Arrhythmias are the most common cardiac complications occurring in pregnancy. Although the majority of palpitations in pregnancy may be explained by atrial or ventricular premature complexes, the full spectrum of arrhythmias can occur. In this article, we establish a systematic approach to the evaluation and management of arrhythmias in pregnancy. Haemodynamically unstable arrhythmias warrant urgent cardioversion. For mild cases of benign arrhythmia, treatment is usually not needed. Symptomatic but haemodynamically stable arrhythmic patients should first undergo a thorough evaluation to establish the type of arrhythmia and the presence or absence of structural heart disease. This will ultimately determine the necessity for treatment given the potential risks of anti-arrhythmic pharmacotherapy in pregnancy. We will discuss the main catalogue of anti-arrhythmic medications, which have some established evidence of safety in pregnancy. Based on our appraisal, we provide a treatment algorithm for the tachyarrhythmic pregnant patient.


Graphical Abstract

Graphical Abstract

Arrhythmias are the most common cardiac complications occurring in pregnancy.1 Advances in clinical medicine have led to an increase in the number of pregnancies in women with pre-existing cardiovascular disease as well as a higher prevalence of obesity and hypertension and rising maternal age.2–4 However, arrhythmias in pregnancy remain a topic with limited evidence. A review of the existing literature provides the best means of synthesizing the current evidence base. Arrhythmias during pregnancy demand careful consideration towards implications of treatment. We establish an approach to the pregnant woman presenting with suspected arrhythmia and appraise key aspects of pathophysiology, epidemiology, diagnosis, and management.
Burden of palpitations and arrhythmia in pregnancy
Cardiovascular adaptations in pregnancy
The maternal heart undergoes major structural and functional changes to accommodate the developing foetus (Figure 1). This combination of vasodilatory, hormonal, structural, and autonomic nervous system, adaptations during pregnancy leads to cardiomyocyte sensitization and cardiac hypertrophy, increase in cardiac output and vascular volume, formation of a hyperdynamic circulation, and decrease in total peripheral resistance.5–8 These haemodynamics may manifest symptomatically as palpitations or be associated with sinus tachycardia.9,10

Figure 1.

Haemodynamic changes in pregnancy. Up arrow, increase; down arrow, decrease. EDV, end-diastolic volume; HR, heart rate; LV, left ventricle; NO, nitric oxide; SV, stroke volume; TPR, total peripheral resistance.


Haemodynamic changes in pregnancy. Up arrow, increase; down arrow, decrease. EDV, end-diastolic volume; HR, heart rate; LV, left ventricle; NO, nitric oxide; SV, stroke volume; TPR, total peripheral resistance.

Prevalence of palpitations

Palpitations are common in pregnancy. However, they do not always indicate underlying arrhythmia. Amongst 822 women referred to an obstetric medicine clinic in Kuwait, 3.3% were due to palpitations. However, only 26% of these women required medical treatment.11 In a Korean study of 261 women, 11.5% reported experiencing palpitations at some point throughout gestation. Of a further 22 patients who underwent 24-h Holter monitoring, 18 experienced palpitations but only 4 (22%) had irregularities on their Holter trace, all of which were benign.12 Namely, they were atrial and ventricular premature complexes and sinus tachycardia.

Palpitations secondary to sinus tachycardia are common. Tachycardia is normal when arising in the context of exercise, emotional stress, coffee, or nicotine. In pregnancy, the physiological increase in heart rate further disposes to tachycardia.6,13 Indeed, the prevalence of palpitations appears to be highest in late second and early third trimesters (Figure 2), which grossly parallels the timing of the final rise in heart rate.7


Figure 2

Palpitations at different stages of gestation.11,12,14,15 This graph depicts the relatively probability of palpitations occurring throughout pregnancy based on limited data.

Most cases of palpitations may be explained by premature atrial complexes (PACs) and premature ventricular complexes (PVCs). These are seen in over 50% of women evaluated for palpitations in pregnancy.16 They are almost always benign. Occasionally, they can trigger brief episodes of non-sustained tachycardia, but these virtually never degrade to an unstable rhythm.6 Concern only arises in the case of a high PVC burden, which refers to the proportion of PVCs occurring in relation to the total number of QRS complexes on a standard 24-h Holter monitor. A recent case–control study compared 53 pregnant women with no pre-existing structural heart disease but with a median PVC burden of 9.2% to 53 women without any cardiac issues.17 Six women (11%), all of whom had a PVC burden >5%, experienced a cardiac event (one heart failure, five sustained ventricular tachycardia). All cases were successfully controlled with medical therapy.

