Atrial fibrillation (AF) in pregnancy is an uncommon phenomenon and the diagnosis is made by excluding any secondary causes like valvular heart disease, structural heart disease, asthma, obstructive sleep apnea, or other cardiopulmonary disease. Pregnant patients presenting as an AF should have an extensive workup including detailed history taking, physical examination, 12-lead electrocardiogram, complete blood count, basic metabolic panel with serum electrolytes, a thyroid function test, urine drug screen, and a transthoracic echocardiogram. Treatment of AF in pregnancy is challenging due to concern for teratogenicity associated with use of medications and side effects of anticoagulation. Direct current cardioversion is the treatment of choice in hemodynamically unstable patients, whereas controlling the heart rate is the primary treatment goal in patients who are hemodynamically stable.

A 40-year-old female with no significant past medical history, P1021 at 29th weeks and 6 days of gestation, presented to the emergency department with a chief complaint of palpitations for 30–45 minutes along with sudden onset of diaphoresis, shortness of breath, and chest pain. In the emergency department, the patient was found to be in an irregularly irregular rhythm, and electrocardiogram showed atrial fibrillation with a ventricular rate of 101 beats per minute (Figure 1), blood pressure was 112/76 mmHg, respiratory rate 14/minute, and oxygen saturation of 98% on room air. The patient’s serum electrolytes, hemoglobin, hematocrit, and thyroid stimulating hormone were within the normal range, and the urine drug screen was negative. The imaging modality of choice for evaluation of pulmonary embolism in pregnant patients, which is the ventilation-perfusion scanning of lungs, ruled out pulmonary embolism. Transthoracic echocardiogram showed an ejection fraction of 60–65%, without any structural or valvular abnormalities.

Initially, three intravenous pushes of Diltiazem were given without any resolution with heart rate going as high as 180 beats per minute with the rapid ventricular rate on the cardiac monitor and was subsequently started on Diltiazem drip at a rate of 10 mg/h. After which the patient’s echocardiogram showed cardioversion to normal sinus rhythm within 24 hours of beginning the Diltiazem drip (Figure 2). No probable cause of AF was found, so the patient was discharged home without any anticoagulation or antiarrhythmics, as risks overweigh the benefits of treatment with anti-coagulants and antiarrhythmics for lone AF.

Lone AF was coined 60 years ago in 1954 by Evans and Swann for patients in whom subsequent investigation shows that heart disease is absent [1].

During pregnancy, arrhythmias are triggered due to several physiological changes like an increase in cardiac output, heart rate, plasma volume, wall tension along with fluctuating hormonal levels, and reduction in systemic vascular resistance or sometimes due to the use of tocolytics [2]. Risk factors like increased maternal age, white race, male sex, obstructive sleep apnea, obesity, consuming alcohol, endurance sports, family history, and several recognized mutations could trigger the development of lone AF [2],[3].

The mechanism behind lone AF is still unclear. However, atrial ectopy, atrial enlargement, fibrosis, increased vagal tone are known to play a role. Genomic variations, microRNAs, and some changes in relevant biomarker levels have also correlated with lone AF [4].

Lone AF is a diagnosis of exclusion and is only confirmed after all the causes of AF are ruled out. Initial emergent workup should include a 12-lead electrocardiogram, complete blood count, basic metabolic panel with serum electrolytes, a thyroid function test, urine drug screen, and a transthoracic echocardiogram, an important implications for both maternal and fetal outcomes in management of lone idiopathic AF during pregnancy. First trimester is the period in which organogenesis takes place, developing fetus is highly sensitive to the potential teratogenic effects of medications. Drugs may have possible effects on fetal growth or lead to fetal arrhythmias in the second and third trimesters [5].

Many commonly used medications in AF like some beta-blockers and anticoagulants such as warfarin have been shown to increase the risks of adverse fetal outcomes [6],[7],[8],[9]. In hemodynamically unstable patients, direct current cardioversion is the treatment of choice; however, in hemodynamically stable patients controlling the heart rate is the primary treatment goal. Beta-blockers, non-dihydropyridine calcium channel blockers can be used as the first choice in pregnant patients. Digoxin can be used, but due to varying serum levels and its toxicity, especially during pregnancy, its use has been limited. Quinidine is one of the safest drugs used in pregnancy and can be used for pharmacological cardioversion as well. Antiarrhythmic drugs like sotalol, flecainide, or propafenone are also reported to be safe in a few studies [10].

Pregnancy is a hyperdynamic state and is associated with vasodilation of the systemic vascular resistance, increase in cardiac output, decrease in arterial pressures including systolic blood pressure, diastolic blood pressure and mean arterial pressure, and increase in heart rate. All these changes may predispose a pregnant patient to arrhythmias. As lone AF is a diagnosis of exclusion in pregnant patients, a careful history, examination, and a thorough workup for a secondary cause of arrhythmias should be ruled out before making a definitive diagnosis of lone AF of pregnancy. It is extremely challengi to treat lone AF of pregnancy because of concern for teratogenicity associated with medications and the use of anticoagulation during pregnancy.