Heart disease pregnancy new dr rabi

CARDIAC DIESEASES IN

PREGNANCY

DR. RABI NARAYAN SATAPATHY

ASST.PROFESSOR

DEPT. OF OBST.& GYNAECOLOGY

SCB MEDICAL COLLEGE, CUTTACK

MOB-09861281510

EMAIL-drrabisatpathy@gmail.com

Epidemiology

Classification of heart diseases

Cardiovascular alterations in normal pregnancy

Effect of pregnancy on heart diseases

Effect of heart diseases on pregnancy

Diagnosis & management of heart diseases in general

Diagnosis & management of cardiac events (arrhythmia, CCF & pulmonary oedema, IE, IHD) complicating heart diseases in pregnancy

Focus on specific cardiac conditions(cong & acquired)

Conclusion

Pregnancy in patients with heart disease is becoming more common due to its early diagnosis and better treatment.

Incidence 0.2-3.7%(avg 1%) (worldwide)

1-3%(USA)

0.5-1%(India)

Developing Countries RHD most common

(upto 95%)

Developed Countries Congenital heart disease

(upto 50%)

The ratio between RHD: CHD has fallen over last 2 decades from 10:1 to about 3 : 1, or even 1 : 1 in developed countries

Acquired - Rheumatic Heart Diseases

Ischaemic Heart Diseases

Cardiomyopathies

Congenital-

Acyanotic(LR) ASD, VSD, PDA

Cyanotic(RL) Tetralogy of Fallot(TOF)

Tricuspid atresia & Ebstein’s anomly

TGA

TAPVC

Obstructive Aortic stenosis

Coarctation of aorta

Pulmonary stenosis

Other important conditions-

Arrhythmia

Infective endocarditis

Marfan’s syndrome

Mitral valve prolapse

Pulmonary hypertension

Eisenmenger syndrome

CLASSIFICATION

Braunwald E et al. Heart Disease. 2001. pg. 2173.

Braunwald E et al. Heart Disease. 2001. pg.

2173.

Normal Physiological Changes in Pregnancy

Braunwald E et al. Heart Disease. 2001. pg.

2172.

Braunwald E et al. Heart Disease. 2001. pg. 2173.

3rd heart sound in upto 90%

Systolic ejection murmur – from hyperkinetic flow

Most auscultatory changes resolved 1-2 weeks postpartum

Cutforth R et al. Heart sounds and mumurs in pregnancy. Am Heart J.

1966;71:741-747.

ECG changes

CXR changes

• Straightening of left upper cardiac border

• Horizontal positioning of heart

• Increased lung marking

• Small pleural effusion at early postpartum

Echocardiogram

• Slightly increased EDV and ESV

• Slightly improved LV function

• Enlargement of ventricular dimensions

• Slight enlargement of left atrial size

• Small pericardial effusion

• Increased tricuspid annulus diameter

• Functional tricuspid regurgitation

Elkayam U et al. Cardiac Problems in Pregnancy.

1990.34-7.

•Left axis deviation(15°)

•Sinus tachycardia

•ST segment and T wave changes in inferior leads

•Small Q, inverted P or T wave in lead III

•Increased R wave amplitude(R/S ratio) in lead V1 & V2

•Atrial or ventricular ectopics

Pain / Anxiety – can increase CO by 50-61%

Uterine contraction – 300-500 mL infusion into central

venous system

Cardiocirculatory effects of uterine contraction:

Parameter Change Comments

Blood Volume Increase 300-500 mL

Cardiac Output Increase 30-60% increase

Heart Rate Increase or

Decrease

Blood Pressure Increase SBP and DBP

Peripheral

Resistance

Unchanged

O2 Consumption Increase 100% increase

Elkayam U et al. Cardiac Problems in Pregnancy. 1990. 16.

• Hemodynamic changes of pregnancy less dramatic in lateral position

• Delivery position depends on cardiac pathology

Parameter Change Comment

Blood Volume Decrease Blood loss

CO Increase 60-80% immediate

increase followed by rapid

decrease, returns to

normal levels in few

weeks

SV Increase

HR Decrease

BP Unchanged

SVR Increase Loss of low resistance

Congestive Heart failure

Pulmonary Oedema

Sudden death

Maternal Mortality –15% of all cardiac patient.

12 - 16 weeks (beginning)

28 - 32 weeks (peak , max cardiac O2 demand)

During labour and delivery (contraction, bearing down)

Immediately after delivery of baby (obstruction to IVC goes away)

4 - 5 days after delivery (decreased SVR, thrombosis)

Group Cardiac disease

Associated mortality risk

I Uncomplicated ASD /VSD /PDA

<1%

Pulmonary/tricuspid valve disease

Corrected TOF

Bioprosthetic valve(Homograft)

MS, NYHA Class I, II

Marfan’s with normal aortic root

II Coarctation of aorta without valvular involvement

5% - 15%

Uncorrected TOF

Mechanical prosthetic valve

MS with AF or NYHA Class III, IV

AS & severe PS

Previous myocardial infarction

III Pulmonary hypertension—primary or secondary

25% - 50%

Eisenmenger syndrome

Coarctation of aorta with valvular involvement

Marfan’s syndrome with aortic involvement

Peripartum cardiomyopathy

1. Puerperial cardiomyopathy

2. Myocardial infarction

3. Aortic dissection

4. Cardiomyopathy and myocarditis

5. Primary pulmonary hypertension

6. Secondary pulmonary hypertension

7. Endocarditis

8. CCF

9. Dysarrhythmias

Preterm delivery

Fetal Growth Restriction

Fetal death

Congenital heart disease (4.5% vs 0.6%)

Clinical-

Symp & sign of Left sided failure

Easy fatigability, shortness of breath, Orthopnoea, PND,

Pulmonary congestion, Cardiac asthma, B/L rales.

