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Cardioversion with lidocaine of vagally associated atrial fibrillation in two dogs

Cardioversion with lidocaine of vagally associated atrial fibrillation in two dogs

Author information

Moïse N.S., Pariaut R., Gelzer A.R., Kraus M.S., Jung S.W. Cardioversion with lidocaine of vagally associated atrial fibrillation in two dogs // J Vet Cardiol. 2005 Nov;7(2):143-8.


Two dogs with acute onset atrial fibrillation (AF) were cardioverted to sinus rhythm by the administration of 2mg/kg lidocaine given intravenously. Each dog was believed to have AF initiated because of elevated vagal tone. This report has potential clinical impact for a subset of dogs because it offers a treatment to circumvent persistent AF. Furthermore, this encouraging result of a pharmacologic cardioversion suggests that further investigation would be of interest to ascertain the effectiveness and mechanism of the antiarrhythmic action of lidocaine in vagally induced AF.

Case report

Dogs with atrial fibrillation (AF) are not uniform in their clinical history and presentation.1 Although most dogs with AF have demonstrable structural and functional abnormalities, subsets of dogs with lone AF should be separated from those with more severe cardiac disease when treatment options are considered.1 For dogs with lone AF, electrical cardioversion of AF to sinus rhythm may provide the optimal long-term treatment.2 The chronicity of atrial fibrillation (AF) is apt to substantially influence the ability to maintain a sinus rhythm due to structural and functional remodeling.3,4 Although the mechanism for dogs developing lone atrial fibrillation (AF) is not proven, factors that influence its initiation and maintenance include (1) critical mass, (2) anatomical or functional blocks, (3) action potential duration (APD), (4) dispersion of repolarization and (5) heterogeneity of refractoriness.5 Consequently, the clinical profile of dogs at risk for AF includes large heart size, myocardial disease or factors that alter the electrophysiological balance.1,2

We have recently demonstrated that German shepherd dogs sedated with fentanyl developed AF with mild perturbations.6 The perturbations (triggers) for the induction of AF included phenylephrine provoked baroreceptor reflex, passage of catheters through the right atrium, touching the atria during surgery or pacing the right atrium. We hypothesized that it was the background high vagal tone associated with the fentanyl that predisposed the dogs to the AF. The vagal influence altered the electrophysiological properties of the atrial myocardium. In all episodes of AF invoked in this way, the administration of 2 mg/kg of lidocaine given intravenously (IV) converted the AF to sinus rhythm within approximately 60 s.6 Only one other study in the dog has reported successful pharmacologic cardioversion of vagally-mediated atrial fibrillation (AF) with lidocaine.7 In that study, AF was induced with pacing under the conditions of increased parasympathetic tone achieved with either morphine and alpha-chloralose anesthesia or pentobarbital anesthesia with direct external electrical vagal stimulation.7

Figure 1 Six lead electrocardiogram recorded from a dog with atrial fibrillation (AF) that was associated with circumstances of elevated parasympathetic tone (laryngeal paralysis and sedation).

Six lead electrocardiogram recorded from a dog with atrial fibrillation (AF) that was associated with circumstances of elevated parasympathetic tone

The atrial fibrillation (AF) was documented for 35 min during which the ventricular response rate had a respiratory rhythmic variation with slower and faster rates indicating the vagal influence on AV nodal conduction. Fibrillation waves (fff) and the irregular RR interval are diagnostic of AF. Lidocaine (2 mg/kg IV) was given 68 s before the first P wave (first P on the left superimposed on the T wave). The lidocaine converted the AF to a sinus rhythm. The second P wave is not conducted but is then followed by a sinus rhythm. Paper speed 50 ms, sensitivity 10 mm/mV.

