Use of Procainamide for Conversion of Acute Onset AF Following Pericardiocentesis in a Dog

Introduction

This case report highlights a complication of pericardiocentesis that requires immediate treatment and demonstrates an effective, inexpensive treatment option for the conversion of acute onset atrial fibrillation (AF). There are no previously published clinical reports documenting the successful conversion of AF to sinus rhythm in dogs using IV procainamide. As such, this case may be useful to any veterinarian who encounters AF acutely that results in hemodynamic changes and requires immediate therapeutic intervention.

Case Report

A 9 yr old spayed female golden retriever weighing 42 kg presented to Texas A&M University Veterinary Medical Teaching Hospital with a 24 hr history of panting, decreased appetite, and suspected food bloat. Approximately 2 hr prior to presentation, the dog appeared uncomfortable and had a distended abdomen (according to the owners). On presentation, the dog was bright, alert, and responsive. The heart rate was 180 beats/min with a regular rhythm, and no cardiac murmur was ausculted. Femoral pulses were strong and synchronous. The dog was panting at 66 breaths/min with clear lung sounds bilaterally. Mucous membranes were moist, pink, and the capillary refill time was < 2 sec. Abdominal palpation revealed a distended stomach and a caudally displaced spleen. The dog had been previously diagnosed with hypothyroidism and was receiving levothyroxine (0.017 mg/kg per os q 12 hr).

Venous blood gas, packed cell volume, total serum protein, electrolyte analysis, blood pressure measurements, pulse oximetry, electrocardiography (EKG), and abdominal radiographs were performed. The results of the venous blood gas were within normal limits. The packed cell volume was 50% (reference range; 35–51%) and total serum protein was 6.5 g/dL (reference range; 6.0–7.5 g/dL). Systolic, diastolic, and mean blood pressures measure by an oscillometric technique were 151 mm Hg, 110 mm Hg, and 125 mm Hg, respectively. Pulse oximetry was 92% on room air. The EKG revealed a sinus tachycardia with a heart rate of 187 beats/min (Figure 1). Abdominal radiographs revealed hepatomegaly, peritoneal effusion, and a possible mass in the caudal left abdomen. There was no evidence of either gastric dilatation or volvulus. The dog was admitted to the intensive care unit for overnight evaluation. An 18 gauge cephalic catheter was placed, and the dog was started on IV fluids^a (with 20 mEq potassium chloride^b) at 100 mL/hr, ondansetron^c (0.19 mg/kg IV q 12 hr), buprenorphine^d (0.02 mg/kg IV q 8 hr), ranitidine^e (1 mg IV q 12 hr), and food was withheld.

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The following morning, the dog had muffled heart sounds and jugular venous distension. Abdominal and thoracic radiographs and thoracic ultrasound were performed to rule out pericardial effusion. Radiographs confirmed a persistent hepatomegaly, increased peritoneal effusion, pleural effusion, and an enlarged cardiac silhouette. Thoracic ultrasound revealed a large amount of anechoic fluid present in the pleural and pericardial spaces. No cardiac masses were visualized, and there was evidence of mild cardiac tamponade.

The dog was positioned in sternal recumbency for pericardiocentesis and a 1 L bolus of IV crystalloid solution^a was administered. The right thorax was clipped and prepared in a surgical manner. A 6-lead EKG was used to monitor heart rate and rhythm during pericardiocentesis. A 14 gauge angiocatheter^f was placed in the pleural space at the level of the sixth intercostal space on the right side of the thorax and 1,280 mL of straw-colored effusion was aspirated. Oscillometric blood pressure, heart rate, and EKG monitoring identified systolic, diastolic, and mean pressures of 155 mm Hg, 85 mm Hg, and 133 mm Hg, respectively with a heart rate of 142 beats/min and normal sinus rhythm. The catheter was removed and a new 14 gauge catheter was advanced into the pericardial space at the level of the fourth intercostal space on the right side of the thorax and 80 mL of hemorrhagic effusion was aspirated. No further effusion could be removed despite persistent effusion so a second attempt was made using a new catheter. This attempt resulted in the aspiration of 450 mL of hemorrhagic effusion, and the catheter was removed. Subsequently, AF with an average ventricular response rate of 260 beats/min was detected on the EKG and oscillometric blood pressure readings decreased (systolic, diastolic, and mean pressures were 122 mm Hg, 87 mm Hg, and 99 mmHg, respectively). Due to the acute onset of AF and reduction in systemic blood pressure, pharmacologic cardioversion to sinus rhythm was attempted.

