Abstract
Cardiac disease is the leading cause of indirect maternal mortality. The optimal management of women with cardiovascular disease begins before conception. Normal physiologic changes of pregnancy and the peripartum and postpartum periods may exacerbate preexisting cardiovascular disease. The anesthetic management of the parturient with cardiovascular disease should be individualized, and a multidisciplinary team should plan care throughout pregnancy and the puerperium.
Keywords
Cardiovascular disease, Valvular heart disease, Anticoagulation during pregnancy, Congenital heart disease, Cardiac monitoring during pregnancy
Chapter Outline
Cardiovascular Physiologic Changes of Pregnancy, 988
Cardiac Examination during Pregnancy, 989
Cardiac Risk Prediction, 990
Cardiovascular Imaging during Pregnancy, 991
Echocardiography, 991
Cardiac Magnetic Resonance Imaging, 992
Cardiac Catheterization, 992
Computed Tomographic Angiography, 992
Ionizing Radiation Risks to the Fetus, 992
Cardiac Drugs and Pregnancy, 993
Angiotensin-Converting Enzyme Inhibitors, 993
Angiotensin Receptor–Blocking Agents, 993
Beta-Adrenergic Receptor Antagonists, 993
Calcium Entry–Blocking Agents, 993
Other Drugs, 993
Aortic Diseases and Aortic Dissection, 993
Marfan Syndrome, 994
Aortic Disease Associated with a Bicuspid Aortic Valve, 994
Ehlers-Danlos Syndrome, 994
Turner Syndrome, 994
Aneurysm-Osteoarthritis Syndrome, 994
Obstetric and Anesthetic Management, 994
Congenital Heart Disease, 995
Atrial Septal Defect, 995
Ventricular Septal Defect, 995
Patent Ductus Arteriosus, 995
Coarctation of the Aorta, 998
Fontan Repair, 998
Transposition of the Great Arteries, 998
Ebstein’s Anomaly, 999
Tetralogy of Fallot, 999
Pulmonary Hypertension, 1001
Infective Endocarditis, 1003
Antibiotic Prophylaxis, 1003
Diagnosis and Treatment, 1003
Neuraxial Anesthesia in Patients with Systemic Infection, 1003
Implantable Cardiac Devices, 1004
Permanent and Temporary Pacemakers, 1004
Implantable Cardioverter-Defibrillators, 1004
Peripartum Management, 1004
Adult Arrhythmias, 1005
Supraventricular Arrhythmias, 1005
Ventricular Arrhythmias, 1006
Congenital Long QT Syndrome, 1006
Antiarrhythmic Drugs, 1006
Electric Cardioversion, 1006
Maintenance of Sinus Rhythm, 1007
Myocardial Infarction, 1007
Valvular Heart Disease, 1009
Aortic Stenosis, 1009
Aortic Regurgitation, 1011
Mitral Stenosis, 1012
Mitral Regurgitation, 1013
Mitral Valve Prolapse Syndrome, 1013
Tricuspid Stenosis and Regurgitation, 1013
Pulmonic Stenosis and Regurgitation, 1014
Prosthetic Heart Valves, 1014
Cardiomyopathies, 1016
Heart Failure Nomenclature, 1016
Peripartum Cardiomyopathy, 1016
Other Nonischemic Cardiomyopathies, 1018
Medical Management of Heart Failure, 1020
Ventricular Assist Devices, 1021
Pericardial Disease, 1021
Pericardial Effusion, 1021
Acute Pericarditis, 1021
Cardiac Tamponade, 1022
Constrictive Pericarditis, 1022
Anesthetic Management, 1022
Cardiopulmonary Resuscitation during Pregnancy, 1022
Pregnancy after Heart Transplantation, 1023
Cardiopulmonary Bypass during Pregnancy, 1023
Evidence suggests that an individual’s sex has a significant impact on cardiovascular disease. The etiology of coronary thrombosis causing acute myocardial infarction is different in women than in men. Plaque erosion, rather than plaque rupture, occurs at a higher rate in women than in men. Coronary artery diameter is smaller in women, and women frequently develop more diffuse atherosclerosis than men. Female aortas appear to be stiffer because of underlying fibrosis or remodeling. Women have more microvascular coronary artery dysfunction than men and frequently demonstrate impaired coronary artery vasodilator response.
Autoimmune rheumatic diseases are associated with premature atherosclerosis; vasculitides such as Takayasu’s arteritis, temporal arteritis, rheumatoid vasculitis, lupus vasculitis, and polymyalgia rheumatica are all more common in women than in men. During exercise stress testing, women more often have atypical and nonanginal pain than men, who more often have typical angina. Women with acute myocardial infarction more frequently do not have chest pain, especially those who have the infarction at a younger age. In-hospital mortality for acute myocardial infarction is higher for women than for men. Although women who have non–ST-segment elevation myocardial infarction have a poorer risk profile than men, the infarction is frequently treated less aggressively. Yet women are more likely than men to summon emergency medical services during a myocardial infarction.
Whether women have poorer outcome after percutaneous coronary intervention has been a matter of debate. At the time of presentation for both percutaneous and surgical coronary revascularization procedures, women are older than men and have more cardiovascular risk factors and comorbid conditions. Older studies demonstrated poorer overall outcome in women than in men; however, more recent studies have demonstrated a narrowing or disappearance of the sex-related outcome gap. Similarly, several studies have demonstrated that female sex was an independent predictor of coronary artery bypass grafting (CABG) operative mortality. However, after extensive baseline risk adjustment, outcomes after CABG or aortic valve replacement have been reported to be similar for men and women.
Number of pregnancies has been associated with the future risk for coronary artery disease and progression of atherosclerosis. Hypertensive disorders of pregnancy, preeclampsia, and gestational diabetes mellitus are risk factors for future development of cardiovascular disease. Earlier identification of these women with an increased lifetime risk for developing cardiovascular disease may present a unique opportunity for prevention of subsequent cardiovascular events.
Historically, rheumatic mitral stenosis represented the most common cardiac condition encountered in pregnant women. This disease continues to be a major problem in the developing world and in certain immigrant populations in the United States. In industrialized countries, congenital heart disease has become the most common cardiac condition complicating pregnancy. This demographic change is a result of significant advances in the treatment of complex congenital heart conditions and survival of these patients into childbearing age. In the United States, maternal mortality caused by hemorrhage and hypertensive disorders of pregnancy has declined, whereas mortality caused by cardiovascular conditions has steadily increased.
