This document discusses cardiovascular diseases in pregnancy. Some key points: - Risk factors for heart disease in pregnancy are increasing and include diabetes, hypertension, and obesity. The number of women with congenital heart disease reaching childbearing age is also rising. - Hemodynamic changes during pregnancy place additional strain on the heart, increasing cardiac output and blood volume. These changes begin in the first trimester and peak in the second. - Women with preexisting heart conditions like pulmonary hypertension face higher risks during pregnancy and delivery. Those with severe disease may require termination of pregnancy for safety. Close monitoring is important for women with heart conditions throughout their pregnancy.

1. PREGNANCY & HEART DISEASE

2. • 0.2–4% of all pregnancies are complicated by
cardiovascular diseases (CVD)
• and the number of the patients who develop
cardiac problems during pregnancy is
increasing

3. RISK FACTORS
• diabetes,
• hypertension,
• obesity
• treatment of congenital heart disease has
improved, resulting in an increased number of
women with heart disease reaching
childbearing age.

4. Poor prognostic indicators
• h/o heart failure, ischemic attack, stroke
• Arrhythmias,
• Base line NYHA class 3 and 4
• MV area below 2cm sq., AV area below 1.5
• Ejection fraction less than 40%

5. • Hypertensive disorders 6–8% of all pregnancies
• congenital heart disease is the most frequent (75–
82%),
• shunt lesions predominating (20–65%).
• Congenital heart disease represents just 9–19% outside
Europe and North America.
• Rheumatic valvular disease dominates in non-western
countries, comprising 56–89% of all cardiovascular
diseases in pregnancy
• Cardiomyopathies are rare, but represent severe
causes of cardiovascular complications in pregnancy.
• Peripartum cardiomyopathy (PPCM) is the most
common cause of severe complications

6. • The hemodynamic changes are profound and
begin early in the first trimester.
• The plasma volume begins to increase in the sixth
week of pregnancy and, by the second trimester
approaches 50% above baseline. The plasma
volume then tends to plateau until delivery.
• This increased plasma volume is followed by a
slightly lesser rise in red cell mass, which results
in the relative anemia of pregnancy.

9. • In early pregnancy increased CO is primarily
related to the rise in stroke volume; however, in
late pregnancy, heart rate is the major factor.
• Heart rate starts to rise at 20 weeks and increases
until 32 weeks.
• It remains high 2–5 days after delivery.
• Systemic BP falls early in gestation and diastolic
BP is usually 10 mmHg below baseline in the
second trimester.

10. • Beginning of labor : > 7 L/min
• Uterine contraction : > 9 L/Min
• Anesthesia : < 8 L/min
• Post partum CO continues to increase up to 72
hours due to auto transfusion from uterus and
reabsorption of edema fluid
• CO falls to non pregnant values in a few wks after
delivery
CO In labor

11. • The heart can increase its size by up to 30%,
which is partially due to dilatation.
• Data regarding systolic and diastolic function
in pregnancy are scarce.
• Systolic function increases first but may
decrease in the last trimester.
• Reports on diastolic function are conflicting.

14. HEMOSTATIC CHANGES
• increase in concentration of coagulation
factors, fibrinogen, and platelet adhesiveness,
as well as diminished fibrinolysis, which lead
to hypercoagulability and an increased risk of
thrombo-embolic events.
• In addition, obstruction to venous return by
the enlarging uterus causes stasis and a
further rise in risk of thrombo-embolism.

16. • SBP and DBP increase 15–25% and 10–15%,
respectively, during uterine contractions.
• Such increases are associated with a rise in pressure in
the amniotic fluid, and in the intrathoracic venous,
cerebrospinal, and extradural fluids.
• CO increases by 15% in early labour,
• by 25% during stage 1,
• and by 50% during expulsive efforts.
• It reaches an increase of 80% early post-partum due to
auto transfusion associated with uterine involution and
resorption of leg oedema.