Initially, a single IV bolus of lidocaine^g (1.2 mg/kg) was administered with no observed effect on either the heart rate or rhythm. After approximately 3 min, procainamide^h was administered (14.3 mg/kg IV) slowly (over 15 min) and conversion to sinus rhythm with a rate of 136 beats/min occurred approximately 12 min after the bolus was finished (Figure 2). Blood pressure improved at the time of conversion (systolic, diastolic, and mean pressures were 141 mm Hg, 89 mm Hg, and 109 mm Hg, respectively). Additional diagnostic tests including echocardiography were recommended to the owner, but were declined. The owner elected humane euthanasia.

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Discussion

This report describes the use of IV procainamide for conversion of acute onset AF following pericardiocentesis in a dog. AF is one of the most common supraventricular tachyarrhythmias in dogs and is characterized by chaotic, disorganized atrial electrical activity resulting in irregular and fast ventricular response rates.¹ The mechanisms of AF induction and maintenance are multifactorial, but three primary theories predominate. The first theory is that rapid firing of an ectopic focus propagates irregularly because of varying ability of different parts of the atrium to respond. The second theory is that a single, very rapid reentry circuit propagates to surrounding atrial tissue irregularly because of spatially varying responsiveness with the atria. The third theory is that there are multiple, coexisting atrial reentry circuits.^2,3

AF can develop either in the presence or absence of underlying cardiac disease. In most dogs, AF develops with primary underlying cardiac diseases that result in atrial enlargement, such as dilated cardiomyopathy, valvular endocardiosis, and various congenital heart defects (e.g., patent ductus arteriosus).^4,5 That said, AF can occur in structurally normal hearts if there is sufficient atrial myocardial mass to support fibrillation.⁵ Additional proposed mechanisms, contributing factors, and concurrent diseases that may reportedly result in the development of AF in structurally normal dog hearts include increased parasympathetic tone, hypothermia, triggered extrasystoles associated with cardiac catheterization, and endocrine diseases such as hypothyroidism and hypoadrenocorticism.^5–7 Pericardiocentesis of large volumes with subsequent IV volume expansion resulting in unequal stretching of the atrial wall also reportedly results in AF.^8,9

Important complications associated with AF are principally related to tachycardia and a reduction in cardiac output resulting in hemodynamic compromise and clinical decompensation. Dogs with AF may develop hypotension, weakness, and heart failure.^10,11 Thromboembolism is a common problem in humans that is rarely recognized in dogs.¹⁰ The dog in this report presented in sinus rhythm and AF developed acutely after pericardiocentesis, resulting in tachycardia and a relative decrease in blood pressure. A complete necropsy was performed in this case that showed no evidence of cardiac enlargement or masses; however, several factors may have contributed to AF in this dog. During pericardiocentesis, the catheter may have inadvertently come into contact with the atrial wall thereby inducing AF. A large volume of pericardial effusion was removed and subsequent IV volume expansion may have occurred, resulting in unequal stretching of the atrial wall. The effective refractory period of the thin portion of the atrium is substantially increased following stretching and the combination of atrial stretch and an increased effective refractory period are thought to be conducive to the development of AF.⁸ Atrial stretching may also lead to localized myocardial hypoxia, which could, in turn, create ectopic foci resulting in AF. The dog had been administered an opioid (buprenorphine) over night and presented initially for gastrointestinal discomfort, potentially enhancing parasympathetic tone. Additionally, ondansetron was administered IV. This medication has been rarely implicated in the development of AF in humans.¹²