Aside from PACs and PVCs, the prevalence of other arrhythmias is variably reported in the literature. The most recent evidence comes from a 12-year US study utilizing the nationwide inpatient sample to examine hospital discharges of pregnant women aged 18–50 between 2000 and 2012.18 Of 57 315 593 pregnancy-related hospitalizations, the overall frequency of arrhythmia was 68 per 100 000 hospitalizations (0.07%). Atrial fibrillation (27 per 100 000), supraventricular tachycardia (22 per 100 0000), and ventricular tachycardia (16 per 100 000) were the most common. The study also found that women 41–50 years of age had overall greater frequency of any arrhythmia (199 per 100 000) compared with women 18–30 years of age (55 per 100 000), although it is unclear which types of arrhythmias were most prevalent within these age brackets. Other smaller studies also report similar rates of arrhythmia, with AF being the most prevalent overall.19,20

Older studies dispute this predominance of AF. However, it is worth noting that, as Vaidya et al.18 also postulates, this discrepancy may be due to the time periods that the studies were conducted. The increase in maternal age over the years, and the associated increase in risk factors, such as hypertension, diabetes, obesity, and structural heart disease, may explain why AF has emerged as the most frequent arrhythmia in pregnancy in more recent studies. For example, an older US study from 1998 to 2007 of 42 602 106 admissions reported the prevalence of supraventricular tachycardia (SVT) to be the highest at 16.4 per 100 0000 and AF at 12.5 per 100 000.21 The majority (86%) of the study population was women aged <35 years of age. This younger population group could also contribute to the reduced prevalence of AF. In another US study from 1992 to 2000 of 136 422 pregnancy-related admissions to a single hospital over 8 years, the rate of AF and atrial flutter (AFL) combined was only 1%.13 About 60% of arrhythmias were one of sinus tachycardia, bradycardia, or arrhythmia (ST, SB, or SA). A further 20% were due to APCs or VPCs and 14% due to supraventricular tachycardia (SVT). Similar to the previous study, the mean age of the study population was 25 years old.

Occasionally, VT can also occur without pre-existing heart disease.22,23 Most cases originate from the right ventricular outflow tract (RVOT) as monomorphic VT. These rarely cause haemodynamic deterioration and only manifest as ectopic beats, bigeminy, or self-limiting bursts of VT.6 Polymorphic VT can also occur without SHD due to QT prolongation and increased catecholaminergic activity.24 Women with long QT syndrome (LQTS) are at high risk, particularly in the postpartum period.25 Syncope in a patient with LQTS can indicate impending cardiac arrest.26


Bradyarrhythmias are also rare in pregnancy but can arise in the setting of SHD.27 First-degree heart block is the most common. It may be seen in women with rheumatic or congenital heart disease.28 Mobitz type 1 is more common and is generally benign, whereas Mobitz type 2 can progress to complete heart block (CHB).29 Complete heart block may be congenital or acquired in origin. Congenital CHB is associated with maternal connective tissue disease. About 30% of such cases may present for the first-time during pregnancy,30 but most women will already have a permanent pacemaker in situ by the time they are pregnant.31 Acquired CHB may occur secondary to infection, valvular disease, or sarcoidosis.32 Sinus bradycardia is rare in pregnancy given the physiological increase in HR.31 However, peripartum cardiomyopathy presenting as bradycardia has been reported and may be an important consideration once more common causes are excluded.33

Figure 3 summarizes the most prevalent types of arrhythmias that need to be considered in a pregnant woman who presents with symptoms concerning such.

Figure 3

Approach to diagnosis in a pregnant patient with symptoms of arrhythmia.6,13,15,31  aSymptoms include palpitations, dizziness, presyncope, and syncope. The likelihood of ‘Other’ arrhythmias is increased in the case of pre-existing structural heart disease. Other, atrial tachycardia, atrial flutter, ventricular tachycardia, ventricular fibrillation, and bradyarrhythmias. PAC, premature atrial complexes; PVC, premature ventricular complexes; SA, sinus arrythmia; ST, sinus tachycardia; SVT, supraventricular tachycardia.

