lecture notes for medical students & student midwifes
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CARDIAC DISEASE
IN
PREGNANCY
DATO DR. Aruku Naidu
MD, FRCOG, CU, AM
Consultant O&G & Urogynaecologist HRPB
Malaysia
PREGNANCY AND HEART DISEASE
Cardiac disease affects 1-2%
of all pregnancies.
One of the leading causes of
maternal mortality and
morbidity
Higher incidence of fetal and
neonatal adverse events
PREGNANCY AND HEART DISEASE
Rheumatic heart disease is the most common
heart disease complicating pregnancy in our
country
Congenital heart disease is encountered as
advances in medical and surgical treatment
have resulted in improved survival.
CAD is expected to grow because of advanced
maternal age and higher incidence of risk
factors
PHYSIOLOGICAL CHANGES IN PREGNANCY
Cardiac output 30-50%
Stroke volume 40% .
Heart rate 10-20bpm .
Systemic Peripheral
resistance 30%
Decrease in both systolic
(3-5mmHg) &diastolic
blood pressure (5-
10mmHg) .
Abrupt hemodynamic changes occur secondary
to pain anxiety and uterine contractions
With each uterine contraction extrusion of
approximately 500ml of blood into central
venous system
CVS Physiology
Periods of greatest risk of cardiac events
24-28 wks
Early 3rd trimester
Delivery
Immediate postpartum
CVS Physiology in Labour
Rapid increase in HR and BP
Cardiac output is often 50% above
baseline during 2
nd
stage, may be even
higher at the time of delivery
After delivery, abrupt increase in venous
return (due to autotranfusion and release of
IVC compression)
CVS Physiology in Labour
Excessive blood loss in normal vaginal
delivery / C-section can alter cardiac status
Cardiovascular adaptations associated with
pregnancy regress by approx. 6wks after
delivery
Decreased exercise capacity
Tiredness
Dyspnoea
Palpitations
Lightheadedness
Presyncope
Symptoms during normal pregnancy
that may mimic cardiac disease
Physical signs
Cardiomegaly
Palpable RV & PA impulse
Loud S1
Exaggerated splitting of S2
Midsystolic ejection murmur at LSB
Continuous murmurs ( mammary
soufflé, cervical venous hum)
ECG
Leftward shift of QRS Axis
ST - T changes
Sinus tachycardia
ECHO DOPPLER-Cornerstone of evaluation
LV / RV dimensions
LA / RA size
Small pericardial effusion
Functional TR / PR / MR/ AR
Investigations
When to suspect heart disease ?
Previous history
Orthopnea and PND
Excessive fatigue
Palpitations with sweating/syncope
Chest pain
When to suspect heart disease -
Signs
Low volume pulse
Tachycardia, Irregular pulse - Atrial
fibrillation
Unequal pulse
Signs of cardiac failure – Raised JVP,
hepatomegaly, pedal edema
Systolic murmurs with Thrill
Diastolic murmurs
Obstetrician and cardiologist should
work together
Prevent an unwanted pregnancy and
asses the risks associated with
pregnancy
Continuation OR Termination
CHD in offspring of a parent with CHD
CHD in a Parent Risk of CHD in Offspring(%)
IC shunts- ASD 3 - 11
VSD 4 - 22
PDA 4 - 11
Obstruction to flow
Lt sided 3 - 26
Rt sided 4 - 15
HCM 50 (AD)
Marfan’s syndrome 50 (AD)
Risk is 4% Vs 0.4 - 0.6% in general population
Maternal mortality risk and cardiac disease
Group Cardiac disease Associated mortality risk
I Mitral /aortic stenosis, NYHA Class I, II
Atrial septal defect* <1%
Aortic/Mitral regurgitation
Pulmonary/tricuspid valve disease
Corrected tetralogy of Fallot
Bioprosthetic valve
Small –moderate VSD/PDA
II Uncorrected tetralogy of Fallot 5% - 15%
Marfan’s syndrome with normal aorta
Mechanical prosthetic valve
Severe Mitral stenosis with AF or NYHA Class III, IV
Severe Aortic stenosis
Previous myocardial infarction
III Pulmonary hypertension—primary or secondary 25% - 50%
Coarctation of aorta with valvular involvement
Marfan’s syndrome with aortic involvement
Peripartum cardiomyopathy
Maternal Risk
Stenotic lesions on the left side are not well
tolerated as cardiac output is markedly reduced.
