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Management of heart failure during pregnancy

Management of heart failure during pregnancy
Literature review current through: Jan 2024.
This topic last updated: Aug 09, 2023.

INTRODUCTION — Pregnancy is associated with substantial hemodynamic changes, including 30 to 50 percent increases in both cardiac output and blood volume. In patients who are pregnant with a history of heart failure (HF) or other cardiovascular disorders, these demands can lead to clinical decompensation. In addition, patients without a history of cardiovascular disease can develop HF due to diseases acquired during pregnancy, such as peripartum cardiomyopathy. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes" and "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis".)

In patients with HF who plan to become pregnant, are pregnant, or are breastfeeding, the medications used to treat HF must be adjusted to avoid toxicity to the fetus or infant. The evaluation and management of HF during pregnancy and breastfeeding will be reviewed here.

The general approach to pregnancy in patients with known congenital or acquired heart disease, treatment of peripartum cardiomyopathy, treatment of hypertrophic cardiomyopathy during pregnancy, and overviews of the management of acute and chronic HF are presented separately:

(See "Acquired heart disease and pregnancy".)

(See "Pregnancy in women with congenital heart disease: General principles".)

(See "Peripartum cardiomyopathy: Treatment and prognosis".)

(See "Treatment of acute decompensated heart failure: General considerations".)

Other causes of HF are discussed separately. (See "Determining the etiology and severity of heart failure or cardiomyopathy".)

EVALUATION — The nature of the initial evaluation in pregnant patients with (or at risk for) HF varies according to the setting. Risk assessment for maternal cardiovascular complications during pregnancy should utilize the modified World Health Organization classifications [1]. Stable as well as decompensated patients require joint cardiac and obstetric care, including baseline and follow-up maternal transthoracic echocardiograms as well as fetal ultrasound examinations [2].

Stable patient — Patients with a history of HF or other cardiovascular disorders often present in a stable, well-compensated condition prior to or in the early stages of pregnancy. The initial approach to such patients involves assessing the cardiovascular risks associated with pregnancy and discussing these risks with the patient [2]. There are increased risks for both the mother and for the fetus and neonate (low birth weight/prematurity). (See "Acquired heart disease and pregnancy", section on 'Assessing risk' and "Pregnancy in women with congenital heart disease: General principles", section on 'Preconception and prenatal care'.)

New or acute heart failure — Patients with new or acute decompensated HF commonly present with progressive dyspnea, chest discomfort, or a range of other HF symptoms. The diagnosis is made using a constellation of clinical signs and symptoms and selected laboratory findings. The general approach to the diagnosis of new or acute decompensated HF is presented in detail separately. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".)

The baseline or initial maternal cardiovascular evaluation usually includes the following:

A careful history (including review of medication list and any preexisting cardiovascular disease or risk factors) and physical examination with consideration of physiologic changes during pregnancy. Findings such as mild pedal edema may be observed during uncomplicated pregnancy.

Assessment of New York Heart Association functional class (table 1).

An electrocardiogram (ECG), which may reveal left ventricular (LV) or right ventricular (RV) hypertrophy, left atrial abnormalities, myocardial ischemia, or atrial fibrillation.

Echocardiography if not recently performed or if there is concern for symptoms or signs of HF, including elevated B-type natriuretic peptides (BNP) or N-terminal pro-BNP (NT-proBNP) (see below).

Echocardiography may reveal previously undetected structural heart disease (eg, valve abnormalities or congenital heart disease) or worsening LV function.

Laboratory tests, including a complete blood count, electrolytes, and renal function tests. Plasma BNP or NT-proBNP level is important for baseline risk stratification and can be used during pregnancy to differentiate HF symptoms from those of normal pregnancy [3]. In patients with HF, we also recommend BNP or NT-proBNP testing each trimester, after delivery, before hospital discharge, within a few weeks of parturition, and at the time of any clinical concern for worsening HF [4]. If there is concern for ischemia, cardiac troponin levels should be drawn. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Diagnostic evaluation'.)