The optimal management of women with cardiovascular disease begins before conception. Normal physiologic changes of pregnancy may exacerbate preexisting cardiovascular disease. For most women with heart disease, pregnancy is associated with favorable outcome; however, even with modern advances in treatment and monitoring, there remains a high incidence of morbidity and mortality for some conditions. Thus, for some women, it may be advisable to avoid pregnancy.
There is significant individual variability in the severity of specific cardiovascular disease entities. Additionally, several cardiovascular conditions may be simultaneously present in one individual. Management may be further complicated by the presence of noncardiovascular pathologic processes. The anesthetic management of the parturient with cardiovascular disease should be individualized, and a multidisciplinary team should plan peripartum care. Some case reports and small series have described the anesthetic management of these patients, but, in general, few data justify choosing one anesthetic technique over another. Therefore, the anesthesiologist must have a thorough understanding of the normal physiologic changes of pregnancy as well as the individual parturient’s pathophysiology, and then plan anesthetic management that best achieves the desired hemodynamic goals. Optimal analgesia is often an important part of safe childbirth in these patients.
The anesthetic care of women with cardiovascular disease does not end with labor and delivery; rather, it continues postpartum when the physiologic changes of pregnancy may be at their greatest. Inadequate postpartum analgesia may be associated with hypertension and tachycardia. Postoperative shivering increases oxygen consumption and may cause myocardial ischemia in patients with limited cardiac reserve.
Cardiovascular Physiologic Changes of Pregnancy
The electrocardiogram (ECG) typically changes during pregnancy. During the third trimester, the enlarging gravid uterus causes upward and lateral rotation of the heart, which may result in left-axis deviation of 15 to 20 degrees. Overall, however, the QRS axis is quite variable during pregnancy. At rest, nonspecific ST-segment and T-wave changes are very common during normal pregnancy. Exercise in healthy pregnant women does not cause distinctive ECG changes compared with nonpregnant subjects.
No repolarization abnormalities are observed with uncomplicated vaginal delivery. ST-segment elevation is never seen in normal pregnancy and should always be considered pathologic. ST-segment depression is seen in 25% to 81% of parturients undergoing cesarean delivery, regardless of the type of anesthesia. Oxytocin administration during the third stage of labor has been associated with ST-segment depression. However, these oxytocin-associated ECG changes are not associated with myocardial damage. Whether these ECG changes are caused by underlying ischemia or some other mechanism remains unclear.
Left ventricular mass increases during normal pregnancy. The increase in left ventricular mass is greater in multiple gestation than in singleton gestation. Preeclampsia also results in a greater increase in left ventricular mass.
Plasma lipid concentrations , including total serum cholesterol, triglycerides, and low-density lipoprotein cholesterol concentrations, increase during pregnancy. Obese pregnant women have an even greater increase in plasma lipids. This increase in plasma lipids results in part from insulin resistance and an increase in estrogen levels during pregnancy. The effects of these physiologic changes in plasma lipid concentrations on long-term cardiovascular outcomes are unclear.
Brain natriuretic peptide (BNP) is a natriuretic hormone synthesized primarily in the heart ventricles. BNP levels increase as a response to increased filling pressures in patients with heart failure. Physiologically, BNP has hypotensive, diuretic, and natriuretic effects. During uncomplicated normal pregnancy, BNP levels are double the nonpregnant level with return to baseline approximately 3 days after delivery. The BNP level appears to be unchanged between the trimesters. BNP levels are increased in preeclamptic women and in pregnant women with heart disease. A correlation exists between BNP and the increases in left ventricular mass and end-diastolic and end-systolic volumes observed in preeclampsia. The increase in BNP with fluid administration in preeclamptic women further confirms that this hormone is secreted in response to increased intracavitary pressures. Intravenous fluid administration does not increase BNP levels in healthy women. BNP is elevated in women with complex congenital heart disease, but it varies considerably among anomalies. Therefore, its role for individual patient management remains unclear.
Cardiac enzyme levels may be altered by pregnancy or pregnancy-associated disease. Myocardial cell death is associated with elevation of sensitive and specific cardiac biomarkers—creatine kinase MB fraction (CK-MB) and cardiac troponins. Cardiac troponin levels are not elevated above the upper limits of normal during uncomplicated pregnancy. Troponin levels are elevated in women with gestational hypertension or preeclampsia. By contrast, CK-MB levels may be elevated up to two to four times the upper limit of normal owing to the presence of these enzymes in the uterus and placenta (see Fig. 46.1 ). Thus, elevated CK-MB levels are not specific for the diagnosis of myocardial infarction during pregnancy. In patients with preeclampsia who have concurrent myocardial infarction, the observed troponin levels are higher than expected for the underlying preeclampsia. Heterophil antibody interference with the troponin assay may cause a false-positive increase in troponin levels during pregnancy. However, both CK-MB and troponin are sensitive markers for the diagnosis of myocardial infarction during pregnancy.
Cardiac output increases as early as 5 weeks’ gestation and continues to increase throughout the second trimester until it is approximately 50% greater than nonpregnant values (see Fig. 2.2 ). Cardiac output does not change from this level during the third trimester; it may actually be reported as decreased in the third trimester if measurements are made in the supine position, which causes aortocaval compression. Both an increase in heart rate and stroke volume contribute to the increase in cardiac output. Distribution of cardiac output to the uterine circulation increases from 1% in the nonpregnant state to 12% during the second half of pregnancy (see Chapter 2 ).
Cardiac Examination during Pregnancy
Pregnant women frequently complain of mild dyspnea at rest and exertion; on occasion, exercise tolerance is decreased. Therefore, it is important to recognize normal changes in the physical examination associated with pregnancy ( Table 41.1 ).