Regurgitant lesions are well tolerated
Congenital heart disease with L-R shunts are
well tolerated due to fall in SVR
R-L lesions and cyanotic lesions not tolerated
Pulmonary HT carries high risk
Risk Index
Preconception history of adverse cardiac events
Poor functional class before pregnancy(NYHA class >II)
Left heart obstruction -MVOA < 1 sqcm
AVA <1.5sqcm
Peak LVOT grd >30mmHg
LV EF <40%
Termination of pregnancy
TERMINATION - <12wks OF PREGNANCY
Eisenmenger's syndrome
Marfan syndrome with aortic involvement
Severe Pulmonary hypertension
Coarctation of aorta
Symptomatic severe AS, MS
Severe left ventricular dysfunction EF<40%
Metallic prosthetic valve -complications
Antepartum Care
NYHA CLASS I or II
1. Limit strenuous exercise
2. Adequate rest
3. Iron and Vitamins to minimize anemia
4. Low salt diet if ventricular dysfunction
5. Regular cardiac and obstetric evaluation
Identify and treat early - infections, anemia,
hypertension, hyperthyroidism & arrthymias
NYHA CLASS III or IV
1.Hospitalisation for bed rest
2.Intensive Close monitoring
3.Cardiac intervention, surgery
4.Termination of pregnancy
PREGNANCY AND DRUGS
STENOTIC LESIONS REGURGITATION LESIONS
•Bblocker: metoprolol ,propranolol
(class C ),atenolol (class D ).
•C channel antagonist: verapamil ,
diltiazem (class C)
•Digoxin : (class C).
•Diuretic: for patient with pulmonary
congestion.
•Vasodilators: only If BP is high :
•Hydralazine:(class C ).
•Nitrate :(class C ).
•Diuretic:
•Thiazide: ( class B).
•Loop diuretic: (class C ).
•Avoid hypotension & placental
hypoperfusion
ACE inhibitor ,ARBS (class X ).
Arrhythmia
Acute atrial flutter or atrial fibrillation, should be
treated promptly.
If possible, all antiarrhythmic drugs should
be avoided during the first trimester, and those
known to be teratogenic should be avoided
throughout pregnancy.
Because of their safety profiles, preferred drugs
include digoxin, beta-blockers and adenosine.
Interventional or surgical Cardiac
management
Optimal time – second trimester
Balloon valvotomies preferred
Open heart surgery-- Higher risk of fetal
malformation and fetal loss in first trimester
(10-30%), Premature labour in third trimester
PROSTHETIC VALVES
DOUBLE JEOPARDY
Mechanical heart valve requires anticoagulation
? Heparin ? Warfarin
ANTICOAGULATION
Adjusted dose UFH bid subcutaneous throughout
pregnancy to achieve mid-interval aPTT at least twice
control
Adjusted dose LMWH bid subcutaneous 1mg/kg
throughout pregnancy to achieve a peak anti-Xa level
of 0.7-1.2 U/ml 4 hours after injection
UFH or LMWH (as above) until 12 weeks' gestation,
change to warfarin until the middle of the third
trimester, and then restart UFH or LMWH
ANTICOAGULATION
Current practical guidelines
Warfarin during entire pregnancy but
substitute heparin during peak teratogenic
period (6th to 12th week)
Warfarin upto 36 wks
Switch over to heparin 2 weeks before labour
ANTICOAGULATION
Heparin discontinued at least 12 hrs before
induction or reversed with protamine &
resumed 6 - 12 hrs post partum
Heparin & LMWH
Heparin does not cross placenta, no teratogenic
effect
Subcutaneous high dose (16,000 to 24,000
units/ day) to maintain APTT 1.5 to 2
Maternal thrombocytopenia, osteoporosis, sterile
abscesses, hematoma, maternal death 6-7%
Heparin & LMWH
LMWH – 1 mg/kg body wt (Enoxaparin)
Effective, easier to use & safe
Expensive, clinical trials needed
Warfarin therapy
Warfarin in the first trimester of pregnancy
is associated with increase -
foetal wastage
prematurity
low birth weight
Risk of valve thrombosis (3.9%)
Warfarin embryopathy in 6.4% of live
births.
