Pregnancy &

Heart Disease
Dr Nithin P G
 Introduction
• 0.2–4% of all pregnancies in western industrialized countries
Am J Obstet Gynecol 1998;179:1643–1653.

• Ht Dis. & Mortality

– In western countries maternal heart disease is now the major cause of
maternal death during pregnancy [UK 2003-2005].
– In South India, 30% H’ge, 17% sepsis, 13% hypertensive disorders
[2001-2003 Special Survey Of Deaths].

• Optimum treatment of both Mother & Fetus must be targeted

Dr Nithin P G
 Introduction
• Hypertensive disorders - most frequent CV events during
pregnancy [6–8% of all pregnancies] Eur. Heart J. 2011:ehr218v1-ehr218

• Among heart diseases,

– Western world Congenital heart disease, most frequent CVD (75–
82%), with shunt lesions predominating (20–65%).
– RHD dominates in non-western countries [56–89% ]; Congenital heart
disease [just 9–19%]. Eur J Heart Fail 2008;10:855-860,
Circulation 2001;104:515-521.

• Cardiomyopathies are rare. Peripartum cardiomyopathy

(PPCM) is the most common.

Dr Nithin P G
Physiological changes in
pregnancy
 CO increases after 5wks, 45% by 24 wks,
Pl. volume- increases by 6 wks, 1.5-2 times normal
decreases to near normal by 10 days PP
by II trimester, plateaus [TBW by 6-8L, Na retension-
SV-increases from 8 to peak at 20wks, decreases
500-900 meq]
to baseline by 2 wks PP
Increased Aortic compliance, A-V shunting in uterus

Dr Nithin P G
•C.O. at labour 7L/min, increases to 9L/min to 10L/min [500 ml autotransfused/
contraction] [Epidural Anesthesia-8L/min, LSCS- 7-8L/min]

•Immediately after delivery- sudden increase in blood volume by abrupt increase in

venous return, autotransfusion, lack of IVC compression autotransfusion continues
for 24-72 hrs [risk of Pulm. Edema]

•Complex interactions of gestational hormones, RAA, PG, NO, ANP, BNP pathways
produce these changes
Dr Nithin P G
 Clinical Findings in Normal
Pregnancy
Elevated JVP [increased
plasma vol.]

S1 Loud [Tachy, increased LV mass], S2 wide split

Reduced B.S. at lung accentuated [P2 delayed], occ S3
bases [diaphragm Flow murm @ aortic, pulm; ESM grade 3 @ LLSB;
moves up] cervical venous hum; mammary souffle @ LLSB,

Apex slight down & out, prominent impulse,

active precordium[volume loaded ventricles]

Tachycardia, low DBP, Pulse Pressure

Pedal oedema increased [bounding pulses]
>60% women Pulsatile fingertips, warm hands, occ.
[increased plasma Quincke
vol., increased
venous pressures]
Dr Nithin P G
 Investigations in normal
pregnancy
Investigation Comments
ECG •Tachycardia
•LAD [ elev. Diaphragm]
•Increased ventricular voltage
•Increased Atrial & Ventricular Arrhythmias [increased repolarization
changes]
CXR •CE
•Horizontal shift of heart
•Fullness of Left cardiac border & pulmonary vasc
Echo •LV mass increased, LVED increased, RV & both Atrial enlarges
•Increased LVOT & RVOT velocities[ gradients less reliable marker
of stenotic severity, 2D valve area best]
•Increased regurgitant lesions
•Pros. Valve- valve gradients, PHT serial changes to be measured

Dr Nithin P G
Pathological conditions &
pregnancy
 Hypertensive disorders
• Hypertension- MC medical problem in pregnancy [15% of
pregnancies & 1/4 of all antenatal admissions]

• Hypertensive disorders in pregnancy have been recognized as an

important risk factor for CVD in women [ Risk for CAD twice; HTN
four times] Circulation 2011;123:1243-1262

