Asymptomatic Postpartum Bradycardia: A Case of Spontaneous Resolution in a 34-Year-Old Woman

Introduction

Cardiac disease in pregnancy can present as heart failure, arrhythmias, conduction abnormalities, hypertensive disorders, congenital heart disease, valvular heart disease, or peripartum cardiomyopathy, all of which require careful monitoring and management, due to potential complications, such as pulmonary hypertension and thromboembolism [1].

As for arrhythmias in pregnancy, although tachyarrhythmias are more common, bradycardia can also occur during the pregnancy, peripartum, and postpartum periods; however, it is infrequent and often underreported [2]. Bradycardia is defined as a heart rate below 60 beats per min (bpm). Although the bradycardia is typically benign and self-limited, it is crucial to identify any underlying pathological causes to prevent potential complications. Certain conditions, such as peripartum cardiomyopathy, can be presented with bradycardia, usually presented within the first 5 months after delivery, and require differentiation from transient postpartum bradycardia [3].

A recent case series and literature review by Tran et al in 2024 examined postpartum maternal bradycardia, highlighting its transient and self-resolving nature [2]. Their study of 24 cases identified sinus bradycardia as the predominant pattern, often linked to preeclampsia, medication effects, and neuraxial anesthesia. This report describes the case of a 34-year-old woman with self-limiting postpartum bradycardia as an incidental finding at a routine day 15 postnatal check-up.

Case Report

A 34-year-old woman, para 3, with no known structural heart disease, presented for her routine postpartum check-up 15 days after childbirth. Her previous 2 pregnancies were uneventful, and her last childbirth was 6 years prior. She had no significant family history of heart disease and was not taking any medications before or during pregnancy, except for prescribed iron therapy.

During pregnancy, at 10 weeks’ gestation, she was hospitalized due to hyperemesis gravidarum and palpitations, leading to a diagnosis of transient gestational thyrotoxicosis. The condition resolved spontaneously by week 13, without requiring medical intervention. At 33 weeks, she developed pregnancy-related anemia, which was unresponsive to oral iron supplementation and necessitated intravenous iron therapy. Her hemoglobin levels improved from 9 g/dL to 11 g/dL following treatment. Her baseline heart rate at admission was 112 bpm, fluctuating between 75 and 96 bpm throughout pregnancy, while her blood pressure measurements were normotensive and ranged from 104 to 126 mmHg systolic and 64 to 72 mmHg diastolic.

She underwent an uneventful spontaneous vaginal delivery at 38 weeks, giving birth to a healthy baby girl, weighing 2.96 kg. She was discharged on postpartum day 2 with stable vital signs. During daily postnatal follow-ups from day 1 to day 14, her heart rate ranged from 65 to 97 bpm, while blood pressure remained from 107 to 115 mmHg systolic and 64 to 78 mmHg diastolic. She remained asymptomatic and was not on any medications postpartum.

On postpartum day 15, she was noted to have sudden-onset bradycardia, with a persistent heart rate of 50 bpm. She denied symptoms such as chest pain, shortness of breath, dizziness, syncope, or fatigue. Upon assessment, she was alert, comfortable, and hemodynamically stable, with a blood pressure of 116/80 mmHg, oxygen saturation of 100% on room air, normal respiratory rate, and a temperature of 36.3 °C. No palpable thyroid enlargement was noted. Cardiovascular examination revealed normal heart sounds, with no murmurs, and lung auscultation was clear. An initial electrocardiogram (ECG) demonstrated sinus bradycardia, with a heart rate of 50 bpm and no evidence of atrioventricular (AV) conduction abnormalities (refer to Figure 1). Given the unexpected nature of persistent bradycardia, she was referred to tertiary care for further evaluation.

Upon admission to a tertiary care center, serial ECG monitoring over 6 days consistently demonstrated sinus bradycardia, with heart rates ranging from 42 to 50 bpm, without AV conduction delay. Further investigations were conducted to exclude reversible and pathological causes. Blood tests, including full blood count to rule out infections, electrolytes (sodium, potassium, calcium, magnesium, phosphate) to rule out electrolyte imbalance and pre-eclampsia, and thyroid function tests to rule out thyroid dysfunction, were all within the reference range (refer to Table 1). A 24-h Holter ECG monitoring was performed, revealing normal sinus rhythm, with no significant bradyarrhythmia, pauses, or conduction abnormalities, ruling out sinus node dysfunction. Echocardiography revealed normal cardiac structure and a left ventricular ejection fraction of 59%, confirming the absence of peripartum cardiomyopathy. An ECG stress test was conducted at 6 weeks postpartum, demonstrating appropriate heart rate response to exercise without ischemic changes or arrhythmias.

