1. What are the normal changes in cardiac physiology during pregnancy?

The normal physiologic changes of pregnancy include: increased blood volume, increased cardiac output, increased heart rate, and decreased blood pressure.

In general, maternal blood volume increases up to 50% above nonpregnant levels. Blood volume begins to increase in the first trimester and continues until approximately 32 weeks’ gestation; it then remains constant until delivery. Maternal plasma volume increases by 50% while maternal red blood cell mass increases by 20%. This discrepancy is responsible for the dilutional anemia of pregnancy. The hormonal mechanisms responsible for this increase include: steroid hormones of pregnancy, increased plasma renin activity, and hyperaldosteronism.

Cardiac output begins to increase in the first trimester and peaks at 30-50% above nonpregnant levels by 20 weeks’ gestation; it then remains constant until term. At 38-40 weeks’ gestation, cardiac output decreases. This change is more pronounced in the supine position due to vena caval compression by the enlarged uterus. Early in pregnancy an increased stroke volume is responsible for the changes in cardiac output, while later in pregnancy an increased heart rate is responsible.

In a normal pregnancy there is a slight decrease in systolic blood pressure and a moderate decrease in diastolic. The nadir occurs in midtrimester, and then there can be a slow increase to the patient’s nonpregnant blood pressure.

2. What are the normal changes in cardiac physiology during labor and delivery?

During a uterine contraction, 300-500 cc of blood is shifted from the uterus to the maternal systemic circulation. As a result of this autotransfusion, systemic venous pressure and right ventricular pressure increase. Maternal mean arterial pressure rises and is followed by a reflex bradycardia. Maternal pain and anxiety result in increased adrenaline, which increases maternal blood pressure and heart rate. Following delivery, vena caval compression is decreased and blood volume is increased. These changes cause a 10-20% increase in circulating cardiac output.

3. Describe the hemodymanic changes caused by regional anesthesia.

Both spinal and epidural anesthesia cause peripheral vasodilation. Peripheral vasodilation can cause a significant decrease in preload. The changes may produce a decrease in cardiac output and blood pressure. In an attempt to diminish the hemodynamic changes of regional anesthesia, most patients are hydrated prior to its administration.

4. What symptoms merit a cardiac evaluation during pregnancy?

During a normal pregnancy it is not unusual for women to experience fatigue, shortness of breath, orthopnea, and peripheral edema. However, progressive limitation of physical activity by shortness of breath, chest pain accompanying exercise or physical activity, and syncope preceded by palpitations or physical exertion should cause the physician to suspect an underlying cardiac condition.

5. How do you take care of a woman with a congenital ventricular or atrial septal defect (VSD, ASD)?

Women with an ASD and a left-to-right shunt usually do well in pregnancy. Peripheral vasodilation of pregnancy decreases the left to right shunt. A small percentage of women have paroxysmal atrial flutter, which recurs when the heart rate is difficult to control. The recommended treatment is catheter ablation-after completion of the pregnancy, since the procedure requires extensive radiation exposure. Women with these defects are not at risk for bacterial endocarditis and do not need antibiotic prophylaxis in labor.

Women with a VSD and a left-to-right shunt also do well in pregnancy. These patients are less prone to arrhythmia, but are at significant risk for bacterial endocarditis. As a result, they need antibiotic prophylaxis during labor and delivery.

6. What is Eisenmenger’s syndrome?

A congenital communication between the pulmonary and systemic circulation causing increased pulmonary vascular resistance (PVR) either to the systemic level or greater than the systemic level. Once the PVR becomes greater than the systemic vascular resistance, a right-to-left shunt develops along with significant pulmonary hypertension. The most common cause of Eisenmenger’s syndrome is a large VSD.

7. What are the risks to a pregnant women with Eisenmenger’s syndrome?

Women with Eisenmenger’s syndrome have a mortality rate of 50%, a fetal mortality rate of 50%, and a preterm delivery rate of 85%. Sudden death can occur at any time; however, the risk is greatest during labor and delivery and the early postpartum period.

Women with Eisenmenger’s syndrome have a high PVR. Management during pregnancy revolves around maintaining pulmonary blood flow. Antenatal care centers on limitation of physical activity, oxygen therapy, and possibly pulmonary vasodilators. Delivery should be planned with central hemodynamic monitoring. It is crucial to maintain preload; therefore, these pregnant women should have an assisted second stage. Cesarean section is reserved for obstetric indications. Despite meticulous care, the mortality rate remains significant, approaching 50%.

8. What is the leading cause of mitral stenosis?

Rheumatic fever is the leading cause of this condition. Congenital mitral stenosis (Lutembacher syndrome) is very rare.

9. What is the pathophysiology of mitral stenosis?

Mitral stenosis impedes the flow of blood from the left atrium to the left ventricle during diastole. These patients normally have a fixed cardiac output. As stenosis worsens, there can be dilation of the left atrium and pulmonary congestion. Normally the mitral valve area is 4-5 cm2. When the valve area is ≤ 2.5 cm2, a women experiences symptoms with exertion, and when the valve area is ≤ 1.5 cm2, a women experiences symptoms at rest.

During pregnancy, the increased blood volume increases venous return. Increased preload in a women with mitral stenosis causes pulmonary congestion instead of increased cardiac output. In addition, tachycardia of pregnancy shortens diastole and decreases left ventricular filling-and, therefore, cardiac output.