17. Clinical Findings in Normal Pregnancy
Elevated JVP [increased
plasma vol.]
Tachycardia, low DBP, Pulse Pressure
increased [bounding pulses]
Pulsatile fingertips, warm hands, occ.
Quincke
Apex slight down & out, prominent impulse,
active precordium[volume loaded ventricles]
Reduced B.S. at lung
bases [diaphragm
moves up]
Pedal oedema
>80% women
[increased plasma
vol., increased
venous pressures]
S1 Loud [Tachy, increased LV mass], S2 wide split
accentuated [P2 delayed], occ S3
Flow murmur @ aortic, pulm; ESM grade 3 @
LLSB; cervical venous hum; mammary soufflé @
LLSB,

18. GENETIC TESTING AND COUNSELLING
• The recurrence risk varies between 3% and
50%
• an autosomal dominant manner (e.g. Marfan
syndrome, hypertrophic cardiomyopathy, or
long QT syndrome) have an inheritance risk of
50%, regardless of gender of the affected
parent.
• Autosomal recessive and X-chromosomal
recessive inheritance are rare.

19. • Genetic testing may be useful:
– In cardiomyopathies and channelopathies, such as
long QT syndromes
– when other family members are affected
– when the patient has dysmorphic features,
developmental delay/mental retardation, or when
other non-cardiac congenital abnormalities are
present,
– in syndromes such as in Marfan, 22q11 deletion,
Williams–Beuren, Alagille, Noonan, and Holt–Oram
syndrome

20. • by chorionic villous biopsy can be offered in the 12th week
of pregnancy.
• All women with congenital heart disease should be offered
fetal echocardiography in the 19th to 22nd week of
pregnancy.
• Measurement of nuchal fold thickness in the 12th to 13th
week of pregnancy is an early screening test for women
over 35 years of age.
• The sensitivity for the presence of a significant heart defect
is 40%, while the specificity of the method is 99%.
• The incidence of congenital heart disease with normal
nuchal fold thickness is 1/1000.

21. Cardiovascular diagnosis in pregnancy
• There is a 15–20 left axis deviation.
• Common findings include
• transient ST segment and T wave changes,
• the presence of a Q wave and inverted T waves in lead
III, an attenuated Q wave in lead AVF, and
• inverted T waves in leads V1, V2, V3.
• Holter monitoring should be performed in patients
with known paroxysmal or persistent documented
arrhythmia [VT, atrial fibrillation (AF), or atrial flutter]
or those reporting symptoms of palpitations.

22. Echocardiography
• can be repeated as often as needed
• is the preferred screening method to assess cardiac
function.
Trans esophageal echocardiography
• in the assessment of complex congenital heart disease.
• Is relatively safe during pregnancy.
• The presence of stomach contents, risk of vomiting and
aspiration, and sudden increases in intra-abdominal
pressure should be taken into account, and fetal
monitoring performed if sedation is used.

23. EXERCISE TESTING
• submaximal exercise tests to reach 80% of
predicted maximal heart rate in asymptomatic
pregnant patients with suspected CVD.
• There is no evidence that it increases the risk
of spontaneous abortion
• Dobutamine stress should be avoided

24. RADIATION EXPOSURE
• Should be delayed till 12 weeks
• No evidence if radiation is < 50 mGy
• Increased incidence of childhood cancer

26. MRI
• Useful to image complex CHD
• Avoid gadolinium
• Should be used in all patient s suspected of
ascending Ao Enlargement
•CT
• Not recommended
• Only in APE if other diagnostic tools are not
helpful

27. • After 4th month in 2nd trimester
• By this time
– Organogenesis is complete
– The fetal thyroid is inactive
– Uterus size small
Percutaneous therapy

28. • Only if Medical therapy and PCI fail & life is threatened
• b/w 20th & 28th weeks
• 1st trimester : high risk of fetal malformations
• 3rd trimester : high incidence of preterm delivery &
maternal complications
• If >26 weeks , LSCS before CABG
• Pump flow >2.5 l /min/m2
• Perfusion pressure >70 mm hg
• Maternal complications are comparable to non-
pregnant
Cardiac surgery with cardiopulmonary
bypass

29. Antenatal Follow up
• Ranging from routine follow up to continuous
hospital admission
• Preferably in Tertiary care centre with cardiac
and cardiac surgical facilities
• Clinical examination and follow up echo
• Saturation

30. Induction of Labour
• Oxytocin and artificial rupture of the membranes
are indicated when the Bishop score is
favourable.
• A long induction time should be avoided if the
cervix is unfavourable.
• Misoprostol or dinoprostone- there is a
theoretical risk of coronary vasospasm and a low
risk of arrhythmias.
• Dinoprostone also has more profound effects on
BP than prostaglandin E1 and is therefore
contraindicated in active CVD.