• Requires high readings on two separate occasions for diagnosis

Severity
• Mild - >140/ 90 mm Hg
• Severe- >160/110 mm Hg

Dr Nithin P G
 Hypertensive disorders
Type Criteria Comments
Pre-existing HTN >140/ 90 mm Hg, either Usu. Persists after 42 days PP;
precedes pregnancy or develops 1-5% of pregnancy
>20 weeks POG
Gestational HTN >140/ 90 mm Hg, develops >20 Usu resolves within 42 days
weeks POG PP; 6-7% pregnancy
Pre-eclampsia Gest HTN + •Upto 25% of prev HTN
proteinuria[>0.3g/day or
>30mg/mmol U. creatinine]
Eclampsia Pre-eclampsia + seizures Immediate termination of
pregnancy required
Pre-existing HTN + Pre-existing HTN+ further
superimposed worsening of BP+ proteinuria
gestational HTN with [>0.3g/day] after 20 wks
proteinuria
Antenatally unclassifiable BP first recorded after 20 wks Re- assessment after 42 days
hypertension PP

Dr Nithin P G
 Pre-eclampsia
• RF- Primi, multiple fetuses, hydatidiform mole or DM

• MC cause for IUGR

Features of Severe Pre-eclampsia

• Right upper quadrant/epigastric pain due to liver oedema + hepatic H’ge
• Headache + visual disturbance (cerebral oedema)
• Occipital lobe blindness
• Hyperreflexia + clonus
• Convulsions (cerebral oedema)
• HELLP syndrome: hemolysis, elevated liver enzymes, low platelet count.

Dr Nithin P G
 Non-pharmacological management
[normal diet without salt restriction, Calcium supplementation of
140-149/ 90-99 at least 1 g daily, Low dose acetylsalicylic acid (75–100 mg/day)
H.S. is used prophylactically in women with a h/o of early-onset
(<28 weeks) pre-eclampsia]
140-149/ 90-99 +
•Gestational HTN
•Pre-existing HTN superimposed
by gestational HTN Pharmacological management
•Subclinical organ damage or a-Methyldopa [SE- PP depression], Labetalol, Metoprolol
symptoms at any time during Nifedipine, isradipine
pregnancy
Or,
≥150/95

Pharmacological management
≥170/110 Nitroprusside [fetal cyanide toxicity], Nitroglycerine, I.V.
Labetalol, oral methyl dopa

Severe Pre- Termination of pregnancy

eclampsia Parenteral Magnesium sulphate to prevent eclampsia

Dr Nithin P G
 Valvular Heart Disease

• Risk Stenotic lesions > Regurgitant lesion

[ increased C.O. increased transvalvular gradient increased upstream

pressures] vs. [ reduced SVR reduces Regurgitant volume]

• Left sided diseases> Right sided disease

Dr Nithin P G
 MS
• Poorly tolerated [ moderate & severe MS] Tachycardia, increased plasma
volume

• PHT, Trans valvular gradients, PAP measurements are less reliable marker
of severity

• Maternal Risks- HF symptoms, Pulmonary edema in II & III trimester. AF

[increases risk of T.Emb, pulmonary edema]

• Fetal risks- prematurity 20-30%; IUGR 5-20%

• Moderate & severe MS counseled against pregnancy without prior

intervention

Dr Nithin P G
Pharmacological management of symptoms
MS with symptoms or PAH, restricted activities and β1-
selective blockers are recommended. Diuretics are
recommended when congestive symptoms persist despite
β-blockers.

BMV
NYHA class III/IV or sys PAP > 50mm Hg, preferably
after 20 weeks POG. [CI in asymptomatic women]

Anticoagulation
•Paroxysmal or Permanent AF, LA thrombus, prior
embolism
•Considered in mod/sev MS with spontaneous echo
contrast, LA > 40ml/m2, low CO, CCF

Delivery
•Vaginal delivery in mild MS, NYHA I/II, no PAH
•LSCS in Mod/Sev MS, NYHA III/IV, PAH despite
medical therapy & BMV cannot be performed or failed.
Dr Nithin P G
 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

Dr Nithin P G
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

Dr Nithin P G
 Regurgitant lesions
• Better tolerated

• Maternal risk- HF, Arrhytmias, Progressive worsening of regurgitations

• Moderate to severe Regurgitant lesions may undergo exercise testing to

decide pre pregnancy intervention

• Severe lesions + symptoms/ impaired LV function/ Ventricular dilatation

 treated surgically, if possible repair

• TV repair if moderate Secondary TR with annular dilatation >40mm, usu

during left sided valve surgeries

Dr Nithin P G
 PS & PR
PS is generally well tolerated
– Complic of sev PS-RV failure & Arrhythmias.
– Prepregnancy balloon valvuloplasty in severe stenosis (peak Doppler
gradient > 64 mmHg)
– LSCS is considered in patients with severe PS and in NYHA class
III/IV despite medical therapy and bed rest, in whom percutaneous
pulmonary valvotomy cannot be performed or has failed.