| Feature | Normal Pregnancy | Implication of Abnormal Findings |
|---|---|---|
| Jugular venous pressure | Normal | Any elevation warrants further evaluation of volume status |
| Carotid pulse | Normal upstroke Normal volume | Decreased or delayed upstroke (aortic stenosis), bifid pulse (hypertrophic cardiomyopathy) |
| Peripheral pulses | Well filled | Diminished or delayed (aortic stenosis, left ventricular outflow obstruction) |
| Point of maximum impulse | Crisp, slightly laterally displaced | Any enlargement or more than slight lateral displacement warrants further evaluation. |
| S1 | Louder and widely split | |
| S2 | Unchanged | Soft/absent/paradoxically split (aortic stenosis) Loud P2, fixed split (pulmonary hypertension) |
| S3 | Normally present | |
| S4 | Rarely heard | |
| Aortic stenosis murmur | Increased | Helpful to confirm physical examination findings with echocardiography |
| Aortic regurgitation murmur | Decreased | |
| Mitral stenosis murmur | Increased | |
| Mitral regurgitation murmur | Decreased | |
| Hypertrophic cardiomyopathy murmur | Decreased | Not all hypertrophic cardiomyopathies have obstructive murmurs; helpful to confirm with echocardiography |
| Peripheral edema | Mild edema normally present | Asymmetric edema warrants further evaluation |
| Stigmata of Marfan syndrome | Risk for aortic dissection | |
| Stigmata of Turner syndrome | Risk for aortic dissection |
Resting heart rate is higher in pregnancy, and peripheral pulses are “well filled” with rapid upstroke and collapse, primarily owing to lower systemic vascular resistance (SVR). Central venous pressure remains unchanged during pregnancy, and any elevation of jugular venous pressure is an abnormal finding. Basilar rales may be heard on lung auscultation; however, these are no longer heard after deep inspiration, a brief breath-hold, or a cough. These evanescent rales likely result from basilar atelectasis.
The heart examination during pregnancy is altered as a result of uterine enlargement. Consequently, the point of maximum impulse (left ventricular apex) is displaced superiorly and laterally during advanced pregnancy. It remains crisp, well defined, and hyperdynamic. In thin women, the right ventricular impulse may become visible owing to an increase in circulating blood volume and the proximity of this chamber to the anterior chest wall.
Recognition of normal auscultatory changes helps distinguish pathologic from physiologic changes. New murmurs are heard in more than 90% of pregnant women. The loudest murmurs are heard between 15 and 25 weeks’ gestation; murmur intensity decreases toward term and increases again during labor and the early postpartum period. This peripartum increase in murmurs is followed by a gradual decrease; most of these pregnancy-associated murmurs are no longer appreciated by 6 weeks postpartum. Importantly, there is no correlation between the disappearance of physiologic murmurs of pregnancy and the return of cardiac output and blood volume to prepregnancy levels.
The first heart sound (S1) becomes louder and is widely split owing to early closure of the mitral valve during pregnancy. The second heart sound (S2) is unchanged. It is quite common to appreciate the third heart sound (S3), although considerable expertise and a quiet environment are necessary because of the presence of underlying tachycardia and an increased basal respiratory rate. The fourth heart sound (S4) is rarely appreciated. Owing to increased cardiac output and increased flow through cardiac valves, a systolic ejection murmur, usually soft (grade 2/6 to 3/6), is appreciated over the upper sternal border and the right side of the heart.
The murmurs of aortic and mitral regurgitation generally decrease and may become inaudible during pregnancy owing to the decrease in SVR. However, administration of phenylephrine or development of hypertension during pregnancy, both of which increase the SVR, increases the intensity of these murmurs.
The murmur associated with aortic stenosis increases in intensity during pregnancy from increased flow through the stenotic valve. A diminished carotid upstroke, soft or inaudible S2, and a grade 4/6 murmur are almost always indicative of severe aortic stenosis. An audible, physiologic split S2 almost invariably rules out severe aortic stenosis. Diastolic murmurs during pregnancy are almost always associated with an underlying pathologic process.
The murmur of hypertrophic cardiomyopathy may have decreased intensity because the pregnancy-associated increase in intravascular volume may result in decreased outflow tract obstruction. The murmur of an atrial septal defect may become more audible during pregnancy.
Mammary souffle (“soo-fuhl”) is a noncardiac sound; it describes the continuous hum heard over the breasts. It becomes audible during late pregnancy and lactation, and it disappears at the end of lactation.
Most pregnant women display some degree of peripheral edema, in part owing to uterine compression of the inferior vena cava, which impedes venous return. This physiologic edema is symmetric and decreases with leg elevation and the left lateral decubitus position. The pathologic edema of preeclampsia should be differentiated from the physiologic edema of pregnancy. Asymmetric lower extremity edema is almost invariably pathologic. A tender and warm lower extremity may suggest deep vein thrombosis or cellulitis.
Funduscopic examination in pregnancy may help differentiate chronic hypertension from hypertensive disease of pregnancy (preeclampsia/eclampsia) and may identify changes caused by long-standing diabetes.
It is important to look for stigmata of Marfan syndrome. Tall stature, large arm span, or other stigmata may alert the practitioner to the presence of a previously undiagnosed condition. Patients with Marfan syndrome frequently demonstrate scoliosis and may have dural ectasia. Turner syndrome is characterized by short stature and webbed neck. Both conditions predispose pregnant women to aortic dissection (see later discussion).
Cardiac Risk Prediction
The New York Heart Association (NYHA) and Heart Failure Stage classifications describe symptoms and predict risk in the nonpregnant population ( Box 41.1 ). Several classifications have been proposed to specifically predict cardiac risk during pregnancy, including the ZAHARA I (Zwangerschap bij vrouwen met een Aangeboren HARtAfwijking), CARPREG (CARdiac disease in PREGnancy), and modified World Health Association (WHO) risk scores ( Box 41.2 ). These classifications may help predict the individual pregnant woman’s cardiac risk and, combined with the clinical constellation and results of cardiac imaging, may help guide clinical management. When studied prospectively, the modified WHO classification outperformed the ZAHARA I and CAPREG risk scores. Implementation of a standardized and guideline-based approach to care, based on risk assessment, provides consistency in treating pregnant women with cardiac disease.
