CARDIOVASCULAR DISORDER PREGNANCY

1. Medical Disorders During
Pregnancy
Shivaom Chaurasia
Internal Medicine
Resident

2. • Each year, approximately 4 million births occur in the United States, and
more than 130 million births occur worldwide.
• A significant proportion of births are complicated by medical disorders.
• Advances in medical care and fertility treatment have increased the number
of women with serious medical problems who attempt to become pregnant.
• Medical problems that interfere with the physiologic adaptations of
pregnancy increase the risk for poor pregnancy outcome; conversely, in
some instances, pregnancy may adversely impact an underlying medical
disorder.

3. HYPERTENSION:
• In pregnancy, cardiac output increases by 40%, with most of the
increase due to an increase in stroke volume.
• Heart rate increases by ~10 beats/min during the third trimester.
• In the second trimester, systemic vascular resistance decreases, and
this decline is associated with a fall in blood pressure.
• During pregnancy, a blood pressure of 140/90 mmHg is considered to
be abnormally elevated and is associated with an increase in perinatal
morbidity and mortality.

4. • In all pregnant women, the measurement of blood pressure should
be performed in the sitting position, because the lateral recumbent
position may result in a lower blood pressure.
• The diagnosis of hypertension requires the measurement of two
elevated blood pressures at least 4 h apart.
• Hypertension during pregnancy is usually caused by preeclampsia,
chronic hypertension, gestational hypertension, or renal disease.

5. PREECLAMPSIA:
• Approximately 5–7% of all pregnant women develop preeclampsia, the new onset
of hypertension (blood pressure >140/90 mmHg) and proteinuria (either a 24 h
urinary protein >300 mg/24 h, or a protein- creatinine ratio ≥0.3) after 20 weeks of
gestation.
• Recent revisions to the diagnostic criteria include: proteinuria is no longer an
absolute requirement for making the diagnosis; the terms mild and severe
preeclampsia have been replaced; and the disease is now termed preeclampsia
either with or without severe features and fetal growth restriction is no longer a
defining criterion for preeclampsia with severe features.
• Although the precise pathophysiology of preeclampsia remains unknown, recent
studies show excessive placental production of antagonists to both vascular
endothelial growth factor (VEGF) and transforming growth factor β (TGF-β).

6. • These antagonists to VEGF and TGF-β disrupt endothelial and renal
glomerular function resulting in edema, hypertension, and proteinuria.
• The renal histological feature of preeclampsia is glomerular
endotheliosis.
• Glomerular endothelial cells are swollen and encroach on the vascular
lumen.
• Preeclampsia with severe features is the presence of new-onset
hypertension and proteinuria accompanied by end-organ damage.

7. • Preeclampsia is associated with abnormalities of cerebral circulatory
autoregulation, which increase the risk of stroke at mildly and moderately
elevated blood pressures.
• Risk factors for the development of preeclampsia include nulliparity,
diabetes mellitus, a history of renal disease or chronic hypertension, a prior
history of preeclampsia, extremes of maternal age (>35 years or <15 years),
obesity, antiphospholipid antibody syndrome, and multiple gestation.
• Low-dose aspirin (81 mg daily, initiated at the end of the first trimester)
modestly reduces the risk of preeclampsia in pregnant women at high risk
of developing the disease.

8. • Features may include severe elevation of blood pressure (>160/110 mmHg),
evidence of central nervous system (CNS) dysfunction (headaches, blurred
vision, seizures, coma), renal dysfunction (oliguria or creatinine >1.5
mg/dL), pulmonary edema, hepatocellular injury (serum alanine
aminotransferase level more than twofold the upper limit of normal),
hematologic dysfunction (platelet count <100,000/L or disseminated
intravascular coagulation [DIC]).
• The HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) is a
special subtype of severe preeclampsia and is a major cause of morbidity
and mortality in this disease.
• Platelet dysfunction and coagulation disorders further increase the risk of
stroke.

9. TREATMENT:
• Preeclampsia:
• Preeclampsia resolves within a few weeks after delivery.
• For pregnant women with preeclampsia prior to 37 weeks of gestation, delivery
reduces the mother’s morbidity but exposes the fetus to the risk of premature
birth.
• The management of preeclampsia is challenging because it requires the clinician
to balance the health of the mother and fetus simultaneously.
• In general, prior to term, women with preeclampsia without severe features may
be managed conservatively with limited physical activity, although bed rest is not
recommended, close monitoring of blood pressure and renal function, and
careful fetal surveillance.

10. • For women with preeclampsia with severe features, delivery is
recommended unless the patient is eligible for expectant management
in a tertiary hospital setting.
• Expectant management of preeclampsia with severe features remote
from term affords some benefits for the fetus, but significant risks for
the mother.
• Postponing delivery beyond 34 weeks gestation in this group of
patients is not recommended.
• In preeclampsia without severe features delivery at 37 weeks is
recommended.

11. • The definitive treatment of preeclampsia is delivery of the fetus and
placenta.
• For women with preeclampsia with severe features, aggressive
management of blood pressures >160/105 mmHg reduces the risk of
cerebrovascular accidents.
• IV labetalol or hydralazine is most commonly used to acutely manage
severe hypertension in preeclampsia; labetalol is associated with fewer
episodes of maternal hypotension.
• Elevated arterial pressure should be reduced slowly to avoid hypotension
and a decrease in blood flow to the fetus.