Symp & sign of Right sided failure :

Weight gain, dependant edema, hepatomegaly, JVP

(increases)

Chest X-Ray

Cardiomegaly,

Pulmonary vascular markings,

Enlargement of pulmonary veins.

ECG -

Cardiac chamber hypertrophy

Arrhythmia

Myocardial ischaemia and infarction

Conduction abnormalities.

Echocardiography.

Detects structural abnormality (ASD, VSD)

Valve anatomy, valves area, function

Lt. ventricular ejection fraction

Pulmonary artery pressure.

• No limitation of physical activity

• No symptom with ordinary exertionCLASS I

• Slight limitation of physical activity

• Ordinary activity causes symptomsCLASS II

• Marked limitation of physical activity

• Less than ordinary activity causes symptom

• Asymptomatic at rest

CLASS III

CLASS IV•Inability to carry out any physical

activity without discomfort

•Symptoms at rest

NYHA FUNCTIONAL CLASSIFICATION

current fitness & status of the pt to embark on a pregnancy

Anticipated complications during pregnancy & delivery & their risks to mother & fetus

Correctable surgery offered

Advice against pregnancy in certain situations including contraception

Information about congenital heart disease in their offspring

Prevent an unwanted pregnancy and avoid the risks associated with pregnancy continuation or termination.

Key points to be addressed

PLACE OF THERAPEUTIC TERMINATION OF PREGNANCY

Absolute Indications

Severe Pulmonary Hypertension

Eisenmenger’s Syndrome

Pulmonary vaso-occlusive Diseases

? Dilated cardiomyopathy with congestive heart failure

? Marfan’s syndrome with dilated aortic root

? Cyanotic congenital heart disease

? Severe aortic stenosis

Relative Indications

? Parous women with Grade III & IV lesions & Gr-I & II with past H/O failure

Termination should be done within 12 wks by S & E /D & E

After 12 wks, risks of termination are greater than those of continued pregnancy & normal delivery at term bcoz of associated risk of infection, fluid overload, or need of anesthesia

Bed rest.

• (a) Rest increases VR ,thereby improves renal perfusion which increases diuresis & elimination of water

• (b) Reduces metabolic need of several organs & decreases work load of heart

Salt Restriction- 4-6 gm /day.

Digoxin (H/O CHF, AF, severe LV dysfunction)

Treatment of precipitating factor for heart failure.

Diuretics may be required

Anticoagulation in AF , prosthetic valves

Fetal growth monitoring.

Anomaly screening in warfarin, diuretic users

Anemia & infections should be treated as it can cause deterioration & can contribute to failure in pregnancy.

ACE Inhibitors should be stopped and switched over to other drugs.

Women with prosthetic valves with PAH and AF on oral anti-coagulants should be on Heparin 5000 U s.c. BD upto12 wks & to be replaced by warfarin upto 36 wks and thereafter to replaced by Heparin

They usually proceed through pregnancy without much morbidity

Special attention given for prevention & early recognition of failure whose 1st signs may be persistent basilar raleswith nocturnal cough

Anemia & infection treated

Smoking prohibited

Pregnancy is to be avoided and interruption is considered in cases with highest mortality risk

If continued prolonged hospitalization and bed rest is often needed

Induction can be done safely

Epidural analgesia recommended except some situations

Vaginal delivery preferred in most cases

Williams :23rd edn / 962-963

Elective:

Grade I: At least two weeks prior to the expected date of delivery.

Grade II: At 28th week specially in case of unfavourable social surroundings

Grade III and IV: As soon as pregnancy is diagnosed. The patient should be kept in the hospital throughout pregnancy.

Emergency:

On deterioration of the functional grading.

Appearance of dyspnoea or nocturnal cough or basal crepitations or tachyarrythymias.

Appearance of any pregnancy complication like anemia, pre-eclampsia.

Timing and mode of delivery

Reducing the effects of tachycardia & increased cardiac

output in labour

Ensuring effective analgesia

Anticoagulation where needed

Endocarditis prophylaxis

Management of PPH

Spontaneous labour at term is the rule rather than exception.

Oxytocin & PGE2 can be used for induction of labour

Lateral supine position

Pain relief(reduces tachycardia,myocardial work, CO)

Restriction of IV fluid 75ml/hr

O2 inhalation & pulse oxymetry

Antibiotic prophylaxis where needed.

Fetal heart monitoring

Prevention of postpartum pulmonary oedema.

