Atrial Fibrillation - Pharmacologic Cardioversion with Intravenous Calcium Gluconate

Ramachandran Muthiah*

*Correspondence to: Ramachandran Muthiah, Morning star hospital, Enayam Thoppu, Kanyakumari District, India.

              
Copyright.

© 2025 Ramachandran MuthiahThis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: 12 Aug 2025

Published: 01 Sep 2025

DOI: https://doi.org/10.5281/zenodo.17053196

Abstract:

A 66 year old known hypertensive and stroke patient presented with sudden onset of tachycardia and  ECG  revealed Paroxysmal Atrial Fibrillation (AF). Echocardiography revealed structurally normal heart with no intracardiac thrombi or spontaneous echo contrast. The arrhythmia was refractory to Diltiazem and  amiodarone and  it was reverted to sinus rhythm by intravenous calcium gluconate.

Introduction

Atrial fibrillation (AF) is the most common serious cardiac arrhythmia in the surgical setting and its incidence varies according to the type of surgery as 3% in adults aged ≥ 45 years undergoing non?cardiac surgery [1], but it is much higher (30%) in thoracic surgery [2]. Most patients developing AF after surgical intervention convert to sinus rhythm spontaneously [3] and this self?limited arrhythmia that usually does not always results hemodynamic compromise and death. However, evidence since the 1980s shows that POAF (postoperative AF) has a poor prognosis, with an increased risk of postoperative complications [4]. The rapid irregular ventricular rate can decrease coronary flow, leading to myocardial ischemia [5], decreased diastolic filling time and cardiac output, loss of atrial contraction [6] and all these effects on the cardiopulmonary hemodynamics can lead to hypotension. Long?term risk of complications such as stroke after non?cardiac surgery is 0.78% during the follow?up period of 2.1 years [7] and the cumulative risk of stroke at 1 year after discharge was 1.47% compared to 0.36% in those with no AF.         

Case Report

The staff nurse in the postoperative surgical care unit noticed sudden onset of rapid irregular heart rate in the ECG monitor in a 66 year old male patient who underwent surgical resection for strangulated right sided inguinal hernia 6 hours before. He is an Asian black, 175 cm height, obese with BMI (body mass index 34 (weight 85 kg), blood pressure 130/80  mmHg with drugs, pulse rate 84 bpm and regular before surgery. He was a known hypertensive, not a smoker, alcoholic and diabetic. He had stroke one year back, but not taking any anticoagulants, antiplatelets and antiarrhythmic drugs before. He had repeated episodes of wheezing before surgery and is on amlodipine for hypertension which is under control. On examination, he was drowsy and not fully recovered from anaesthesia,  afebrile, not anemic, not cyanosed, no clubbing and no pedal edema. Peripheral pulses were normally felt. Bruit over both carotids, Jugular venous pressure not elevated, No precordial bulge and apical impulse in the normal location. First heart sound varying in intensity. No murmurs or additional sounds, emphysematous chest  with scattered rales and rhonchi in the lung fields and had right sided hemiparesis with aphasia. He suffered from right sided inguinal hernia for which he never underwent surgery before. He developed sudden onset of acute abdominal pain and referred to the surgical specialist.   

 Blood, liver and renal parameters were normal. Troponin T was < 0.01 ng/ml. X-ray chest showed emphysematous changes in the lung fields. Echocardiography revealed normal study. His ECG shown in Figure (1) before surgery seems to be normal. The ECG taken at the onset of rapid heart rate (180 bpm) was shown in Figure (2). He was treated with intravenous diltiazem 5 mg three bolus doses at 5 minutes interval. The ECG taken after intravenous diltiazem  shown in Figure (3) revealed persistence of arrhythmia with a heart rate of 136 bpm. Then he was treated with intravenous amiodarone 150 mg bolus followed by 300 mg infusion. Following intravenous amiodarone, the patient developed hypotension with respiratory distress suddenly and the ECG taken was shown in Figure (4) revealed persistence of arrhythmia (nodal rhythm) with a heart rate of 115 bpm. The patient was supported with dopamine infusion and oxygen. Hypotension persisted and then he was supported with noradrenaline infusion. Hypotension still persisted with worsening of respiratory function and persistence of arrhythmia with the heart rate of 110 bpm. 10 ml of 10% solution of calcium gluconate (1 mL of 10% calcium gluconate contains 9.3 mg of elemental calcium) was given intravenously slowly on an emergency basis. Cardiopulmonary function was restored immediately with the reversion of arrhythmia to sinus rhythm as shown in Figure (5) and blood pressure was maintained at 120/70mm Hg. The heart rate was regular at a rate of 107 bpm.

Figure 1- 66 years old male with normal ECG before surgery.