In select cases, cardiovascular magnetic resonance imaging or other cardiac imaging studies may be required (eg, congenital heart disease with RV dilation/dysfunction). The use of gadolinium contrast should be avoided during pregnancy. (See "Diagnostic imaging in pregnant and lactating patients".)

A chest radiograph may not be necessary to establish the diagnosis of HF if there is clear clinical evidence of pulmonary edema; however, a radiograph should be performed when needed due to the low risk of fetal radiation [5]. (See "Diagnostic imaging in pregnant and lactating patients" and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Chest radiograph'.)

Differential diagnosis — The differential diagnosis for HF symptoms during pregnancy or in the peripartum period includes the following conditions:

Uncomplicated pregnancy is commonly accompanied by breathlessness, easy fatigability, decreased exercise tolerance, and peripheral edema. Physical examination (elevated jugular venous pressure and persistent rales) and laboratory findings (eg, elevated BNP and/or NT-proBNP levels, evidence of elevated intracardiac pressures, and systolic and/or diastolic dysfunction on echocardiography) distinguish benign symptoms and signs of normal pregnancy from HF. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes".)

Pulmonary edema due to preeclampsia/eclampsia (hypertension plus proteinuria or other characteristic findings) may be present. (See "Acute respiratory failure during pregnancy and the peripartum period", section on 'Pulmonary edema'.)

Amniotic fluid embolism is suggested by abrupt onset of hypotension, hypoxemia, disseminated intravascular coagulation, and coma or seizures. (See "Amniotic fluid embolism".)

Pulmonary embolism may be distinguished from HF by physical examination, chest radiograph, and computed tomographic imaging. Of note, acute large pulmonary embolus can cause elevations in BNP or NT-proBNP (similar to levels seen with HF) and a dilated hypokinetic RV on echocardiogram. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Acute respiratory failure during pregnancy and the peripartum period", section on 'Pulmonary embolism'.)

Pneumonia is suggested by clinical history and physical examination. If a pregnant or postpartum patient has signs and symptoms of HF, a chest radiograph interpreted as pneumonia should be questioned. Echocardiography and BNP should be assessed if there is concern for pulmonary edema. (See "Acute respiratory failure during pregnancy and the peripartum period", section on 'Pneumonia' and "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".)

Myocardial infarction is diagnosed based upon ischemic symptoms, characteristic ECG abnormalities, and elevations in cardiac biomarkers. (See "Acute myocardial infarction and pregnancy" and "Diagnosis of acute myocardial infarction".)

COUNSELING — Management of a woman with HF (or at risk for HF) contemplating pregnancy includes counseling the patient regarding the expected prognosis and potential risks of pregnancy. The discussion should be based upon an individualized assessment of risk. Counseling should ideally occur prior to pregnancy by a team with expertise in cardio-obstetrics.

Specifically, patients with a preexisting dilated cardiomyopathy should be informed about the risk of deterioration during and after pregnancy, which is dependent upon the severity of systolic dysfunction [1,4]. Since the risk of maternal morbidity and mortality is high during pregnancy for patients with dilated cardiomyopathy with LVEF <30 percent, avoidance of pregnancy is advised.

For those patients at very high risk who become pregnant, termination of pregnancy should be discussed with the patient and reliable contraception should be offered, noting there are no cardiovascular contraindications to most forms of birth control [1,6-8].

Discussion of prognosis with patients with peripartum cardiomyopathy is discussed separately. (See "Peripartum cardiomyopathy: Treatment and prognosis", section on 'OUTCOMES'.)

MANAGEMENT GOALS — Management goals for pregnant patients with HF and for patients with HF contemplating pregnancy are similar to those in nonpregnant patients. These include the following:

Relief of symptoms.

Optimizing hemodynamic status. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults".)

When possible, continuation (or initiation) of chronic therapies that improve long-term outcomes (including mortality) in patients with chronic cardiovascular disorders (eg, beta blocker therapy to treat HF with reduced ejection fraction and antihypertensive therapy in patients with hypertension).