Given the remarkable consistency of pharmacological cardioversion of AF in experimental dogs, we wished to determine if lidocaine would be a successful treatment in clinical cases of atrial fibrillation (AF). We knew that the conditions underlying AF would need to be specific to approximate those seen experimentally. Therefore, we treated with lido- caine two consecutively seen dogs with acute onset AF in which the modulating factor for AF induction likely was elevation in vagal tone. Lidocaine successfully converted AF to sinus rhythm in both dogs. We report these cases to document an easy and successful treatment of AF when the situation mimics that described herein.

Figure 2 Six lead electrocardiogram recorded from a dog during pacemaker implantation for treatment of collapsing with long sinus pauses

Six lead electrocardiogram recorded from a dog during pacemaker implantation for treatment of collapsing with long sinus pauses

These 3 frames, although not exactly continuous, were recorded over a total time period of 36 s. In frame A the fibrillation waves (fff) of atrial fibrillation (AF) are seen. A narrow QRS complex conducts through the AV node (CB = conducted beat). When the AV nodal conduction slows below a ventricular response rate of 80 bpm, the bipolar temporary pacemaker with the lead positioned in the right ventricle captures the heart (PB = paced beat). In frame B approximately 45 s after a bolus of 2 mg/kg lidocaine was given, AV nodal conduction is evidenced by the conducted beats (CB) and associated with atrial waveforms that are variable in morphology and rate (possibly atrial flutter to atrial tachycardia). Then, the baseline flattens as the tachyarrhythmia ceases. The pacemaker initiates a rhythm (PB) because the ventricular rate is less than 80 bpm. P waves (P) indicate the return of a sinus rhythm. In frame C the return of a sinus rhythm with AV nodal conduction is documented. In subsequent ECGs the relatively deep Q waves and left axis shift of the sinus beats persisted and was believed to be due to the orientation of the heart in the thorax of this Doberman. Paper speed 50 ms, sensitivity 10 mm/mV.

By intervening early in such cases, prevention of persistent AF is more likely.8

A 10-year-old 55 kg castrated male Labrador retriever was admitted with severe laryngeal paralysis and nonspecific cervical pain. The dog was treated by the referring veterinarian with acepro- mazine (0.04 mg/kg IV), butorphenol (0.2 mg/kg IV), dexamethazone and furosemide. On admission to Cornell University, the dog had profound inspiratory stridor and exhibited severe pain with cervical manipulation. Additional subcutaneous (SC) doses of acepromazinea (0.01 mg/kg) and butorphenolb (0.2 mg/kg) were given. A sinus arrhythmia (not confirmed by ECG) and heart rate of 60 bpm were auscultated. Chemistry panel and thoracic radiographs were unremarkable for organ dysfunction. Two hours later when the dog was examined in preparation for surgery, AF was suspected from auscultation and confirmed by electrocardiography. Sustained AF was documented with a continuous ECG monitor for 35 min. A bolus of 2 mg/kg of lido- cainec was given IV and the atrial fibrillation (AF) was converted to sinus rhythm in 68 s (Fig. 1). Echocardiography performed during the restored sinus rhythm revealed a normal heart. The following day the dog underwent successful left arytenoid lateralization under general anesthesia with isofluraned which included premedication with glycopyrolatee and oxy- morphonef and induction with propofol.g Recovery was satisfactory and the dog was clinically improved and in sinus rhythm when rechecked 2 months later. The reason for the cervical pain was not determined, but did not persist.

