Cardiac disease in pregnancy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Anjan K. Chakrabarti, M.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]

Approximately 1-4% of pregnancies in the United States occur in women with maternal cardiovascular disease. In fact, pregnancy can “unmask” underlying cardiovascular disease, due to the hemodynamic changes associated with pregnancy. ^[1] With a careful pre-pregnancy evaluation, most women with cardiovascular disease can carry a pregnancy to term with proper care.

There are significant hemodynamic changes associated with pregnancy that begin early, reach their peak during the second trimester, and persist through delivery. These changes include a 40% increase in blood volume expansion, reductions in both the systemic vascular resistance and pulmonary vascular resistance, a 30% rise in cardiac output and little change in the blood pressure. These changes can have a significant impact on both the mother and the fetus, particularly when there are maternal cardiac disorders.

Increasing numbers of women with congenital heart disease are now reaching childbearing age, making congenital heart disease the most common form of heart disease complicating pregnancy in the United States. Rheumatic heart disease is still prevalent in the developing world and in immigrant populations. Overall, maternal death during pregnancy in women with heart disease is rare, but certain conditions are associated with an increased mortality.^[2]

Maternal cardiovascular disease includes (most commonly) congenital heart disease. Other cardiovascular disorders encountered during pregnancy include cardiomyopathies, both dilated and hypertrophic, and valvular heart disease, such as bicuspid aortic valve and mitral valve prolapse. Less common cardiovascular disorders include pulmonary hypertension and, rarely, coronary artery disease. The above cardiovascular disorders require a strategy regarding the frequency of follow-up by the cardiologist and a plan for labor and delivery.^[3]

The following clinical characteristics are independent predictors of adverse outcomes in a risk score for maternal cardiac complications^[4]:

• Prior cardiac events or arrhythmia
• Poor functional class or cyanosis
• Left ventricular outflow tract obstruction
• Left ventricular systolic dysfunction

Pulmonary hypertension is a well recognized risk factor during maternal pregnancy. In particular the presence of Eisenmenger syndrome places the mother particularly high risk.

A history should be taken to assure that the patient does not have a condition that would place them at high risk during the pregnancy such as Marfan’s syndrome, Eisenmenger’s syndrome, congestive heart failure, a prior history of peripartum cardiomyopathy or pulmonary arterial hypertension.

Common symptoms present during pregnancy include: fatigue, decreased exercise capacity, hyperventilation, dyspnea, tachycardia and palpitations.

Secondary to inferior vena caval compression by the gravid uterus resulting in reduced venous return from the lower extremities, patients may even experience orthostatic lightheadedness and syncope.

Pedal edema is often observed during the last trimester and may lead to an erroneous diagnosis of heart failure.

Normal physical exam signs of pregnancy include an “innocent” systolic flow murmur in 96% of patients due to the hyperdaynamic circulation, a diastolic murmur in 18% of patients, jugular venous distension and a displaced cardiac apex due to volume expansion, an S₃ in 84% of patients, an occasional S₄, varicose veins and pedal edema.

The common electrocardiographic findings that occur secondary to physiological changes during pregnancy include: tachycardia, short PR interval and left axis deviation.

Echocardiograhy does not carry the risk of fetal irradiation and is a safe and a preferred screening method to assess cardiac function and valvular lesions.

Performance of routine chest x-rays should be avoided, especially in the first trimester of pregnancy. A chest x ray may be indicated in the pregnant patient with dyspnea ^[5] or cough ^[5]. Among patients with dyspnea, a chest x-ray may be obtained to eavluate the patient for the presence of heart failure due to peripartum cardiomyopathy. In this scenario, the chest x ray may show cardiomegaly, Kerley B lines, pleural effusion and cephalization of blood vessels.

There are no known safety hazards associated with the performance of an MRI, especially after the first trimester.^[6] However, data evaluating the safety of MRI during pregnancy is limited and an MRI is indicated only when other imaging modalities such chest x-ray and echocardiography are inconclusive.^[7] Currently, the FDA recommends prudent use of MRI during pregnancy.

Contrast MRI using gadolinium is contraindicated as gadolinium crosses the trans-placental membrane and exposes the fetus to teratogenicity.