Severe PR with impaired RV function

– pre-pregnancy pulmonary valve replacement (preferably bioprosthesis)
should be considered.

Dr Nithin P G
 Prosthetic valves
Mechanical valves
• Excellent H.D.
Performances
• Long term durability
• Thrombogenic
Dr Nithin P G
Bioprosthetic valves
• Good H.D Performances
• Much less thrombogenic
• High risk of valve
degeneration [~50% women
<30yrs at 10 yr post
implant]
– M> A,T position
– Reoperation mortality risk
addl 5%
 Anticoagulation Strategies
Valve thrombosis Maternal mort.
3.9 % OAC 2%

9.2 UFH OAC 4

35 UFH 15

9 LMWH

3.6 LMWH OAC

Arch Intern Med 2000;160:191-196

Dr Nithin P G
 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 H

6 wks 12 wks 36 wks 6 hrs 6 hrs

Dr Nithin P G
Peripartum cardiomyopathy

Eur J Heart Fail 2010;12:767–778.

Dr Nithin P G
 Etiology
Fas/Apo-1, C-reactiveprotein,
Cathepsin D in response to IFN-g and IL-6
oxidative stress cleaves
Prolactin into angiostatic &
Viruses
proapoptotic fragment 16 kDa
Prolactin
Autoimmune

Dr Nithin P G
Differential diagnosis

Eur J Heart Fail 2010;12:767–778.

Dr Nithin P G
SA- 6m & 2yr
mortality LV func.
rates 10% & returns
28%. to normal in
Brazil & Haiti 23–41%
6m rate 14–
16%
Turkey- 4yr
rate 30%

Dr Nithin P G Eur J Heart Fail 2010;12:767–778.

 Natural history
N Engl J Med 2001;344:1567-71.
•Group 1 (28) EF after index pregnancy > 50%
Group 2 (16) EF <50 %
•More HF symptoms in group 2 [44 vs. 21%]
•Group 2- 3 deaths during subsequent pregnancy

Am J Obstet Gynecol 2008;199:415.e1-415.e5.

Dr Nithin P G
 Other cardiomyopathies
DCM
• Typical symptoms of HF, LV dilation, and LV systolic dysfunction of
unknown origin.
• Differentiation from PPCM is supported by the ‘time of manifestation’
– If not known before conception, the condition is unmasked during the I or II
trimester when hemodynamic load is increasing.
– Family history of DCM
• Secondary cardiomyopathies, such as infiltrative , toxic CM & storage
diseases manifest themselves in pregnancy.
• Maternal risk- Risk of deterioration of DCM during gestation and PP.
LVEF < 40% is a predictor of high risk. LVEF is <20% MTP may be
considered.

Dr Nithin P G
 Other cardiomyopathies
HCM

• Frequently diagnosed for the first time in pregnancy by echocardiography.

• Characterized by diastolic dysfunction due to hypertrophied non-compliant

myocardium[ HF, Pulmonary congestion] , severe LVOTO [syncope] and
arrhythmias [SVT & VT].

• Maternal risk -usually tolerate pregnancy well. Risk is increased in those

symptomatic before pregnancy and in those with a high outflow gradient .

