Cardiovascular Changes

Circulating volume increases by about 40%. Plasma volume increases slightly more than red cell volume, resulting in mild anemia. Cardiac output also increases by about 40% through a combination of increased preload (increased blood volume), reduced afterload (systemic vasodilation), increased heart rate (10 to 15 beats/min), and a slight increase in contractility. Blood pressure falls by 10% to 15%. Near term, uterine blood flow is 600 to 700 ml/min (10% to 15% of cardiac output). From about week 20, when the mother is in the supine position, the enlarged uterus is capable of compressing the inferior vena cava (causing maternal hypotension) and the aorta (causing reduced placental blood flow).

Pregnancy is a state of hypercoagulability during which there are increased levels of certain coagulation factors (II, VII, X) and a reduction in anticoagulant factors (e.g., protein S). This is of particular importance for mothers at increased risk for thromboembolism, such as those with mechanical heart valves, atrial fibrillation, or cyanotic heart disease.

Respiratory Changes

Displacement of the diaphragm by the enlarging uterus decreases functional residual capacity by approximately 20%. Minute ventilation increases by about 40%, resulting in mild respiratory alkalosis, which is compensated for by renal bicarbonate loss. In late pregnancy, the normal value for arterial carbon dioxide tension is about 4 kPa (30 mmHg). Edema of the upper airway and larynx may occur, particularly in the presence of preeclampsia.

Renal and Gastrointestinal Changes

Glomerular filtration rate and creatinine clearance increase, resulting in a mild reduction in serum creatinine and urea. Thus, levels of these substances at the upper limit of “normal” represent significant renal dysfunction. Pregnancy is associated with relaxation of the lower esophageal sphincter which, together with the expanding uterus, renders the mother at increased risk for gastroesophageal reflux.

Labor

Cardiac output rises throughout labor, particularly during uterine contractions. Contractions cause the expulsion of blood from the uteroplacental capacitance vessels, resulting in an autotransfusion of 300 to 500 ml of blood. Cardiac output remains elevated by 10% to 20% above predelivery levels for 24 to 48 hours after delivery, then slowly declines to prepregnancy levels over the next 10 to 14 days. Uterine contractions are associated with acute increases in heart rate and blood pressure. These hemodynamic effects are exacerbated by maternal pain and anxiety and minimized by epidural analgesia. Maternal blood loss averages 300 to 400 ml in a normal vaginal delivery and 500 to 800 ml in a cesarean section.

Mitral Stenosis

Rheumatic mitral stenosis (see Chapter 10) is the valve lesion that most commonly complicates pregnancy. The increased circulating volume and heart rate that occur during pregnancy can cause pulmonary congestion or frank pulmonary edema. The development of rapid atrial fibrillation can precipitate acute cardiac decompensation.

Aortic Stenosis

Aortic stenosis (see Chapter 10) is an uncommon problem in pregnancy. Patients with known severe aortic stenosis should undergo valve replacement prior to conception—preferably involving a homograft or tissue valve, thus eliminating the need for warfarin.

Patients with mild or moderate aortic stenosis can usually be managed conservatively and allowed to undergo a trial of labor. If an epidural is used, it is essential to titrate the block carefully so as to avoid hypotension.

Severe aortic stenosis presents a very high risk for maternal and fetal mortality. If symptoms related to aortic stenosis are present in the first trimester, termination of the pregnancy should be considered. If the pregnancy proceeds, intervention in the form of percutaneous valvuloplasty or valve replacement will be required during the second trimester. In contrast to percutaneous mitral valvuloplasty, aortic valvuloplasty is associated with a high rate of procedural complications (particularly aortic regurgitation) and provides only limited benefit. Patients with bicuspid aortic valve are at increased risk for aortic dissection during pregnancy.

