This document discusses the cardiovascular changes that occur during pregnancy and how they impact women with underlying heart disease. It notes that the incidence of heart disease complicating pregnancy is approximately 1% globally. The most common types seen in India are rheumatic heart disease (78%) and congenital heart disease (18.7%). The document outlines the normal anatomical and physiological changes pregnancy has on the cardiovascular system. It then discusses how certain heart conditions are classified based on their risk during pregnancy, from WHO class 1 (lowest risk) to WHO class 4 (highest risk). The document provides guidance on evaluating and managing women with heart disease throughout their pregnancy.

1. MODERATOR: Dr. MUNIKRISHNA
PRESENTED BY: Dr SUNANDA

2.  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)

3.  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

4. ANATOMICAL CHANGES
 Due to elevation of diaphragm consequent to
the enlarged uterus, the heart is pushed
upwards & outwards with slight rotation to
left.

5.  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

6.  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

7.  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.

8.  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)

9.  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

10.  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

11.  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

12.  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%

13.  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.)

15.  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

16.  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

17. SYMPTOMS
 progressive dyspnoea or orthopnoea
 Nocturnal cough
 Hemoptysis
 Syncope
 Chest pain

18. SIGNS
 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

19. LEFT VENTRICULAR
FAILURE OR PULMONARY
VENOUS HYPERTENSION
Easy fatigability
Shortness of breath
Orthopnea
Pulmonary congestion
RIGHT SIDED HEART
FAILURE
Weight gain
Dependent oedema
Hepatomegaly
Increase JVP

20. grade symptoms
Grade 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
activity
Comfortable at rest but less that
ordinary activity causes symptoms
Grade 4 Severly compromised
Inability to perform any physical
activity without symptoms

21. 1. Prior cardiac event( TIA, stroke, heart
failure)
2. Baseline NYHA class > 2 or cyanosis
3. 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)

22.  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%

23. RISK CLASS RISK OF PREGNANCY BY
MEDICAL CONDITION
WHO 1 risk no higher than general
population
WHO 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

24. Uncomplicated, small or mild:
 Pulmonary stenosis
 VSD
 PDA
 Mitral valve prolapse with no more than
trivial mitral regurgitation
Successfully repaired simple lesions
 Ostium secondum ASD
 VSD
 PDA
 Total anomalous pulmonary venous drainage

25. If otherwise uncomplicated:
 Unoperated ASD or VSD
 Repaired tetralogy of fallot
 Most arrhythmias

26.  Mild LV impairment
 Hypertrophic cardiomyopathy
 Native or tissue valvular heart disease not
considered WHO4
 Marfan syndrome without aortic dilation
 Heart transplantation

27.  Mechanical valve
 Systemic right ventricle
 Post fontan operation
 Cyanotic heart disease
 Other complex congenital heart disease

28.  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.

29.  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.

30.  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

31.  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

32.  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

33. ABSOLUTE
 Eisemenger’s syndrome
 Primary pulmonary hypertension
 Single ventricle
 marfan’s syndrome with aortic root
diameter>7cm
 Peripartum cardiomyopathy
 Pulmonary veno occlusive disease

34.  Relative
 Severe obstructive lesion
 Parous women with NYHA III&IV
 History of cardiac failure
When to do?
Termination should be done using S&E
Before 12wks preferably 8wks

35.  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

36.  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.

37.  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

38.  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

40. 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%

41.  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

42. CHEST 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

43. ELECTROCARDIOGRAPHY
 Main role is in the diagnosis of arrhythmias
ECG 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

44. 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.

45.  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

46.  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.

47. 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.

48. LEFT TO RIGHT SHUNTS-
 septal defects that result in volume overload-
ASD, VSD, PDA
STENOTIC 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

49. Cardiac lesion Previous sibling
affected
Father affected Mother affected
Marfan syndrome NS 50 50
Aortic stenosis 2 30 15-18
Pulmonary
stenosis
2 2 6-7
VSD 3 2 10-16
ASD 2.5 1.5 5-11
PDA 3 2.5 4
COA NS NS 14
TOF 2.5 1.5 2-3
CONGENITAL HEART DISEASE IN FETUS(%)
NS = NOT STATED
DATA FROM LUPTON, 2002

50. LEFT 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

51.  Commonest congenital lesion
 Repaired ASD- WHO risk class 1
 Unoperated ASD- WHO risk class2
 Unrepaired ASD- risk of pre- eclampsia &
IUGR increased

52. 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.

53.  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

54.  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

55.  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.

56.  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

57.  Account for 3% of all congenital cardiac
malformations
 Compared with simple defects, complications
are more frequent during pregnancy

58.  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.

59.  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

60. 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

61.  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 hypertrophy
de swiet 5th ed

62.  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.

63.  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

64.  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.

65.  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

66. 1. MODE OF DELIVERY
2. ANALGESIA & ANAESTHESIA
3. INDUCTION OF LABOUR
4. MANAGEMENT OF LABOUR

67.  Vaginal delivery is the safer route.
 cesarean section should be generally
performed for obstetric reasons.

68.  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 dissection
4. Acute intractable heart failure
5. Severe aortic stenosis
6. 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

69.  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.

70.  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

71.  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.

72.  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

73.  Antibiotic prophylaxis- to prevent bacterial
endocarditis
 Prevent thromboembolic complications- early
ambulation, compression bandage, prophylactic
low dose heparin during labour,delivery &
immediate postpartum periods

74.  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

75.  If labour starts prematurely & urgent delivery
is unavoidable in pt with mechanical valves on
full anticoagulation with LMWH or UFH
1. Protamine sulphate
2. FFP should be given prior to LSCS to achieve
INR<2
3. Oral vit K (0.5- 1mg) but takes 4-6 hrs to
affect INR
4. Newborns of mothers on OAC – FFP & vit K

76. 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.

77. 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.

78. SECOND STAGE
 Cut short
 Assisted with forceps or ventouse

79. 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.

80. 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

81.  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

82. Thank you