Cardiovascular Disease
Mladen I. Vidovich MD, FACC, FSCAI
Chapter Outline
CARDIOVASCULAR PHYSIOLOGIC CHANGES OF PREGNANCY
CARDIAC EXAMINATION DURING PREGNANCY
CARDIOPULMONARY RESUSCITATION DURING PREGNANCY
Evidence suggests that gender 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,1 and women frequently develop more diffuse atherosclerosis than men. Female aortas appear to be stiffer due to 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.2 Women with acute myocardial infarction more frequently do not have chest pain, especially women who have the infarction at a younger age. In-hospital mortality for acute myocardial infarction is higher for women than for men.3 Although women who have non–ST-segment elevation myocardial infarction have a worse risk profile than men, the infarction is frequently treated less aggressively.4 Yet women are more likely than men to summon emergency medical services during a myocardial infarction.
Whether women have worse outcome after percutaneous coronary intervention has been a matter of debate.5 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.5 Older studies demonstrated worse overall outcome in women than in men; however, more recent studies have demonstrated a narrowing or disappearance of the gender outcome gap. Similarly, several studies have demonstrated that female gender was an independent predictor of coronary artery bypass (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.
The number of pregnancies has been associated with the future risk for coronary artery disease6 and progression of atherosclerosis.7 Hypertensive disorders of pregnancy, preeclampsia, and gestational diabetes mellitus are risk factors for future development of cardiovascular disease.8,9 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 the 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 due to hemorrhage and hypertensive disorders of pregnancy has declined, whereas mortality due to cardiovascular conditions has steadily increased.10
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.11 Exercise in healthy pregnant women does not cause distinctive ECG changes when 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.12,13 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.14
Left ventricular mass increases during normal pregnancy.15,16 The increase in left ventricular mass is greater in multiple gestation than in singleton gestation.17 Preeclampsia also results in a greater increase in left ventricular mass.18
Plasma lipid concentrations, including total serum cholesterol, triglycerides, and low-density lipoprotein cholesterol concentrations, increase during pregnancy.19 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 unchanged (< 20 pg/mL).20 The lack of change in BNP levels during normal pregnancy suggests that the heart adapts to the increased volume load associated with pregnancy. By contrast, BNP levels are increased in preeclamptic women20 and in pregnant women with heart disease.21 A correlation exists between BNP and the increases in left ventricular mass and end-diastolic and end-systolic volumes observed in preeclampsia.18 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.22,23 BNP is elevated in women with complex congenital heart disease, but it varies considerably among anomalies. Therefore, its use for individual patient management remains unclear.24
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.25 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.26,27 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 Figure 47-1). Thus, elevated CK-MB levels are not specific for the diagnosis of myocardial infarction during pregnancy.27,28 In patients with preeclampsia who have concurrent myocardial infarction, the observed troponin levels are higher than expected for the underlying preeclampsia.29 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 Figure 2-1). 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 42-1).
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). The 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.30 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.31
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 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.32
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 due to 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)33 and Heart Failure Stage34 classifications describe symptoms and predict risk in the nonpregnant population (Box 42-1). Several classifications have been proposed to specifically predict cardiac risk during pregnancy (Boxes 42-2, 42-3, and 42-4).35–38 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.35,37–39 Implementation of a standardized and guideline-based approach to care, based on risk assessment, provides consistency in treating pregnant women with cardiac disease.
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.35,39
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.
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.40 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.17
