Arrhythmias in Pregnancy

Pregnant women often experience symptoms of dizziness or palpitations, most of which are benign. These can be due to arrhythmias that are either new or due to underlying conditions that have been unmasked by pregnancy. Understanding the physiologic changes and the types of arrhythmias that occur during pregnancy can help the practitioner identify when further interventions are necessary.

Physiology

Several hemodynamic changes occur during normal pregnancy, including an increase in blood volume and cardiac output, and decreased systemic vascular resistance and blood pressure (BP). The total blood volume increases about 50 percent above the normal level, which provides some reserve for peripartum blood loss. Although both the plasma volume and red cell volume increase during pregnancy, the plasma volume increases to a greater extent, resulting in a modest reduction in hematocrit or a physiologic anemia, most apparent at 30-34 weeks.⁴ This results in decreased blood viscosity, increased perfusion of the placenta, and less myocardial workload. Cardiac output increases by 30-50 percent above baseline, primarily due to increased preload from the rise in blood volume, reduced afterload from decreased systemic vascular resistance, and increased heart rate (by about 15-20 beats/minute).^5,6 The resting heart rate also increases about 10 beats per minute.⁷ Blood pressure decreases due to reduced systemic vascular resistance and decreased afterload, as a result of peripheral vasodilation and the low-resistance, high-flow circulation of the uterus and placenta.⁵ The overall decrease in diastolic BP and MAP is about 5-10 mmHg.⁸ Myocardial contractility is preserved during pregnancy.⁹ In late pregnancy, supine hypotension can result from compression of the inferior vena cava by the uterus, resulting in dizziness and syncope, resolving in the lateral recumbent position.¹⁰

ECG Changes

Some 4 to 14 percent of women develop nonspecific ST segment and T-wave changes that are most commonly seen in the left precordial leads, which typically resolve after delivery.^11,12 These changes often recur with subsequent pregnancies. There may also be a slight leftward or rightward axis deviation due to rotation of the heart from elevation of the diaphragm and/or the gravid uterus.^13,14 With the increased heart rate of pregnancy, the PR and QT intervals shorten.

Premature Beats

Atrial (APBs) and ventricular premature beats (VPBs) are not usually associated with symptoms, and their overall incidence during pregnancy is unknown. However, among pregnant women with symptoms of palpitations, presyncope, or syncope, the incidence of APBs and VPBs was found to be 56 and 59 percent, respectively.¹⁵ During labor, APBs and VPBs were detected in 90 and 50 percent of women, respectively.¹⁶ APBs are more common during labor, but during pregnancy there is usually no increased incidence of premature beats as compared to non-pregnant women without structural heart disease. Overall, premature beats carry a benign prognosis, and no therapeutic interventions are warranted in the absence of structural heart disease, such as coronary artery disease or heart failure.

Supraventricular Tachycardia

Supraventricular tachycardias (SVT) often occur during the reproductive years, but there are conflicting study results about whether there is an increased incidence during pregnancy.^17-21 These arrhythmias are usually benign and occur in pregnant women with or without heart disease. The most common SVT is atrioventricular nodal reentrant tachycardia (AVNRT), irrespective of pregnancy or structural heart disease. Although usually benign, in the presence of underlying heart disease, AVNRT can cause hemodynamic instability. Atrioventricular reentrant tachycardia (AVRT) is the second most common SVT. AVRT is due to the presence of an accessory pathway, and an increased incidence of orthodromic tachycardia has been noted in pregnancy, which can cause significant symptoms due to the rapid rate.¹⁹ For example, congenital heart disease such as Ebstein s anomaly is associated with rapidly conducting antegrade accessory pathways causing symptomatic SVT.²² Women with underlying congenital heart disease and AVRT are more likely to require pharmacologic or electrical conversion to improve their symptoms and cardiac function.²³ Atrial fibrillation and atrial flutter rarely occur during pregnancy and are usually associated with underlying metabolic disturbances such as thyrotoxicosis or congenital or valvular heart disease. When these arrhythmias do occur, it is important to treat them promptly due to the increased risk of thromboembolism and the risk to the fetus due to the hemodynamic effects of ventricular tachycardia (VT). Atrial fibrillation can also cause hemodynamic deterioration in patients with heart failure, congenital heart disease, or accessory pathways. Usually, either rhythm or rate control is an acceptable goal. Maintenance antiarrhythmic treatment is not usually necessary. The safety profile of antiarrhythmics is discussed below, but it is important to note that amiodarone, in particular, is contraindicated in pregnancy. In the setting of mitral stenosis, atrial fibrillation is more common, and is also more dangerous as it can rapidly precipitate into pulmonary edema. This is most common in late pregnancy and in the setting of ventricular tachycardia. The preferred treatment includes beta-blockers and digoxin.²⁴ SVT may be initially managed by vagal maneuvers. Adenosine can also be used to terminate reentrant tachycardias involving the atrioventricular node if the patient is hemodynamically stable, since this is generally well-tolerated by the fetus. Digoxin, beta-blockers, and calcium channel blockers can also be used to terminate SVT. Lidocaine and procainamide can be used in pregnancy. Amiodarone should be avoided due to its long half-life and potential to cause thyroid abnormalities and bradycardia in the fetus.