Figure 2- 66 years old male with tachycardia after surgery

Figure 3- 66 years old male with tachycardia after IV diltiazem

Figure 4- 66 years old male with tachycardia after IV amiodarone

Figure 5- 66 years old male with normal sinus rhythm after IV calcium gluconate

Etiopathogenesis

Following non?cardiac surgery, AF usually occurs during the first 4 days and its pathophysiology  is not well understood [8]. The possible mechanisms are shown in Table 1.

Table 1. Mechanisms of postoperative atrial fibrillation in non cardiac surgery

Hypoxia leads to pulmonary vein vasoconstriction and increase right ventricular pressure and right atrial stretch. Also, hypoxia can cause ischemia of the myocardial atria cells and alters its conductivity. Hypervolemia increases the intravascular volume, which causes stretching of the right atrium. The independent predictors are increased age (55-74 , > 75 years), male gender, preoperative heart rate ≥ 72 beats/minute [9] and increased extent of operation [10]. Elevated preoperative B?type natriuretic peptide (BNP) measurements are independent predictor of POAF (postoperative atrial fibrillation) after thoracic surgery [11].

The prevalence of atrial fibrillation is much greater in aged population.  Elderly patients > 40 years presenting with AF may have occult or masked hyperthyroidism (apathetic hyperthyroidism) in 10 to 30% of cases [12] Measurement of total T4 and T3 may be misleading since these concentrations are reduced in patients with heart disease or other serious illnesses. and a measurement of serum TSH provides a good evidence of Thyrotoxicosis [13],[14],[15].

Many elderly patients tolerate atrial fibrillation well without therapy because the ventricular rate is slow as a result of concomitant AV nodal disease [16]. The autonomic nervous system can trigger AF in susceptible patients through heightened vagal or adrenergic tone called as neurogenic AF. In adrenergic AF, the ventricular response is rapid and flutter does not occur. Beta-blockers are the first-line choice because of their beneficial effects in the hyper-adrenergic post-operative state [17] and patients usually are resistant to class Ia and Ic drugs. Intravenous diltiazem or metoprolol are commonly used for AF with a rapid ventricular response and Landiolol received FDA approval in November 2024, a beta adrenergic blocker indicated for short-term reduction of ventricular rate in adults with supraventricular tachycardia (including atrial fibrillation/atrial flutter) [18]. Sinus node dysfunction presents with a tachycardia, most commonly AF that terminate abruptly and is followed by a long offset pause before the resumption of sinus rhythm. For older patients with AF of unknown cause, the term "idiopathic AF" is often used. ‘Lone’ AF is the term which is often used to describe AF of unidentifiable cause in patients younger than 60 years [19] and it is distinguished from idiopathic AF [20], which implies uncertainty about its origin without reference to the age of the patient or associated cardiovascular pathology [21] and its prevalence varies from 1.6% to 31%. However, with modern diagnostic methodologies, many experts now feel that a cause for atrial fibrillation can be found in virtually all patients and the most recent major-organization guidelines state that the term “lone AF” should no longer been used [22]. Persistent AF is a prolonged episode of AF that typically lasts more than seven days and requires medical intervention to restore sinus rhythm [23]. AF burden varies considerably among individuals, moreover, even in patients with paroxysmal AF, AF patterns range from multiple short AF bursts (staccato rhythm) to a few long AF episodes (legato rhythm) [24],[25]. The age at the onset of vagal AF is 40 to 50 years and the ventricular response is relatively low (100 to 120 bpm). Digoxin and β blockers may aggravate the syndrome and class Ia agents may be particularly beneficial because of their vagolytic effects. The anticholinergic activity of long-acting disopyramide makes this a relatively attractive choice for patients with vagally induced AF and propafenone is not recommended because its (weak) intrinsic beta-blocking activity which may aggravate this type of paroxysmal AF. Familial AF with autosomal dominant mode of inheritance due to an abnormal genetic chromosomal loci was identified at chromosome 10q region [26] and in vagal fibrillation, the paroxysmal AF does not progress to chronic AF.

The proportion of stroke rising from 6.5% for ages 50 to 59 years to approximately 31% for ages 80 to 89 years and nonvalvular AF is the most powerful precursor of stroke in this population up to 15% [27]. Carotid artery disease is believed to be responsible for  10 to 20% [28] and  most of them are related to embolism from a vulnerable plaque [29]. Thus patients with AF who experience symptoms of cerebral ischemia require careful evaluation of other causes, especially if they have been therapeutically anticoagulated.

Controlling risk factors is essential to prevent the onset of AF, and to try to maintain sinus rhythm over the long term [30].  In this patient systemic hypertension was well controlled with drugs and prophylactic anticoagulants and antiarrhythmic drugs were not prescribed to attribute AF as the etiology  for the neurologic deficit. Carotid artery disease as evidenced by bruit over both carotids [31] is the clinically documented etiology for the neurological deficit happened before in this patient.