Classification of Heart Failure
Class I
No limitation of physical activity
Class II
Mild limitation of physical activity; regular physical activity causes symptoms
Class III
Marked limitation of physical activity; no symptoms at rest; minimal activity causes symptoms
Class IV
Symptoms at rest
Stages in the Development of Heart Failure
Stage A
At risk for heart failure but without structural heart disease or symptoms (e.g., hypertension, coronary artery disease, obesity)
Stage B
Structural heart disease but without signs or symptoms (e.g., previous myocardial infarction, asymptomatic valvular heart disease)
Stage C
Structural heart disease with prior or current symptoms of heart failure (e.g., known structural heart disease and symptoms)
Stage D
Refractory heart failure requiring specialized interventions (e.g., marked symptoms at rest with maximal medical therapy)
Class I (no increase or a mild increase in morbidity)
Mild pulmonic stenosis
PDA
Mitral valve prolapse
Repaired ASD, VSD, PDA, anomalous pulmonary venous return
Class II (small increase in maternal mortality, moderate increase in maternal morbidity)
Unrepaired ASD or VSD
Repaired tetralogy of Fallot
Most arrhythmias
Mild left ventricular dysfunction
Hypertrophic cardiomyopathy
Marfan syndrome without aortic dilation
Bicuspid aortic valve with aortic diameter < 45 mm
Class III (significant increase in maternal mortality and severe increase in maternal morbidity)
Mechanical valve(s)
Systemic right ventricle
Fontan circulation
Unrepaired cyanotic heart disease
Complex congenital heart disease
Marfan syndrome with aortic dilation 40 to 45 mm
Bicuspid aortic valve with aortic dilation 45 to 50 mm
Class IV (pregnancy is not recommended or is contraindicated)
Pulmonary arterial hypertension of any cause
Severe left ventricular dysfunction
Previous peripartum cardiomyopathy with residual left ventricular dysfunction
Severe mitral stenosis
Severe aortic stenosis
Marfan syndrome with aortic dilation > 45 mm
Bicuspid aortic valve with aortic dilation > 50 mm
Severe unrepaired aortic coarctation
PDA, Patent ductus arteriosus; ASD, atrial septal defect; VSD, ventricular septal defect.
Maternal cardiac disease is associated with an increased incidence of neonatal complications. The most widely accepted associations are cyanosis, NYHA functional class greater than II, presence of a mechanical valve prosthesis, heparin or warfarin use during pregnancy, multiple gestation, smoking during pregnancy, left-sided heart obstruction, and use of cardiac medications before pregnancy. At the current time, the risk-estimation models to predict neonatal events will require further refinement to afford clinical utility.
Cardiovascular Imaging during Pregnancy
Echocardiography
Echocardiography allows for safe and noninvasive assessment of heart structure and function. Both transthoracic and transesophageal echocardiography can be performed at any stage of pregnancy. Echocardiography helps predict overall cardiac risk and guides anesthetic management in pregnant women with cardiac disease. Echocardiography also allows assessment of intravascular volume and may obviate the need for right-sided heart catheterization to determine ventricular filling pressures. Contemporary evidence suggests that for most common cardiac conditions, handheld transthoracic echocardiography provides more accurate diagnosis than physical examination.
One of the most commonly used echocardiographic assessments of left ventricular function—left ventricular ejection fraction—remains unchanged during pregnancy. Echocardiographic measurements of cardiac output increase during pregnancy owing to increases in stroke volume and heart rate. Importantly, stroke work is increased during pregnancy, which is consistent with augmented myocardial fiber function. Both the right and left ventricular chamber size are increased in end-diastole and end-systole, and the heart becomes more globular. This increase in chamber size results in increased left ventricular end-systolic and end-diastolic volumes and is accompanied by an increase in left ventricular wall thickness (eccentric left ventricular hypertrophy). These parameters return to baseline within 3 to 6 months postpartum. Left ventricular end-diastolic and end-systolic volumes are further increased with multiple gestation; the stroke volume is increased an additional 15%. Combined with a small additional increase in heart rate, this change results in a 20% greater increase in maternal cardiac output with multiple gestation compared with singleton gestation.
Left atrial size is increased during pregnancy ; the increase is even greater with multiple gestation than with singleton gestation. Preeclampsia results in an adaptive concentric hypertrophy and an increase in left ventricular mass caused by increased afterload.
In normal pregnancy, left ventricular diastolic function is increased in the first two trimesters and declines in the third trimester. Twenty percent of women with preeclampsia have evidence of global diastolic dysfunction. Diastolic function is most commonly assessed echocardiographically by evaluating mitral valve inflow, pulmonary venous flow, and myocardial tissue motion (tissue Doppler imaging).
Cardiac Magnetic Resonance Imaging
The risks associated with magnetic resonance imaging (MRI) in pregnant women are similar to those in nonpregnant patients, and there is no evidence that MRI causes harm to the fetus. Similar to the use of all imaging modalities during pregnancy, cardiac magnetic resonance (CMR) imaging should be performed during pregnancy only after consideration of both the maternal and fetal benefits and risks. However, given the quality of images and diagnostic yield, CMR is preferable to any modality that uses ionizing radiation. Gadolinium crosses the placenta and has been found to be teratogenic in animal models. Currently available human data suggest that gadolinium should be used in pregnant women only if it significantly improves diagnostic performance and is expected to improve maternal or neonatal outcome.
Cardiac Catheterization
Coronary angiography remains the “gold standard” for diagnosis of coronary artery disease, and it can be performed at any time during pregnancy. Radial arterial access is preferable to femoral access because it is associated with earlier ambulation, increased patient comfort, and a significant reduction in access-related bleeding complications. Additionally, during the procedure, the left lateral decubitus position can be more easily maintained with radial access. Cardiologists should strictly adhere to the ALARA principle (as low as reasonably achievable) to limit both maternal and fetal ionizing radiation exposure.
The use of pulmonary artery catheterization has significantly declined in the United States in recent years. Similar information can be obtained noninvasively by transthoracic or transesophageal echocardiography. However, thermodilution and Fick cardiac output measurements can be obtained only with the use of a pulmonary artery catheter. Similarly, right-sided heart catheterization is required for vasoreactivity testing in patients with pulmonary hypertension.
Iodinated Contrast Use during Pregnancy
The use of iodinated contrast media in pregnant women appears safe. To date, there has been no report of fetal teratogenic or mutagenic effects after maternal administration of iodinated contrast media. Free iodide in the contrast medium administered to the mother may depress fetal, and subsequently neonatal, thyroid function. Therefore, it has been suggested that neonatal thyroid function be checked during the first week postpartum. Minimal amounts of iodinated contrast media are excreted in breast milk; even smaller amounts are absorbed by the neonate’s gastrointestinal tract. The slight potential risk associated with absorption of contrast medium is thought to be insufficient to recommend interruption of breast-feeding after maternal administration of iodinated contrast media.
Computed Tomographic Angiography
Multidetector computed tomography (CT) allows noninvasive imaging of the coronary arteries along with cardiac structure and function. Use of contemporary CT with aggressive dose-reduction techniques can significantly limit the radiation dose. The overall radiation dose of coronary CT angiography may be equivalent to, or even lower than, radiation doses delivered with conventional invasive coronary angiography. Although soft cardiac structures not seen by conventional coronary angiography are well visualized by CT angiography, the intravenous contrast medium load is greater with CT angiography, and coronary intervention cannot be performed at the time of imaging. Thus, in pregnancy, invasive coronary angiography appears preferable under most circumstances.