Dr Nithin P G
 Management
• Managed as in non pregnant states
• Hydralazine & nitrates instead of ACEI, b1- selective blockers should be used
[n/b- hypoglycemia, bradycardia, resp. depression]. Diuretics used judiciously
[ Aldosterone antagonists avoided]. Anticoagulation- I/C thrombus, AF

HCM
• b-Blockers - >mild LVOTO and/or wall thickness >15 mm to prevent sudden
pulmonary congestion. Delivery under b-blockers recommended
• b-Blockers- rate control in AF & to suppress ventricular arrhythmias. Verapamil
second choice (AV block in the fetus). Cardioversion for persistent arrhythmia
because AF poorly tolerated. Therapeutic anticoagulation as indicated
• Severe LVOTO- Epidural anaesthesia must be used with caution
• I.V. fluids given judiciously [in view of diastolic dysfunction]
• Syntocinon slow infusion [hypotension, arrhythmias, and tachycardia]

Dr Nithin P G
 Congenital Heart diseases and
PAH
(Elective)

(>20 weeks)

• Miscarriage rate higher in more complex diseases

• Maternal cardiac complications in 12% of completed pregnancies & pts are at higher risk
of late cardiac events after pregnancy
• Offspring mortality (4%) more frequent than general population
Eur. Heart J. 2011:ehr218v1-ehr218
Dr Nithin P G
 Shunt lesions
• Hemodynamically significant shunt best repaired pre
pregnancy
• Insignificant lesions, good LV function no indication for closure
during pregnancy
• Severe PAH/ eisenmenger syndrome – high risk
• Pre-pregnancy evaluation of the severity of a shunt, residual
defect in case of repair, estimation of pulmonary pressures,
cardiac dimensions & function
• Increase in Arrhythmias, T. Emb. and worsening of NYHA class,
higher incidence of preeclampsia
• Hemodynamically significant shunt – SGA baby, fetal mortality

Dr Nithin P G
 Coarctation of Aorta
• Unrepaired native CoA and those repaired with residual HTN, residual
CoA, or aortic aneurysms have an increased risk of aortic rupture and
rupture of a cerebral aneurysm during pregnancy and delivery
• Risk Factors to be screened for- aortic dilatation and bicuspid aortic
valve
• HTN should be treated[ aggressive treatment avoided to prevent
placental hypoperfusion]
• Percutaneous intervention for re-CoA associated with a higher risk of
aortic dissection than outside pregnancy [indic- severe HTN despite
max medical Rx and there is maternal or fetal compromise] [covered
stents may lower the riskof dissection].
• Vaginal delivery with epidural analgesia preferred

Dr Nithin P G
 Cyanotic congenital heart
disease
• Maternal complications (HF, pulmonary or systemic thrombosis, SVT, IE)
occur in 30% of cyanotic pregnant patients.

• If resting O2 sat. <85%- substantial maternal and fetal mortality risk

expected and pregnancy is contraindicated. If 85–90%, measure it during
exercise Significant and early decrease  pregnancy has poor
prognosis.

• With resting maternal blood saturation >90%, fetal outcome is good (<10%
fetal loss).

Dr Nithin P G
 Cyanotic congenital heart
disease
Tetralogy of Fallot
• In unrepaired patients, surgical repair is indicated before pregnancy [ Repaired TOF
usually tolerate pregnancy well]
• Cardiac complications during pregnancy upto 12% of patients. [Arrhythmias & HF-
MC; Thr. Emb., progressive aortic root dilatation, & IE].
• Risk Factors  RV Dysfunction &/or mod to sev. PR [Pregnancy associated with
persisting increase in RV size]
• In repaired symptomatic TOF, RV dilatation due to severe PR, pre-pregnancy PVR
(homograft)
Ebstein’s anomaly
• Ebstein’s anomaly without cyanosis & HF, pregnancy is often tolerated well.
• Symptomatic + Cyanosis and/or HF should be treated before pregnancy or
counselled against pregnancy. In severe symptomatic TR  pre-pregnancy repair .
[haemodynamic status depends on TR severity & RV function]
• Associated ASD & WPW syndrome. (Incidence of arrhythmias increased)
• Other complications- shunt reversal and cyanosis; paradoxical emboli
Dr Nithin P G
 Cyanotic congenital heart
disease
TGA
• Atrial switch operation (Senning or Mustard repair)
– Increased risk of arrhythmias & HF
– Underlying bradycardia or junctional rhythmB-blockers with caution.
– Irreversible decline in RV function in 10% cases. Pts with > moderate impairment of RV
function or severe TR should be advised against pregnancy.
• Arterial switch surgeries – usually normal pregnancy