Fetal intracranial bleeding: 4 - 10%
throughout pregnancy, during vaginal
delivery
Study of 55 pregnancies – Warfarin < 5 mg
No cases of embryopathy
ANTICOAGULANT THERAPY IN PREGNANCY
MATERNAL
DEATH
THROMBO
EMBOLISM
EMBRYOPATHY THERAPY
1.8% 3.9% 6.4-10% Vit k antagonist
throughout
pregnancy
40% 60% 0% Low dose UFH
throughout
pregnancy
6.7% 25% 0% Adjusted dose
UFH throughout
pregnancy
4.2% 9.2% 3.4% UFH in 1
st
trimester then Vit k
antagonist up to
36wk
Warfarin is the favored anticoagulant during
the 2
nd
, 3
rd
trimesters until the 36
th
wk
(Class IC ESC guidelines).
Warfarin is favored in the 1
st
trimester if the
dose <5mg /24hrs(Class IIaC ECS guidelines)
ESC Guidelines
MODE OF DELIVERY
Normal vaginal delivery is advised in
patients who are hemodynamically stable
class IC (ESC guidelines)
Cesarean section is indicated in:
1.Aortic dissection.
2.Marfan syndrome with dilated aortic root.
3.Hemodynamically Unstabillity in particular
case of severe AS.
4.Obstetric causes .
MODE OF DELIVERY
Intensive Hemodynamic monitoring is
recommended in case of severe stenotic lesions
or low EF.
Admit few days before labour
Monitor pulse, BP, Oxygen saturation
Oxygen inhalation
Careful attention to volume status is
essential
NS < 75 ml/hr 30ml/hr
Inj. Frusemide , Digoxin
Asses pulmonary basal crepts, JVP
Treatment of arrhythmias
Epidural analgesia to provide analgesia
and thus avoid I in CO due to pain and
anxiety,
Obstetric procedures (ventouse / forceps) to
cut short the 2
nd
stage of labour will
decrease the hemodynamic consequences
Left Lateral decubitus position is preferred to
attenuate the hemodynamic effect of the
supine position .
Slight blood loss is beneficial, Inj Frusemide
ENDOCARDITIS PROPHYLAXIS
Required in patients of prosthetic valve / cardiac
device implants
Previous history of IE
Used routinely in all pts as an uncomplicated
delivery cannot always be anticipated (not
recommended by AHA)
POSTPARTUM CARE
Hemodynamics do not return to baseline for
many days after delivery
Patients at intermediate or high risk may
require monitoring for at least 72 hours
postpartum.
Lactation should be encouraged unless
patient is in failure.
POSTPARTUM CARE
Cardiac output is not compromised during
lactation.
Lactation is a pathway for fluid excretion
and diuretic requirement may actually fall.
CONCLUSION
PREPREGNANCY COUNSELLING AND RISK
STRATIFICATION SHOULD BE DONE TO ALL WOMEN
WITH HEART DISEASE
TREATMENT OPTIONS AT PROPER SHOULD BE GIVEN
SUCCESSFUL PREGNANCY IS POSSIBLE FOR GROUP I
& II PATIENTS WITH HEART DISEASE
OPTIMAL CARE REQUIRES A MULTIDISCIPLINARY
TEAM APPROACH