Ionizing Radiation Risks to the Fetus
The ionizing radiation dose to the fetus can be limited by the use of echocardiography, intracardiac echocardiography, reduced fluoroscopy frame rates, and contemporary image noise-reduction technology. Because the fetus is not directly within the radiation beam for cardiac procedures, the fetal exposure occurs through indirect scatter radiation. Therefore, external shielding of the fetus is ineffective. The fetal radiation dose cannot be measured and is therefore estimated; however, it is reassuring that the estimated fetal doses are low. Nonetheless, the safest approach is to avoid ionizing radiation during pregnancy if possible, and to assess both the maternal and fetal risks and benefits before deciding on the most appropriate imaging modality.
Cardiac Drugs and Pregnancy
Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE) inhibitors are the mainstay treatment of coronary artery disease, left ventricular dysfunction, and hypertension in nonpregnant patients. These drugs are particularly useful in nonpregnant patients with diabetes mellitus.
In the first trimester, the use of ACE inhibitors has been associated with an increased risk for fetal cardiovascular and central nervous system malformations. Use of ACE inhibitors during the second and third trimesters of pregnancy has also been associated with adverse fetal and neonatal outcomes as a result of the ACE inhibitors’ effect on fetal renal vascular tone. These drugs cause fetal kidney malfunction and decreased fetal urine output, which results in oligohydramnios. Positional limb deformities, skull ossification retardation, and lung hypoplasia are seen with ACE inhibitor–associated oligohydramnios. Thus, despite the exceptionally useful profile of ACE inhibitors in nonpregnant patients with cardiovascular disease, their use in pregnancy is contraindicated (see Chapter 14 ).
Angiotensin Receptor–Blocking Agents
Fewer data are available on the use of angiotensin receptor–blocking agents in pregnancy. Nonetheless, given the adverse outcomes associated with use of ACE inhibitors in pregnancy and the mechanism of action of angiotensin receptor–blocking agents, the use of these drugs is not recommended in pregnancy.
Beta-Adrenergic Receptor Antagonists
Beta-adrenergic receptor antagonists are often used for treatment of coronary artery disease, myocardial infarction, hypertension, many arrhythmias, and a wide spectrum of cardiomyopathies. There is no evidence that beta-adrenergic receptor antagonists are teratogenic. Prolonged and high-dose use of these drugs has been associated with fetal growth restriction; however, the overall risk is likely small. Neonatal bradycardia, hypotension, and hypoglycemia are rarely encountered.
Calcium Entry–Blocking Agents
First-trimester maternal use of verapamil and diltiazem is likely not teratogenic. Both drugs appear to be safe and effective treatments for cardiac arrhythmias in the second and third trimesters. The use of amlodipine, a dihydropyridine calcium entry–blocking agent, appears safe during pregnancy.
Other Drugs
Hydralazine is used in the treatment of cardiomyopathy and is also an excellent antihypertensive agent. It has a long track record of safe use during pregnancy.
The use of nitrates for treatment of angina during pregnancy appears safe. Nitrates likely can be safely used long term in pregnant women with cardiomyopathy.
Digoxin may be useful for the treatment of various cardiomyopathies and some arrhythmias. Digoxin freely crosses the placenta, but its use has not been associated with congenital abnormalities or untoward fetal effects. Digoxin’s pharmacokinetics are altered during pregnancy, and monitoring of blood levels is recommended.
Eptifibatide, tirofiban, and abciximab are potent intravenous platelet aggregation inhibitors (IIB/IIIA receptor inhibitors) used to inhibit platelet aggregation during percutaneous coronary intervention. Both the American Society of Regional Anesthesia and Pain Medicine (ASRA) and the European Society of Anaesthesiology (ESA) guidelines strongly advise avoidance of neuraxial anesthesia until platelet function has recovered after administration of these agents.
Statins interrupt cholesterol synthesis and result in a lowering of plasma cholesterol levels. The widespread use of statins (which are associated with exceptionally robust cardiovascular outcome data) has transformed the treatment of coronary artery disease. Nonetheless, given the critical importance of cholesterol synthesis in the normal development of the embryo and placenta, and thus their potential for teratogenicity, statins are contraindicated in pregnancy.
Thiazide diuretics do not appear to be teratogenic. Long-term use may result in a reduction in uteroplacental perfusion, which may be associated with fetal growth restriction and oligohydramnios. Neonatal hypoglycemia and thrombocytopenia have been reported.
Loop diuretics are likely not teratogenic. Similar to thiazide diuretics, fetal growth restriction may be associated with long-term use during pregnancy. Spironolactone is an aldosterone antagonist frequently used in the treatment of patients with congestive heart failure and cardiomyopathy, but because of its antiandrogenic potential its use during pregnancy is not recommended.
Aortic Diseases and Aortic Dissection
The cardiovascular changes of pregnancy may to lead to increased arterial wall tension and intimal shear forces. However, the full impact of pregnancy on changes in aortic wall structure is not fully understood. Estrogen-induced changes in collagen deposition, as well as circulating elastases and relaxin, may weaken the aortic media and thus predispose the aorta to dissection during pregnancy. Approximately one-half of aortic dissections and ruptures in women younger than 40 years of age are associated with pregnancy. Dissection of the ascending aorta (Stanford type A or DeBakey type I or II) is a surgical emergency, whereas dissection of the descending aorta (Stanford type B or DeBakey type III) is predominantly treated medically.
Conditions that predispose women to aortic dissection during pregnancy include Marfan syndrome, Ehlers-Danlos syndrome, bicuspid aortic valve, Turner syndrome, and non–Marfan syndrome–associated familial thoracic aneurysms. Aortic dissection has been associated with preeclampsia and chronic hypertension in pregnancy. Most aortic dissections that occur during pregnancy are type A (ascending aorta); the average aortic diameter at the time of dissection is 4.8 cm. The majority of dissections occur in the third trimester of pregnancy, but aortic dissections may also occur at the time of delivery or in the early postpartum period. It has been hypothesized that contraction of the uterus causes outflow resistance, thus predisposing to aortic dissection after delivery.
Marfan Syndrome
Marfan syndrome is an autosomal-dominant connective tissue disorder. The penetrance is high, but the expression is variable. Marfan syndrome is caused by a mutation in the FBN1 gene encoding fibrillin-1, a glycoprotein. Sporadic mutations are seen in approximately 25% of patients without a family history of this syndrome. Aortic dilation and aortic dissection contribute significantly to cardiovascular complications in these patients. In addition to aortic disease, affected patients often have valvular disease (e.g., aortic regurgitation, mitral regurgitation, mitral valve prolapse). Aortic dissection has been observed during pregnancy and in the peripartum period. Most patients have type A aortic dissection; type B aortic dissection and abdominal aortic aneurysm are less commonly seen.