Treatment of precipitating factors (eg, anemia, arrhythmias, infection, thyroid disorders).

General discussions of the treatment of acute and chronic HF are presented separately. (See "Treatment of acute decompensated heart failure: General considerations" and "Overview of the management of heart failure with reduced ejection fraction in adults".)

TREATMENT REGIMENS

Chronic heart failure — Components of therapy for chronic HF include lifestyle modification, review of drugs, vaccinations (pneumococcal, coronavirus 2019, and annual influenza), pharmacologic therapy, and device therapy (including cardiac resynchronization therapy and/or implantable cardioverter-defibrillator therapy).

HFrEF – Drugs used to treat chronic HF with reduced ejection fraction (HFrEF) during pregnancy include diuretics, beta blockers, hydralazine plus nitrate, and digoxin. (See 'Drugs' below.)

During pregnancy, clinical HF including pulmonary congestion is treated with a diuretic. (See 'Diuretics' below and "Use of diuretics in patients with heart failure".)

Beta blockers are generally continued during pregnancy in patients with chronic HFrEF who are taking a beta blocker as part of a chronic regimen to improve long-term outcomes. (See 'Beta blockers' below.)

For pregnant patients with symptoms of HF, hydralazine plus isosorbide dinitrate is a reasonable alternative to vasodilators contraindicated in pregnancy. (See 'Vasodilators' below.)

For pregnant patients with symptoms of HF due to systolic dysfunction that persist despite diuresis and vasodilator therapy, digoxin can be used to treat symptoms. (See 'Digoxin' below.)

We avoid the following agents due known toxicities and effects or the absence of safety data:

Angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, and sacubitril-valsartan are contraindicated. (See 'Avoid angiotensin inhibition' below.)

We avoid mineralocorticoid receptor antagonists. (See 'Aldosterone antagonists' below.)

We avoid sodium-glucose co-transporter 2 (SGLT2) inhibitors during pregnancy given the absence of human safety data supporting use during pregnancy. (See 'Sodium-glucose co-transporter 2 inhibitors' below.)

If indicated, implantation procedures for cardiac resynchronization therapy or implantable cardioverter-defibrillator therapy are performed prior to or following pregnancy, if possible, to avoid the risk of radiation to the fetus. (See "Diagnostic imaging in pregnant and lactating patients".)

HFpEF – For the treatment of HF with preserved ejection fraction (HFpEF), we avoid the use of mineralocorticoid receptor antagonists, sacubitril-valsartan, and SGLT2 inhibitors. (See 'Aldosterone antagonists' below and 'Sodium-glucose co-transporter 2 inhibitors' below and 'Avoid angiotensin inhibition' below.)

Acute heart failure — Components of therapy for acute HF include supplemental oxygen therapy and pharmacologic therapy (including diuretic therapy in patients with clinical HF including those with pulmonary edema). (See "Treatment of acute decompensated heart failure: Specific therapies".)

Pregnant patients with severe decompensated HFrEF and hypotension may require intravenous inotropic therapy. (See 'Inotropes' below and "Inotropic agents in heart failure with reduced ejection fraction".)

For pregnant patients hospitalized with severe decompensated HF in whom further afterload reduction may be beneficial, options for therapy include intravenous nitroglycerin, hydralazine, and sodium nitroprusside. If nitroprusside is selected for therapy, we measure thiocyanate levels to mitigate maternal and fetal toxicity, though levels that cause toxicity are ill-defined in adults and in the fetus. Further details on the use of these agents in acute decompensated HF can be found separately. (See 'Vasodilators' below and "Treatment of acute decompensated heart failure: Specific therapies", section on 'Vasodilator therapy'.)