Mitral and Aortic Regurgitation

Mitral regurgitation (see Chapter 10) as a complication of pregnancy is most commonly caused by mitral valve prolapse. Chronic aortic regurgitation in young women is usually associated with aortic root dilatation (e.g., Marfan syndrome) or with a bicuspid or rheumatic valve. In patients who are in NYHA functional class I or II prior to conception, mitral and aortic regurgitation are usually well tolerated during pregnancy. Treatment involves diuretics and, if vasodilation is required, hydralazine or a calcium channel blocker. Angiotensin-converting enzyme inhibitors are associated with fetal toxicity secondary to fetal hypotension and decreased renal blood flow, resulting in anuria-associated oligohydramnios. Thus, angiotensin-converting enzyme inhibitors are contraindicated in pregnancy. Surgery for mitral or aortic regurgitation during pregnancy should be considered only for patients with NYHA class III or IV symptoms.

Marfan Syndrome

Patients with Marfan syndrome⁵ (see Chapter 11) are at increased risk for aortic dissection and rupture during pregnancy, even in the absence of aortic aneurysm. An ascending aortic dimension greater than 5 cm is an indication for elective repair prior to conception. Patients with Marfan syndrome who are considering pregnancy should undergo an echocardiogram prior to becoming pregnant and should receive prophylactic β blockers during pregnancy. In the absence of any detectable cardiac abnormalities, it is reasonable to plan on vaginal delivery. A carefully titrated epidural and an assisted delivery reduce the need for pushing during labor. Thus, acute increases in blood pressure, which put the patient at risk for aortic dissection, are avoided. If an aortic root diameter greater than 4 cm is discovered during pregnancy, some authorities recommend termination of the pregnancy and surgical repair. If the pregnancy proceeds, blood pressure should be tightly controlled. It may be prudent to avoid labor by performing an elective cesarean section.

Cardiopulmonary Bypass During Pregnancy

Cardiac surgery is only rarely required during pregnancy,^10,11 most commonly for a decompensated valvular lesion. Although cardiac surgery and cardiopulmonary bypass (CPB) can be carried out with a relatively low maternal mortality rates (around 3%), fetal mortality rates are high (around 20%). If possible, surgery should be delayed until the fetus is viable (≥24 weeks’ gestation) and for 48 hours after corticosteroids have been administered to promote fetal lung maturity, at which time cesarean section and cardiac surgery can be carried out as a combined procedure, with the cesarean section being performed first.

If surgery cannot be delayed until after delivery, a number of techniques have been proposed to reduce the risk of fetal loss. They include:

Anticoagulation

Anticoagulation^5,12,13 during pregnancy is required for patients with mechanical heart valves, atrial fibrillation, or both. However, anticoagulation in pregnancy is problematic for a number of reasons. Pregnancy represents a hypercoagulable state. Maternal thromboembolism occurs in 4% to 14% of patients with mechanical heart valves, despite adequate anticoagulation, and it has high maternal mortality rates. Warfarin can cause fetal hemorrhage and is teratogenic if used during weeks 6 through 12 of pregnancy. Heparins do not cross the placenta and are not teratogenic, but there are problems with their use in pregnancy. Unfractionated heparin has been used extensively for anticoagulation during pregnancy. However, it is difficult to maintain satisfactory anticoagulation with this drug, and its use has been associated with catastrophic valve thrombosis resulting in maternal death. Furthermore, prolonged use of unfractionated heparin is associated with thrombocytopenia and osteoporosis. Low molecular weight heparins (LMWHs) are an attractive option because of their prolonged duration of action, their more predictable antithrombotic effects, and their minimal bone and platelet effects. Because the pharmacokinetics of LMWHs change during pregnancy, the monitoring of antifactor Xa levels and dose adjustment to ensure therapeutic anticoagulation are recommended. However, there are only limited data to support their use and, at least for enoxaparin, use in pregnancy is not supported by the manufacturer.¹⁴