Avoid IV methergin or bolus oxytocin but control PPH

Avoid difficult instrumental delivery

General objectives of treatment

• Shunts: avoid favoring R to L shunting, lower PA pressures, avoid hypoxemia, avoid prolonged valsalva

• Obstructive Lesions: β-blockers, avoid volume depletion, maintain preload

• CHF: diuretics (only with pulmonary edema), reduce afterload(NTG, hydralazine)

• Arrhythmias: rate and rhythm control, anticoagulation as necessary, higher dose digoxin

• Marfan’s, aortic dissection: β-blockers

It is individualized according to the severity of maternal disease and any associated fetal compromise

In cyanotic HD significant IUGR may warrant preterm delivery

Steroids considered for <34 wks .At risk of pulm edema ,monitoring to be done for 24-48 hrs in fear of fluid retention & cardiac decompensation responsive to diuretics

TIMING OF DELIVERY

Vaginal delivery is safer except certain situations & unless there is an obstetric indication for CS

Induction done for obstetric reasons.

And usually done by

• Oxytocin infusion in the form of a concentrated drip with fluid restriction.

• Amniotomy deferred for fear of ascending infection and chorioamnionitis.

• PGE2 used for cervical ripening but its a potent vasodilator and may increase C.O pulmonary edema

Cardiac indication for CS

aortic root dilatation in Marfan’s: progressive enlargement or >4.5 cm

Aortic dissection

severe peripartum cardiomyopathy or severe LV dysfunction

Coarctation of aorta to prevent aortic rupture or cerebral aneurysm rupture

However in class - IV pts. elective CS may be considered d/t better control of ventilation, fluids & cardiac stress.

Arulkumaran’s Best Practice in Labour and Delivery ;1st edn / 228

Lithotomy results in increased VR (CCF risk)

Supine position reduces VR (fetal risk)

Positioning the patient on her left side lessens the hemodynamic fluctuations during contractions

Position best tolerated is with the women sitting upright with her legs lower than her abdomen and her feet supported on foot rests or on reversed lithotomy poles

Arulkumaran’s Best Practice in Labour and Delivery ;1st edn / 228

MATERNAL POSITIONING

• Consider lateral decubitus position with obstructive lesions

• Consider supine position with CHF (reduce VR and so cardiac workload)

SUPINE VERSUS LATERAL

DECUBITUS POSITION

During labour, the mother with significant heart disease

should be kept in a semirecumbent position with lateral

tiltWilliams 23rd edn /

962

Oxytocin bolus avoided

Methergin & prostodin avoided

Misoprostol can be safely given rectally

Mechanical compression sutures , such as B-Lynch brace sutures , can be used prophylactically in a woman with severe heart disease on CS as an adjunct to medical treatment

Arulkumaran’s Best Practice in Labour and Delivery ;1st edn / 229

INDICATIONS FOR CONSIDERING PA CATHETER

• NYHA Functional Class II, III, IV

• Mitral stenosis

• Aortic stenosis

• Pulmonary hypertension

• Pulmonary edema

• Hypoxemia

• Ischemic heart disease

• Intractable hypertension

• Oliguria unresponsive to fluids

Risk of PA catheter:

• Increased procedural fear and pain leading to increased CO

Invasive monitoring is rarely indicated

Williams 23rd edn / 962

Systemic vasodilation

Decrease CO 25-45% even in normal patients

Well tolerated (often beneficial):

• AR, MR, L to R shunts

Poorly tolerated:

• Limited ability to increase SV

• R to L shunts

• AS, MS

• Hypertrophic CM

• Pulmonary hypertension without ASD

PLACE OF EPIDURAL ANESTHESIA

MANAGEMENT DURING LABOUR

FIRST STAGE

Should be confined to bed with lateral recumbent position to minimize aorto- caval compression.

O2 inhalation 6 ltrs/min.

Analgesia ,majority by epidural

Fluid infusion should not be more than 75ml/hr. to prevent pulmonary edema.

Careful watch of pulse & resp. rate, if pulse > 100/min b/w uterine contractions, then rapid digitalization may be done

Cardiac monitoring & pulse oximetry can detect arrythymias & hypoxaemia

Williams 23rd edn / 961-962

Increases in PR much above 100 bpmor respiratory rate above 24 per min ,

particularly when associated with dyspnoea ,may suggest impending

ventricular failure

Most important predictors are prior heart failure and decreased LV ejection

fraction

SECOND STAGE

Delay in 2nd stage of labour to be curtailed by forceps / ventouse application under pudendal and / or perineal block.

Ventouse preferred as it can be applied in lateral recumbent position.

i.v. ergometrine to be withheld after delivery of shoulders.

Prolonged valsalva increase PA pressures, increases R to L shunting

THIRD STAGE

Conventional management to be followed.

It is preferable to administer oxytocin in an i.v. drip to all cases who are not in failure and simultaneously furosemide 40mg. i.v. to relieve volumetric load.

Slight blood loss is beneficial and if in excess oxytocin infusion may be continued.

Episiotomy wound repaired early. Pt kept in propped up position, Inj. morphine & O2 supply through out.

If resp. distress develops secondary to pulm. congestion , should be treated aggressively as pulm edema in I.C.U.

MANAGEMENT DURING PUERPERIUM

Close observation for 1st 24hrs.

Signs of pulm congestion & Edema to be looked for.