Therapeutic goals for the management of AF are ventricular rate control with antiarrhythmic drugs (β-blockers, calcium channel blockers, digoxin, amiodarone) or conversion to normal sinus rhythm with either antiarrhythmic drugs or synchronized direct current cardioversion to restore cardiac output and improve clinical signs. In veterinary medicine, the conversion of acute AF (< 24 hr) to sinus rhythm has been reported with IV lidocaine and direct cardioversion.^13,14 Conversion of recent-onset and chronic AF has been reported with the use of amiodarone (IV and per os), IV verapamil, IV diltiazem, and oral quinidine sulfate.^15–18 Although these methods have been successful, there are factors that may limit their widespread use. Direct current cardioversion requires general anesthesia, technical expertise, and specialized equipment. Although antiarrhythmics preclude the need for general anesthesia and special equipment, many of the available drugs used to convert AF to a sinus rhythm are limited by important adverse effects. In dogs, reported adverse effects of oral amiodarone include bradycardia, increased hepatic enzyme activity and hepatopathies, neutropenia, thrombocytopenia, and positive Coombs’ test results.^16,19 IV amiodarone has been associated with tachypnea, severe skin reactions, anaphylaxis, and life threatening hypotension in dogs.²⁰ The IV calcium channel blockers diltiazem and verapamil can cause bradycardia, decreased cardiac output, and vasodilation.²¹ To the authors’ knowledge, there are no previously published reports documenting successful conversion of AF to sinus rhythm in dogs using IV procainamide in clinical studies; however, an experimental study showed an 83% success rate for converting experimentally induced AF in six dogs.²²

Procainamide is a class 1a antiarrhythmic drug that prolongs the action potential duration and effective refractory period, raises the threshold of excitability, and has no effect on resting membrane potential.²³ Procainamide is capable of terminating AF in dogs with experimentally induced AF. Procainamide’s mechanism of action for terminating AF is related to increases in wavelength at short cycle lengths, slow atrial activation, and increases in the size of reentry circuits. The resulting increase in the size of functional reentry circuits decreases the total number of circuits within the atria, and the arrhythmia is terminated when the remaining circuits fail to sustain themselves allowing for recovery of the remaining portions of the atria.²⁴ Multiple human studies report the efficacy of various doses of IV procainamide for the conversion of AF.^25–28 Successful conversion rates are variable, ranging from 51% to 82% when the duration of AF is < 48 hr. When the duration of AF is < 2 wk, the conversion rate is 21–75%. Regardless of the duration of AF, the average time to conversion is 60 min.²⁵ The wide range in conversion rates can best be explained as a result of patient selection (structural versus nonstructural heart disease), duration of AF, and procainamide dose. Side effects of IV procainamide reported in those studies were uncommon and included systemic hypotension and nonsustained ventricular tachycardia. Additional side effects associated with IV procainamide described in humans include QRS and QT widening, atrioventricular block, vagolytic effects leading to transient increases in ventricular response rates, and proarrhythmia (e.g., torsades de pointes).^25–28 Side effects of IV procainamide in the dog are similar to those reported in humans and include hypotension, increased ventricular rates from enhanced atrioventricular nodal conduction, and atrioventricular nodal block; however, no adverse side effects occurred in the dog in this report and the dog’s hemodynamics improved once sinus rhythm was reestablished.^4,29

Conclusion

AF is a common supraventricular tachyarrhythmia that can be encountered in a variety of clinical settings. The dog in this report presented to the hospital in sinus rhythm and developed AF acutely following pericardiocentesis resulting in hemodynamic changes that were immediately recognized and addressed therapeutically with IV procainamide. Many cases of acute AF resolve spontaneously (within several hours or days). In the dog described herein, the close temporal relationship of conversion associated with procainamide infusion make pharmacologic conversion likely. This report highlights a complication of performing a pericardiocentesis that requires immediate treatment and demonstrates a potentially effective, inexpensive treatment option for the conversion of acute onset AF in dogs. Future prospective clinical studies are necessary to determine the percentage of dogs in which IV procainamide would show a similar beneficial effect.