CARDIAC DISEASE IN

PREGNANCY

Dr. K. N. Georgewill
Department of Obstetrics and Gynaecology, UPTH.
SYNOPSIS
– INTRODUCTION
– HEMODYNAMIC CHANGES IN
PREGNANCY
– SYMPTOMS OF HEMODYNAMIC CHANGES
THAT MIMIC CARDIAC DISEASE
– CLASSIFICATION OF CARDIAC DISEASES
– BURDEN OF HEMODYNAMIC CHANGES
ON THE CARDIAC PATIENT**
 INTRODUCTION
Cardiovascular disease is the most important
non-obstetric cause of disability and death in
pregnant women, occurring in 0.4 – 4% of
pregnancies.
It is not surprising that the added hemodynamic
burden of pregnancy, labour and delivery can
aggravate symptoms and precipitate
complications in a woman with pre-existing
cardiac disease.
Many of these women may be able to sustain a
successful pregnancy, but in specific situations,
potential risks may arise and should be
anticipated.
 HEMODYNAMIC CHANGES OF
PREGNANCY, LABOUR & DELIVERY
The major cardiovascular changes that occur during
pregnancy include:
▲Blood volume (25 – 50%) = Plasma vol + RBC mass
▲Plasma vol (30 – 50%): Na+ and fluid retention by
the action of progesterone, rennin, aldosterone and
prolactin
▲ RBC mass (20 – 40%)
Plasma vol > RBC mass = dilutional anaemia
▲Cardiac output (30 – 50%) = ▲stroke vol + ▲ heart
rate = ▲myocardial contractility
▲stroke vol (10%)
▲Heart rate (10 – 20%)
▼Peripherial vascular resistance (30 – 50%): due to
vasodilatation (oestrogen, progesterone, PgE2, PgI2)
and placenta acting as an arteriovenous shunt
Blood pressure: systolic is unchanged; diastolic ▼in
1st and 2nd trimester but ▲in 3rd trimester, returning
to the non-pregnant state
In multiple pregnancy there is ▲▲ in these
physiologic variables mentioned above
Additional hemodynamic changes occur during the
various stages of labour & delivery & include:
▲cardiac output (20%) with each uterine contraction.
Pain, fear & anxiety contribute further to an increase in
cardiac output.
▲systolic blood pressure with each contraction,
increasing the load on the left ventricle by 10%, while
the heart rate falls.
Both the blood pressure and cardiac output are ▼
during epidural analgesia in labour
Oxytocic drugs can produce further hemodynamic
changes
 Following delivery, in the absence of post-partum
haemorrhage, the cardiac output & plasma vol
increase by 20 – 60% due to shift of blood from the
uterus & placenta into the vascular space as well as
resorption of interstitial fluid

The hemodynamic changes of normal pregnancy can

result in symptoms & signs that mimic those of heart
disease, often making it difficult to differentiate the two.
It is therefore, the severity & persistence of symptoms
that suggest underlying organic heart disease. Eg
 SYMPTOMS OF HEMODYNAMIC CHANGES
THAT MIMIC CARDIAC DISEASE