Based on observational studies, current guidelines recommend that women with Marfan syndrome who are planning pregnancy undergo replacement of the ascending aorta and the aortic root if the diameter is greater than 4.0 cm (class IIa, level of evidence C). The aortic root dilation rate increases during pregnancy and does not return to baseline after delivery. Subsequent pregnancies further increase the aortic dilation rate.
Aortic Disease Associated with a Bicuspid Aortic Valve
Bicuspid aortic valve has been associated with dissection during pregnancy. Affected women are slightly younger, and the dissection occurs earlier in pregnancy than in patients with Marfan syndrome. Because the disease is familial, first-degree relatives of patients with a bicuspid aortic valve should be screened for this disease.
Ehlers-Danlos Syndrome
Ehlers-Danlos syndrome is an inherited connective tissue disorder. Ehlers-Danlos syndrome type IV has been associated with severe complications and maternal mortality. Rupture of the bowel, aorta, vena cava, and uterus may occur. Pregnancy outcomes in patients with Ehlers-Danlos syndrome types I, II, and III are generally favorable, although these women may have a higher incidence of pelvic instability, preterm delivery, perineal lacerations, and postpartum hemorrhage than the general population.
Turner Syndrome
Turner syndrome is caused by complete or partial absence of an X chromosome. In addition to short stature, webbed neck, and characteristic facial features, Turner syndrome is associated with aortic coarctation and hypertension. Approximately 30% of patients with Turner syndrome have a bicuspid aortic valve. During pregnancy, the syndrome is associated with aortic dissection. Preconception echocardiographic evaluation of patients with Turner syndrome is recommended. Given the frequent aortic abnormalities in these patients, preconception MRI is also recommended. Because of short stature in some patients with Turner syndrome, absolute aortic root measurements may not accurately predict the risk for aortic dissection. Cesarean delivery is frequently required in these patients because of cephalopelvic disproportion.
Aneurysm-Osteoarthritis Syndrome
Aneurysm-osteoarthritis syndrome is a recently described autosomal-dominant condition caused by mutations in the SMAD3 gene. Mutations in the SMAD3 gene lead to increased aortic expression of several components in the TGF-β pathway and subsequent aneurysm formation. In addition, visceral and iliac aneurysms, arterial tortuosity, and early-onset joint abnormalities may be present. In a cohort of 17 patients and 34 pregnancies, no maternal mortality or aortic dissection was observed. Cesarean delivery was performed for mainly obstetric indications without increased bleeding complications. The type of anesthesia was not reported.
Obstetric and Anesthetic Management
Given the inherent risk for aortic dissection, parturients with aortic disease should deliver in a center that has immediate access to a cardiothoracic surgeon with expertise in aortic endovascular repair techniques. Current guidelines are based on expert opinion, case reports, and current standard of care (level C evidence) ( Box 41.3 ; Table 41.2 ). The 2010 American College of Cardiology (ACC) Foundation/American Heart Association (AHA) guidelines recommend the following for pregnant women with chronic aortic dilation: (1) strict blood pressure control; (2) monthly or bimonthly echocardiographic measurement of aortic dimension; (3) cesarean delivery in women with significant aortic enlargement, dissection, or severe aortic valve regurgitation; and (4) prophylactic surgery in the setting of progressive aortic dilation and/or advancing aortic valve regurgitation.
a All recommendations are Level of Evidence C (very limited populations have been evaluated, and recommendations are based on consensus opinion of experts, case studies, or standard of care).
Class I b
b Class I: Procedure/treatment should be performed/administered; Class IIa: It is reasonable to perform procedure/administer treatment; Class IIb: Procedure/treatment may be considered.
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Women should be counseled about the risk for aortic dissection as well as the heritable nature of the disease before pregnancy.
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Strict blood pressure control, specifically to prevent stage 2 hypertension, is recommended. c
c Stage 2 hypertension: blood pressure ≥ 160/100 mm Hg.
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Monthly or bimonthly echocardiographic measurements of the ascending aortic dimensions are recommended to detect aortic expansion.
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For imaging of pregnant women, magnetic resonance imaging (without gadolinium) is recommended over computed tomography to avoid both maternal and fetal radiation exposure. Transesophageal echocardiography is an option for imaging of the thoracic aorta.
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Women should be delivered in a center where cardiothoracic surgery is available.
Class IIa b
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Cesarean delivery is reasonable for patients with significant aortic enlargement, dissection, or severe aortic valve regurgitation.
Class IIb b
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If progressive aortic dilation and/or advancing aortic valve regurgitation is documented, prophylactic surgery may be considered.