Thus, anticoagulation during pregnancy is controversial, and a number of regimens are used. Warfarin may be used throughout the pregnancy (aiming for INR 2.5 to 3.5 for mechanical valves) except during weeks 6 through 12 and beyond 36 weeks, when heparin can be substituted. Unfractionated heparin may be administered either subcutaneously (17,500 to 20,000 IU twice daily, adjusted to prolong the aPTT to 2 to 3 times normal) or as a continuous intravenous infusion (dose-adjusted to prolong the aPTT to 2 to 3 times normal). LMWH is also used subcutaneously twice daily, adjusted to maintain therapeutic antifactor Xa levels. Adjunctive aspirin is also recommended with all regimens. Delivery should be planned and the patient converted to intravenous heparin at least 36 hours prior to induction of labor or cesarean section. Heparin should then be stopped at least 4 hours prior to labor or surgery. If labor begins while the mother is receiving warfarin, anticoagulation should be reversed and cesarean delivery should be performed.⁸ Heparin is restarted 4 to 6 hours after delivery and warfarin is resumed the night after delivery if there are no bleeding complications.

Endocarditis Prophylaxis

The American College of Cardiology/American Heart Association guidelines⁵ do not recommend that antibiotic prophylaxis be given to patients with valvular heart disease who are undergoing uncomplicated vaginal or cesarean delivery unless infection is suspected. However, antibiotics may be considered in patients at high risk for endocarditis (Table 10-8).

General Issues

Beyond the twentieth week of pregnancy, a wedge should be placed under the right side of a woman so as to prevent aortocaval compression. Graduated compression stockings and sequential compression devices are indicated in pregnant patients at increased risk for deep venous thrombosis, especially in those confined to bed. Because of the teratogenic (during the first trimester) and oncogenic (increased risk for childhood leukemia) effects of radiation exposure, the fetus should be shielded by a lead apron while maternal radiographs are obtained.

Fetal Monitoring

Critical illness in the mother is highly likely to precipitate hypoxia and acidosis in the fetus. If the fetus is viable (>24 weeks), continuous monitoring of fetal heart rate under the supervision of a midwife and obstetrician is indicated. Persistent fetal bradycardia (>120 beats/min) is indicative of serious fetal hypoxia. If an abnormal heart rate pattern is identified, a fetal ultrasound examination should be performed to obtain a biophysical profile (a measure of fetal well-being). If the mother is in labor and has a dilatated cervix, fetal acid-base status may be monitored by a scalp pH electrode—assuming there are no concerns about fetal anticoagulation, because warfarin takes 7 to 10 days to be cleared from fetal circulation after the mother discontinues treatment. A pH less than 7.2 constitutes important fetal acidosis.

Maternal Cardiac and Respiratory Decompensation

The management of maternal cardiac or respiratory decompensation is essentially the same as it is for the nonpregnant patient—with a few caveats. Fetal hypoxia may be avoided or reversed by increasing maternal oxygen delivery. Thus, routine use of supplemental oxygen is indicated; the hemoglobin concentration should be kept above 80 to 90 g/l, and low cardiac output should be treated with inotropic drugs. An improvement in maternal blood pressure should not be achieved at the cost of uterine vasoconstriction.

Data concerning the effects of inotropic agents on placental blood flow are conflicting and are derived mainly from animal studies.³ Catecholamines with α₁-receptor activity cause uterine vasoconstriction. Drugs with β₂-receptor activity cause uterine vasodilatation but may exacerbate hypotension and cause uterine relaxation, which may be good in the presence of premature labor but bad during the postpartum period. In one study, milrinone did not adversely affect uterine blood flow.¹⁵ It is interesting to note that, in contrast to common opinion, the use of the α₁-agonists metaraminol and phenylephrine to treat hypotension due to spinal anesthesia has been associated with improved fetal pH measurements as compared to ephedrine, a mixed α and β agonist.^16,17 For the treatment of low cardiac output, an inodilating drug (e.g., dobutamine, milrinone, low-dose epinephrine) may be used. Inoconstricting drugs such as norepinephrine should be avoided unless there is documented inappropriate vasodilatation.

The indications for mechanical ventilation are the same as those for the nonpregnant patient. Intubation should be performed as a rapid-sequence induction (see Chapter 40), and the clinician should be prepared for brisk desaturation (due to the low functional residual capacity and high metabolic rate), difficult intubation (due to body habitus, the lateral tilt position, and airway edema), and the reflux of gastric contents. A smaller than usual endotracheal tube should be available (i.e., 7.0 to 7.5 mm internal diameter). Minute ventilation must be 20% to 40% higher than normal. Assuming high airway pressures are not required, it is reasonable to ventilate to an arterial carbon dioxide tension of 4 kPa (30 mmHg), the normal value for pregnancy.

