Mini Review Volume 11 Issue 3
1Professor of Obstetrics and Gynecology, Creighton University School of Medicine, Clinical Professor of Obstetrics and Gynecology, University of Arizona College of Medicine, USA
2Director, Maternal Fetal Medicine, Valleywise Medical Center, USA
Correspondence: Linda R. Chambliss, BSN, MD, MPH, Director, Maternal Fetal Medicine, Valleywise Medical Center, Professor of Obstetrics and Gynecology, Creighton University School of Medicine, Clinical Professor of Obstetrics and Gynecology, University of Arizona College of Medicine, USA
Received: September 18, 2025 | Published: October 20, 2025
Citation: Chambliss LR. Cardiac disease in pregnancy: What nurses need to know. Nurse Care Open Acces J. 2025;11(3):89‒93. DOI: 10.15406/ncoaj.2025.11.00326
Pregnancy is a time of significant physiological changes. Perhaps the most significant changes are in the cardiovascular system. Obstetrical providers are seeing more and more patients with heart disease as the obesity epidemic has increased the risk of hypertension, more children with congenital cardiac defects are surviving to adulthood and more women are becoming pregnant at older ages. Providers need to understand the changes in cardiac physiology in pregnancy to best care for these patients. Maternal mortality due to direct obstetrical causes such as hemorrhage are decreasing but deaths due to co-existing diseases are increasing and most deaths due to cardiac disease are thought to be preventable.
Keywords: pregnancy, heart disease, physiology
Maternal mortality continues to increase in the United States. Cardiac disease is the leading cause of indirect maternal deaths, i.e. deaths from an underlying condition made worse by the pregnancy. Congenital heart disease accounts for 2/3 of the heart disease seen in pregnancy. Acquired heart disease is increasing due to the obesity epidemic leading to more hypertension. Since some women delay childbearing until they are older, there is more risk of coronary artery disease. These deaths disproportionally occur in non-Hispanic Black women. Most of the deaths occur in women who were not diagnosed with a cardiac condition prior to their deaths and in some series as many as 80% of the cardiac related deaths are thought to have been preventable. A major factor in these deaths was a lack of a multidisciplinary team to care for the patient. Providers should recognize the cardiac decompensation in pregnancy is often subtle at first one needs to be vigilant as to a change in symptoms or physical findings. Women have long suffered from being excluded from trials on cardiac disease. Even studies in rats only included male animals. Data has been extrapolated from the results in males to females without regard to physiological differences.1
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a) Class I No limitations on activity; ordinary activity does not result in cardiac sx. |
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b) Class II Slight limitation of physical activity; ordinary activity results in sx that resolve with rest. |
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c) Class III Less than ordinary activity causes symptoms markedly limiting activity but comfortable at rest. |
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d) Class IV Symptoms with any physical activity and symptoms present at rest. |
Table 1 New York Heart Association Classification of Heart Disease
Cardiac disease has implications not only for the mother but for the fetus as well. This is particularly true if the patient has a New York Heart Association (NYHA) disease class II or higher, smokes or has more than a singleton. Table 1 lists the NYHA classes. When a mother has a congenital lesion there is an increased risk that the fetus will be affected with a congenital lesion. Several cardiac lesions such as Marfan’s or DiGeorge syndrome are inherited in an autosomal dominant fashion putting the fetus at a 50% risk of being affected. In other conditions where the mother has a known congenital condition that is not inherited in an autosomal dominant fashion, this increased the risk of a congenital lesion in the fetus from the background risk of 1% to a risk of 4-6%. If the mother has an autosomal dominant condition such as Marfan’s or DiGeorge syndrome, the fetus has 50% of being affected. If this is not the case, the fetus may not have the same problem as the mother and studies suggest that their lesions are only concordant about 50% of the time. The fetus may not have adequate blood flow due to cardiac disease in the mother. If the mother has cyanotic heart disease only about 85% of the pregnancies will result in a live birth. The fetus may need to be delivered prematurely due to the mother’s decompensation. And lastly the fetus may be exposed to medications or procedures that incur some risk.2
There are some lesions that are considered to be a contraindication to pregnancy. Table 2 lists the conditions that are contraindicated since the maternal mortality reaches 25-50%.