The preferable estimated fetal exposure from ionizing radiation should be below 50 mGy and with CT, the exposed radiation is 0.3 mGy and therefore contra-indicated during pregnancy.^[8]

The only exception for the use of CT during pregnancy include to diagnosis pulmonary embolism, for which a low-radiation CT is recommended.^[9][10]

The preferred route of delivery is vaginal, but indications for a C-section include:

• Traditional obstetric indications
• Warfarin anticoagulation
• Severe pulmonary hypertension
• In the presence of fixed obstructive congenital lesions sudden BP changes may be dangerous
• Unstable aorta

If a pregnant patient is radiated with less than five rads, then they can be reassured that there is a very low likelihood of risk. If a pregnant patient is exposed to more than 15 rads, termination of the pregnancy is recommended. A routine chest x-ray is associated with radiation of 20 millirads to the chest. Standard fluoroscopy delivers 1-2 rads per minute. Cineangiography delivers 5-10 rads per minute. Only 5% of the radiation delivered is absorbed by the fetus. A lead apron should be used over the mother’s pelvis to minimize the risk of radiation exposure. With the use of nuclear medicine procedures the radiopharmaceuticals collect in the bladder which is in close proximity to the placenta and is directly across from the fetus. The expected radiation with thallium-201 or Tc imaging is less than one rad per examination.

Absolute and relative contraindications to pregnancy include severe pulmonary arterial hypertension; severe fixed valve stenoses (AS,MS,PS,HOCM, coarctation; Class III or IV congestive heart failure with a left ventricular ejection fraction of < 40%; a history of peripartum cardiomyopathy; a dilated aorta such as in Marfan’s syndrome with an aortic arch >40-45 mm; and severe cyanosis.

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Anjan K. Chakrabarti, M.D. [3]; Lakshmi Gopalakrishnan, M.B.B.S. [4]

There are significant hemodynamic changes associated with pregnancy that begin early, reach their peak during the second trimester, and persist through delivery. These changes include a 40% increase in blood volume expansion, reductions in both the systemic vascular resistance and pulmonary vascular resistance, a 30% rise in cardiac output and little change in the blood pressure. These changes can have a significant impact on both the mother and the fetus, particularly when there are maternal cardiac disorders.

• During early stages of pregnancy, prior to full placentation, progesterone is produced by the corpus luteum.
• Increased progesterone decreases smooth muscle tone which decreases the systemic vascular resistance (SVR).^[1]

• Elevated estrogen levels may increase myocardial contractility.^[2]

• Peripheral vasodilation subsequently causes renal vasodilation and activation of the renin-angiotensin-aldosterone system,^[1] which results in:

• Increased sodium and water retention.
• Compensation for the decreased systemic vascular resistance.

• Increased renin and aldosterone levels are caused by increased estrogen

• Plasma volume expansion starts as early as 6-weeks of gestation and is increased to approximately 40-45% by the mid trimester.
• Plasma volume expansion → hemodilution → anemia
• Despite the development of anemia, the total red cell mass is not decreased because the rate of rise in plasma volume is more than rate of rise in red cell mass. This occurs until 30-weeks of gestation and is referred to as the physiologic anemia of pregnancy.
• The hematocrit may drop to 33-38%.^[3]
• A greater increase in blood volume may be observed among multigravidas.^[3]
• An increase in atrial natriuretic peptide levels is observed in response to changes in intravasular volume.^[1]

• There is a higher volume of more dilute blood to circulate.^[2]
• There is approximately a 50% increase in cardiac output which is required to oxygenate the fetus.
• The increase in cardiac output begins as early as the 5^th week of gestation and steadily increases up to the 24^th week of gestation after which time it plateaus.^[2][4]

• The initial increase in cardiac output is attributed to an increase in stroke volume, whereas during late trimesters, it is attributed to an increase in heart rate and a reduction in systemic vascular resistance.^[2]

• Increase in resting heart rate by 10 to 15 beats per minute is observed during the first and second trimester suggesting an initial increase in venous return.^[2] Higher rates of increase in heart rate is observed with multiple gestation.

• Several factors influence the changes observed in cardiac output during pregnancy. Serial hemodynamic measurements performed in the supine position may be erroneous secondary to the compression of the inferior vena caval by the enlarging uterus which subsequently decreases the venous return from the lower extremities. Therefore, owing to the caval compression, cardiac output has been shown to decline in the supine position whereas the cardiac output increases in the left lateral position.^[5][6]

• Precipitation of high cardiac output failure may be observed in some patients secondary to the shunting of blood within the placenta where it may pass from arterioles to venules bypassing the capillaries.

• Arterial blood pressure begins to fall during the first trimester, reaching a nadir during the mid trimester (usually 10 mm Hg below baseline) and returns toward pre-gestational levels before term.^[7][8]

• A widened pulse pressure is present because there is a more substantial reduction in the diastolic blood pressure when compared with the systolic blood pressure.