Approach to the pregnant woman with palpitations


History-taking to establish severity and cause is important in determining whether to initiate drug therapy, particularly with regard to dizziness, syncope, or dyspnoea, as well as to evaluate the need to exclude underlying heart disease.6,34 Syncope occurring in the first trimester may be associated with higher rates of preterm birth, congenital anomalies, and an increased incidence of maternal arrhythmias and syncope in the first-year postpartum.35 Symptoms of other causes of arrhythmia or tachycardia, such as hyperthyroidism, drugs, anxiety, anaemia, pulmonary embolism, and infection should also be ascertained.

An antenatal history should follow the cardiac history. The physiological drop in blood pressure is maximal in the second trimester, so episodes of syncope during this period may be attributed to hypotension.6 A past medical or family history of SHD or other predispositions to arrhythmia (previous episodes, hypertension, pulmonary disease, etc.) assists in risk stratification.6,31,34


The cardiac examination should be conducted as for a non-pregnant patient. However, some exceptional findings may be considered normal in pregnancy. The hyperdynamic circulation can cause a soft systolic flow murmur and a widely split first heart sound. In late pregnancy, splitting of the second heart sound and mild peripheral oedema may also occur.36 The presence of a displaced apex beat, added heart sounds, and mitral regurgitation can indicate heart failure secondary to cardiomyopathy.37


The electrocardiogram (ECG) is the key initial investigation. There are several changes considered normal in pregnancy (Figure 4). The increased HR typically causes a shortening of the PR, QRS, and QT intervals, whilst the gravid uterus and the elevation of the diaphragm can cause a physiological left axis deviation.6,38–40 An increased QRS amplitude is occasionally seen.38 Q-waves in leads II, III, aVF, and V4–V6 and flat or inverted T waves in leads III and V1–V3 are found in the second and particularly third trimester.40 Associated with the latter, sagging of the ST segment may also be noted. However, other changes, such as a ‘delta’ wave suggestive of WPW, or a prolonged QT interval indicating LQTS should be treated as pathological findings.

Figure 4

Physiological electrocardiographic changes in pregnancy.38–40 A left-axis deviation (not depicted) can also occur. Q, Q-wave; P, P-wave; R, R-wave; S, S-wave; T, T-wave; V1–V6, chest leads; lead I–III, limb leads.

A transthoracic echocardiogram is essential to exclude structural and functional causes of heart disease and to establish the state of ventricular function prior to choosing drug therapy, if indicated. As with the ECG, the normal echocardiographic findings in a pregnant patient can vary from the non-pregnant counterpart (Figure 5). Most of the changes gradually increase until peaking in the third trimester and reverse in the postpartum period.41
Figure 5

Structural echocardiographic changes in pregnancy.42,43 Up arrow, increase; down arrow, decrease.

In cases where no acute pathology is found but palpitations occur on a regular basis, a Holter monitor or an event loop recorder should be requested in order to capture the rhythm during symptomatic episodes.6 Electrolyte and thyroid hormone levels should be measured to exclude other causes.6

Principles of management of arrhythmias in pregnancy

The approach to managing arrhythmias is based on its aetiology and rhythm during symptoms. Any patient with sustained arrhythmias resulting in haemodynamic compromise needs urgent stabilization with intravenous fluids, anti-arrhythmics and electrical cardioversion.44 Asymptomatic arrhythmias, unless deemed life-threatening, do not require treatment.

Anti-arrhythmic drugs in pregnancy carry multiple risks. As the most critical in utero development occurs in the first trimester, with 5–9 weeks being the most critical period with respect to structural abnormalities,45 drug therapy should ideally be avoided in the first trimester.46 When necessary, as few medications as possible should be used from the limited catalogue of drugs that have some evidence of safety in pregnancy. The current evidence base pertaining to the side effect profiles of classes I through IV anti-arrhythmics in pregnancy is summarized in Table 1.