12. • Magnesium sulfate is the preferred agent for the prevention and
treatment of eclamptic seizures.
• Large, randomized clinical trials have demonstrated the superiority of
magnesium sulfate over phenytoin and diazepam in reducing the risk
of seizure and, possibly, the risk of maternal death.
• Magnesium may prevent seizures by interacting with N-methyl-d-
aspartate (NMDA) receptors in the CNS.

13. • The universal use of magnesium sulfate for seizure prophylaxis in
preeclampsia without severe features is no longer recommended by
most experts.
• There is consensus that magnesium sulfate should be used in all cases
of preeclampsia with severe features, or in cases of eclampsia.
• Women who have had preeclampsia appear to be at increased risk of
cardiovascular and renal disease later in life.

14. CHRONIC ESSENTIAL HYPERTENSION:
• Pregnancy complicated by chronic essential hypertension is associated with
intrauterine growth restriction and increased perinatal mortality.
• Pregnant women with chronic hypertension are at increased risk for
superimposed preeclampsia and abruptio placentae.
• Women with chronic hypertension should have a thorough prepregnancy
evaluation, both to identify remediable causes of hypertension and to ensure
that the prescribed antihypertensive agents (e.g., angiotensin-converting enzyme
[ACE] inhibitors, angiotensin-receptor blockers) are not associated with an
adverse outcome of pregnancy.
• Labetalol and nifedipine are the most commonly used medications for the
treatment of chronic hypertension in pregnancy.

15. • The target blood pressure is in the range of 130–150 mmHg systolic
and 80–100 mmHg diastolic.
• Should hypertension worsen during pregnancy, baseline evaluation of
renal function (see below) is necessary to help differentiate the
effects of chronic hypertension from those of superimposed
preeclampsia.
• There are no convincing data that the treatment of mild chronic
hypertension improves perinatal outcome.

16. GESTATIONAL HYPERTENSION:
• The development of elevated blood pressure after 20 weeks of
pregnancy or in the first 24 h post-partum in the absence of
preexisting chronic hypertension or proteinuria is referred to as
gestational hypertension.
• Mild gestational hypertension that does not progress to preeclampsia
has not been associated with adverse pregnancy outcome or adverse
long-term prognosis.

17. RENAL DISEASE:
• Normal pregnancy is characterized by an increase in glomerular filtration
rate and creatinine clearance.
• This increase occurs secondary to a rise in renal plasma flow and increased
glomerular filtration pressures.
• Patients with underlying renal disease and hypertension may expect a
worsening of hypertension during pregnancy.
• If superimposed preeclampsia develops, the additional endothelial injury
results in a capillary leak syndrome that may make management
challenging.

18. • In general, patients with underlying renal disease and hypertension benefit
from aggressive management of blood pressure.
• Preconception counseling is also essential for these patients so that
accurate risk assessment and medication changes can occur prior to
pregnancy.
• In general, a prepregnancy serum creatinine level <133 μmol/L (<1.5
mg/dL) is associated with a favorable prognosis.
• When renal disease worsens during pregnancy, close collaboration
between the internist and the maternal-fetal medicine specialist is
essential so that decisions regarding delivery can be weighed to balance
the sequelae of prematurity for the neonate versus long-term sequelae for
the mother with respect to future renal function.

19. CARDIAC DISEASE:
• VALVULAR HEART DISEASE:
• Mitral Stenosis:
• This is the valvular disease most likely to cause death during pregnancy.
• The pregnancy-induced increase in blood volume, cardiac output, and
tachycardia can increase the transmitral pressure gradient and cause
pulmonary edema in women with mitral stenosis.
• Women with moderate to severe mitral stenosis (mitral valve area ≤1.5
cm2) who are planning pregnancy and have either symptomatic disease or
pulmonary hypertension should undergo valvuloplasty prior to conception,
preferably with percutaneous balloon valvotomy (PBV).

20. • Pregnancy associated with long-standing mitral stenosis may result in
pulmonary hypertension.
• Sudden death has been reported when hypovolemia occurs.
• Careful control of heart rate, especially during labor and delivery,
minimizes the impact of tachycardia and reduced ventricular filling
times on cardiac function.

21. • Pregnant women with mitral stenosis are at increased risk for the
development of atrial fibrillation and other tachyarrhythmias.
• The immediate postpartum period is a time of particular concern
secondary to rapid volume shifts.
• Careful monitoring of cardiac and fluid status should be observed.

22. • Mitral Regurgitation and Aortic Regurgitation and Stenosis
• The pregnancy-induced decrease in systemic vascular resistance reduces the risk
of cardiac failure with these conditions, especially in women with chronic lesions.
• Acute onset of mitral or aortic regurgitation may not be well tolerated during
pregnancy.
• For women with severe aortic stenosis, treatment before pregnancy should be
considered for a peak-to-peak valve gradient >50 mmHg.
• In women with aortic stenosis and a mean valve gradient <25 mmHg, pregnancy
is likely to be well tolerated.
• For women with mitral or aortic regurgitation and left ventricular dysfunction
(LVEF <30%) pregnancy should be avoided.

23. CONGENITAL HEART DISEASE:
• Reparative surgery has markedly increased the number of adult
women with surgically repaired congenital heart disease.
• Maternal morbidity and mortality are greater among these women
than among those without surgical cardiac repair.
• When pregnant, these patients should be jointly managed by a
cardiologist and an obstetrician familiar with these problems.

24. • The presence of a congenital cardiac lesion in the mother increases
the risk of congenital cardiac disease in the newborn.
• Prenatal screening of the fetus for congenital cardiac disease with
ultrasound is recommended.