The patient remained asymptomatic throughout hospitalization, maintained a normal blood pressure range, and was discharged with a diagnosis of asymptomatic postpartum sinus bradycardia. Her heart rate gradually returned to normal, ranging from 64 to 87 bpm by 6 weeks postpartum. Subsequent follow-ups at the cardiology clinic showed stable sinus rhythm, with no further cardiac concerns, and she was eventually discharged from cardiology care.

Discussion

This case highlights the rare occurrence of postpartum bradycardia, which can be a physiological adaptation but requires careful evaluation to exclude pathological causes. Physiological bradycardia is often seen in well-conditioned athletes or during sleep, when a slower heart rate is normal and benign. However, pathological causes, including autonomic dysfunction, cardiomyopathies, infections, ischemia, medications, metabolic and endocrine disorders, and rheumatologic diseases, warrant thorough evaluation to distinguish between normal adaptation and underlying pathology, ensuring appropriate management, while avoiding unnecessary interventions [4]

Postpartum bradycardia may be underreported, but its occurrence has been documented in a study as 1 in 20 000 reproductive women, making it relatively rare compared to maternal tachycardia [5]. This postpartum period, often termed the “fourth stage of labor”, comprises 3 overlapping phases: an acute phase within the first 6 to 12 h with rapid physiological changes and potential complications, a subacute phase lasting 2 to 6 weeks involving continued recovery and self-identified concerns, and a delayed phase extending up to 6 months, with gradual bodily adjustments and minimal pathology [6]. During pregnancy, the cardiovascular system undergoes significant changes, including increased blood volume and cardiac output, which elevate the heart rate [7]. After delivery, as the body reverts to its pre-pregnancy state, the vagus nerve exerts a greater influence, increasing vagal tone and slowing the heart rate [8]. Scientific literature, including a large cohort study from the United Kingdom, indicates that postpartum bradycardia is rare, with maternal heart rates typically stabilizing around 75 bpm by postpartum day 14 [9].

The largest recent published case series of postpartum bradycardia by Tran et al reported that most patients were symptomatic; however, our patient was asymptomatic, and the bradycardia was detected incidentally. The most common symptoms documented are chest discomfort, dyspnea, and dizziness [2]. Cases associated with preeclampsia [11] or anesthesia exposure [5] were more likely to present with symptoms requiring medical intervention. Generally in asymptomatic individuals, bradycardia is often detected incidentally during a routine checkup or on an ECG performed for unrelated reasons, with the most common finding in about 80% of the cases being sinus bradycardia, as seen in our patient [2,10].

Another key difference between our case and the cases reported by Tran et al is the timing of onset. Most cases reported that postpartum sinus bradycardia typically appeared within the first 48 h after delivery. However, in contrast to these findings, the patient in the present case unexpectedly developed bradycardia on postpartum day 15, deviating from the typical pattern. This delayed onset raises the question of whether late-onset postpartum bradycardia is a distinct, under-recognized phenomenon, which raises concerns, as it could be indicative of a more serious underlying condition and can potentially lead to severe complications.

Although limited studies on postpartum bradycardia are available, various causes have been identified. In one of the largest case series on maternal bradycardia during the postpartum period, over 50% of cases were linked to preeclampsia, which contrasts with the findings of a literature review in which the authors noted that most cases described in prior reports were attributed to medications or neuraxial anesthesia [2]. The exact cause of preeclampsia-induced bradycardia remains unclear, but one hypothesis suggests it results from an imbalance between sympathetic and parasympathetic function. This mechanism proposes that a baroreceptor reflex in response to hypertension triggers parasympathetic activation from the medulla, leading to bradycardia, which resolves once blood pressure is stabilized [11]. Medication-induced bradycardia typically occurs and resolves shortly after administration. Commonly implicated drugs include ergotamine, betamethasone, magnesium sulphate, and anesthetic agents. Based on these etiologies, thorough history and physical examination are essential in evaluating bradycardia, as they provide critical insights into the underlying cause, guiding focused diagnostic work-ups to refine the differential diagnosis [4]. Our patient had no identifiable risk factors, such as preeclampsia, medication use, or recent anesthesia exposure. Her pregnancy was largely uneventful, aside from transient gestational thyrotoxicosis at 10 weeks, which resolved by week 13 without intervention. She also had pregnancy-related anemia, requiring intravenous iron therapy at 33 weeks, which improved her hemoglobin levels. However, neither condition is known to predispose individuals to postpartum bradycardia. Other reports described postpartum bradycardia with different underlying mechanisms. Acharya and Shrestha reported postpartum transient hyper-vagotonic sinus node dysfunction, in which excessive vagal tone caused transient bradycardia, similar to our case, as it was also asymptomatic and self-resolving [12].