Table 1

Foetal and neonatal side effects of commonly used anti-arrhythmic medications in pregnancy47–68

ClassDrugFDA categorya

Notable foetal and neonatal side effects

Other comments
Good quality evidenceLow-quality evidence
I—sodium channel blockers Quinidine None described Torsades, preterm labour, neonatal thrombocytopenia, ototoxicity  
Procainamide Limited evidence Torsades, preterm labour Can cause lupus-like syndrome with long-term use 
Lignocaine Foetal bradycardia Increase myometrial tone, placental hypoperfusion, foetal bradycardia  
Flecainide None described Maternal QTc requires close monitoring with use 
Propafenone Limited evidence  
II—beta blockers Beta-blockersb LBW, IUGR, preterm birth Neonatal hypoglycaemia, neonatal bradycardia All beta-blockers other than atenolol are considered safe in pregnancy 
III—potassium channel blockers Amiodarone Hypothyroidism, IUGR, preterm birth Pregnancy loss, congenital nystagmus, synchronous head titubation, neonatal hypotonia, hypertelorism, micrognathia, aggravation of heart failure Hypothyroidism more prominent when administered only in third trimester rather than throughout gestation 
Sotalol Torsade de pointes, hypotension, bradycardia, LBW, IUGR, prematurity With early pregnancy exposure—teratogenic effects, LBW Maternal QTc requires close monitoring with use 
Ibutilide Limited evidence  
IV—calcium channel blockers Diltiazem Limited evidence  
Verapamil Maternal hypotension, neonatal convulsions Cardiac malformations (in animal studies only) Generally well tolerated in pregnancy 
V—other Adenosine Limited evidence Foetal bradycardia, preterm labour First-line pharmacological option for SVT in pregnancy 
Digoxin Unreliable serum levels None described Considered the safest anti-arrhythmic in pregnancy 

IUGR, intrauterine growth restriction; LBW, low birth weight.

a. The former Food and Drug Administration (FDA) classification of drugs in pregnancy: (A) no demonstrated risk to the foetus based on well-controlled human studies; (B) no demonstrated risk to the foetus based on animal studies; (C) animal studies have demonstrated foetal adverse effects, no human studies, potential benefits may warrant use of the drug; (D) demonstrated human foetal risk, potential benefits may warrant use of the drug; and (X) demonstrated high risk for human foetal abnormalities outweighing potential benefit.

b. Not including atenolol which should be avoided in pregnancy.

Treatment of specific arrhythmias in pregnancy

Haemodynamically unstable arrhythmia

All haemodynamically unstable patients with arrhythmia warrant urgent electrical cardioversion.51 Cardioversion is considered safe throughout pregnancy.69 It has a high success rate of 93.2%.70 There is some limited evidence to suggest an increased risk of foetal arrhythmia,6 preterm labour in late pregnancy,48 and cases of foetal distress necessitating emergency caesarean section.70 Having access to an operating theatre is a prerequisite for attempting cardioversion.70,71 Foetal monitoring during cardioversion (only if time permitting) and post-cardioversion are also recommended69; however, this should never delay cardioversion or initiation of treatment. The woman should receive 100% oxygen, early intravenous access, and be placed in the left lateral position to minimize vena caval compression.70 As for non-pregnant adults, the usual position of pad placement is anterolateral with the lateral pads being placed under the left breast tissue.72

Benign arrhythmias

For PACs, PVCs and sinus tachycardia, reassurance, and expectant management are appropriate. The woman may be advised to avoid potential stimulants, such as smoking, caffeine, and alcohol if not already doing so.73 Gentle exercise and good hydration are also beneficial.74 If symptoms prove intolerable, a cardioselective beta-blocker (e.g. metoprolol) can be commenced, preferably after the first trimester.48 Metoprolol and propranolol are the beta-blockers of choice in pregnancy. Atenolol should be avoided altogether due to a higher association with low birth weight.75 Additionally, in women with a high PVC burden (>5%), a precautionary referral to a cardiac-obstetric or arrhythmia clinic should be made.17

Supraventricular tachycardia

For haemodynamically stable SVT, a conservative approach with vagal manoeuvres, such as carotid sinus massage and Valsalva should be trialled first. If persistent, first-line medical therapy with intravenous adenosine is shown to be 89–100% effective.13,76 All narrow complex tachycardias can be treated with intravenous adenosine as it will either resolve or at least reveal the underlying arrhythmia.