10. How are patients with mitral stenosis managed during pregnancy, labor, and delivery?

In the antepartum period, management focuses on maintaining cardiac output while decreasing pulmonary congestion. This balance is achieved with diuretics and beta-blocker therapy. Good pain control is important during labor and delivery to reduce the maternal heart rate and increase diastole. Patients should be given antibiotic prophylaxis for bacterial endocarditis. In addition, most women cannot tolerate the second stage due to a decreased preload with pushing. As a result, an operative vaginal delivery is necessary. Finally, the postpartum autotransfusion can produce massive pulmonary edema in a woman with mitral stenosis. Immediate and aggressive diuresis postpartum can significantly decrease this complication.

11. Describe the pathophysiology of aortic stenosis.

The majority of aortic stenosis is a combination of congenital lesions and rheumatic fever. The normal aortic valve area is 3-4 cm2. Aortic stenosis becomes significant when the valve area is ≤ 1 cm2. As stenosis progresses, the left ventricle initially hypertrophies in response to the increased pressure gradient. Eventually the left ventricle dilates. A patient will present with angina, near-syncope/syncope, and congestive heart failure.

12. How is a patient with aortic stenosis managed during pregnancy, labor, and delivery?

Women with aortic stenosis have a fixed cardiac output. It is essential that their preload be maintained during pregnancy, labor, and delivery. Any hypotension can cause sudden death, and women with a valve gradient > 100 mmHg are at greatest risk. During labor and delivery, women with severe disease may require central hemodynamic monitoring. In addition, regional anesthesia should be used with caution because of the risks for hypotension. These women cannot tolerate the second stage due to a decreased preload with pushing, and an operative vaginal delivery is necessary. Postpartum blood loss can also significantly reduce preload, and volume resuscitation with fluid or blood may be necessary. Finally, patients should be given antibiotic prophylaxis for bacterial endocarditis.

Key points: cardiovascular disease in pregnancy

  • Cardiac output increases in pregnancy, first by increased stroke volume then by increased heart rate.
  • Do not forget subacute bacterial endocarditis prophylaxis at the time of delivery in women with cardiac valvular disease and ventricular septal defects.
  • Eisenmenger’s syndrome, severe mitral or aortic stenosis, primary pulmonary hypertension, and Marfan syndrome with a dilated aortic root carry the greatest risk of maternal mortality.
  • Labor and delivery is a critical time for women with cardiac disease due to significant changes in hemodynamics and volume status.

13. What are the management issues for a women with primary pulmonary hypertension?

Women with severe pulmonary hypertension have an obstruction to right ventricular outflow. The major physiologic concern is maintenance of pulmonary blood flow. Anything that decreases preload decreases pulmonary blood flow. Antenatal care revolves around limitation of physical activity, oxygen therapy, and possibly pulmonary vasodilators. Despite meticulous care, the mortality rate remains significant, approaching 50%. Women with this condition should be strongly advised against pregnancy.

14. What is Marfan syndrome?

Marfan syndrome is an autosomal dominant genetic disorder with a prevalence of 4-6/10,000. An abnormal fibrillin gene on chromosome 15 causes the disease. Abnormal fibrillin causes connective tissue abnormalities all over the body, the most significant being aortic root dilation, optic lens dislocation, long limbs, scoliosis, and joint laxity. These patients have an increased mortality from aortic dissection or rupture.

15. What is the optimum management for pregnant women with Marfan syndrome?

Women with an aortic root < 4 cm can attempt pregnancy with a modest risk. Women with an aortic root > 5.5 cm should have aortic graft and aortic valve replacement prior to attempting pregnancy.

Women with an aortic root 4.0-5.5 cm have the greatest risk during pregnancy because cardiac surgery is premature. During pregnancy, beta blockade should be used to protect the aortic root from the increased hemodynamic forces of pregnancy. The goal is to maintain a resting pulse of 70 bpm. Follow the aortic root with sequential echocardiograms.

During labor and delivery, women with an aortic root < 4 cm can have a vaginal delivery with prevention of tachycardia. In women with dilated aortic roots, the delivery management is controversial. Some authorities recommend a cesarean delivery to minimize the increased pressures that occur during pregnancy. At the present there are no data to support or refute this delivery plan.

16. What are the diagnostic criteria for peripartum cardiomyopathy?

  • Heart fainure within the last month of pregnancy or 5 months postpartum
  • Absence of prior heart disease
  • No determinable cause
  • Echocardiographic indication of left ventricular dysfunction: ejection fraction < 45%, fractional shortening < 30%, or left ventricular end-diastolic dimension > 2.7cm/m2.

17. What is the treatment of peripartum cardiomyopathy?

Women with peripartum cardiomyopathy should be treated with diuretics and afterload reduction. If a patient is pregnant, use hydralazine as the afterload-reducing medication; if the patient is postpartum, an ACE inhibitor is preferred.

18. What is the prognosis for women with peripartum cardiomyopathy?

Women with peripartum cardiomyopathy whose left ventricular (LV) size and function remain abnormal 6 months after delivery have a 5-year mortality of 50-85%. These women should be counseled against subsequent pregnancies.

Women whose LV size and function normalize within 6 months of delivery have a greatly reduced 5-year mortality. However, they also have a 25% recurrence rate during a subsequent pregnancy.

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