| Disease | Modifier | Anesthetic Considerations | Monitoring |
|---|---|---|---|
| Ascending aortic dilation/aneurysm | Bicuspid aortic valve Marfan syndrome Turner syndrome | Meticulous attention to blood pressure control Maintain beta-adrenergic receptor antagonist therapy Possible dural ectasia (Marfan syndrome) may increase risk for failed spinal anesthesia | Low threshold for invasive blood pressure monitoring |
| Unrepaired ASD | PAP < 40 mm Hg | Pregnancy/labor usually well tolerated Meticulous attention to de-airing all venous access tubing Consider potential for air embolism with loss-of-resistance-to-air epidural technique | |
| PAP ≥ 40 mm Hg | High-risk group Maintain preload Positive-pressure ventilation decreases preload and increases intrathoracic pressure, which is deleterious to RV function | Low threshold for invasive blood pressure monitoring and central venous access/filling pressure monitoring | |
| Repaired ASD | PAP < 40 mm Hg | Pregnancy well tolerated | |
| PAP ≥ 40 mm Hg | High-risk group Maintain preload Positive-pressure ventilation decreases preload and increases intrathoracic pressure, which is deleterious to RV function | Low threshold for invasive blood pressure monitoring and central venous access/filling pressure monitoring May require pulmonary vasodilators | |
| Unrepaired or repaired VSD | PAP < 40 mm Hg | Pregnancy well tolerated | |
| PAP ≥ 40 mm Hg | High-risk group | Invasive blood pressure monitoring Central venous access/filling pressure monitoring May require pulmonary vasodilators | |
| Patent ductus arteriosus | Pregnancy well tolerated | Echocardiographic evaluation to rule out pulmonary hypertension (rare) | |
| Fontan repair | Meticulous attention to preload; low and high preload poorly tolerated Positive-pressure ventilation poorly tolerated because increased intrathoracic pressure impedes venous return | Continuous telemetry monitoring indicated because of high incidence of arrhythmias | |
| Transposition of the great arteries | Complete/repaired | Caution with preload because of propensity for RV dysfunction Meticulous attention to preload in early postpartum period | Low threshold for central venous access/filling pressure monitoring in patients with RV dysfunction Continuous telemetry monitoring indicated because of high incidence of arrhythmias |
| Congenitally corrected | Pregnancy well tolerated | Echocardiographic assessment of ventricular function is helpful | |
| Ebstein’s anomaly | Pregnancy well tolerated with normal RV function May have associated ASD detected by echocardiography (see above for ASD considerations) | Low threshold for continuous telemetry monitoring because of high incidence of arrhythmias | |
| Tetralogy of Fallot (repaired) | Pregnancy well tolerated | Echocardiographic assessment of RV structure and function and evidence of pulmonary hypertension | |
| Pulmonary hypertension | Mild-moderate | Attention to preload | Low threshold for central venous access/filling pressure monitoring |
| Severe | Very high-risk group Maintain SVR Maintain preload/venous return Prevent/treat pain, hypoxemia, hypercarbia, and acidosis Avoid myocardial depression | Multidisciplinary approach Echocardiography May require pulmonary vasodilators Invasive blood pressure monitoring Central venous access/filling pressure monitoring Caution with pulmonary artery catheterization without fluoroscopic guidance | |
| Aortic stenosis | Transvalvular gradient < 25 mm Hg, valve area > 1.5 cm 2 , normal LV function | Neuraxial anesthesia generally well tolerated Attentive preservation of preload and afterload Monitor closely for volume overload during the first 24 hours after delivery | Low threshold for invasive blood pressure monitoring |
| Transvalvular gradient ≥ 25 mm Hg, valve area < 1.0 cm 2 , LV dysfunction | High-risk group Consider risks/benefits of neuraxial versus general anesthesia Avoid myocardial depressants and vasodilators Meticulously maintain preload and afterload Avoid abrupt decrease in SVR with sympathectomy Maintain sinus rhythm Address new-onset atrial fibrillation (rate control, consider cardioversion) Monitor very closely for volume overload during first 24 hours after delivery | Low threshold for invasive blood pressure monitoring and central venous access/filling pressure monitoring | |
| Mitral stenosis | Valve area > 1.5 cm 2 , no pulmonary hypertension | Neuraxial anesthesia generally well tolerated Maintain sinus rhythm and prevent tachycardia Increase in preload not well tolerated Address new-onset atrial fibrillation (rate control, consider cardioversion) Monitor closely for volume overload during first 24 hours after delivery | Low threshold for central venous access/filling pressure monitoring |
| Valve area ≤ 1.5 cm 2 , pulmonary hypertension | High-risk group Consider percutaneous mitral valvuloplasty before labor/delivery Maintain sinus rhythm and prevent tachycardia Increase in preload not well tolerated Address new-onset atrial fibrillation (rate control, consider cardioversion) Prevent/treat pain, hypoxemia, hypercarbia, and acidosis | Low threshold for invasive blood pressure monitoring and central venous access/filling pressure monitoring | |
| Pulmonary stenosis | Mild-moderate | Pregnancy well tolerated | |
| Severe | High-risk group Consider balloon valvuloplasty Prevent tachycardia Mitigate increase in pulmonary artery resistance (e.g., hypoxemia, positive-pressure ventilation) | Low threshold for invasive blood pressure monitoring and central venous access/filling pressure monitoring | |
| Hypertrophic cardiomyopathy | Without LVOT obstruction | Pregnancy well tolerated | |
| With LVOT obstruction | Maintain beta-adrenergic receptor antagonist therapy Low preload and low afterload worsen outflow gradient Treat hypotension with phenylephrine Maintain sinus rhythm and prevent tachycardia Address new-onset atrial fibrillation (rate control, consider cardioversion) | Low threshold for invasive blood pressure monitoring and central venous access/filling pressure monitoring Echocardiography helpful to follow outflow tract gradient | |
| Cardiac tamponade | Meticulous attention to preload Maintain spontaneous ventilation Positive-pressure ventilation is deleterious to preload Volatile anesthetic agents depress ventricular function | Invasive blood pressure monitoring Central venous access/filling pressure monitoring |
All patients with Marfan syndrome should receive beta-adrenergic receptor antagonist therapy throughout pregnancy to decrease the rate of aortic dilation. The risk for major aortic complications during pregnancy appears low if the aortic root diameter is less than 4.0 cm. In the event of a type A aortic dissection in the first or second trimester, surgical repair should be performed with the knowledge of fetal risk during hypothermic circulatory arrest. If the dissection occurs in the third trimester and the fetus is deemed viable, an urgent cesarean delivery followed by aortic surgery may be performed.
Both neuraxial and general anesthesia may be safely performed in these patients, with emphasis on meticulous blood pressure stability and control. Invasive blood pressure monitoring is recommended to facilitate tight hemodynamic control. Dural ectasia and scoliosis may complicate neuraxial anesthetic techniques in parturients with Marfan syndrome. The increase in lumbar cerebrospinal fluid volume associated with dural ectasia may cause unpredictable and inadequate spread of intrathecal local anesthetic solutions; thus, it may be prudent to obtain lumbar spine MRI before planned pregnancy.
Congenital Heart Disease
Atrial Septal Defect
Patients with an atrial septal defect may remain asymptomatic until the fourth decade of life. Not infrequently, women with an atrial septal defect may become symptomatic during pregnancy. The most common defect is the secundum-type atrial septal defect (80%), whereas the primum, sinus venosus, and coronary sinus types of atrial septal defect are less common. Right ventricular overload leads to pulmonary hypertension and Eisenmenger syndrome in less than 5% of patients with an atrial septal defect. In women with both an atrial septal defect and Eisenmenger syndrome, pregnancy carries a significant risk for both maternal and fetal mortality, and is not recommended. In the absence of pulmonary hypertension, pregnancy is overwhelmingly well tolerated in women with an atrial septal defect.
Cardiac complications are similar in women with unrepaired and repaired atrial septal defects. Preeclampsia, fetal demise, and small-for-gestational-age infants are more common in pregnant women with an unrepaired atrial septal defect than in the general obstetric population. Pregnant women with an atrial septal defect are more likely to develop supraventricular and ventricular arrhythmias than women who are not pregnant.