Ventricular Tachycardia

Ventricular tachycardia that presents during pregnancy should raise suspicion for underlying cardiac disease. In the absence of heart disease, VT is usually monomorphic, well-controlled with beta-blockers, and follows a benign course with a good prognosis. Exacerbating factors include exercise, emotional stress, or other provocative stimuli. It is usually idiopathic and more commonly originates from the right ventricle.²⁵ VT (sustained or nonsustained) that presents during the last trimester of pregnancy or within six months of delivery should raise suspicion for the development of peripartum cardiomyopathy.²⁴ Metabolic derangements from thyrotoxicosis and hyperemesis gravidarum can also precipitate episodes of VT, which resolves with resolution of the underlying disorder. Nonsustained VT can also occur in the setting of severe hypertensive crises due to increased catecholamine levels or myocardial ischemia.²⁶

Underlying Heart Disease

Wolff-Parkinson-White

Women with Wolff-Parkinson-White (WPW) may experience more frequent episodes of tachycardia,¹⁹ but not all studies support this observation.²¹ Women may also manifest with their first symptoms of WPW during pregnancy, since those with accessory pathways are at the highest risk of developing SVT, which can also increase as women age.

Congenital Long QT Syndrome

Congenital long QT syndrome is an important entity during pregnancy and can be difficult to control, particularly in the postpartum period.²⁷ During pregnancy, the increased heart rate can be protective by shortening the QT interval. However, in the postpartum period, the heart rate decreases, and the patient may experience increased stress from sleeplessness and caring for a newborn, increasing the risk of torsade de pointes. Beta-blockers are the treatment of choice and should be continued both during and after pregnancy in patients with long QT syndrome.²⁴

Hypertrophic Cardiomyopathy

Women with hypertrophic cardiomyopathy usually tolerate pregnancy without complications. Increased fluid retention is compensated for by a reduction in afterload, and the heart can maintain an increase in cardiac output. Increased incidence of symptomatic nonsustained VT and a case of fatal arrhythmia have been reported.²⁸ Most women tolerate pregnancy and can be successfully managed with beta-blockers, without requiring anti-arrhythmic treatment that could be toxic to the fetus.^29,30

Management

To date, there is no strong evidence supporting the safety of antiarrhythmic medications in pregnancy. As such, the use of antiarrhythmics should be restricted to those with severe symptoms or hemodynamic instability. In these extreme cases, the fewest number of antiarrhythmics at the lowest possible doses should be used.³¹ The use of antiarrhythmics is further complicated by the pharmacokinetic changes that occur during pregnancy. Alterations in drug absorption can be attributed to decreased gastrointestinal motility and changes in gastric pH. An increase in maternal intravascular volume can be seen during pregnancy and may affect the distribution of a drug, warranting increased doses of antiarrhythmics during this period. Reductions in serum protein levels may also increase the amount of free drug circulating in the body. Enhanced drug elimination also occurs due to increased renal elimination and increased hepatic metabolism. As a result of these factors, an increase in monitoring needs to occur to ensure that the appropriate doses of antiarrhythmics are being used.³¹ Fetal risk varies over the course of the pregnancy. It is known that the greatest risk of teratogenicity occurs during the first 8 weeks after fertilization.³² After this period, the risk of teratogenicity is reduced although the risk of decreased fetal growth and development still remains. If at all possible, the use of antiarrhythmics should be avoided during the first trimester.³³ The risks associated with individual antiarrhythmics are not well defined. Most of the drugs fall within the Food and Drug Administration s pregnancy category C (Table 1). This means that there are either no controlled studies in humans or that there has been animal studies demonstrating adverse effects.³⁴ There are few antiarrhythmics outside this category including pregnancy category B agents, lidocaine and sotalol. Lidocaine has been shown in human studies to have no significant adverse affects, while sotalol s safety is based on conflicting animal studies.^35-37 Antiarrhythmics that have documented risks include the category D agents atenolol and amiodarone. Amiodarone s adverse effects on the fetus include hypothyroidism, growth retardation, and premature delivery.³⁸ The lack of data makes use of antiarrhythmics in pregnancy difficult. Although there is no definitive first-line agent during pregnancy, those with the greatest clinical data regarding safety and use should be employed first. While radiofrequency ablation is contraindicated during pregnancy, implantable cardioverter-defibrillators (ICDs) can be considered for patients with recurrent ventricular tachycardia or fibrillation. Women with ICDs do not have an increased risk of major complications nor do they have a high number of shocks; these women can consider pregnancy unless the underlying heart disease is a contraindication.³⁹ External cardioversion can also be used when clinically indicated in pregnant women who are hemodynamically unstable.

Conclusions

Several hemodynamic changes during pregnancy can predispose women to the development of new or underlying arrhythmias. While many arrhythmias are benign and self-limited, the risk increases with the presence of underlying cardiac disease. Many tachyarrhythmias can be managed during pregnancy with beta-blockers and digoxin. Antiarrhythmic medications should generally be avoided due to the potentially adverse effects on the fetus.