Second-line therapy for SVT is a cardio-selective beta-blocker (e.g. metoprolol),51 and third-line therapy is either verapamil50 or procainamide.69 For long-term SVT prophylaxis, an oral beta-blocker (with or without digoxin) or verapamil is appropriate.50 However, in patients with WPW syndrome, flecainide or propafenone should be used instead.51 Verapamil and digoxin can increase risk of rapid accessory pathway conduction (due to AF) in these patients and should be avoided.48 Finally, amiodarone should only be considered as a last resort for potentially life-threatening and/or refractory SVT.50,69

Atrial fibrillation and atrial flutter

In haemodynamically stable AF or AFL with a structurally normal heart, chemical cardioversion with intravenous ibutilide or flecainide can be trialled.51 Otherwise, rate-control with a cardioselective beta-blocker (intravenous in the acute setting and oral for long-term therapy) is appropriate. Digoxin and verapamil can also be considered for long-term rate-control if beta-blockers fail.77 Should all these agents fail, flecainide, propafenone, or sotalol can be used as rhythm control.48,51 It is important to establish the duration of AF or AFL prior to proceeding with rhythm control and assess the need for anticoagulation based on the patient’s thromboembolic risk.

Additionally, AF in the setting of pre-excitation (e.g. WPW) manifests as a wide-complex tachycardia and should be treated with intravenous procainamide.48 Additionally, AFL in patients with CHD is not well tolerated and may require electrical cardioversion.51

Anticoagulation in pregnancy is a challenging dilemma but warrants consideration in the setting of persistent AF and AFL. The utility CHA2DS2-VASc score, the standard stroke risk calculator for those with AF, is poorly validated in the pregnant population.78 Nevertheless, the latest guidelines still recommend its application for risk stratification of pregnant patients with AF.51,77 Those with non-valvular AF, a low CHA2DS2-VASc score, or lone AF may not require anticoagulation.79

The choice of anticoagulation, namely low molecular weight heparin (LWMH) or vitamin K antagonists (i.e. warfarin), depends on the stage of gestation.51 Direct oral anticoagulants (DOACs) are contraindicated altogether because of a lack of safety and efficacy data in pregnancy.80 Heparin compounds, namely low molecular weight heparin (LWMH) and unfractionated heparin (UH), are best in the first trimester and during the last month of pregnancy.51 Weight-based LWMH is the most preferred regimen as it has fewer side effects compared to UH such as thrombocytopenia, bleeding, and osteoporosis.48,79 Warfarin is preferred for anticoagulation from the second trimester until 1 month before the expected delivery date.51 It is best avoided in the first trimester due to its teratogenicity. However, the latest consensus is that lose-dose warfarin (daily doses of 5 mg or less) is the best anticoagulation regimen for women with high thrombotic risk, such as those with mechanical heart valves, even in the first trimester.81 This is because warfarin is a more effective anticoagulant than heparin and the risk of embryopathy is minimized (<3%) with low doses. Its adverse other adverse outcomes neurological complications, miscarriage, and stillbirth also appear to be dose-dependent.82,83 Those requiring warfarin doses >5 mg in the first trimester should be switched to LWMH by the sixth week.81 By 36 weeks and beyond, all women requiring anticoagulation during pregnancy should be changed to (if not already on) LWMH or UH.50 Heparin should be withheld 12 h before planned induction of labour. Anticoagulation can resume 12 h after vaginal delivery or 24 h after caesarean delivery.79

Ventricular tachyarrhythmias

Treatment of VT in the setting of SHD should be tailored to the underlying cardiac condition. Immediate electrical cardioversion is recommended for unstable sustained VT.51 Stable cases can also undergo either electrical or chemical cardioversion (with lidocaine).50,51 Procainamide or quinidine can be used if lidocaine is ineffective.48 Patients with VT and SHD require suppressive therapy, often with beta-blockers. Sotalol, quinidine, and mexiletine (despite limited evidence) are offered as second-line options.48,50 In all cases ventricular arrhythmia, amiodarone is once again considered last-line pharmacotherapy.51

Polymorphic VT has a high risk of progressing to VF. Emergency treatment involves removing all potential causes by correcting electrolytes and removing precipitating drugs—Classes I and III anti-arrhythmics, macrolides, non-sedating anti-histamines, anti-depressants, and anti-psychotic drugs.6 Magnesium sulphate is particularly effective at suppressing torsade de pointes. It is associated with few side effects, but maternal hypothermia and foetal bradyarrhythmias are observed to occur.84

Idiopathic VT originating from the RVOT is typically haemodynamically stable and responds to beta-blockers.48 Flecainide, procainamide, or sotalol is suitable alternatives.4,48,51 For the less common form of VT arising from the left ventricular outflow tract, verapamil is most effective.85

A treatment algorithm summarizing the main approach to the tachyarrhythmic pregnant patient is depicted in Figure 6.