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a) Pulmonary arterial hypertension of any kind |
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b) Marfan’s syndrome with an aortic root > 40 mm |
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c) Aortic dilation > 50 mm in bicuspid aortic valve |
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d) Severe left heart obstructive lesions |
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e) Severe mitral stenosis, severe symptomatic aortic stenosis, severe coarctation |
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f) Severe systemic left ventricular dysfunction |
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g) Left ventricular EJ < 30%, NYHA class III or IV |
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h) Prior peripartum cardiomyopathy with residual impaired LV function |
Table 2 Lesions that are considered to be a contraindication to pregnancy
Lastly contraception is more difficult in women who have heart disease. The presence of severe hypertension may limit the use of oral contraceptives. For some patients with reduced cardiac output or arrythmias oral contraceptives present too much of a risk of thrombosis.
Physiological changes in pregnancy
Pregnancy and labor and delivery have important and frequently predictable changes in cardiac function. Pregnancy is a time of dramatic changes in cardiac function which start early in the first trimester and peak in labor. There is a 30-40% increase in blood volume which is essential to allow for adequate fetal growth. In a singleton pregnancy the volume increases by an average of 1500 cc while in twins it increases by about 2000 cc. Plasma volume and red cell mass increase but since the plasma volume increases more than the red cell mass, there is the so called “physiological anemia of pregnancy”. Heart rate increases by 10-15 beats/minute. Maternal stroke volume rises by 30%, while systemic and pulmonary vascular resistance both decreases. Cardiac output increases 30-50%. Maternal position can have a dramatic effect on cardiac output. The ejection fraction on the echocardiogram does not change. In about 10% of women being supine is enough to cause hypotension even in the absence of any type of illness. Many of the clotting factors increase in pregnancy to protect the mother from a postpartum hemorrhage. The enlarging uterus can compress venous return. These changes lead to an increased risk of thrombotic events.
The most significant physiological change in pregnancy is the cardiac changes in the first 30 minutes postpartum. Cardiac output is a function of stroke volume and heart rate. Stroke volume is dependent upon preload or the amount of blood returning to the heart. Since the vena cava is no longer compressed by the enlarged uterus, there is better venue return to the heart. This, combined with the 500 cc of blood volume added to the circulation from the contracted uterus, allows for a 60% increase in stoke volume. Since the stroke volume increases, the heart rate can decrease and still maintain adequate cardiac output. All of these changes are even further accentuated in multiple gestations and labor. There is limited information about the changes in twins and scant information about the changes in higher order multiples such as triplets or quads.3
Diagnostic challenges in pregnancy
Many of the usual signs of cardiac disease overlap with normal pregnancy complaints. Most women have peripheral edema due to the 6–8-liter increase in water and the decrease in colloid osmotic pressure which allows for third spacing of fluid. Many women will report dyspnea due to the progesterone mediated effects on pulmonary function. Most patients will have a systolic ejection murmur, but the usual murmur is a 2/6. Louder murmurs are abnormal. About 10% of patients also have a diastolic murmur but in general these should be investigated. Chest pain is never normal and needs evaluation as does worsening dyspnea or a decrease in exercise tolerance.
Due to the changes in cardiac position with the enlarging uterus, the heart appears to be enlarged on a chest Xray. The diagnosis of cardiomegaly should not be made on the basis of the chest Xray alone but needs confirmation with an echocardiogram. The EKG is changed as well. There is an increase in heart rate so as a result there is a shortening of the PR, QRS and QT intervals. More ectopy is reported most likely from stretch. The shift in position leads to a left axis deviation. When there is “lightening” or the fetal head drops into the pelvis, there is sometimes a right axis deviation. Since the heart is moved, the usual lead placement can show a Q wave in II, III and AvF. Inverted T waves are normal in III and V1-V6. The echocardiogram can show trivial tricuspid and pulmonic regurgitation as well as an increase in atrial size, an increase in left ventricular end diastolic dimensions and a small pericardial effusion. Cardiac catheterization is not usually needed to diagnose or manage patients unless there is suspected acute coronary syndrome.4
Even considering these changes there are recognized scenarios to indicate the need for further evaluation in pregnant women. They would include patients with a history of a known cardiac disease, symptoms that are more than what would be expected in pregnancy, a systolic murmur that is greater than a 2/6, a diastolic murmur, cyanosis or evidence of oxygen desaturation or evidence of cardiac failure. It is critical to ask patients at risk about symptoms during prenatal care as patients may not recognize the significance of what they are experiencing. Patients should be asked about exercise tolerance, whether they go up a flight of stairs, how many pillows they use, if they experience palpitations and if they have chest pain with either exercise or at rest. Table 3 lists common conditions that help predict complications.