31. Vaginal or caesarean delivery
• The preferred mode of delivery is vaginal
• Caesarean delivery should be considered for
obstetric indications
• Cardiac Indications-
– Dilatation of the ascending aorta >45 mm,
– Severe aortic stenosis,
– Pre-term labour while on oral anticoagulants
– Eisenmenger syndrome,
– Severe OR worsening heart failure
– Mechanical prosthesis

32. Labour
• Once in labour, the woman should be placed in a
lateral decubitus position to attenuate the
haemodynamic impact of uterine contractions.
• Avoid maternal pushing, to avoid the unwanted
effects of the Valsalva
• Delivery may be assisted by low forceps or
vacuum extraction.
• Continuous electronic fetal heart rate monitoring
is recommended.

33. Anaesthesia
• Lumbar epidural analgesia is recommendable
to reduce pain related sympathetic activity,
• Reduces the urge to push
• Regional anaesthesia can cause systemic
hypotension and must be used with caution in
patients with obstructive valve lesions.

34. Delivery in ant coagulated women with
prosthetic valves
• OACs should be switched to LMWH or unfractionated
heparin (UFH) from the 36th week.
• Women treated with LMWH should be switched to i.v. UFH,
at least 36 h before the induction of labour or caesarean
delivery.
• UFH should be discontinued 4–6 h before planned delivery,
and restarted 4–6 h after delivery if there are no bleeding
complications
• Urgent delivery in a patient with a mechanical valve taking
therapeutic anticoagulation may be necessary, and there is
a high risk of severe maternal hemorrhage.
• If emergent delivery is necessary while the patient is still on
UFH or LMWH, protamine should be considered

35. • In the event of urgent delivery in a patient on
therapeutic OACs, caesarean delivery is preferred to
reduce the risk of intracranial hemorrhage in the fully
ant coagulated fetus.
• If emergent delivery is necessary, fresh frozen plasma
should be given prior to caesarean delivery to achieve
a target international
• normalized ratio (INR) of ≤2.4 Oral vitamin K (0.5–1
mg) may also be given, but it takes 4–6 h to influence
the INR.
• If the mother was on OACs at the time of delivery, the
anticoagulated newborn may be given fresh frozen
plasma and should receive vitamin K.
• The fetus may remain anticoagulated for 8–10 days
after discontinuation of maternal OACs

36. Post-partum care
• Slow i.v. infusion of oxytocin
• Prostaglandin F analogues to treat post-
partum haemorrhage
• Meticulous leg care, elastic support stockings,
and early ambulation are important to reduce
the risk of thrombo-embolism

37. IE prophylaxis
• Not recommended

48. • Regular antihypertensive medications not effective in
preventing preeclampsia.
• When preeclampsia develops,
– bed rest usually is initiated,
– with salt restriction and close monitoring,
– and magnesium sulfate prevent eclamptic seizures and to
prolong the pregnancy.
• Urgent delivery usually is necessary,
• after which the blood pressure usually normalizes rapidly.
• Beta blockers, particularly labetalol have been used with
good effect, although a long safety record has been accrued
with methyldopa, which has no adverse effect on mother
or baby.

50. Cyanosis
• Fetal and maternal hypoxia
• Increased thromboembolism
• Increased right to left shunt
• Worsening desaturation
• Paradoxical embolism

51. Cyanosis management
• Restriction of physical activity
• Monitoring oxygen saturation
• Supplemental oxygen
• Prevention of venous stasis
– Use of compression stockings
– Avoiding the supine position
– For prolonged bed rest, prophylactic heparin
administration

52. • Common L to R shunt complicating pregnancy
• Prognosis
– Pulm hypertension
– Functional status
– Size of shunt
• Elective closure of an atrial septal defect by
device or operative repair is preferable before
pregnancy
ASD

53. Ventricular septal defect
• Patients with small VSD tolerate pregnancy
without difficulty
• If large VSD with severe PAH , counselling
regarding the termination.