Beta blocker therapy in pregnant patients with acute decompensated HFrEF is managed in the same manner as in nonpregnant patients with decompensated HFrEF. Beta blockers are not initiated in the setting of acute decompensated HFrEF. Similarly, patients on chronic beta blocker therapy who develop acute decompensated HFrEF often have the dose reduced or therapy withheld during initial treatment. (See 'Beta blockers' below and "Treatment of acute decompensated heart failure: General considerations".)

Refractory heart failure — For patients with acute or chronic HF that is refractory to treatment, specialized strategies include intravenous inotropic therapy and temporary mechanical circulatory support. (See "Management of refractory heart failure with reduced ejection fraction".)

Limited experience with pregnancy and delivery in patients with LV assist devices has been described [9,10]. Concerns include maternal and fetal risks such as thromboembolism and the need for anticoagulation and the risk of bleeding exacerbated by the occurrence of acquired von Willebrand syndrome.

DRUGS — Due to the unique issues related to pregnancy and lactation, each medication to treat HF must be carefully considered in these clinical settings [11]. Since there are changes in the volume of distribution and glomerular filtration rate during pregnancy, dosing of certain medications may need to be increased during pregnancy.

The following discussion addresses the role of medications commonly used for the treatment of HF during pregnancy and lactation.

Avoid angiotensin inhibition — Angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and sacubitril-valsartan, which are part of the standard long-term therapeutic regimen in nonpregnant patients with HF with reduced ejection fraction (HFrEF), are contraindicated during pregnancy. These drugs are associated with a high risk of adverse effects in the fetus during all trimesters of pregnancy, particularly the second and third trimesters. Consequences include fetal renal failure and even neonatal death [12-15]. (See "Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy".)

During preconception consultation, the risks of stopping HF medications should be addressed. If a patient plans to become pregnant, we will typically stop any ACE inhibitor, ARB, or angiotensin receptor-neprilysin inhibitor (ARNI), and repeat echocardiography (in some cases also with stress testing or strain imaging) to determine whether LV dilation or function has worsened. If this occurs or the clinical status worsens, the risks of pregnancy should be readdressed.

If an ACE inhibitor, ARB, or ARNI is inadvertently taken during the first trimester, immediate discontinuation of the medication and periodic fetal monitoring are required [6].

Levels in breast milk of ACE inhibitors are low and not expected to cause adverse effects in breastfed infants [16]. An ACE inhibitor that has been studied in breast milk or breastfed infants (such as enalapril, captopril, quinapril, or benazepril) is preferred [17]. There are no data on ARB or ARNI safety during breastfeeding, and therefore we do not recommend using an ARB or ARNI during breastfeeding. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Drug options during breastfeeding'.)

Beta blockers — Beta-adrenergic blocking agents, such as extended-release metoprolol, carvedilol, and bisoprolol, are important components of the treatment regimen for patients with chronic HF due to systolic dysfunction.

During pregnancy — Beta blockers are used frequently in pregnancy for the treatment of hypertension, arrhythmias, and other cardiac conditions. These agents are generally safe and effective during pregnancy, although there may be an increased risk of fetal growth restriction when they are administered [18,19]. In general, agents that are beta-1 selective (eg, metoprolol) are preferable, since these agents are less likely to interfere with beta-2 mediated uterine relaxation and peripheral vasodilation. However, atenolol should not be used during pregnancy since its use is associated with fetal growth restriction [20].

Continuation of chronic beta blocker therapy in stable patients with HFrEF who are pregnant is suggested. Fetal growth should be monitored by ultrasound. Beta blockers are not associated with an increased risk of congenital anomalies, although occasional cases of neonatal bradycardia and hypoglycemia have been reported.

Beta blockers are not initiated in the setting of acute decompensated HFrEF. Similarly, patients on chronic beta blocker therapy who develop acute decompensated HFrEF often have the dose reduced or therapy withheld during initial treatment. Once the patient with an episode of acute decompensation has stabilized, chronic beta blocker therapy may be initiated. (See "Treatment of acute decompensated heart failure: General considerations".)