Sedation and analgesia of the ventilated pregnant patient is the same as those for the nonpregnant patient. Meperidine is the most widely used intravenous opioid during labor, but in reality, all opioids can cause maternal and fetal respiratory depression. No fetal risk has been ascribed to propofol, but the data are limited.

Cardiac Arrest

Several factors make cardiac resuscitation difficult in the pregnant patient.^18,19 Aortocaval compression contributes to hemodynamic instability when the patient is in the supine position, but external cardiac massage is less effective when in the lateral tilt position. Hypoxemia develops rapidly, and there is a high risk for aspiration of gastric contents. Endotracheal intubation may be difficult. External cardiac compression and bag-mask ventilation are unable to meet the high metabolic requirements of the mother and the fetus. Epinephrine causes marked uterine vasoconstriction. Despite these problems, standard resuscitation protocols should be employed. In addition to placing a wedge under the right hip, manual sideways traction may be applied directly to the abdomen to reduce the effect of aortocaval compression.

If the fetus is viable (<24 weeks), consideration should be given to emergency cesarean section. Survival of the fetus is directly proportional to the time taken for delivery. If delivery is begun within 5 minutes of a cardiac arrest, delivery of a viable fetus is possible and resuscitation of the mother becomes easier. Even after 35 minutes of resuscitation, 25% of fetuses will survive neurologically intact.

Arrhythmias

Amiodarone use has been associated with premature birth, growth retardation, and fetal hypothyroidism and should be avoided if possible. Adenosine, digoxin, β blockers, lidocaine, and magnesium may be used for maternal arrhythmias. Electrical cardioversion is considered safe if required.

Hypertension

Hypertension may be treated with oral β blockers, methyldopa, and calcium channel blockers. If intravenous therapy is needed, hydralazine (5 mg bolus doses repeated as required) or labetalol (5 mg bolus doses repeated as required) may be used. Angiotensin-converting enzyme inhibitors should be avoided (see earlier discussion). Sodium nitroprusside can be used in the short term for hypertensive emergencies, but it has the potential to cause fetal cyanide toxicity. Nitroglycerin may be used but, like β₂ agonists, it inhibits uterine contractions.

Premature Labor

The onset of premature labor is commonly treated with a tocolytic drug such as nifedipine or a β₂-sympathomimetic drug (e.g., terbutaline or ritodrine). Other agents with tocolytic properties such as magnesium and indomethacin are now rarely used for this purpose. β₂ sympathomimetics are associated with a number of adverse effects, including hypokalemia, tachycardia, and hyperglycemia. In addition, for reasons that are not entirely clear, intravenous β₂ sympathomimetics administered during labor are associated with acute pulmonary edema. If delivery of a very premature infant (>34 weeks gestation) is unavoidable, corticosteroids should be administered to promote fetal lung maturity.

Planned Labor

The majority of maternal deaths resulting from cardiac disease occur during labor and delivery. Most patients benefit from epidural analgesia and a shortened second stage that includes an assisted delivery. If labor is prolonged or stalled, cesarean section is indicated.

Patients with significant cardiac symptoms prior to labor should have invasive monitoring (arterial and central venous catheters) during labor. If there is a high risk for pulmonary edema (e.g., moderate mitral stenosis), the insertion of a pulmonary artery catheter should be considered.

Oxytocin is commonly used to augment labor but can occasionally cause profound hypotension. Fluid retention and hyponatremia may also occur. The drug should be administered as a dilute infusion rather than as a bolus. Prophylaxis against acid aspiration should be administered in case emergency cesarean section and general anesthesia are required.

Postpartum Care

The risk for cardiac decompensation, particularly pulmonary edema, extends into the postdelivery period. Thus, monitoring in the intensive care unit should be maintained for 24 to 48 hours after delivery.