• A drop in the blood pressure is caused by a decline in systemic vascular resistance secondary to reduced vascular tone.^[9][10] This is mediated by gestational hormone activity, increased circulating levels of prostaglandins and atrial natriuretic peptides,^[1] as well as endothelial nitric oxide.^[11][12]

• The blood pressure remains relatively unchanged when measured in the left lateral recumbent position. However, the supine hypotensive syndrome of pregnancy occurs in approximately 11% of pregnant women and is often associated with weakness, lightheadedness, nausea, dizziness and even syncope. Acute compression of the inferior vena cava by the gravid uterus is a possible explanation for this syndrome. Symptoms usually subside when the patient changes from the supine position.^[13]

• An increased respiratory rate is present secondary to increased abdominal pressure and accompanying elevation of the diaphragm.
• An increased respiratory rate subsequently lowers the carbon dioxide tension.

• Reduced gastric emptying secondary to reduced gastrointestinal motility is observed during pregnancy.

• An incompetent gastro-oesophageal sphincter leads to gastro-oesophageal reflux with an increased risk of aspiration of gastric contents into the trachea.

• Intra-gastric pressure increases during the last trimester.^[14]

• There is an increase in clotting factor concentration
• There is an increase in platelet adhesiveness
• There is a decrease in fibrinolysis and protein S activity
• As a result of all of the above, there is an increased risk of thormbosis and embolism

• Flared ribs.
• Breast hypertropy which may impede effective resuscitation.^[15]

• Hemodynamics are altered substantially during labor and delivery secondary to increased sympathetic tone caused by anxiety, pain, and uterine contractions.

• These changes include:

• Oxygen consumption increases by threefold.
• Cardiac output rises progressively during labor owing to an increase in both stroke volume and heart rate. The work of labor has also shown to increase cardiac output by 60% over the baseline.
• Blood pressure is higher in the left lateral position. During uterine contractions, a marked increase in both the systolic and diastolic blood pressure is observed with a greater augmentation during the second stage of labor. The form of anesthesia impacts the blood pressure.^[16]

• During the second stage of labor, an increase in venous stasis, heart rate (greater than 120 beats/min) and blood pressure (more than 150 mmHg) is observed.^[17]

• By the time of delivery, cardiac output has increased by 50%, the plasma volume has increased by 40% and the red cell mass has increased by 25% to 30%.

• Immediately following delivery, the uterus contracts and delivers a sudden bolus of 500-750 cc of blood to the circulatory system which may result in pulmonary edema in patients with coronary heart disease.

• To avoid the hemodynamic changes associated with vaginal delivery, cesarean section is frequently recommended for women with cardiovascular disease.

• Cesarean section is also associated with hemodynamic fluctuations that are related to intubation, analgesia and the choice of anesthesia. Most common form of anesthesia used is epidural which significantly reduces pain but is also associated with significant peripheral vasodilation and subsequent hypotension.

• Cesarean section is associated with greater extent of blood loss as well as provides relief of caval compression.^[18]

• There can be a temporary increase in venous return immediately after delivery due to relief of caval compression in addition to blood shifting from the contracting uterus into the systemic circulation.^[19]

• Effective increase in venous return and blood volume, despite the blood loss occurred during delivery, results in a substantial increase in ventricular filling pressures, stroke volume, and cardiac output that may lead to clinical deterioration.

• Both heart rate and cardiac output return to pre-gestational values by an hour after delivery. However, it takes about 24-hours for the blood pressure and stroke volume to return to baseline.

• Hemodynamic adaptation of pregnancy persists postpartum and gradually returns to pre-gestational values within 12-24 weeks after delivery.

• Uterine blood flow increases by a factor of 50 during pregnancy.
• The uterine blood vessels remain dilated throughout pregnancy.
• Transfer of oxygen across the placenta is flow-limited.
• Fetal oxygen tension is normally quite low (30 to 40 mmHg).
• Supplemental oxygen to the mother is quite effective in increasing fetal oxygen, particularly with fetal distress.
• Normal fetal pH is 7.35. Fetal scalp pHs <7.25 are abnormal.
• Labor can precipitate fetal distress because during uterine contractions, uterine blood flow is nearly occluded.
• In a mother with cyanosis, it is easier for problems to arise during labor because of the reduced reserve in oxygen delivery.
• With contractions, there may normally be a reduction or deceleration in the fetal heart rate, but this rapidly returns to normal.
• In fetal distress, the decelerations are later in the contraction and persist, i.e. late decelerations.
• Fetuses do not die suddenly during labor, and there are many minutes or hours of fetal distress before death so that there is time to intervene.
• Placing the mother in the left lateral recumbent position and oxygen will relieve many cases of fetal distress.
• Fetal monitoring should be used in the presence of maternal heart disease, cardiac surgery, cardioversion.

