Obstetric Events That Affect Cardiac Patients

Antenatal Period

In the antenatal period, circulating blood volume increases by 50% to 70%. Systemic vascular resistance falls starting at about 5 weeks and continues until about week 32, when it begins to rise. This is caused by circulating prostacyclin (PGI ₂ ) and shifting of blood to the low-resistance placental circulation. Pulmonary vascular resistance also drops significantly. Cardiac output typically increases 30% to 50%. Women who are unable to increase their cardiac output or who require increased filling pressures to do so may develop heart failure. Heart rate typically increases by 20 to 30 beats/min above prepregnancy levels. Oxygen consumption typically rises 20% to 30%, which may lead to myocardial ischemia in women with coronary artery disease.

Peripartum Period

The first stage of labor involves uterine contractions, which expel up to 500 cc of blood into the circulation. This phenomenon is sometimes called the autotransfusion effect. Increased catecholamine levels during labor cause increases in heart rate, blood pressure, and cardiac output; the latter increases about 10% during labor. Immediately after delivery and when the vena cava is no longer obstructed, cardiac output may increase as much as 80% above prepregnancy levels. It returns to normal about 60 minutes after delivery.

Postpartum Period

Complete resolution of the hemodynamic changes of pregnancy may take 3 to 6 months. Blood volume decreases by 10% within 3 days postdelivery. Blood pressure initially falls and then increases from day 3 to day 7 postpartum, and then it returns to prepregnancy levels by 6 weeks. Systemic vascular resistance increases over the 2-week postpartum period and achieves values about 30% over that at delivery. Heart rate decreases to baseline in about 2 weeks. Cardiac output increases as much as 80% in the first few hours after delivery and then gradually declines to baseline over the next 6 months.

Analgesia and Anesthesia

The method of anesthesia used during labor and delivery may have profound effects on hemodynamics. Regional anesthesia using epidural or spinal anesthesia blunts the stress response, resulting in less catecholamine release, which results in less tachycardia and hypertension. The denser neural blockade required for cesarean section is associated with greater autonomic blockade, which can lead to vasodilation and hypotension. Regional anesthesia cannot be used safely in the presence of a coagulopathy or in the presence of active anticoagulation therapy.

General anesthesia also significantly reduces catecholamine release, resulting in less tachycardia and hypotension. It may depress respiration in the newborn. There is an increased risk of blood loss in cesarean section performed under general anesthesia because volatile anesthetics relax the uterus.

Assisted Delivery

Assisted delivery is the use of instruments such as forceps or ventouse. It is performed most often when patients fail to progress during the second stage of labor, but it also may be performed to avoid the adverse effects of pushing in a cardiac patient. Both pushing and the stress of nonassisted delivery cause significant increases in peripheral vascular resistance, which may be harmful to women with significantly dilated aortas or severe left ventricular dysfunction.

Cesarean Delivery

Cesarean delivery avoids the fluctuations in blood pressure associated with vaginal delivery, but the anesthesia it requires does cause blood pressure to fluctuate. Spinal anesthesia blocks the sympathetic nerves, causing vasodilation and hypotension. Rarely, general anesthesia may be required. General anesthesia also may cause hypotension. The blood loss with cesarean delivery is double that with vaginal delivery. Moreover, with cesarean delivery, there is an increased risk of wound and uterine infection and an increased risk of thromboembolic complications.

Deep Vein Thrombosis

Pregnancy is a hypercoagulable state, and the compression of the pelvic veins by the expanding uterus creates stasis; both of these (the hypercoagulable state and stasis) predispose the patient to DVT. The risk of venous thromboembolism is fivefold higher in pregnant women than nonpregnant women. Puerperium is the time of greatest risk, with an up to 20 times greater relative risk. Approximately 80% of events occur in the first 3 weeks after delivery. DVT in pregnancy is more commonly left sided and is most likely to involve the iliofemoral veins. It can present with various combinations of pain and swelling in the leg, lower abdominal pain, low-grade fever, and an elevated white count.

Many (>50%) women who present with symptoms suggesting DVT do not actually have it, so it is imperative to confirm the diagnosis with objective testing. Duplex scanning is the usual first-line test. If the test result is negative but clinical suspicion is high, it is usually recommended to treat for 1 week and then repeat the duplex scan. If the scan result is again negative, treatment is stopped unless clinical suspicion remains high. In that case, either magnetic resonance venography or conventional venography may be considered.

D-dimer measurements may be unreliable in the diagnosis of DVT during pregnancy. D-dimer levels increase during normal pregnancy and increase with complications such as preeclampsia and placental abruption. Furthermore, false-negative D-dimer results have been reported during pregnancy.

The standard treatment for DVT in pregnancy is low-molecular-weight heparin (LMWH). Treatment should be provided for a minimum of 3 months and for at least 6 weeks postpartum. Usually, leg elevation and early mobilization with compression stockings also are recommended.

Pregnant women who develop DVT should be screened for a hypercoagulable state. It is difficult to evaluate coagulation parameters during pregnancy, so only a limited screening, for antithrombin deficiency and antiphospholipid antibodies, is recommended.

Multiple-Gestation Pregnancies

Multiple-gestation pregnancies are associated with significantly higher maternal complication rates than singleton pregnancies. The risks of hypertensive disorders, heart failure, and myocardial infarction are increased. The risks of other pregnancy-related complications, such as premature rupture of the membranes, abruptio placenta, and postpartum hemorrhage, are increased as well.

Multiple-gestation births also are associated with an increased risk for the fetuses, including premature birth, low birth weight, and intrauterine growth restriction.

In women pregnant with twins, the size of the uterus is roughly the same as for singletons until about 18 weeks of gestation, when it rapidly enlarges so that it is twice normal size by 35 weeks.

Weight gain in the mother is greater with multiple-gestation pregnancies. The increase in amniotic fluid is greater, as are the increases in cardiac output and maternal blood volume.

Preeclampsia and Eclampsia

Preeclampsia is a disease that occurs in pregnant women and is characterized by hypertension and proteinuria. It is diagnosed when a woman who was not hypertensive before pregnancy develops hypertension (blood pressure >140/90 mm Hg) after 20 weeks of pregnancy and proteinuria of at least 0.3 g/24 hours. In recent years, it has been recognized that proteinuria is not universally present in patients with preeclampsia. The 2013 American College of Obstetricians and Gynecologists guidelines state that in the absence of proteinuria, preeclampsia is diagnosed as hypertension in association with thrombocytopenia (platelet count <100, 000/μL), impaired liver function (elevated blood levels of liver transaminases to twice normal), the new development of renal insufficiency (elevated serum creatinine >1.1 mg/dL or a doubling of serum creatinine in the absence of other renal disease), pulmonary edema, or new-onset cerebral or visual disturbances. Preeclampsia, which occurs in 1% to 3% of pregnancies, is a leading cause of maternal death and is responsible for about half of all preterm deliveries. In the following paragraphs, we summarize available information about its etiology, risk factors, maternal and fetal effects, diagnosis, management, and treatment.