Heart disease in pregnancy

15,390 views 47 slides Jun 09, 2021
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About This Presentation

lecture notes for medical students & student midwifes


Slide Content

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

Management
1.Pre-conceptional counselling, Risk
stratification

2.Antepartum management

3.Peripartum management

Pre-conceptional counselling

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%


Estimated risk of adverse cardiac event
0 ------- 5%
1 ------- 27%
>1 ------- 75%

Multicentric Canadian Study . Circulation104;155,2001

First Visit
Detailed history

The patient’s functional status as per
New York Heart Association(NYHA)

Cardiology consultation

ECG , ECHO

6/9/2021 20
NEW YORK HEART ASSOCIATION
FUNCTIONAL CLASSIFICATION OF CARDIAC DISEASE

CLASS I No functional limitation of activity.
No symptoms of cardiac decompensation with activity.

CLASS II Patients are asymptomatic at rest. Ordinary physical
activity results in symptoms.

CLASS III Limitation of most physical activity.
Asymptomatic at rest
Minimal physical activity results in symptoms.

CLASS IV Severe limitation of physical activity results in
symptoms.
Patients may be symptomatic at rest/heart failure
at any point of pregnancy.

ASSESSMENT OF PREGNANT
PATIENTS
HISTORY
•Dyspnea : NYHA classification, onset.
•Prior events : (HF ,TIA ,STROKE).
•Associated diseases : (anemia ,thyrotoxicosis ,Hpt).
•Drugs : (kind ,compliance ,education).
•Arrhythmia.
EXAMINATION
•Murmurs.
•Signs of heart failure.
ECG&ECHO
•ECG: arrhythmia.
•ECHO: valve (anatomy ,area ,pre gradient), diameter of ascending aorta ,
systolic pulmonary artery pressure ,EF .

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

Treat precipitating events – infections,
arrhythmia, anemia, hyperthyroidism

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
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