CCTGA
• Risk depends on functional status, ventricular function, presence of arrhythmias,
and associated lesions.
• Complications- arrhythmias& HF
– Pre-disposed to developing AV block B-blockers with caution.
– Irreversible decline in RV function in 10% cases.
– Patients with NYHA functional class III or IV, EF < 40% or severe TR should be
counseled against pregnancy

Dr Nithin P G
 Cyanotic congenital heart
disease
Fontan patient

• Moderate to high risk pregnancies [Esp. if the Fontan circuit is not optimal]

• Atrial arrhythmias & NYHA class deterioration

• Pregnancy C.I. - O2 saturation < 85% at rest, depressed ventricular

function, mod to sev AV regurgitation or with protein-losing enteropathy

• Premature birth, small for gestational age, and fetal death in up to 50%.

• Therapeutic anticoagulation should be considered.

Dr Nithin P G
 Pulmonary Hypertension&
Eisenmenger
• Low pregnancy-independent exercise
capacity, superimposed on the
gestational CV demands, Insufficient
adaptation of the right heart and Poorly
compliant pulmonary vasculature. J
Am Coll Cardiol 1998;31:1650 –7
• Even moderate PAH can worsen during
pregnancy - decrease in SVR and
overload of RV& “no safe cut-off
value”
• High maternal mortality risk is
reported (30–50% in older series &
17–33% in more recent papers) in pts
with severe PAH and Eisenmenger
syndrome. Eur Heart J 2009;30:256– Eur Heart J 2009;30:256–265.
265.

Dr Nithin P G
 Pulmonary Hypertension&
Eisenmenger
J Am Coll Cardiol 1998;31:1650 –7
Dr Nithin P G
• Maternal death occurs in “the last
trimester of pregnancy & in the first
months after delivery”
– pulmonary hypertensive crises
– pulmonary thrombosis
– refractory right heart failure.
• This occurs even in patients with
little or no disability before or during
pregnancy.
• Risk factors for maternal death are:
late hospitalization, severity of PAH,
and GA.
• Neonatal survival rates are reported
to be 87–89%. Eur Heart J
2009;30:256–265.
 Management
• Avoid Pregnancy & MTP
• Maintain circulating Volume, and to avoid systemic Hypotension, Hypoxia, and
Acidosis which may precipitate refractory HF
• Supplemental O2 therapy if hypoxaemia; Haemodynamic monitoring by Swan–Ganz
catheter not indicated now [PA rupture]
• Diuretics must be used judiciously and at the lowest E.D. to avoid
haemoconcentration and intravascular volume depletion. Microcytosis and iron
deficiency should be treated with supplemental oral or i.v. iron
• Anticoagulation- Continued in patients were there is indication for use outside
pregnancy. Used with caution in Eisenmenger syndrome [prone to haemoptysis and
thrombocytopenia]- used in PE or HF
• I.V. Prostacyclin or aerosolized Iloprost [to improve haemodynamics during delivery]
• Continue drugs for PAH [Bosentan-teratogenic, Sildenafil-category B]
• Planned LSCS and vaginal delivery with incremental regional anaesthesia are
favoured over emergency LSCS delivery.

Dr Nithin P G
 Management of cyanotic
mothers
• Medical
– Restriction of physical activity and supplemental oxygen are recommended.
– Because of the increased risk of paradoxical embolism, prevention of venous
stasis (use of compression stockings & avoiding the supine position) is
important. For prolonged bed rest, prophylactic heparin administration should be
considered.
– Haematocrit and Hb levels are not reliable indicators of hypoxaemia.
– Diuretics and iron therapy are indicated in patients with Eisenmenger syndrome.