Sedatives to be given in 1st few days to relieve Anxiety Related tachycardia with Adequate Bed Rest.

Any Infection however during puerperium should be seriously viewed.

Not too many visitors.

Breast feeding is not contraindicated unless there is failure.

Pts. on warfarin should be allowed to Breast feed as secretion through Breast milk is extremely small.

Lactation should be encouraged unless patient is in failure.

Cardiac output is not compromised during lactation.

Lactation is a pathway for fluid excretion and diuretic requirement may actually fall.

CONTRACEPTION

Steroidal contraception is C/I , may ppt. thrombo-embolic phenomenon

IUDs cause infection.

Barrier method are best

Sterilization considered completion of family of the end of 1st week in Puerperium

If Heart is not well compensated, husband to be advised for vasectomy.

If unwilling to take a permanent method ® post natal contraception achieved by 3 monthly Injection of medroxyprogesterone acetate 150mg.

Low Doses OCP's may be given 6 months after Delivery.

Heart failure

Pulmonary oedema

Arrythymia

TIA & stroke

Thromboembolism

Sudden death

Anaemia

Increased physical activity

Fluid or dietary excess

Infection

Acute rheumatic carditis

SABE

PIH

Cardiac enlargement > 55% lung space on CXR

Twins/Hydramnios

Excessive weight gain

β-adnenergic agents

Age > 30 years

Gestational age > 20 weeks

Arrhythmias

N

NYHA functional class > 2

O(valvular & outflow tract obstruction)

Aortic valve area < 1.5 cm2

Mitral valve area < 2 cm2

Left ventricular outflow tract peak gradient > 30 mm HgPPrior cardiac events (heart failure, arrhythmia, TIA, stroke)E(ejection fraction)

Myocardial dysfunction (LVEF < 40% )

PREDICTORS(NOPE)

High risk pregnancy & delivery : Fernando Arias;3rd

edn/507

The estimated risk of a cardiac event with score 0,1 or more than 1 was 5%, 27% and 75% respectively

High risk pregnancy & delivery : Fernando Arias;3rd

edn/507

principles

Reduction of work load with bed rest, passive leg exercise-pneumatic compression stockings & heparin to prevent thromboembilism

Reduction of preload with Diuretics(furosemide is the choice)

Augmentation of cardiac contractility with digitalis or other agents like dopamine and dobutamine(digoxin 0.25mg,5/7 days is the choice)

Reduction of afterload with vasodilators(NTG is the choice)

Correction of precipitating factors.

Life threating situation

Mobilization of fluid from pulmonary interstitial space to alveolar space

Impairment of gas exchange

Oxygen desaturation & accumulation of CO2

Tissue hypoxia

Acidosis

Death

1. Stop the offending drug & treat underlying problems.

• 2. IV administration of furosemide

• 3. Oxygen by mask

• 4. Back rest

• 5. Parenteral morphine & deriphylline

&

SECOND LINE ACTIONS

NTG if SBP >100mm Hg

Dopamine if SBP 70-100 with signs & symptoms of shock

Dobutamine if SBP>100 with no signs & symptoms of shock

SBP defines second line of action

FIRST LINE ACTIONS

Oxygen & intubation

NTG sublingual

Furosemide iv 0.5-1.0 mg/kg

Morphine iv 2-4 mg

Acute pulmonary edema and or CCF

Clinical signs shock, hypoperfusion, CCF, pulm edema

Most likely problem ?

Haarrison’s;17th

edn/1704

Pregnancy may exacerbate the frequency and hemodynamic severity of pre-existing arrhythmiaas well as cause de-novo arrhythmias.

The risk of arrhythmias is relatively higher during labour and delivery.

Most arrhythmias in young women are not associated with structural heart disease

Drug therapy should be avoided during the 1st trimester if possiblePSVT- vagal stimulation, adenosine, cardioselective beta blockers Ventricular arrhythmias – i.v.lidocaine, procainamide ,electrical cardioversionAmiodarone is contraindicated

Pregnancy is associated with a higher myocardial oxygen consumption and reduced supply.

incidence of AMI is 1 in 35,700 deliveries, with a maternal mortality rate of 7.3%.

Delivery within 2 weeks of acute myocardial infarction was associated with up to 50% maternal mortality.

Etiology: coronary spasm-43%,atherosclerosis-47%,coronary artery dissection-10%

Treatment same as nonpregnantwomen thrombolysis , angioplasty and stenting

60 min of fluoroscopy exposes the fetusto 1300 mrad

Morbidity during subsequent pregnancy is20% -50%, including congestive heart failure and unstable angina

medication Potential adverse effects FDA category Compatible

with

breastfeeding

ACE inhibitors Teratogenesis,skull

ossification defects,renal

defects,oligohydramnios

C(1st

trimester)D(2n

d,3rd

trimester)

Enalapril,capto

pril yes

amiodarone Hypothyroidism,growth

retardation

D No

coumarin Warfarin embryopathy,cns

abnormalities,haemorrhag

e, spontaneous abortion

D(X ) yes

digoxin Accelerated labor,LBW C yes

diuretics Placental

hypoperfusion,jaundice

Furosemide C

hydrochlorthia

zide B

unknown

heparin Maternal

haemorrhage,osteoporosis

,

C yes

Metoprolol No teratogenesis,possible

bradycardia

B yes

Antibiotic prophylaxis for endocarditis is not routine.