The risk for paradoxical embolism is increased in patients with an unrepaired atrial septal defect. It is critically important to ensure that intravenous catheters are de-aired. Transesophageal echocardiography demonstrates the presence of microbubbles in the right-sided cardiac chambers within 15 seconds of the epidural injection of air or fluid. Therefore, it seems prudent to avoid using the loss-of-resistance-to-air technique to identify the epidural space (see Table 41.2 ). Both neuraxial and general anesthesia are appropriate for patients with a repaired or unrepaired atrial septal defect.
Ventricular Septal Defect
There are four types of ventricular septal defects; the most common type is a perimembranous ventricular septal defect. Pregnancy is well tolerated in women with a repaired ventricular septal defect or a small ventricular septal defect in the absence of pulmonary hypertension. An unrepaired ventricular septal defect with Eisenmenger syndrome is associated with a high risk for maternal cardiac complications (see later discussion). Pregnancy is not recommended in patients with a ventricular septal defect and Eisenmenger syndrome. Preeclampsia is encountered more frequently in women with an unrepaired ventricular septal defect. Echocardiography allows assessment of right-sided pressures and shunt fraction.
Patent Ductus Arteriosus
Pregnancy is well tolerated in patients with patent ductus arteriosus, and complications are rare. A left-to-right shunt may cause pulmonary hypertension. Pregnancy is not recommended in women with patent ductus arteriosus with Eisenmenger syndrome.
Coarctation of the Aorta
Women with repaired coarctation of the aorta tolerate pregnancy well. Systemic arterial hypertension is often observed during labor. The coarctation may be associated with a bicuspid aortic valve in more than half the patients. Prepregnancy evaluation of the coarctation, including the residual degree of obstruction and associated anomalies (e.g., bicuspid aortic valve), is recommended.
Vaginal delivery with neuraxial anesthesia is the preferred mode of delivery; cesarean delivery is reserved for obstetric indications. Epidural anesthesia has been successfully administered in a patient with an uncorrected coarctation. One report described the use of remifentanil to control blood pressure during administration of general anesthesia for cesarean delivery.
Fontan Repair
The Fontan repair is a surgical procedure that establishes blood flow from the venous system to the pulmonary artery by bypassing the right ventricle ( Fig. 41.1 ). It can be performed for valvular defects such as tricuspid or pulmonic atresia, or other anomalies with a single ventricle. Because there is no functional right ventricle, blood flow from the periphery to the lungs occurs at very low pressure gradients. Owing to the presence of surgical scar tissue in the atrium, patients with a Fontan repair are prone to supraventricular and, less commonly, ventricular arrhythmias. The Fontan repair is associated with the highest prevalence of arrhythmias during pregnancy of any congenital heart condition. Deterioration in the NYHA functional status during pregnancy can occur.
Administration of neuraxial analgesia/anesthesia for labor and vaginal delivery and emergency cesarean delivery has been described. Administration of neuraxial anesthesia, with meticulous attention to maintenance of normal intravascular preload, appears to be the preferred anesthetic technique for cesarean delivery. Use of neuraxial anesthesia avoids the adverse effects of myocardial depression and positive-pressure ventilation on the Fontan circulation, which lacks a functioning right ventricle (see Table 41.2 ).
Transposition of the Great Arteries
Transposition of the great arteries comprises two distinct groups: complete transposition of the great arteries (d-transposition) and congenitally corrected transposition of the great arteries (l-transposition). In both conditions, the aorta originates from the right ventricle and the pulmonary artery originates from the left ventricle. Complete transposition of the great arteries manifests as neonatal cyanosis.
Pregnant women born with d-transposition of the great arteries have undergone surgical correction—traditionally an atrial switch procedure (Senning or Mustard) or the more contemporary arterial switch procedure (Jatene or Rastelli). In the atrial switch procedure, the right ventricle functions as the systemic ventricle. Atrial arrhythmias, right ventricular (systemic ventricle) dysfunction, tricuspid regurgitation (systemic atrioventricular valve), atrial baffle obstruction or leaks, and pulmonary hypertension are some of the long-term complications of the traditional atrial switch surgical repair of d-transposition of the great arteries. The advantage of the Jatene and Rastelli procedures is that the left ventricle functions as the systemic ventricle. However, myocardial ischemia may occur after arterial switch operations, because the coronary arteries are reimplanted during these procedures.
All women with repaired d-transposition of the great arteries require detailed echocardiography and, ideally, CMR imaging before planned pregnancy. Owing to the propensity for arrhythmias in these patients, continuous telemetry monitoring during labor and delivery seems appropriate. Women who have undergone the Mustard operation tolerate pregnancy well ; however, there is a risk for right ventricular dysfunction that may be irreversible. The physiologic changes of pregnancy and/or the natural progression of disease result in an increased right ventricular volume in pregnant women who have undergone a Mustard procedure. There are limited data about pregnancy in patients who have undergone an arterial switch operation. Overall, pregnancy outcomes after arterial switch operations appear favorable.
Patients with congenitally corrected transposition (l-transposition) of the great arteries tolerate pregnancy well. Thorough echocardiographic evaluation before and throughout pregnancy is advisable.
Both neuraxial and general anesthesia appear to be reasonable options for parturients with surgically corrected and congenitally corrected transposition of the great arteries (see Table 41.2 ). Successful cesarean delivery with general anesthesia has been reported in a parturient with d-transposition of the great arteries corrected with a Jatene procedure.
Ebstein’s Anomaly
In Ebstein’s anomaly, the tricuspid valve is displaced toward the apex of the right ventricle, which results in severe tricuspid regurgitation and right atrial enlargement ( Figs. 41.2 and 41.3 ). It is commonly associated with an atrial septal defect and preexcitation syndromes. Accessory pathways result in arrhythmias in approximately 30% of patients; the most commonly observed arrhythmias include atrial tachycardia, atrial flutter, and atrial fibrillation. Pregnancy appears to be well tolerated in patients with Ebstein’s anomaly, especially in women with preserved ventricular function (see Table 41.2 ). Patients with a concomitant atrial septal defect and cyanosis have an increased risk for fetal loss and low infant birth weight.
Related posts:
Patient Safety and Team Training
Systemic Analgesia: Parenteral and Inhalational Agents
Anesthesia for Cesarean Delivery
Maternal Mortality
Psychiatric Disorders
Practice Guidelines for Obstetric Anesthesia: an Updated Report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia and the Society for Obstetric Anesthesia and Perinatology
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