54. PDA
• small ducts with normal or near-normal
pressures usually cause no hemodynamic
perturbations during pregnancy.
• With a large shunt, the added volume load of
pregnancy may precipitate left ventricular
failure.
• Patients with pulmonary hypertension should
be counseled that pregnancy is
contraindicated.

55. Pulmonary hypertension
• When the pulmonary hypertension exceeds
approximately 60% of systemic levels, more likely
to be associated with complications.
• The volume load may compromise the poorly
functioning right ventricle
• fall in peripheral resistance augments R-L
shunting =cyanosis
• Labor and delivery are particularly dangerous,
• the highest incidence of maternal death is during
parturition and the puerperium.

56. Pulmonary hypertension
• Termination of pregnancy safer option, this is
more complex procedure, and cardiac anesthesia
• successful maternal outcome with the use of
pulmonary vasomodulator drugs.
• Nitric oxide can be administered through nasal
cannula or facemask, and successful pregnancy
also has been reported with intravenous
epoprostenol.
• Sildenafil also has been used, but with all of these
agents, maternal death may still occur days or
weeks after delivery

57. • In summary, the mortality for pregnant
patients with severe pulmonary hypertension
is high.
• Appropriate advice about contraception
• Estrogen-containing contraceptives are
contraindicated

58. Pulmonary valve stenosis
• Relatively well tolerated if the right ventricular
pressure is less than 70% of systemic pressure
• Right ventricular failure
• Arrhythmias.
• Balloon valvuloplasty if PG>64
• CS- severe PS and in NYHA class III/IV despite
OMT

59. Cyanosis
• Fetal and maternal hypoxia
• Increased thromboembolism
• Increased right to left shunt
• Worsening desaturation
• Paradoxical embolism

60. Cyanosis management
• Restriction of physical activity
• Monitoring oxygen saturation
• Supplemental oxygen
• Prevention of venous stasis
– Use of compression stockings
– Avoiding the supine position
– For prolonged bed rest, prophylactic heparin
administration

62. Eisenmenger
• The risks and benefits of anticoagulation
considered on an individual patient basis.
• Diuretics
– The lowest effective dose
– Avoid haemoconcentration
– Intravascular volume depletion.
• Microcytosis and iron deficiency
– Supplemental iron.

63. Tetralogy of Fallot
• Pre repair
– Arrhythmias , heart failure , thrombo-embolism
– Progressive aortic root dilatation,
– Endocarditis
• Post repair
– Palliation – depends on the degree of cyanosis
– Dysfunction of the right ventricle
– Moderate to severe pulmonary regurgitation
– Screening for 22q11 deletion - %

64. Pulmonary regurgitation
• Severe pulmonary regurgitation
– An independent predictor of maternal
complication
– Bad outcome with impaired ventricular function
• Pulmonary valve replacement
– Pre -pregnancy
– Preferably bioprosthesis
– TPVI – for refractory heart failure

65. Ebstein’s anomaly
• Outcome depend on
– The severity of the TR
– right ventricular function
– Cyanosis
– Previous cardiac event
• Usually be managed medically during pregnancy.
• Echocardiographic surveillance of RV function
• Early caesarean delivery If RV function
deteriorates
• After T valve replacement pregnancy is well
tolerated

66. Transposition of the great arteries
• Post operative- WHO risk class III.
• Atrial repair
– Atrial arrhythmia
– Severe impairment of RV function
• Great arterial repair
– Obstruction
– Regurgitation
• Bradycardia or junctional rhythm - b-blockers
cautious
• An irreversible decline in RV function in 10%

67. Congenitally corrected transposition of
the great arteries
• WHO risk class III .
• Pre -disposed to developing AV block
• B-blockers must be used with extreme caution.
• An irreversible decline in RV function has been
described in 10%
• Class 4
– NYHA III or IV,
– EF < 40%
– severe TR

68. Fontan circulation
• Successful pregnancy is possible in selected
patients with intensive monitoring - class III
• Class 4
– Patients with oxygen saturation ,85% at rest,
– Depressed ventricular function, and/or moderate
to severe AV regurgitation

70. AS
• Usually congenital bicuspid aortic valve [ always
assess aortic diameters]
• Even severe AS may be asymptomatic
• Maternal risk HF 10%, Arrhythmias 3-25%
• Fetal risk- Preterm Labour, IUGR, LBW