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a) A prior cardiac event such as a MI or CVA |
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b) NYHA classes III or IV |
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c) Left outflow obstruction |
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d) A reduced ejection fraction |
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e) A mechanical prosthesis |
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f) Moderate to severe valvular regurgitation |
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g) Need for cardiac medications prior to pregnancy |
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h) Cyanotic heart disease |
Table 3 conditions that help predict adverse outcomes
Care during labor
Labor places enormous demands on the heart. It is critical to have an accurate diagnosis of whatever underlying cardiac condition the patient has and how she has been managed as an outpatient. Generally the mode of delivery should be based on obstetrical indications. It is very important to have adequate pain control so as to not have pain increase cardiac demand. Patients benefit from early epidural anesthesia with levels of anesthesia increased gradually to reduce the risk of hemodynamic instability. Patients should always have mechanical compression devices to reduce the risk of thrombosis. The indications for prophylactic antibiotics to reduce the risk of endocarditis have changed recently. Only those at the highest risk of endocarditis should receive antibiotic prophylaxis. Prophylaxis is restricted to women with prosthetic valves or prosthetic material used in the repair, those with a prior episode of endocarditis, women with unrepaired cyanotic heart disease, if the congenital heart lesions was repaired within the last 6 months, those with repaired lesions with residual defects at the site of a prosthetic patch or patient who have had a cardiac transplant and have valvular regurgitation due to an abnormal valve. Prior to labor there should be a multidisciplinary decision as to whether the patient should push in the second stage of if there should be an assisted delivery. Many suggest aggressive management of the third stage to avoid a postpartum hemorrhage. The volume changes that occur in the immediate postpartum period can be particularly challenging for patients with stenotic valvular lesions who cannot tolerate the sudden increase in blood volume and providers need to be alert to the possibility of pulmonary edema. It is important to continue mechanical compression devices as the postpartum period has the highest risk of thrombosis.5
Cardiac arrest in pregnancy
Thankfully, cardiac arrest rarely occurs in pregnancy. The estimates are it complicates 8.5 patients/100,000 deliveries. About 60% of patients survive to discharge but since arrests are so rare there is not a lot of data about factors that affect survival. However, it is very clear that immediate, effective chest compressions are the key to maternal and fetal survival. In non-pregnant patients the estimates are that even excellent compressions only produce a cardiac output that is about 30% of normal. Given the effects of aortic compression from the enlarged uterus, compressions in pregnancy probably generate even less. Hands are placed slightly higher on the sternum, and the compression rate should be 100-120/minute to a depth of 2 inches. When compressions are started it is optimal to have a second provider manually displace the uterus to the left rather than place the patient in a left lateral tilt. The left lateral tilt reduces the force of the compression which is a key component in survival. Compressions should only be interrupted for 10 seconds or less to assess a shockable rhythm, to administer the shock or to change CPR providers. Providers should be changed frequently, probably about every 2 minutes to maximize the strength of the compression and avoid provider fatigue.
The compression: ventilation ratio is 30:2. Some authors suggest that bag-mask ventilation should be minimal, and preparations should be made for rapid endotracheal intubation. Intubations are much more difficult in pregnant patients due to the pregnancy induced edema of the airway. In addition, maternal oxygen consumption is markedly increased, intrapulmonary shunting is increased and there is a 20% reduction in the functional residual capacity. The functional residual capacity is what allows one to have a buffer and these changes lead to a rapid oxygen desaturation with apnea. As such, the most experienced person should be the one to intubate. The general rule is that a c-section should begin after 4 minutes of resuscitation. However, If the CPR is ineffective or the cause of the arrest is probably not reversible (a pulmonary or amniotic fluid embolism for example), the c-section should begin immediately.
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a) Failure to use a backboard |
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b) Failure to start effective compressions immediately |
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c) Stopping the compressions for more than 10 seconds or for reasons such as starting an IV or doing the c section |
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d) Failure to notify the NICU immediately |
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e) Moving the patient somewhere before beginning the c section |
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f) Failure to do a left lateral displacement (preferably manual, not left tilt) |
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g) Failure to disconnect the fetal monitor before using the defibrillator |
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h) Waiting too long to start the c section; delivery within 4- 5 minutes and sooner if the cause of the arrest is likely irreversible |
Table 4 Common mistakes in providing CPR in pregnancy
With careful multidisciplinary care most women with cardiac disease do well. Ideally patient should be counseled as to their risks prior to pregnancy and advised if they have one of the conditions considered to be a contraindication to pregnancy. It is critical to carefully evaluate the patient at frequent prenatal visits, be aware of physiological changes, to understand how testing can change and how to manage the labor and delivery as that is an especially risky time. However, it is also important to remember that most women with appropriate care will do well and have successful pregnancies.
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