Palpitation: ▲HR, SV
Dyspnea, shortness of breath, orthopnea:
hyperventilation from ▲progesterone, ▼alveolar CO2
tension, upward displacement of diaphragm
Easy fatigability: ▲cardiac output at rest
Epigastric pain, bloating, heartburn: displacement of
diaphragm , stomach & liver by enlarging uterus,
▼GIT motility
Dizziness, syncope: ▼venous return due to
compression of IVC by enlarging uterus
Heat intolerance, sweating & flushing: ▲cutaneous
blood flow & ▲metabolic rate
Bounding pulse: ▲cardiac output, ▼peripherial
resistance, widened pulse pressure, ▲cutaneous
blood flow
Widely split S1 & S2: ▲cardiac output, ▲veneous
return, delayed right ventricular emptying
Third heart sound: ▲cardiac output, rapid ventricular
filling
Systolic murmur (precordial or left sternal edge):
▲cardiac output, ▲veneous return, ▲mammary flow,
turbulent flow through pulmonary valve
Varicose veins: incompetent valve following
obstruction of IVC, ▲venous distensibility
Edema ( legs occasionally hands & face): ▲venous
pressure in legs following obstruction of IVC
 CLASSIFICATION OF CARDIAC
DISEASES
CONGENITAL
– Left to right shunt (volume overload)
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Truncus arteriosus
– Obstructive lesions of the outflow tract (pressure
overload)
– Bicuspid aortic valve stenosis
– Pulmonary valve stenosis
– Coarctation of the aorta
– Cyanotic heart disease
Tetralogy of fallot
Eisenmenger’s complex
Transposition of the great vessels
Ebstein’s anomaly
Complex cyanotic heart disease
ACQUIRED
– Rheumatic/Valvular heart disease
Mitral stenosis / regurgitation
Aortic stenosis / regurgitation
Tricuspid valve disease
– Myocardial disease
Cardiomyopathy
Ischaemic heart disease
Myocarditis
– Pericardial disease
Acute pericarditis
– Infective endocarditis
– Arrhythmias
Supraventricular
Ventricular
– Aortic dissection
 NEW YORK HEART ASSOCIATION
CLASSIFICATION OF DEGREE OF
FUNCTIONAL DISABILITY OF CARDIAC
DISEASE
Class I: Asymptomatic with normal activity
Class II: Slightly symptomatic with normal
activity but asymptomatic at rest
Class III : Markedly symptomatic with less than
normal activities but asymptomatic at rest
Class IV: Symptomatic at rest or with minimal
activity
 BURDEN OF HEMODYNAMIC CHANGES
ON THE CARDIAC PATIENT
▲in cardiac output & stroke vol increase preload on
the heart. Augmented preload may not be tolerated by
obstructive cardiac lesions, such as mitral or aortic
stenosis.
In the setting of pulmonary hypertension, this
additional blood volume and preload burden could
result in right-sided heart failure.
A decrease in afterload (systemic vascular resistance)
from vasodilation in a woman with aortic stenosis may
further increase the gradient across the aortic valve,
adding to the left ventricular work – left heart failure
Conversely, certain lesions may benefit from
the afterload reduction, such as mitral
regurgitation and aortic insufficiency.
Regurgitant murmurs may soften and the
echocardiographic severity of regurgitation
decrease during pregnancy.
During labour, the augmented preload may
exacerbate certain cardiac problems.
Often the left-lateral position is recommended
for labour, this may prove deleterious
(augmented preload) for patients with certain
types of cardiac lesions.
 VENTRICULAR SEPTAL DEFECT &
PREGNANCY

The ventricular septal defect is the most common

congenital heart disease anomaly identified at birth
Less common in adults & therefore in pregnant
women b/c they tend to close spontaneously b/4 the
women reach adulthood
Women with small – moderate sized V.S.D tolerate
pregnancy well, although they are at risk of infective
endocarditis, Such women generally require antibiotic
prophylaxis
With large V.S.D, the risk of pulmonary hypertension
increases progressively with pregnancy
Late complications of V.S.D: ventricular arrhythmias,
aortic insufficiency, heart block, sudden death
 MITRAL STENOSIS & PREGNANCY

Most common type of RHD in young women

Most patients with mild – moderate M.S tolerate
pregnany well
Those with severe disease are likely to dev
complications (pul. venous congestion or frank pul.
edema, rt ventricular failure, pul hypertension
hemoptesis, thromboembolism, atrial fibrillation)
Patients with any degree of M.S can dev
complications during pregnancy
Symptoms can be aggraviated by associated anaemia
& tarchycardia resulting from anxiety, fear & stress
The risk of developing heart failure increases
progressively throughtout pregnancy & is further
increased during labour & delivery & immediately
postpartum.
The risk of infective endocarditis remains throughout
pregnancy, delivery & early puerperium
The mortality rate in pregnant women with M.S is 1%
overall & 3 – 4% in those with severe disease
Previously rheumatic heart disease was the most
common type of heart disease in pregnant
women. Because of advances in the medical and
surgical treatment of children born with congenital
heart disease, an increasing number of such
women reach childbearing age. Therefore,
congenital heart disease now represent a larger
percentage of cardiac disease encountered in
pregnancy. It is important, therefore, that obstetricians
understand the late complications of operated or
unoperated congenital heart disease in pregnancy.
However, it is important to state that the sequelae of
rheumatic heart disease still remain a problem in the
third world.