71. Pharmacological management of symptoms
HF- treat with diuretics
AF- b-blockers, CCB to control HR, Digoxin also may be
used
Pre- pregnancy intervention
•Symptomatic severe AS
•LVEF<50%, severe LVH (PW> 15mm)
•TMT- symptoms or fallin BP
•Recent progression of AS
•Asc. Aorta> 50 MM (27.5mm/m2)
During Pregnancy
Severe symptomatic AS + refractory to medical therapy/
life threatening symptoms Non calcified valve may be
subjected to BAV/o.w. emergency AVR
Delivery
•Vaginal delivery + regional anesthesia in non-sev AS
•LSCS in Sev AS

72. Coarctation of the aorta
• Repaired
– Restenosis
– Site rupture
• Unrepaired
– Hypertension
– Risk of aortic rupture
– Rupture of a cerebral aneurysm
– PIH
– Associated bicuspid aortic valve- aortic dilation

73. Coarctation of the aorta
• Close surveillance of BP
• Avoid aggressive treatment to prevent placental
hypoperfusion.
• PCI is associated with a higher risk of aortic
dissection
• Should only be performed if severe hypertension
persists despite maximal medical therapy and
there is maternal or fetal compromise.
• The use of covered stents may lower the risk of
dissection.

76. Hypertrophic cardiomyopathy
• Frequently diagnosed for the first time in pregnancy by
echocardiography.
• Intermittent high catecholamine state of pregnancy ↑ LVOT
obstruction
• Epidural anaesthesia causes systemic vasodilation and
hypotension in severe LVOTO
• Fluids must be given judiciously and volume overload must
be avoided
• The implantation of an ICD should be considered in patients
with high risk factors for sudden cardiac death
• All other management is the same, except for amiodarone
for rhythm control
• Atenolol - class d

77. Peripartum Cardiomyopathy
• A form of dilated CMP with LV systolic dysfunction that results in
the signs and symptoms of heart failure
• Criteria
■ Development in last month of pregnancy or the first 5 months after
delivery
■ Absence of heart disease prior to last month of pregnancy
■ Absence of identifiable cause of heart failure
■ LV systolic dysfunction
 Etiology is unknown
 Theories
■ Genetic predisposition
■ Autoimmunity
■ Viral infection

78. Peripartum Cardiomyopathy
• Associated risk factors:
■ Age - over 35
■ twin pregnancy
■ gestational hypertension
■ Multiparity
■ use of tocolytic therapy
• Motality rate 25-50%

79. Peripartum Cardiomyopathy
• clinical course varies
■ 50-60% of patients demonstrate complete recovery within the
first 6 months
■ The rest of the patients demonstrate either further clinical
deterioration, or premature death, or persistent LV
dysfunction and chronic heart failure
■ Pregnancy contraindicated
• Persistent cardiomegaly
• Cardiac dysfunction

80. Peripartum Cardiomyopathy
• Management
■ Acute heart failure treatment with O2, diuretics,
digoxin and vasodilators (hydralazine is safe)
■ Because of the increased incidence of
thromboembolic events, anticoagulation therapy
is recommended

81. Anticoagulation Strategies
• OAC throughout pregnancy best strategy [esp. if warf <5 mg, Acitrom
(acenocoumarol) <2 mg]
• Discontinuation of OAC b/w 6 &12 wks and replacement by UFH (a PTT ≥2×
control; infusion in high risk pts) or LMWH twice daily (according to weight and
target anti-Xa level 4-6 hours post-dose 0.8-1.2 U/mL in patients with a warfarin
dose required of >5 mg/day
• OAC discontinued and UFH (a PTT ≥2× control) or adjusted-dose LMWH (anti-Xa
level 4-6 hours post-dose 0.8-1.2 U/mL) started at the 36th week
• LMWH replaced by i.v. UFH at least 36 hours before planned delivery. UFH should
be continued until 4-6 hours before planned delivery and restarted 4-6 hours after
delivery if there are no bleeding complications
• If delivery starts while on OACs, caesarean delivery is indicated to prevent fetal
bleed
OAC UFH/L OAC UFH/L UFH
36 wks12 wks6 wks 6 hrs
H
6 hrs