1st two weeks of puerperium

ELECTROCARDIOGRAPHY Main role is in the diagnosis of arrhythmiasECG CHANGES IN NORMAL PREGNANCY Mechanical changes in the size & position

of the heart -shift in the QRS axis to the left or right during a normal pregnancy.

non specific ST-T wave changes

ECHOCARDIOGRAPHY Best method to detect structural

abnormality of the heart in all types of cardiac disease & to assess its severity.

TRANSTHORACIC used most frequently to determine

ventricular function,to assess status of native & prosthetic valve disease & to assess pulmonary artery pressure.

TRANSOESOPHAGEAL not routinely performed in pregnancy may be necessary to provide more

detailed imaging of valvular disease, the presence or absence of a shunt or intracardiac thrombus or in suspected infective endocarditis to facilitate the detection of a valvular vegetation or perivalvular abscess

Two dimentional doppler is considerd safe for both mother & fetus.

There is increase in left & right ventricular end diastolic dimentions which returns to normal after pregnancy.

The atria may be slightly dilated. Small pericardial effusions are found in

about 40% of normal women in late pregnancy.

MRI Useful in diagnosis of pathology of aorta

& complex heart disease but it should be performed when other measures have failed.

Gadolinium should be avoided as data on fetal safety is not available.

CECT is usually not indicated in pregnancy because of the risk of ionic radiation.

The only indication is for accurate diagnosis or exclusion of pulmonary embolism.

CONGENITAL HEART DISEASELEFT TO RIGHT SHUNTS- septal defects that result in volume

overload- ASD, VSD, PDASTENOTIC LESIONS- aortic & pulmonary stenosis, COA,

hypertrophic sub aortic stenosis that result in pressure overload

RIGHT TO LEFT SHUNTS- TOF & Eisenmenger syndrome that result

in cyanotic heart disease

RISKS FOR FETAL HEART LESIONS RELATED TO AFFECTED FAMILY MEMBERS

Cardiac lesion Previous sibling affected

Father affected

Mother affected

Marfan syndrome

NS 50 50

Aortic stenosis 2 30 15-18Pulmonary stenosis

2 2 6-7

VSD 3 2 10-16ASD 2.5 1.5 5-11PDA 3 2.5 4COA NS NS 14TOF 2.5 1.5 2-3

CONGENITAL HEART DISEASE IN FETUS(%)

NS = NOT STATEDDATA FROM LUPTON, 2002

CONGENITAL HEART DISEASELEFT TO RIGHT SHUNTS Usually well tolerated Main problem- pulmonary HTN & shunt

reversal & production of cyanosis Echocardiogram should be done before

or immediately after pregnancy is discovered to rule out pulmonary HTN

ASD Commonest congenital lesion Repaired ASD- WHO risk class 1 Unoperated ASD- WHO risk class2 Unrepaired ASD- risk of pre- eclampsia &

IUGR increased

CLINICAL FEATURES: Signs of RV hypertrophy and pulmonary

hypertension in advanced and severe cases.

On auscultation wide split s2 that is fixed with respiration. Flow murmur due to increased right sided flow.

MANAGEMENT No surgical intervention needed during

pregnancy If maternal condition deteriorates

catheter device closure can be performed in pts with ostium secondum type defect

Care to avoid air entry into IV lines- risk of systemic air embolism due to rt to left shunt

Paradoxical embolism- entry of venous thrombus through septal defect & into systemic arterial circulation- embolic stroke.

Early ambulation adviced after delivery If prolonged bedrest adviced-

anticoagulation Endocarditis prophylaxis- not indicated

(in repaired or unrepaired ASD) Uneventful spontaneous vaginal

delivery occurs in most pts

VSD Ventricular septal defects (VSD) are

common at birth (0.3–3 /1000 livebirths). The most common type of defect occurs in

the membranous septum Small defects with diameter< aortic valve

i.e 1.25cmsq- pulmonary HTN & heart failure do not develop.

If the effective defect size exceeds that of aortic valve orifice symptoms rapidly develop.

If pulmonary artery pressure reaches systemic levels - reversal or bidirectional flow or Eisenmenger syndrome

Bacterial endocarditis more common with unrepaired defects- antimicrobial prophylaxis

CLINICAL FEATURES Exercise intolerance, dyspnea or congestive

heart failure. The flow across a VSD produces a loud

systolic ejection murmur

ATRIOVENTRICULAR SEPTAL DEFECTS Account for 3% of all congenital cardiac

malformations Compared with simple defects,

complications are more frequent during pregnancy

PDA It is the persistence of the direct connection

between the pulmonary and arterial circulation

Incidence of Isolated PDA 1:2000 newborns, but rarely in adults.

The residual embryonic shunt is from the descending aorta to the proximal left pulmonary artery.

Clinical symptoms and complications are also similar to VSD.

Physical examination - grade 4–6/6 continuous(diastolic and systolic), “machinery” murmur that is best heard at the upper left sternal border or infraclavicular area.

Risks of pregnancy - related to shunt size and degree of pulmonary hypertension

COMPICATIONS Theoretical risk of shunt reversal With large shunts - enlargement of the

pulmonary artery and left-sided chambers and can develop high-output heart failure.