During nursing — The excretion of beta blockers into breast milk appears to be higher for drugs with low protein binding. Risk of accumulation of beta blocker in infants rises with degree of renal excretion. Despite these variations, the amount of beta blocker that would be ingested by a nursing infant is generally small and measured serum beta blocker levels in breastfed infants have generally been very low or undetectable, with limited exceptions (eg, atenolol) [16,21].

Among the three beta blockers recommended to treat stable HFrEF, we suggest use of metoprolol in nursing mothers, based upon the following considerations:

Though metoprolol (which is 10 percent protein bound and 40 percent renally excreted) is excreted into breast milk, breastfed infants have had very low or undetectable serum levels [16,21]. Limited studies on the use of metoprolol during breastfeeding have reported no adverse reactions in breastfed infants.

Since carvedilol is highly protein bound (95 percent) and has low renal excretion (1 percent), carvedilol likely presents a low risk for accumulation in breastfed infants [16]. In patients with hypertension or on stable doses of carvedilol, it may be reasonable to use carvedilol despite less published experience than metoprolol.

Since bisoprolol has relatively low protein binding (30 percent) and moderately high renal excretion (50 percent), it presents a moderately high risk for accumulation in breastfed infants [16]. Since there is little published experience with bisoprolol during breastfeeding, other agents may be preferred when nursing a newborn or preterm infant.

We avoid atenolol with lactation, as other agents are preferred.

Aldosterone antagonists — The aldosterone antagonists spironolactone and eplerenone, which compete with aldosterone for the mineralocorticoid receptor, prolong survival in selected patients with HF. However, in animal studies, the antiandrogen effects of spironolactone caused feminization of the male fetus [22,23]. There are neither data nor clinical experience to support the safety of these agents during pregnancy. Thus, we suggest that these agents not be used during pregnancy.

Limited data suggest that spironolactone use is acceptable during breastfeeding since the maternal diuretic effect is unlikely to be potent enough to affect lactation, and the dose to the breastfeeding infant is low [16]. In patients with HF who are breastfeeding, we generally avoid eplerenone due to lack of data.

Sodium-glucose co-transporter 2 inhibitors

During pregnancy — Sodium-glucose co-transporter 2 (SGLT2) inhibitors should be avoided during pregnancy. There are inadequate safety data in pregnant patients to determine the drug-associated risk for major birth defects or miscarriage. Based on animal studies, adverse effects on renal development may be seen in a timeline that correlates with the second and third trimesters of human pregnancy.

During nursing — The SGLT2 inhibitors dapagliflozin and empagliflozin are uncharged molecules that are highly protein bound and unlikely to pass into breastmilk in clinically important amounts [16]. However, due to lack of published data, we do not recommend these medications while nursing a newborn or preterm infant.

Digoxin — Digoxin is generally considered safe in pregnancy, despite anecdotal reports of adverse effects [24,25]. Dosing may need to be increased to achieve a therapeutic effect during pregnancy. The decision to do so should be based upon the perceived adequacy of the therapeutic effect rather than purely on serum levels [26]. Transplacental passage of digoxin has been documented, and this pharmacokinetic property has been used for the in-utero treatment of fetal tachyarrhythmias [27].

During pregnancy, digoxin can be particularly useful for two reasons:

The use of conventional HF therapies is limited.

The increased physiologic demands of pregnancy can exacerbate HF symptoms.

Similar to nonpregnant patients, reasons to consider adding digoxin in pregnant patients include:

The persistence of symptoms (such as fatigue, dyspnea, and exercise intolerance) despite optimal treatment with agents safe for use during with pregnancy.

For control of the ventricular rate in HF patients with atrial fibrillation who cannot achieve adequate control on beta blockers alone.

During nursing — Digoxin levels in breast milk are low; the dose to a breastfed infant is small and no adverse effects have been reported in newborns [16]. If an intravenous dose of digoxin is administered to a nursing mother, avoidance of breastfeeding for two hours will lessen the dose ingested by the infant.

Ivabradine — Given lack of evidence of safety during pregnancy and nursing, we suggest avoiding ivabradine use in pregnant or nursing patients.