The diagnostic approach in the present case followed a stepwise evaluation to exclude metabolic, endocrine, and structural cardiac abnormalities. These tests are routinely conducted in the clinical management of bradycardia to rule out underlying pathological causes [4]. A 12-lead ECG, essential for assessing rhythm, conduction disturbances, and structural abnormalities [13], returned normal results in our patient, excluding pathological causes. Echocardiography demonstrated no structural abnormalities, with a normal left ventricular ejection fraction effectively ruling out peripartum cardiomyopathy (PPCM) as a cause of bradycardia. The importance of echocardiography in evaluating postpartum bradycardia has been highlighted in previous reports. In 2017, Codsi et al described a case of PPCM presenting as bradycardia, underscoring the role of echocardiography in differentiating PPCM from other causes of postpartum bradycardia [14]. In contrast, our patient had no clinical signs of heart failure, and echocardiography confirmed normal left ventricular function, reinforcing that her bradycardia was not secondary to PPCM. This aligns with case series by Tran et al from 2024, in which echocardiographic assessments were part of the diagnostic workup; however, no significant structural abnormalities were identified in most cases, further supporting the benign and self-limiting nature of postpartum bradycardia [2].

To further assess the persistence of bradycardia and rule out underlying conduction abnormalities, 24-h Holter monitoring was performed in our case. This revealed normal sinus rhythm with no pauses, bradyarrhythmia, or AV conduction defects, effectively ruling out sinus node dysfunction. These findings reinforce that most cases of postpartum bradycardia, including ours, are benign and self-limiting, with no underlying arrhythmogenic pathology detected on extended cardiac monitoring [2]. While Holter monitoring is essential for capturing intermittent bradyarrhythmia and correlating symptoms with heart rhythm [15], the absence of abnormalities in both our case and the cases in the series of Tran et al supports the hypothesis that postpartum bradycardia is often a transient autonomic adaptation rather than an indicator of structural or electrical heart disease [2].

In our patient, at 6 weeks postpartum, an ECG stress test showed an appropriate heart rate response to exercise, with no ischemic changes or arrhythmias, further confirming the absence of conduction abnormalities or autonomic dysfunction. This parallels the findings of Tran et al, in which most cases resolved spontaneously, reinforcing that postpartum bradycardia is typically benign [2]. However, the later onset and incidental detection in our patient suggest that some cases can remain undiagnosed unless actively screened.

The treatment of bradycardia lies on the underlying condition and the severity of the presentation. In more severe or symptomatic cases, especially when bradycardia is linked to conduction disorders or sinus node disease, pharmacological treatment with atropine, a parasympatholytic that blocks muscarinic acetylcholine receptors, can be necessary [14]. For patients with hemodynamic instability, temporary pacing might be required [15]. A literature review highlighted that most cases of maternal postpartum bradycardia are benign and self-limiting and rarely require intervention, with normal findings in investigations [2]. This aligns with the present case, in which monitoring was the primary management approach. However, it is essential to document this history for future pregnancies, to ensure enhanced postnatal care. This is also important as to prevent unnecessary intervention, such as pacemaker insertion. Early multidisciplinary collaboration involving primary care physicians, cardiologists, and obstetricians is crucial for comprehensive care in such cases [2].

Conclusions

This report highlights the condition of postpartum maternal bradycardia and emphasizes the importance of clinical history, targeted investigations, and follow-up in guiding appropriate management. While postpartum bradycardia is rare and typically self-limiting, differentiating it from pathological causes is crucial to prevent unnecessary interventions. Given its variable presentation and potential under-recognition, increased awareness among clinicians is essential to ensure timely evaluation and appropriate management when bradycardia is encountered in routine postpartum monitoring.