Arrhythmia-centered treatment review of tachy-arrhythmia during pregnancy

The risk related to arrhythmias is highest in patients with:
1) known structural heart disease,
2) established arrhythmias or
3) congenital heart disease (1,2).

Mechanism is likely related to increase :
1) intravascular volume and stretch of atria and ventricles
2) and baseline heart rate (3,4). 

Likewise, arrhythmias are either:
1) supraventricular - atrial premature beats (APBs) paroxysmal supraventricular tachycardias (AVNRT & AVRT), focal atrial tachycardia, atrial fibrillation or atrial flutter, or
2) ventricular - premature beats (VPBs), tachycardia (VT) or fibrillation (VF).
Only haemodynamically unstable patients may receive anti-arrhythmic medications as they have adverse effects on the fetus (5,6,7).

Management includes:
1) clinical assessment with a detailed history and examination,
2) blood count, renal function, electrolytes (potassium, magnesium) & thyroid function assessments
3) ECG and telemetry/holter monitoring
4) echocardiogram and if required,
5) fetal monitoring.

I. Supraventricular arrhythmias 

Atrial premature beats are frequent and mostly cause few or no symptoms: reassurance and avoidance of the precipitating factors that are smoking, alcohol and caffeine is to be advised. Should symptoms be intolerable, cardioselective beta blockers may be prescribed. 
Paroxysmal supraventricular tachycardia (PSVT) (with no structural heart disease) is the most common tachyarrhythmia (8) and is most often 1) atrioventricular nodal reentrant tachycardia (AVNRT) or 2) atrioventricular reciprocating tachycardia (AVRT). The symptoms (palpitations and/or dizziness), are as in the non-pregnant and are tolerated well if there is no structural heart disease.
Electrical cardioversion (DCCV) is recommended in haemodynamically unstable patients while vagal manoeuvres and adenosine is recommended in stable patients, with 90% reverted to sinus rhythm (9). Intravenous beta blockers (propranolol and metoprolol), also to achieve sinus rhythm, are second-line agents (10).
Significant symptoms may require combination therapy i.e. beta blockers and digoxin for AVNRT, and class IA antiarrhythmic drug (AAD) with digoxin for concealed accessory pathways (AVRT). Refractory arrhythmias should have radio-frequency ablation prior to pregnancy or in selected cases during pregnancy.

Focal atrial tachycardias are rare and mainly occur in those with structural heart disease. Although focal atrial tachycardias (FAT) are often persistent and refractory to treatment including to DCCV, FAT are well tolerated and therefore urgent DCCV and multiple intravenous drugs are not recommended in hemodynamically stable patients. 
Aim of treatment is heart rate control through medications which are digoxin, beta blocker and dihydropyridine calcium channel blockers (11,12). In refractory cases, sotalol, flecainide or amiodarone can be effective nevertheless decision regarding AAD should be made after discussion with the electrophysiologist. 
Incessant FAT should be referred to electrophysiologists to consider radio-frequency ablation (13).
Atrial fibrillation/atrial flutter is less common than PSVT but more common with structural heart disease. Metabolic disturbances including hyperthyroidism and electrolyte imbalance may contribute to AF and should be ruled out. 
Risk of systemic embolism is high due to AF and structural and haematological changes. There is no standardised anticoagulation regimen and the choice of anticoagulation should be tailored to the individual - with none of the novel agents being recommended.
Thromboembolism risk should be assessed with CHADS2 score. (See here a previous article on CH2ADS2-VASc which includes stroke). If the CHADS2 Score <2, and in presence of lone and nonvalvular atrial fibrillation, aspirin may be appropriate. CHADS2 Score 2 or above calls for low molecular weight heparin. Low dose aspirin and heparin are safe but should be stopped prior to delivery. Warfarin should be avoided due to its potential teratogenicity (it is reserved for complex risk cases such as mechanical valves). Dabigatran is not safe due to risk of fetotoxicity (14).
New onset atrial fibrillation and failure of rate control, calls for a rhythm control strategy preferably. If rhythm control is unsuccessful then rate control with digoxin, beta blocker and non dihydropyridine calcium-channel blockers CCB is instituted. Pharmacological cardioversion can be done with Class IA AAD or amiodarone (rarely) (15). In atrial fibrillation and pre-excitation = Class IA and IC (less commonly used due to safely profile) AAD are most useful in blocking accessory pathways and preventing tachycardia. Electrical cardioversion (emergency or elective electrical cardioversion) can be performed at all stages and should be used for any sustained arrhythmia with hemodynamic compromise (16). Electrical cardioversion can also be considered for drug-refractory arrhythmias. Although risk to induce arrhythmias in fetus is small, fetal rhythm monitoring is recommended during cardioversion (17). 
Patients at risk of worsening arrhythmias can be considered for catheter ablation before pregnancy. Radiofrequency catheter ablation is generally avoided given the need for fluoroscopy and is delayed until after delivery. 