Vericiguat — We do not use vericiguat in patients who are pregnant, who seek to become pregnant, or who are breastfeeding.

Diuretics — Diuretics are given for HF during pregnancy for symptomatic relief of congestion, pulmonary edema (eg, paroxysmal nocturnal dyspnea or exertional dyspnea), or peripheral edema. For treatment of HF, loop diuretics are generally preferred over thiazide diuretics and potassium-sparing diuretics. (See "Use of diuretics in patients with heart failure".)

Treatment with loop diuretics (without waiting for response to sodium restriction) is recommended for patients with any degree of pulmonary congestion. Potential maternal complications of loop diuretic use are similar to those of nonpregnant patients and include volume contraction, metabolic alkalosis, decreased carbohydrate tolerance, hypokalemia, hyponatremia, hyperuricemia, and pancreatitis. Potential risks to the fetus are related to the potential for intravascular volume contraction and reduced placental perfusion.

A thiazide diuretic may be added if volume cannot be adequately controlled with a loop diuretic alone. However, there are reports of bleeding disorders and hyponatremia among neonates of patients who have taken thiazide diuretics during pregnancy [28].

Volume contraction caused by diuretics might decrease lactation [16]. No information is available on the use of loop diuretics during breastfeeding. Moderate doses of thiazide diuretics (eg, up to 50 mg daily of hydrochlorothiazide) are acceptable during lactation.

Vasodilators — Vasodilator therapy improves cardiac output in moderate to severe HF and slows the rate of myocardial deterioration at all stages by inducing afterload reduction.

Hydralazine plus nitrate — Because ACE inhibitors, ARBs, and sacubitril-valsartan are contraindicated in pregnancy, the combination of hydralazine plus nitrate (isosorbide dinitrate) is the vasodilator therapy of choice during pregnancy. Hydralazine has been used for many years in the treatment of hypertension during pregnancy and appears to be safe for both the mother and fetus [29-31].

The combination of hydralazine plus nitrate (isosorbide dinitrate) is the vasodilator therapy of choice in pregnant patients with HF [6,32]. The evidence for hydralazine plus nitrate therapy for HFrEF is not as strong as the evidence for ACE inhibitor therapy. Therefore, we suggest that hydralazine not be routinely started when ACE inhibitor, ARB, or ARNI therapy is discontinued in patients who are clinically stable and normotensive. Hydralazine plus nitrate therapy should be used instead of ACE inhibitors, ARBs, or ARNI in pregnant patients with HF who are hypertensive, have severe LV systolic dysfunction, or have evidence of congestion and decompensated HF.

Limited data on breast milk and breastfed infant serum levels suggest that use of hydralazine is acceptable in nursing mothers [16]. Evidence is lacking on use of isosorbide dinitrate during breastfeeding. Since we usually restart ACE inhibitor therapy postpartum, we seldom use hydralazine plus nitrate to treat HF in nursing mothers.

Intravenous agents — A separate issue is the use of intravenous vasodilators (eg, nitroglycerin and nitroprusside) in pregnant patients with decompensated HF, particularly if associated with hypertension. Intravenous afterload reduction should be undertaken with great care in this setting given the risk of deterioration of the fetal heart rate with rapid and profound drop in maternal blood pressure. Continuous fetal monitoring is recommended if viability has been achieved.

Nitroglycerin or nitroprusside — In pregnant patients with decompensated HF, particularly those with hypertension, cautious use of intravenous nitroglycerin can be attempted [33]. However, nitroprusside should be used only when all other interventions have failed and when it is essential for maternal well–being. Even under these conditions, the dose and duration of therapy should be minimized due to the metabolism of this agent to thiocyanate and cyanide, which has resulted in fetal cyanide poisoning in animal models [34]. Experience with nitroglycerin and nitroprusside in pregnant patients comes largely from treatment of hypertensive emergencies. (See "Drugs used for the treatment of hypertensive emergencies", section on 'Nitroprusside' and "Treatment of hypertension in pregnant and postpartum patients", section on 'Nitroprusside' and "Treatment of acute decompensated heart failure: Specific therapies".)