AHA guidelines do not recommend routine endocarditisprophylaxis for cesarean section delivery or for uncomplicated vaginal delivery without infection.

However, some centers do administer endocarditis prophylaxis for vaginal delivery in women with structural heart disease, as an uncomplicated delivery cannot always be anticipated.

Infective endocarditis prophylaxis

American heart association guidelines are according to the risk levels:

Benefits most in highest risk cases

1.Mechanical prosthetic heart vlave

2.Natural prosthetic heart valve obtained from animals

3. A prior history of endocarditis

4. Congenital heart abnormities TGA, Tetralogy of fallot

Moderate risk

1.Hypertrophic cardiomypathy

2.Mitral valve prolapse

4. Unrepaired VSD or PDA

5. Acquired valvular dysfunction – MR or AR or AS

6. ASD, VSD, PDA

Low risk: No antibiotics prophylaxsis is required

1.Physiologic, functional murmers

2.MVP without regurgitation

3.Mild TR,ASD, VSD ,PDA(closed more than 6 months before)

4.Coronary arterial disease – (old CABG)

7. Previous rheumatic fever

8. People with pacemakers or defibrillatorsA pregnant women who has high risk of IE usually does not need antibiotic prophylaxis before normal delivery or LSCS but need to give to prevent infection due to Group B streptococcusIE prophylaxis :

Ampicillin 2gm IV or IM, or,

Ceftriaxone or cefazolin 1gm IM or IV, or,

Clindiamycin –600mg IM or IV, or,

Azithromycin – 500mg

Vancomycin

ACC & AHA recommend antibiotic prophylaxis for any congenital or acquired lesion in women with suspected bacteremia or active infection

Optional for women undergoing an uncomplicated delivery who are at high risk for endocarditis

Ampicillin 2g/cefazolin 1g/ceftriaxone 1g iv. Or if hypersensivity clindamycin 600mg iv . Or Amoxycillin 2g PO. vancomycin if enterococcus recommended 30 to 60 min before the procedure

ACC & AHA 2007, ACOG

2008Williams 23rd edn / 975

TISSUE VALVES:

less thrombogenic,require no anticoagulation

degeneration requires reoperation

MECHANICAL VALVES:

greater longevity

require anticoagulation

greater chance of fetal loss,placental haemorrhage and valve thrombosisco-existing heart disorders requiring anticoagulationeg: atrial fibrillation, apical thrombus, RHD, thromboembolism

Women with mechanical prosthetic valves must be anticoagulated & when not pregnant, warfarin is recommended

Overall maternal mortality is 3-4% with mechanical valves & fetal loss is common

Porcine tissue valves are much safer during pregnancy , because anticoagulation is not required as thrombosis is rare

Williams;23rd edn/963

Anticoagulation

3 common anticoagulant agents used during pregnancy are: Unfractionatedheparin(UH), low molecular weight Heparin (LMWH), warfarin .

The 6th American college of chest physicians (ACCP) conference on antithrombolysis recommends Heparin during first trimester & after 36th week of gestation & warfarin during the middle period of pregnancy to achieve INR 2-3, (also Euro Soc of Cardio)

Warfarin

It crosses the placental barrier and can harm fetus but is safe during breast feeding.

The incidence of Warfarin embryopathy is 4 to 10 %(avg6%)

Williams;23rd

edn/964

ACOG (2002) advised against LMWH during pregnancy for those with prosthetic valves because of sporadic reports of vascular thrombosis

Williams 23rd edn / 975

Heparin may cause maternal thrombocytopenia and osteopenia and is less effective in preventing thrombosis in patients with prosthetic valves.

It has no fetal ill effects as it can’t cross placenta

Warfarin in 1st trimester causes chondrodysplasia punctata ,fetal warfarinsyndrome hypoplasia of nose, eye socket, hand bones; risk max between 6-12 wks

When used in 2nd or 3rd trimester it can cause fetal CNS abnormalities which are less when low dose <5mg of warfarin is used per day .

Fetal intracranial bleeding is a risk throughout, particularly during vaginal delivery, unless stopped before labour

Safe during breast feeding

WARFARIN EMBRYOPATHY

Braunwald E et al. Heart Disease. 2001. pg. 2186.

CARDIAC DISEASE IN PREGNANCY:

PROSTHETIC VALVES

Heparin discontinued just before delivery

If delivery supervenes then protamine sulfate (1mg needed for 100 U heparin) given iv as an antidote to prevent extensive bleeding

Heparin / warfarin resumed 6 hrs after VD & 24 hrs after CS

Williams;23rd

edn/964

LMWH should be stopped at onset of contractions & 24 hrs before induction or CS. Regional analgesia given after 24 hrs of last dose.

Heparin/ LMWH resumed 6 hrs after delivery. Conversion back to warfarinshould be delayed for 3-7 days to minimise 2° PPH.LMWH continued till INR ≥2 for VTE & ≥2.5 for mechanical valves

Arulkumaran’s Best Practice in Labour and Delivery ;1st edn / 230-

232

Warfarin reversed with FFP & vit-K(1mg iv) and UFH with protamine sulfate.