II. Ventricular arrhythmias 

Ventricular premature beats are frequently seen and produce few or no symptoms - these are usually palpitations or dizziness. No therapy is needed in asymptomatic patients. Symptomatic patients should be reassured and precipitating factors addressed. Symptoms not tolerated may call for beta blockers. Metoprolol is preferred, as it has no effect on the fetus.
Ventricular tachycardia and ventricular fibrillation are both rare. The former is usually associated with structural heart disease however cases have been reported in the structurally normal heart (18). Risk of recurrent ventricular tachycardia (VT) is high (27%) in patients with previous VT and structural heart disease (19). Women with primary electrical disease such as Long QT syndrome (20) and Brugada syndrome (21) are also at risk.
Other causes of VT are hypomagnesemia, hypertensive crises and thyrotoxicosis (hyperthyroidosis).
Idiopathic ventricular tachycardia in a structurally normal heart. Most commonly, it is right ventricular outflow tract (RVOT) and less frequently, left ventricular outflow tract (LVOT). These are usually catecholamine-sensitive and they rarely degenerate into unstable rhythm; they usually have a benign prognosis (22).
Repetitive monomorphic RVOT VT is treated with cardioselective beta blockers; sotalol is the alternative (23). LVOT VT can be treated with verapamil (24).
Ventricular tachycardia in Long-QT syndrome with a structurally normal heart (25): increased heart rate and shortened QT interval during pregnancy is protective and therefore VT is high postpartum (26). Treatment with beta blockers is effective and should be continued postpartum unless there is definitive contraindication.
Hypertrophic cardiomyopathy: patient usually tolerates pregnancy well but there are several reports describing complications and death during pregnancy (27).
Congenital Heart Disease in a patient with structural heart disease; the prevalence of sustained VT in those with congenital heart disease is 4.5 to 15.9, depending on the type of cardiac lesions.
Peripartum cardiomyopathy: the prevalence of sustained VT is unknown as it is rare. Ventricular tachycardia can be refractory to medications such as metoprolol, amiodarone, lidocaine, and DC cardioversion may be required (28).
Sustained VT with hemodynamic compromise in a patient with structural heart disease can be treated safely with electrical cardioversion at all stages. Although small, there is a theoretical risk of inducing arrhythmias in fetus, and therefore fetal monitoring is recommended.

Sustained VT without hemodynamic compromise can be managed pharmacologically with IV amiodarone or Lidocaine.
Structural heart disease requiresprophylaxis and risk is higher in cases of LV dysfunction. Cardioselective beta blockers, amiodarone or combination can be effective. Sotalol can be an alternative in certain cases.
If a patient is at high risk of sudden death, the external defibrillator (lifeVest) can be used. Data for implantation of ICDs is limited (29). Patients implanted with ICDs can have a successful pregnancy with no fetal compromise and there is no increase in ICD shocks or ICD related complications (30,31).

Conclusions 

All pregnant women with complaints of palpitations/diziness call for a detailed clinical assessment to identify the nature of dysrrhythmia. Investigations should include full blood count, renal function, electrolytes & thyroid function, ECG and echocardiogram. 
All sustained arrhythmias with hemodynamic compromise should be electrically cardioverted (DCCV).
Paroxysmal supraventricular tachycardia is the most common arrhythmia in the structurally normal heart; it is well tolerated. and can be safely treated with vagal manoeuvres and AV node blocking agents.
For AF, rhythm control strategy is preferred in new onset cases but rate control with AV node blocking agents is reasonable. Anticoagulation with aspirin or low molecular weight heparin is preferred choice based on the CHADS2 score.
Ventricular arrhythmias are rare and can be managed as in non-pregnant women.
Electrical cardioversion is safe and can be performed at all stages with fetal monitoring.

Table 1 - Identification and treatment flowchart of tachy-arrhythmias during pregnancy.

Table 2 - Therapy according to tachy-arrhythymia.