Since thiocyanate is excreted into breast milk and cyanide may also enter breast milk, nursing should be avoided if nitroprusside therapy is required [16]. Since intravenous use of nitroglycerin has not been studied during breastfeeding [16], nursing should be avoided when intravenous nitroglycerin is used.

Inotropes — Patients with acute decompensated HF and systolic dysfunction who are hypotensive or who remain in pulmonary edema despite oxygen, diuresis, and, if tolerated, vasodilators, may benefit from intravenous inotropic support. As each of these medications has slightly different properties, in a seriously ill pregnant woman, the selection of a specific agent should be based upon the clinical scenario. (See "Inotropic agents in heart failure with reduced ejection fraction".)

Dobutamine is a beta agonist with both inotropic and vasodilator properties. Dopamine has an inotropic effect and variable effects on the peripheral vasculature, depending upon the dose administered. Like dobutamine, the phosphodiesterase inhibitors such as milrinone have vasodilatory properties. Drugs with both inotropic and vasodilatory properties address the two hemodynamic problems that most commonly lead to low cardiac output in severe HF (ie, poor cardiac contractility, peripheral vasoconstriction).

No information is available on the use of dopamine or dobutamine during breastfeeding [16]. Intravenous dopamine infusion may decrease milk production, but this has not been directly studied.

Vasopressors — Vasopressors (eg, norepinephrine and phenylephrine) are usually avoided in patients with HF, since such patients usually have high systemic vascular resistance at baseline and further peripheral vasoconstriction may impair cardiac output. In pregnant patients, vasopressors carry the additional risk of impairing uterine blood flow. In critically ill, hypotensive patients, however, blood pressure may need to be supported. There are few data to guide selection of an appropriate vasopressor in a pregnant woman. Animal studies suggest that dopamine may have less deleterious effects on uterine blood flow than norepinephrine or phenylephrine. (See "Critical illness during pregnancy and the peripartum period", section on 'Vasopressors'.)

No information is available on the use of dopamine, norepinephrine, or phenylephrine during breastfeeding [16]. These drugs may decrease milk production.

Anticoagulants — The role of anticoagulation to manage thromboemboli and thromboembolic risk in pregnant patients is described elsewhere:

Deep vein thrombosis. (See "Venous thromboembolism in pregnancy: Prevention" and "Venous thromboembolism in pregnancy and postpartum: Treatment".)

LV thrombus. (See "Antithrombotic therapy in patients with heart failure".)

Atrial fibrillation, atrial flutter, and other supraventricular tachycardias. (See "Supraventricular arrhythmias during pregnancy".)

Valve disease and prosthetic valves. (See "Pregnancy and valve disease".)

Prophylactic anticoagulation in peripartum cardiomyopathy. (See "Peripartum cardiomyopathy: Treatment and prognosis", section on 'Antithrombotic therapy'.)

DELIVERY — Management of delivery in patients with heart disease is discussed separately. (See "Acquired heart disease and pregnancy", section on 'Management of labor and delivery'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Management of cardiovascular diseases during pregnancy" and "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

Evaluation of heart failure during pregnancy

Patients with a history of heart failure (HF) or cardiac disorders that put them at risk for HF should undergo a thorough initial evaluation prior to or in the early stage of pregnancy. (See 'Evaluation' above.)

Patients who develop signs or symptoms of HF during pregnancy should undergo an initial evaluation similar to that generally recommended for patients with suspected HF. B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) levels should be measured in all patients with known or suspected HF, with a low threshold for echocardiography. (See 'New or acute heart failure' above and "Heart failure: Clinical manifestations and diagnosis in adults".)