If a fully anticoagulated pt requires CS ,GA should be administered & wound drains and interrupted skin sutures to be considered

Arulkumaran’s Best Practice in Labour and Delivery ;1st edn / 232

Monitoring

With LMWH administered sc. twice daily maintain anti-Xa level between 0.7 and 1.2 U/ml 4 hours after admn.

With dose adjusted UFH, the aPTT should be at least twice control.

Those on warfarin, the INR goal should be 3.0(range 2.5 to 3.5)

Mitral stenosis

Most common valvular disorder in pregnancy.

Normal mitral valve area - 4-6 cm2

Symptoms develop - < 2.5 cm2

Mild - 1.5-2.5 cm2

Moderate - 1.5-1 cm2

Severe - <1 cm2

Critical - < 0.5cm2

25% - Detected for first time during pregnancy

MITRAL STENOSIS:

The severity of MS assessed by measurement of the mitral valve area by echo-Doppler is the most powerful predictor of maternal pulmonary edema.

Pregnancy-associated hypervolemia and tachycardia result in increase of the functionality of the mitral valve stenosis, increased left atrial pressure, risk of atrialfibrillation, and heart failure.

Marked increase in maternal morbidity and unfavourable effect on foetal outcome. Mortality is rare

BMV is safe and effective and appears to be preferable during pregnancy.

MVR indicated when associated with severe MR & previously distorted valves due to prior manipulation & has a high fetal loss rate

MITRAL STENOSIS:

Progressively worsening cardiac status

Progressive pulmonary hypertension

Pulmonary edema

Failure to respond to conservative treatment

Massive hemoptysis

Critical MS

h/o CCF in last pregnancy

INDICATIONS FOR BMV

Prerequisites (1) No MR (2) Valves should not be calcified.

Best done between Pregnancies but if indicated b/w 24 - 28 wks of Pregnancy.

Mitral valve prolapse (MVP) is the most common cardiac abnormality found in pregnant women, affecting 12–17% (6-8% in India) of women of child bearing age.

Mostly asymptomatic, present with MR; may present with chest pain , palpitation & syncope with arrhythmia

Most pregnants with MVP don’t require treatment, only those with recurrent severe arrhythmias need beta blockers

There is no need for IE prophylaxis

MITRAL VALVE PROLAPSE

The cause of mitral regurgitation may be rheumatic heart disease or myxomatousdegeneration

The disease is usually well tolerated in pregnancy as with decrease in systemic vascular resistance there is decrease in regurgitation.

One should always remain cautious of atrialfibrillation or severe hypertension.

Women with severe MR should be advised to undergo operative repair prior to pregnancy.

MITRAL REGURGITATION

The cause may be RHD, congenitally deformed valve, infective endocarditis, connective tissue disease.

Ideally women with severe AR should undergo operation prior to conception.

They are at increased risk for aortic dissection.

Congestive heart failure with MR or AR is treated with digoxin, diuretics, vasodilators such as hydralazine, NTG. Beta blockers are safe.

AORTIC REGURGITATION

It is a disease of old age but in females under 30 yrs ,the cause is congenital bicuspid valve.

Mild to moderate AS is well tolerated.

In cases of severe AS there is increased risk and may present with dyspnea, angina or syncope in 3rd trimester.

Ideally surgery should be done prior to conception. In severe symptomatic AS cases during pregnancy percutaneous aortic balloon valvuloplasty should be preformed prior to labor & delivery.

This is high risk condition in which pregnancy should not be advised. If pregnancy occurs therapeutic termination should be considered.

AORTIC STENOSIS

CONGENITAL HEART DISEASE

Classified as

• Acyanotic (Lt to Rt)

• - ASD

• - VSD

• - PDA

• Cyanotic (Rt to Lt. shunts)

• - TOF.

• - Eissenmengers Syndrome

• Others

• - Co-arctation of Aorta

• - Primary Pulmonary HTN.

• - Marfan's syndrome.

Majority already corrected, hence pose less risk, but uncorrected cyanotic group pose major risk.

Non-cyanotic cardiac disease

• NYHA Functional Class

• Maternal mortality

• Class I and II: 0.4%

• Class III and IV: 6.8%

• Fetal mortality

• Class I: negligible

• Class IV: 30%

Cyanotic cardiac disease

• 45% rate of fetal death

• Low birth weight and immaturity

OUTCOMES

Is determined by :

-- nature of disease & surgical repair

-- cyanosis & Hb-- PVR

-- functional capacity

CV deterioration favorised by :

- exercise, heat, humidity, anemia, infections, and arrhythmias

GOOD in most non-cyanotic cases

UNFAVOURABLE if cyanosis ,impaired functional status ( IE, CCF, HTN, arrhythmia, thromboembolism )

MATERNAL OUTCOME

Is determined by maternal

-- cyanosis

-- functional capacity

Fetal wastages (20% noncya vs 45% cya )

Low birth wt & prematurity (correlate with Hb )

CHD ( 10 % ) ( VSD: 22%, AS: 20% , Fallot: 3-17%)