Discussion

Etiologically AV conduction system disease is unlikely since the heart rate was rapid. Elderly patients who are felt to have lone AF actually have a sick sinus syndrome [32] as the underlying cause. Sinus node dysfunction (SND) is most often related to age-dependent progressive fibrosis of the sinus nodal tissue and surrounding atrial myocardium [33]. Intravenous calcium gluconate may inhibit the sinus node and can cause cardiac arrest particularly in patients with sinus node dysfunction andso it is not the cause for AF in this case. Troponin T  was normal and so coronary artery disease is not contributing. Thyroid function tests were normal and there was no left ventricular hypertrophy and diastolic dysfunction to attribute the etiology. Systemic hypertension was controlled with drugs. Triggering foci for paroxysmal AF from the pulmonary veins are more often in younger individuals. Increased vagal or sympathetic tone may cause AF in susceptible individuals. Vagal AF is characterized by slow ventricular response and sympathetic AF tends to disappear at rest. Severe infection is uncommon since the patient was afebrile with normal blood leukocyte count. The clinical and Echocardiographic features are not favourable for massive pulmonary embolism. X-ray chest revealed emphysematous changes in the lung fields attributing pulmonary pathology as the possible etiology of paroxysmal AF in this patient and surgery is the stress related precipitating factor.

Eventhough Ic agents (Flecainide) is the most appropriate drug for paroxysmal AF in structurally normal heart [34], it is not preferred since neurological dysfunction is the most frequent side effect of Flecainide. Diltiazem  act as an arteriolar dilator by inhibiting  calcium entry and a dose related fall in peripheral vascular resistance leading to drop in blood pressure. On intravenous amiodarone, patient developed hypotension refractory to vasopressors with respiratory distress suddenly and a marked reduction in heart rate as shown in Figure (4). Amiodarone has a significant negative dromotropic effect on AV conduction due to its intrinsic β blocking property and also has an appreciable calcium channel blocking effect. Pulmonary toxicity is the most serious adverse effect of amiodarone due to a hypersensitivity reaction [35]. The mechanism for the refractory hypotension may be due to the combined calcium channel blocking effects of both diltiazem and amiodarone. The respiratory distress is may be due to the hypersensitivity reaction of amiodarone in the lungs [36] which was aggravated by the preexisting lung disease.

10 ml of 10% solution of calcium gluconate was given intravenously on an emergency basis. Cardiopulmonary function was restored immediately with the reversion of arrhythmia to sinus rhythm as shown in Figure (5) and blood pressure was maintained at 120/70mm Hg. The heart rate was regular at a rate of 107 bpm. Calcium has a positive inotropic effect on the myocardium, increasing both the force of contraction and the maximum unloaded shortening velocity of cardiac muscle and rises the blood pressure and heart rate [37]. The rise in heart rate abolished the arrhythmia having the low heart rate and restore the sinus rhythm by overdrive suppression [38]. Calcium has a definite role in the stimulation of corticosteroid production [39],[40] and a significant increase in 11-hydroxy cortcosteroids can be demonstrated after intravenous calcium gluconate administration. These steroids may neutralize the hypersensitivity reaction occurred due to amiodarone therapy in the setting of preexisting lung disease manifested as increased respiratory distress. Thus the pulmonary function was restored at optimum with the normalization of blood pressure, rhythm and heart rate. Stunned atrium is defined as a state of temporary mechanic atrial dysfunction with preserved bioeletrical function. It may follow up to 38-80% successful cardioversions performed to convert atrial fibrillation to regular sinus rhythm. Lack of effective atrial contractility leads to hemodynamic changes, which may result in thrombus formation with subsequent thromboembolic events [41]  and so the patient was advised warfarin for a minimum period of 4 weeks with maintaining the therapeutic INR of 2 to 3 to prevent thromboembolic episodes due to atrial stunning [42] following pharmacologic cardioversion with intravenous calcium gluconate.

Electrical cardioversion was not preferred since the patient is having chronic obstructive lung disease in the form of emphysematous changes. Emphysema can cause air trapping and reduced lung capacity, making it harder for the lungs to recover after the electrical shock [43].  In pulmonary disease, electrical cardioversion may not restore the sinus rhythm and may result in frequent recurrence of AF. Pharmacologic and electrical cardioversion may be ineffective in the management of atrial fibrillation in patients with COPD(chronic obstructive pulmonary disease) until respiratory decompensation has been corrected [44]. Calcium gluconate prevent the fall in blood pressure induced by calcium channel antagonists and  restore the blood pressure to control values [45],[46].

Conclusion

Thus intravenous calcium gluconate play a role for Pharmacologic Cardioversion of Paroxysmal Atrial Fibrillation refractory to drugs having calcium channel blocking properties, resulting to hemodynamic compromise in pulmonary disease.

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