Figure 6

Pharmacotherapy for tachyarrhythmia in pregnancy. This algorithm provides a summary of treatment pathways that may utilized according to the patient’s haemodynamic state, type of arrhythmia, and the presence or absence of structural heart disease. There are other factors which need to be considered prior to initiating therapy, such as the stage of gestation as drug therapy should ideally be avoided in the first trimester. If refractory to pharmacotherapy, then invasive measures need to be considered. aBeware of pre-excitation syndromes (e.g. Wolf–Parkinson White) in which case long-term therapy should be with flecainide or propafenone. Flecainide and propafenone should only be used in cases without structural heart disease. bMagnesium sulphate can also be administered in the case of polymorphic VT to suppress deterioration to VF. AF, atrial fibrillation; IV, intravenous; LWMH, low molecular weight heparin; NCT, narrow complex tachycardia; SHD, structural heart disease; VT, ventricular tachycardia.


Invasive interventions

For pharmacotherapy-refractory arrhythmias, invasive interventions may be considered. Catheter ablation, if needed, should be performed in the second trimester, after which organogenesis is complete, the foetal thyroid is still inactive, and the volume of the uterus is sufficiently small to maximize distance from the chest.16 Ablation without fluoroscopy altogether, a technique known as zero fluoroscopy ablation, has also emerged in recent years and mitigates any risk of radiation exposure.86,87 Women with unstable ventricular arrhythmias and at high risk for sudden cardiac death may benefit from an implantable cardioverter-defibrillator (ICD).48,88 On the other hand, for symptomatic sinus bradycardia not responding to conservative therapy a temporary pacemaker should be considered.51 With CHB diagnosed for the first time in pregnancy, the emerging consensus is that asymptomatic cases without other evidence of conduction or structural heart disease can be managed expectantly.48,89

ICDs and pacemakers are well-tolerated in pregnancy,90 although concerns regarding the lack of coordinated guidelines have been raised.91 Studies, albeit limited, report positive outcomes overall.92,93 They can be successfully implanted during pregnancy, especially beyond 8 weeks, either with or without fluroscopy.51,94 In the event of a caesarean delivery, the ICD’s defibrillator function should be deactivated (either via a programmer or placement of a magnet to inhibit sensing) as the use of electrocautery can prompt inappropriate shocks.92

Postpartum considerations

In the first 48 h after delivery, the mother endures the most dramatic physiological changes in haemodynamics. This phase requires vigilant monitoring of maternal fluid status.95 It takes 2–6 weeks postpartum for the cardiac output to return to non-pregnant levels.7,96–98 Structural adaptations, such as the physical growth of the heart muscle may even take up to 12 weeks to revert.7 In women with LQTS type 2, the risk of arrhythmias is increased in the post-partum period and up to the first 9–12 months after delivery.99 The mother may be susceptible to further arrhythmias during this time and require ongoing treatment whilst breastfeeding.

The treatment of arrhythmias during lactation is beyond the scope of this review. Briefly, metoprolol remains the beta-blocker of choice.34 However, caution is advised with sotalol and adenosine due to minimal safety data.48 Amiodarone should also be used with caution and only if necessary as it concentrates in breast milk and can predispose to harmful foetal outcomes.100


Most palpitations in pregnancy are benign and usually occur due to atrial or ventricular premature complexes. Rarer and more insidious arrhythmias warrant vigilant evaluation and management. Careful consideration should be given to the stage of gestation and the haemodynamic state of the patient. The clinician must also be aware of the drugs that are appropriate for use during pregnancy in order to minimize maternal and foetal risk.

Fuente: https://doi.org/10.1093/europace/euab297