Counseling – Management of a woman with HF (or at risk for HF) contemplating pregnancy includes counseling the patient regarding the expected prognosis and potential risks of pregnancy. The discussion should be based upon an individualized assessment of risk utilizing the modified World Health Organization classification of maternal cardiovascular risk. Counseling should ideally occur prior to pregnancy by an experienced cardio-obstetrics team. (See 'Counseling' above.)

Treatment regimens – Patients with HF during pregnancy should be treated for HF, except for avoiding contraindicated medications such as angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitor (ARNI), aldosterone antagonists, vericiguat, and ivabradine. We also suggest avoiding use of sodium-glucose co-transporter 2 (SGLT2) inhibitors during pregnancy, given lack of evidence of safety during pregnancy. (See 'Chronic heart failure' above.)

Drugs used to treat chronic HF with reduced ejection fraction (HFrEF) during pregnancy include diuretics, beta blockers, hydralazine plus nitrate, and digoxin. (See 'Drugs' above.)

-During pregnancy, clinical HF including pulmonary congestion is treated with a diuretic. (See 'Diuretics' above and "Use of diuretics in patients with heart failure".)

-Beta blockers are generally continued during pregnancy in patients with chronic HFrEF who are taking a beta blocker as part of a chronic regimen to improve long-term outcomes. (See 'Beta blockers' above.)

-For pregnant patients with symptoms of HF, hydralazine plus isosorbide dinitrate is a reasonable alternative to vasodilators contraindicated in pregnancy. (See 'Vasodilators' above.)

-For pregnant patients with symptoms of HF due to systolic dysfunction that persist despite diuresis and vasodilator therapy, addition of digoxin may be considered for treatment of symptoms. (See 'Digoxin' above.)

Acute decompensated HF during pregnancy is managed with supplemental oxygen therapy and pharmacologic therapy (including diuretic therapy in patients with clinical HF including those with pulmonary edema). (See 'Acute heart failure' above and "Treatment of acute decompensated heart failure: Specific therapies".)

-Beta blocker therapy in pregnant patients with acute decompensated HFrEF is managed in the same manner as in nonpregnant patients with decompensated HF. (See 'Beta blockers' above and "Treatment of acute decompensated heart failure: General considerations".)

-Pregnant patients with unstable, severe decompensated HFrEF and hypotension may require intravenous inotropic therapy. (See 'Inotropes' above and "Inotropic agents in heart failure with reduced ejection fraction".)

Treatment of HF with preserved ejection fraction (HFpEF) during pregnancy remains empiric and includes control of systolic and diastolic hypertension, control of pulmonary congestion and peripheral edema with diuretics, and control of heart rate if elevated.

-Antihypertensive agents that may be used to treat HFpEF during pregnancy include beta blockers and heart rate limiting calcium channel blockers.

-Digoxin is not indicated in patients with HFpEF.

For patients with refractory HF, specialized strategies include intravenous inotropic therapy, mechanical circulatory support (eg, left ventricular [LV] assist device), and cardiac transplantation. Limited data are available on LV assist device use during pregnancy. Cardiac transplant recipients are generally advised to avoid pregnancy during the first year posttransplantation when the risk of rejection is greatest and immunosuppressive therapy most aggressive. (See "Heart transplantation in adults: Pregnancy after transplantation".)

Drugs to avoid during pregnancy Drugs that should not be used in patients who are pregnant or who are planning to become pregnant include:

ACE inhibitors, ARBs, and sacubitril-valsartan (see 'Avoid angiotensin inhibition' above)

Mineralocorticoid receptor antagonists (see 'Aldosterone antagonists' above)

SGLT2 inhibitors (see 'Sodium-glucose co-transporter 2 inhibitors' above)

Ivabradine (see 'Ivabradine' above)

Vericiguat (see 'Vericiguat' above)

Anticoagulation – Indications for anticoagulation in patients with HF during pregnancy include standard indications for anticoagulation, such as evidence of systemic embolism or LV thrombus, presence of a mechanical prosthetic heart valve, and select cases of atrial fibrillation. (See 'Anticoagulants' above.)

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Topic 3507 Version 25.0

References

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