Other physical & mental abnormalities

CHD - FETAL OUTCOME

Parameter No. of

pregnancies

No. of live births % born alive

Haemoglobin

gm/dl

<16 28 20 71

17-19 40 18 45

>20 26 2 8

Arterial oxygen

saturation(%)

<85 17 2 12

85-89 22 10 45

>90 13 12 92

FETAL OUTCOME IN CYANOTIC

CHD

POORLYINTERWELL

NYHA IVNYHA II-IIINYHA I

R-L shunt,

Unrepaired +cyanosis

Ebstein`s anomalyL-R shunt - PH

PHT/ P vascular

disease

Repaired TGA

Fontan repair

Repaired TF

PS (severe) ?PS (mild to moderate)

Marfan`s

Coarctation Aorta

PR,TR (even severe

if low pressure)

AS, MS (severe)AS, MS (moderate)AR, MR ( mild to

moderate)

ASD

MC type is ostium secundum

Even uncorrected ASD tolerate Preg. & Labourwell.

CCF unresponsive to Medical therapy need surgical mgtShunt Reversal is a threat in case of systemic hypotension (eg. Hemorhage or Epidural Analgesia)Paradoxical embolus chance is there(by RL shunt)

Isolated VSD: well tolerated

With PHT : ( marked reduction in BP shunt reversal )

Post-op :(offspring : 22% CHD, 50% of them VSD )

VSD

Pregnancy & Labour well toteroted.

CCF & Pulm. Hypertension develop when defect > 1.25cm2.

Major Risk of shunt Reversal when circulatory collapse & cyanosis.

Total fetal loss upto 20%

Mild & moderate-sized :

- risk of IE during delivery

Moderately restrictive :

- decrease in SVR decrease L-R shunt, shunt reversal if PHT

- risk of HF ( > Age 30 )

Non restrictive (+ PV disease & R-L shunt) :

- decrease in SVR increase R-L shunt low uterine flow fetal risk

PDA

Majority of PDA pts. tolerate pregnancy well

Pulm HTN can cause death.

Surgical correction possible in the absence of pulm. HTN.

Epidural analgesia avoided d/t to fear of shunt Reversal.

Total Loss upto 7%

4% chance of child suffering from the same abnormality.

Well tolerated ( even severe occasionally )

IE prophylaxis advisable

Severe PS :

- Should be corrected prior to conception

- Balloon dilatation during pregnancy efficacious

( progressive RV failure despite drug therapy )

Post-op :

- Low risk of IE

- Mild to moderate PR not a concern

Hypertension (comparatively low incidence of toxemia )

Increased risk of aortic rupture or dissection

Increased risk of cerebral hemorrhage

LVF exceptional under age 40 (except infants)

Risk of IE if bicuspid aortic valve

Coarctation is to be corrected prior to pregnancy

Steps for limiting physical activity & controlling BP

Surgical correction during pregnancy successful in cases of uncontrollable HTN or CCF

Low incidence among women, cardiac defects in 20% of infants

Stenosis : mild to moderate generally well tolerated

severe (+ dyspnea, angina) high risk

Regurg : generally well tolerated even severe(with good LV function)

High risk of IE : prophylaxis during labor & delivery

Risk of aortic root dissection

Severe AS :

balloon dilatation ( provided thin, mobile& not calcified )

Mild to moderate AS & significant AR :

advice pregnancy before replacement ( provided good LV function)

Severe AS and/or AR ( replacement indicated ) :

advice a tissue valve

Post-op : risk of IE and aortic root dissection persist

Severe aortic stenosis ( pregnant patient) : high risk of decompensation in the 2nd or 3rd trimester

early abortion :

+ valvuloplasty or replacement

continuation of pregnancy :

+ medical treatment, hemodynamic monitoring during labor & delivery & appropriate anesthesia

+ balloon valvuloplasty or

+ surgical replacement

Four components

Ventricular septal defect

Pulmonic stenosis

Overriding or dextroposed aorta

Right ventricular hypertrophy

TOF is the commonest cyanotic CHD, 17% in India

Ghai pediatrics;7th edn/408

Patients with prior surgical repair, good exercise capacity & minimal residual disease pregnancy is well tolerated.

Without surgical repair or palliative surgery risk depends on degree of cyanosis

Risk of fetus having congenital heart disease is 5-6%.

Severity of cyanosis is directly proportional to severity of PS

Pregnancy :

- exacerbate R-to-L shunt and cyanosis.

poor prognostic signs : Hct > 60%, SaO2 <80%, RV HTN, syncope ,shorter systolic murmur

Labor & delivery :

- sudden decrease in SVR intense cyanosis, syncope & death

Downward displacement of TV leaflet into rtventricle with anomalous attachment leading to

TR (due to dysplastic TV leaflet)

Hypoplastic rt ventricle (atrialised rt ventricle)

Harrison’s;17th edn/1464

Risk of TR & RV dysfunction, AF, R->L shunt leading to cyanosis, paradoxical embolus

*** Outcome depends on severity of TR, RVF, and cyanosis

*** successful pregnancy reported in the majority of patients

Surgery :

improve RV function

eliminate the risk of paradoxical emboli & bypass tracts

reduce the risk of IE & supraventricular arrhythmias

High maternal morbidity

Inheritance 50%

Majority manifest during pregnancy (AR, HF ,Aortic dissection)