Associated pulmonary hypertension significantly increases maternal and fetal morbidity and mortality rates

TETRALOGY OF FALLOT Most common cyanotic congenital heart

defect in pregnant women 3.9 per 10,000 births. The four diagnostic abnormalities are- VSD- Deviation of the aorta to the right so that it

over-rides the VSD, - Infundibular pulmonic stenosis- Secondary right ventricular hypertrophyde swiet 5th ed

Preconception repair is preferred Repair usually involves relief of the right

ventricular outflow obstruction & closure of the VSD

Corrected patients should have a preconception functional assessment.

Prophylaxis with aspirin to reduce the risk of thrombosis and paradoxic emboli.

Patients with corrected lesions, good residual right ventricular function and good functional status usually tolerate the stress of pregnancy.

Uncorrected lesions - clinical deterioration during pregnancy, resulting in increased maternal and fetal complications

de swiet 5th ed

EISENMENGER’S SYNDROME Severe pulmonary vascular obstructive

disease and hypertension resulting from septal communication between the systemic and pulmonary circulations is termed Eisenmenger’s syndrome.

The degree of pulmonary HT determines the amount of shunting and cyanosis.

endstage of this process when equalization of pressures in the right and left heart causes the previous shunting to reverse so that unoxygenated blood enters the systemic circulation

The hemodynamic changes of pregnancy and parturition are poorly tolerated in Eisenmenger’s syndrome .The maternal mortality rate may be as high as 39–52%; thus, pregnancy is contraindicated

LABOUR AND DELIVERY

1. MODE OF DELIVERY2. ANALGESIA & ANAESTHESIA3. INDUCTION OF LABOUR4. MANAGEMENT OF LABOUR

MODE OF DELIVERY Vaginal delivery is the safer route. cesarean section should be generally

performed for obstetric reasons.

Non obstetric indications of elective cesarean section include:

1. Marfans syndrome with aortic diameter>45mm.

2. Patients on oral anticoagulants in preterm labour

3. Acute or chronic aortic dissection4. Acute intractable heart failure5. Severe aortic stenosis6. Severe forms of pulmonary

hypertension(eisenmenger syndrome)7. Urgent delivery in a pt on oral anticoagulants

to reduce risk of intracranial haemorrhage in the fully anticoagulated fetus

ANALGESIA & ANAESTHESIA should have effective pain relief during

labour During early labour IM or IV labour

analgesia may be used Later if the pt is not on anticoagulation, the

analgesia/anaesthesia of choice is epidural blockade.

It limits the extent of sympathetic blockade & its effect on intravascular volume pooling & blood pressure.

preferable to administer epidural narcotic( eg. Fentanyl) than epidural anaesthesia.

Epidural analgesia –causes hypotension & therefore must be used with caution in pts with obstructive valve lesions

Epidural narcotics may be given in situations where epidural administration of local anaesthetics is a relative contraindication such as:

AS, MS, COA, marfan syndrome with dialated aortic root or hypertrophic obstructive cardiomyopathy.

INDUCTION OF LABOUR oxytocin infusion is appropriate when

Bishop score is favourable Unripe cervix- PGE2 has a more profound

effect on BP thus misoprostol is preferable Mechanical methods like foleys catheter

may be preferred in cyanotic heart disease. Long induction- delivery interval & early

amniotomy to be avoided- risk of ascending infection

MANAGEMENT OF LABOUR Antibiotic prophylaxis- to prevent bacterial

endocarditis Prevent thromboembolic complications-

early ambulation, compression bandage, prophylactic low dose heparin during labour,delivery & immediate postpartum periods

oral anticoagulants- switched over to LMWH or UFH from 36th week.

UFH -discontinued 4-6 hrs before planned delivery or at the start of labour &

restarted 4-6 hrs after delivery if there are no bleeding complications

If labour starts prematurely & urgent delivery is unavoidable in pt with mechanical valves on full anticoagulation with LMWH or UFH

1. Protamine sulphate2. FFP should be given prior to LSCS to

achieve INR<23. Oral vit K (0.5- 1mg) but takes 4-6 hrs to

affect INR4. Newborns of mothers on OAC – FFP & vit K

1st stage Semirecumbent position with left. lateral

tilt. I/V fluids restricted to 75ml/hr except in AS. Oxygen inhalation 5-6 l/min. Labour analgesia/ (morphine/epidural ). CVP monitoring in high risk patients.

Monitoring for signs of CCF as follows:- pulse>100/min RR>24 Dyspnea Elevated JVP Cyanosis Basal crepitations Invasive monitoring by PAC in high risk

cases.

SECOND STAGE Cut short Assisted with forceps or ventouse

THIRD STAGE iv bolus doses of oxytocin - fall in SVR &

subsequent hypotension which may be difficult to tolerate for some pts.

Oxytocin to be given by slow iv infusion (<2mU/min)

Ergot alkaloids for prophylaxis of uterine atony- intense vasoconstriction & elevation of blood pressure

Judicious use of diuretics.

PUERPERIUM 1st 12hrs crucial. Bed rest in propped up position. Increases blood volume- may exceed the

pumping ability of heart- acute pulmonary edema

sitting position following delivery- more gradual adaptation to postpartum haemodynamic changes- venous pooling in lower extremities – decreased venous return

CONTRACEPTION Barrier methods advised. Progesterone only pills. DMPA good option. IUCD relatively contraindicated. Oral contraceptive pills contraindicated. Vasectomy of husband or mini laprotomy Laproscopic sterlisation not advisable

Thank you