- History of heart disease.
- Symptoms and signs of heart disease.
- Echocardiographic or other objective evidence of heart disease.
Cardiovascular disease occurs in approximately 1% of pregnancies, but the incidence is increasing due to improved prognosis
of women with congenital heart disease and a trend toward older
maternal age. The unique hemodynamic changes associated with pregnancy
make diagnosis and management of heart disease in pregnant patients
a challenge to the physicians, who must consider not only the patient
but also the risks to the fetus.
In general, the normal hemodynamic changes associated with pregnancy are well tolerated by those who have a normal cardiovascular system,
valvular regurgitation, and left-to-right intracardiac shunts. On
the other hand, the highest maternal and fetal morbidity and mortality
is seen with severe obstructive valvular lesions, severe aortic
disease (dilated thoracic aorta or uncorrected coarctation), New
York Heart Association (NYHA) class III or IV heart failure, uncontrolled
hypertension, and cyanotic congenital heart disease. As a rule,
spontaneous vaginal delivery, often with use of vacuum extraction
or forceps to facilitate stage 2 of labor to avoid the hemodynamic stress
associated with pushing, is preferred. Cesarean section, with few
exceptions, should be reserved for obstetric indications.
Stout KK et al. Pregnancy in women with valvular
heart disease. Heart. 2007 May;93(5):552–8.
Normal pregnancy is accompanied by significant physiologic changes, although underlying mechanisms remain virtually unknown (Table 31–1). The normal signs and symptoms associated with pregnancy, such as shortness of breath, fatigue, and exercise intolerance, may obscure the diagnosis of heart disease. The clinician must, therefore, have a thorough knowledge of these normal changes and the aspects of the history and physical examination that suggest the presence of heart disease.
Table 31–1. Cardiovascular Changes in Normal Pregnancy.
| Save Table
Table 31–1. Cardiovascular Changes in Normal Pregnancy.
| First Trimester|| Second Trimester|| Third Trimester||At Term|
|Blood volume||+||+ +||+ + +||↑ 30–50%|
|Heart rate||+||+ +||+ + (+)||↑ 15–20 beats/min|
|Stroke volume||+||+ + (+)||+|
|Cardiac output||+||+ + (+)||+||↑ 30–50%|
|Systolic blood pressure ||–||–||No change||↓ 5–10 mm Hg mid pregnancy|
|Diastolic blood pressure ||–||– –||–|
|Systemic vascular resistance||–||– – –||– –|
|Pulmonary vascular resistance||–||– –||–|
|Left ventricular end-diastolic pressure||+||+ +||No change|
|Venous compliance and volume||+||+ +||+|
|Red blood cell mass||+||+||+||↑ 15–20%|
The increase in maternal blood volume begins as early as the sixth week of pregnancy, peaks at approximately 32 weeks of gestation,
and stays at that level (40–50% higher than pregestational levels) until delivery. The plasma volume shows a more rapid and significant rise than the red blood cell mass, accounting for the appearance of physiologic anemia during pregnancy. The
increased blood volume is maintained until after delivery, when a spontaneous diuresis occurs. At the same time, there is an increased venous return due to the relief of vena caval compression after
delivery. These rapid postpartum changes in blood volume are critical
for patients with underlying heart disease.
One of the most significant changes during pregnancy is the increase in cardiac output, which begins to rise during the first trimester
and peaks around the twenty-fifth week of gestation and then levels
off. Total cardiac output increases up to 50% over pregestational
levels. Cardiac output is the product of stroke volume and heart
rate. During the early part of pregnancy, the increase in cardiac
output is predominantly the result of an increase in stroke volume,
augmented by increased intrinsic myocardial contractility. Numerous
studies have shown a gradual increase in left ventricular
systolic function attributed to left ventricular afterload reduction
due to the low-resistance runoff of the placenta. The rise in left
ventricular systolic function begins in early pregnancy, peaks in
the twentieth week, and then remains constant until delivery. As
pregnancy advances, heart rate increases and stroke volume mildly decreases.
The increased cardiac output in late pregnancy is maintained because of
the increased heart rate.
A unique aspect of pregnancy is the hemodynamic changes induced by a change in a patient’s position. When the patient is
in the supine position, the gravid uterus induces profound mechanical
compression of the inferior vena cava, decreasing venous return
to the heart, and thus, cardiac output. A change from the supine
to the left lateral position results in a 25–30% increase
in cardiac output because of an increase in stroke volume.
Intravascular Pressures and Vascular Resistance
Systolic and diastolic pressures drop during pregnancy. A small decrease in systolic blood pressure begins in the first trimester,
peaks at midgestation, and returns to near prepregnancy levels at term.
The diastolic blood pressure decreases more than the systolic blood pressure,
due to a significant fall in systemic vascular resistance, and results
in a wider pulse pressure. The systemic blood pressure increases
during pregnancy with the patient’s age and parity. It also
varies with the patient’s position. The highest levels
are recorded early in the pregnancy when the patient is upright,
and lowest when she is supine. During the latter part of pregnancy,
the effect of position on systemic blood pressure depends on the
relative degrees of inferior vena cava and aortic compression. Total
vascular resistance, including both the systemic and the pulmonary, decrease
during pregnancy. The mechanism for the fall in resistances is poorly understood
but is attributed to the low-resistance circulation of the pregnant uterus
and to hormonal changes associated with pregnancy.
Fujitani S et al. Hemodynamic assessment in a
pregnant and peripartum patient. Crit Care Med. 2005 ...