Aortic root < 40 mm :In general, favorable outcome

Periodic follow up, prophylactic beta blockers recommended, limited physical activity

Dilatation of the aorta >4cm or progressive

advise against conception

during pregnancy : Significant aortic dilatation

therapeutic abortion

surgical intervention

During delivery : Significant cardiac complication

LSCS

high risk for maternal morbidity and mortality(50%)

poor fetal outcome(prematurity,IUD,IUGR,perinatal death)

to be advised against pregnancy, termination indicated

death due to RV failure with cardiogenic shock

Severe PAH resulting in RtLt shunt at ASD / VSD /PDA

Eisenmenger complex= PAH+VSD (RtLt shunt)

If a patient decide to proceed to term :

- Close follow-up

- Restriction of physical activity

- Anticoagulation

- Hospitalization for any sign of premature uterine activity

- Early elective hospitalization recommended

- Spontaneous labor preferred to induction

- BP, ECG, blood gas monitoring essential

- High concentration O2 may be helpful

- Vaginal delivery mostly tolerated( + forceps & vacuum extraction)- Cesarean section ( GA with minimal negative inotropic or segmental epidural )

Idiopathic DCM : should not have pregnancy if EF<40%.

Ventricular function must be assessed without ACEI

Exercise testing may be helpful.

Hydralazine, diuretics, bed rest for heart failure

DILATED CARDIOMYOPATHY:

PERIPARTUM CARDIOMYOPATHY (ALL FOUR OF FOLLOWING NEEDED)

1. Cardiac failure occurring in the last month of pregnancy, or within 5 months postpartum

2. Absence of an identifiable cause for the cardiac failure

3. Absence of heart disease prior to the last month of pregnancy

4. Left ventricular systolic dysfunction by echographic criteria:

left ventricular ejection fraction <45% and/or

decreased fractional shortening <30%

+ end diastolic dimension >2.7 cm/m2

National Heart, Lung, & Blood Institute and Office of Rare

Diseases : 1997

Age : 20-35 years

Present in : 2nd or 3rd postpartum month

C/o : weakness, breathlessness, orthopnoea, palpitation, PND, palpitation

Examination: tachycardia, arrhythmias, pulmonary rales, peripheral oedema

Investigation: Chest X-Rayenlarged heart, pulm vascular redistribution, ECHOenlargement of all cardiac chambers mainly LV, LVEF & CO decreased, PCWP increases

T/t. bed Rest, Digitalis, Diuresis (Pre-load Reduction), Hydralazine (Post - Load Reduction)

Beta Blocker & Anti-coagulation therapy.

Immunosuppressive therapy, Heart transplantation

Vaginal delivery Preferred.

Epidural Anesthesia ideal.

Recurrence in subsequent Pregnancies is 21% with normal LV function & 44% in persistent LV dysfunction

Immunosuppresive therapy in biopsy proven myocarditis who fail to improve within 2 weeks .

Implantable cardioverter defibrilator or cardiac transplantation may be helpful

Mortality:25-50% with 50% of deaths in the first 3 months postpartum.

Cause of death:

CHF, arrhythmias, thromboembolism

MANAGEMENT

Characterised by LV myocardial hypertrophy with LV outflow pressure gradient

AD inheritance

Pregnancy well tolerated but CCF common

Strenous exercise prohobited, abrupt positional changes avoided

Beta blockers & CCBs given but diuretics & dilators contraindicated

Spinal anaes contraindicated, EA controversial

Rare inheritance of lesion in infants

PRIMARY PULMONARY HYPERTENSION

Characterised by thickening of muscular layer of pulm. arterioles.

Maternal Mortality 50%

Fetal outcome very poor

Termination of Pregnancy indicated.

Bed rest from 20wks. of GA, avoidance of supine position

Heparin administered.

Nifedipine , Prostacyclin helps as pulmonary vasodilatation.

Epidural Morphine given.

Commonest cause is Eisenmenger’s syndrome.

If pulmonary hypertension >60% of systemic levels, complications are likely

Maternal mortality 50%, perinatal 28%, 80% death during 1st postpartum month

Highest incidence during labor and puerperium.

Mode of delivery: caesarean section probably preferable.

Dihydropyridine CCBs nifedipine,amlodipinePO

Endothelin receptor antagonist bosentan PO

Phosphodiesterase-5 inhibitor sildenafil PO

Prostacyclin analogues ilioprost inhalation, epoprostenol iv, treprostinil iv or sc

Lung transplantation in refractory cases

Harrison’s;17th edn/1576-1579

Pregnancy causes significant haemodynamic changes and imposes an additional burden on the cardiac patient, especially around the time of labour and in the immediate puerperium.

To achieve a successful pregnancy outcome, a clear understanding of these haemodynamic adaptations as well as meticulous maternal and foetal surveillance for risk factors and complications throughout the pregnancy is essential.

CONCLUSION

Appropriate contraceptive and family planning advice as well as pre-conceptional counselling are also important.

Referral to a higher centre especially in presence of moderate to severe disease.

The concerted efforts of a team consisting of the obstetrician, cardiologist, anaesthesist, cardiothoracic surgeon, neonatologist, and paediatric cardiologist are mandatory to ensure optimal results.