• Vaginal delivery is advised in most cases [timely hospital admission,

planned elective delivery, and incremental regional anaesthesia] If the
maternal or fetal condition deteriorates, an early caesarean delivery
should be planned. [risks of anesthesia]

Dr Nithin P G
 Aortic Diseases
• Pregnancy is a high risk period for all patients with aortic
pathology, and aortic pathology is reported as one of the
leading causes of maternal mortality

• Causes-
– Heritable Aortic diseases- pre-disposing patients to both aneurysm
formation and aortic dissection. [ Marfan syndrome, bicuspid aortic
valve, Ehlers–Danlos syndrome, Turner syndrome, and familial forms
of aortic dissection, aneurysm, or annuloaortic ectasia]
– Congenital heart disease (TOF, aortic coarctation) may be accompanied
by aortic dilatation or aneurysm formation.
– non-heritable aortic pathology

Dr Nithin P G
 Aortic Diseases
• Susceptibility to dissection- hormonal changes during
pregnancy [most often in the last trimester of pregnancy (50%)
or the early postpartum period (33%)]
– an enlarged aortic root diameter [Marfan > 45mm ;Bicuspid AoV>50mm
(>27mm/m2)]
– previous aortic dissection

• Imaging of entire aorta performed before pregnancy

• Vaginal delivery in < 40 mm, Vaginal delivery with epidural

anesthesia in 40-45mm, LSCS in >45mm [ In non-marfan,
>40mm]
Dr Nithin P G
 Arrhythmia
• Premature extra beats and sustained tachyarrhythmias become more frequent
and may even manifest for the first time during pregnancy
• PSVT in 20-44% of pregnancy Am J Cardiol 2006;97(8):1206-1212

• Immediate electrical cardioversion is recommended for a/c Rx of any

tachycardia with haemodynamic instability
• For acute conversion of PSVT, vagal manoeuvre followed by I.V. adenosine
is recommended. I.V. metoprolol or propranolol can also be considered
• For long-term management of SVT oral digoxin or metoprolol/propranolol
is recommended. If not successful oral sotalol or ecainide may be used

Dr Nithin P G
 Arrhythmia
• Immediate electrical cardioversion of VT is recommended for sustained,
unstable & stable VT .
• I.V. Sotalol or Procainamide may be considered for a/c conversion of sustained,
haemodynamically stable, and monomorphic VT. Not responding 
Amiodarone
• Oral metoprolol, propranolol or verapamil is recommended in idiopathic
sustained VT (Long-term management). If unsuccessful  oral sotalol,
ecainide, propafenone
• β-blockers recommended during pregnancy and also postpartum in congenital
long QT syndrome.
• ICD implantation, if clinically indicated, is recommended prior to pregnancy
but if required, during pregnancy also. Implantation of PPI or ICDs (preferably
one chamber) should be considered with echo guidance, especially if the fetus
is beyond 8 weeks gestation.

Dr Nithin P G
 CAD
• Coronary dissection [LAD] as a cause for MI

• ECG & Troponin measurements in all patients with chest pain

• Aortic dissecction also to be ruled out in pregnant women with

chest pain

• PCI treatment of choice in STEMI. STK do not cross placenta

but can lead to increased H’ge

• PCI in high risk NSTEMI only

Dr Nithin P G
 General
Management
 Risk
stratification

Circulation 2001;104:515-521

Dr Nithin P G
Dr Nithin P G
 General Management
• Best time for percutaneous intervention in pregnancy-
– After 4th month in the second trimester [ organogenesis complete, fetal
thyroid still inactive, volume of uterus small]
– ACT b/w 200-300s

• Best time for CPBypass-

– 13th & 28th week POG [Fetal malformation in I trim & Preterm delivery
& maternal complication in III trim]
– 3-6% late neurological impairment in children, high fetal mortality
hence Sx only when refractory to medical therapy, interventional
procedures fail, mother’s life threatened

Dr Nithin P G
 General Management
• Vaginal delivery in most cases [lumbar epidural anesthesia]
• LSCS in preterm labour on anticoagulants, Marfan >45 mm
aorta, a/c or c/c dissection, intractable HF [also considered in
severe AS ,severe PAH including Eisenmenger syndrome &
a/c HF]
Post Partum-
– slow i.v. infusion of oxytocin (<2 U/min), PG F analogues
[Methylergonovine C.I. [vasoconstriction & HTN]
– Elastic support stockings, and early ambulation [reduce the risk of T.
Emb]
– First 12–24 h [HF] hence, hemodynamic monitoring continued for at
least 24 h after delivery.

Dr Nithin P G
Thank you
Dr Nithin P G