heart disease pregnancy new dr rabi
TRANSCRIPT
CARDIAC DIESEASES IN
PREGNANCY
DR. RABI NARAYAN SATAPATHY
ASST.PROFESSOR
DEPT. OF OBST.& GYNAECOLOGY
SCB MEDICAL COLLEGE, CUTTACK
MOB-09861281510
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.