Template:WikiDoc Sources CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Anjan K. Chakrabarti, M.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]

Cardiovascular diseases, including heart disease and stroke, account for more than one-third (33.6%) of all U.S. deaths.[4]Approximately 1-4% of pregnancies in the United States involve maternal cardiovascular disease. Heart disease along with deep venous thrombosis and pulmonary thromboembolism has surpassed hemorrhage, hypertensive disorders^[1] and infection as the leading cause of maternal mortality.^[2] 13% of pregnancies will be complicated by a cardiovascular event such as pulmonary edema, cardiac arrhythmia, stroke or cardiac death.

• A pregnancy-related death is defined as the death of a woman while pregnant or within one year of pregnancy termination regardless of the duration or site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management, but not from accidental or incidental causes.

• In the United States—

• Of the 3,319 deaths within a year of pregnancy termination that occurred in 2006-2007, 1,294 were found to be pregnancy-related.
• The pregnancy-related mortality ratio was 15.1 deaths per 100,000 live births for the period 2006–2007.

• Considerable racial disparities in pregnancy-related mortality exist and during the 2006–2007 period, the pregnancy-related mortality ratios were:

• 11.0 deaths per 100,000 live births for white women.
• 34.8 deaths per 100,000 live births for black women.
• 15.7 deaths per 100,000 live births for women of other races.

• The graph below depicts the causes for pregnancy-related deaths in the United States for the year 2006-2007.

• Increasing numbers of women with congenital heart disease are now reaching childbearing age.
• Congential heart disease is now the most common form of heart disease complicating pregnancy in the United States.
• Rheumatic heart disease still predominates in developing countries and in immigrant populations in the United States.
• Maternal death during pregnancy in women with heart disease is rare; conditions that are associated with increased mortality includeEisenmenger syndrome, pulmonary vascular obstructive disease, and Marfan syndrome with aortopathy.^[3]
• In a prospective study of 562 pregnant women with heart disease (aged 28 ± years) at 13 Canadian cardiac and obstetric teaching hospitals, a primary cardiac event occurred in 80 completed pregnancies (13%), the most common complications being pulmonary edema and cardiacarrhythmia.^[4]

• CDC: Pregnancy-related Mortality in the United States, 2006-2007
• CDC: Pregnancy-related mortality in the United States, 1998–2005

• CDC: Pregnancy-related mortality in the United States, 1991–1997

• CDC: Pregnancy-related mortality in the United States, 1987–1990.^[5]

Template:WikiDoc Sources CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Anjan K. Chakrabarti, M.D. [2]

Women with acquired or congenital heart disease have a higher risk of cardiac complications during pregnancy than the general population. In general, a full evaluation including history, physical examination, echocardiogram, and electrocardiogram should be considered in the patient maternla patient with underlying heart disease. Further risk stratification and monitoring are dictated by a number of factors, including the presence of prior cardiac events, heart failure, valvular heart disease, and systolic or diastolic dysfunction.

A prospective study performed by Siu and colleagues identified four predictors of maternal cardiac events.^[1] These include:

• A prior cardiac event (e.g., heart failure, transient ischemic attack, arrhythmia or stroke) before pregnancy
• A baseline New York Heart Association (NYHA) class higher than Class II heart failure or cyanosis
• A left-sided heart obstruction (mitral valve area smaller than 2 cm², aortic valve area less than 1.5 cm², or peak left ventricular outflow tract gradient more than 30 mm Hg by echocardiography
• Reduced left (or systemic) ventricular systolic function (ejection fraction) less than 40%

Based on this study of approximately 600 patients, the estimated risk of a cardiac event in pregnancies with 0, 1, and more than 1 point was 5%, 27%, and 75%, respectively. The authors recommended that those with a low cardiac risk of 0 could safely be delivered in a community hospital, but those at intermediate or high cardiac risk (risk score of 1 or more) should be delivered at a regional center.

It should be noted that severe pulmonary hypertension is associated with a 30-50% risk of maternal mortality.

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines designate the following valvular lesions as high risk during pregnancy^[2]:

• Severe aortic stenosis
• Symptomatic mitral stenosis
• Aortic regurgitation or mitral regurgitation with NYHA class III to IV symptoms
• Aortic and/or mitral valve disease with left ventricular dysfunction (left ventricular ejection fraction < 40%)
• Aortic and/or mitral valve disease with severe pulmonary hypertension (pulmonary artery (PA) pressure > 75% of systemic pressure)
• Marfan syndrome
• Mechanical prosthetic valve requiring anticoagulation

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