A 2-year-old 34 kg castrated male Doberman pincher was admitted for frequent syncope. A 24-h ambulatory ECG recording revealed sinus arrhythmia with an average heart rate of 79 bpm (range 36—231 bpm). A total of 2107 sinus pauses of greater than 2 s were recorded with the longest pause of 8.5 s. AV nodal conduction was normal. Thoracic radiographs and echocardiogram were normal. The dog underwent pacemaker implantation under general anesthesia with isofluraned which included premedication with morphineh (1 mg/kg SC), midazolami (1.5 mg/kg IV), and induction with midazolam (1.5 mg/kg IV) and eto- midatej (0.8 mg/kg IV). A temporary pacing lead was positioned in the right ventricle with the rate programmed at 60 bpm. Forty minutes after the induction of anesthesia the heart rate suddenly increased to 90 bpm and the rhythm was irregular. The ECG revealed AF with intermittent AV nodal conduction that at times was slow enough to permit the pacemaker to capture the rhythm (Fig. 2A). After 40 min of documenting sustained AF, a bolus of 2 mg/kg of lidocaine was given IV. The atrial fibrillation (AF) ceased 45 s after the IV bolus of lidocaine and a slow sinus rate was initiated (Fig. 2B and C). Pacemaker implantation continued uneventfully. A sinus rhythm was confirmed 6 months later.

In each of the dogs reported herein an elevation in parasympathetic tone potentially contributed to the environment in which AF could be triggered. In the first dog the combination of the laryngeal paralysis and potential cervical lesion could have increased the vagal tone. Parasympathetic tone was likely further enhanced with the sedation, particularly butorphenol. High vagal tone was evidenced by the slow heart rate and sinus arrhythmia initially auscultated. Additionally, continued high vagal tone was probable given the continued bradycardia and heart block present after restoration of the sinus rhythm. The second dog was pretreated with morphine which is known to increase vagal tone.9,10 Both dogs had structurally and functionally normal hearts as judged clinically. Atrial fibrillation thus far has not recurred in either dog. The frequency in which atrial fibrillation (AF) develops in presumed clinically normal dogs with enhanced vagal tone is unknown. However, experimental dogs simply sedated with drugs that increase vagal tone are easily induced to AF.6,7 The experimental dogs lacked a disease substrate, but did have modification to their autonomic tone and usually a premature atrial complex to trigger the AF.6 In the clinical cases reported herein, we did not document the onset of AF to know if a premature atrial complex triggered the arrhythmia. Moreover, we do not know if subclinical atrial disease made these dogs more susceptible to AF. Usually such a disease substrate is present with AF1; however, in the large dog perhaps high vagal tone and a trigger (premature atrial complex) are the only requisite ingredients for expression of the arrhythmia. Admittedly a speculative hypothesis, but yet plausible, is that lone AF in some giant and large breed dogs1 is induced by inciting circumstances (not necessarily drugs) of high parasympathetic tone (e.g. sleep) with simply a spontaneous single premature atrial complex to trigger the AF.

Vagally induced atrial fibrillation (AF) in dogs has been extensively used to investigate the mechanisms of AF.5 As reported, direct vagal nerve stimulation, acetylcholine infusion, or alpha-chloralose anesthesia creates an environment favorable to AF induction and mainte- nance.7,11,12 The propensity for AF particularly during direct vagal stimulation results from parasym- pathetically induced atrial APD shortening and increase in heterogeneity of refractoriness.13 Abbreviation of APD is related to the activation of /K(Ach) current. Heterogeneity of vagal nerve ending distribution, muscarinic receptor or potassium channel density to the atrium may explain the dispersion of refractoriness.11 Both effects promote reentry which is thought to be the most common mechanism for AF occurrence and maintenance.10 The use of opiates as sedatives may mimic vagal models of AF.7,9,10 Indeed, opiates are known to alter synaptic neurotransmission to cardiac vagal nerves through the inhibition of presynaptic release of gamma- aminobutyric acid (GABA), resulting in increased vagal tone.14 Moreover, the imbalance between sympathetic and parasympathetic tones could be implicated in AF induction. Similar to high parasympathetic tone, increase in sympathetic nerve activity shortens APD but does not promote effective refractory period (ERP) dispersion and therefore is less effective as a trigger for AF.11 Nevertheless, heterogeneous cardiac sympathetic nerve distribution may in some cases contribute to dispersion of refractoriness.11 For example, the predominance of vagal influence in puppies, whose sympathetic innervation is not completely functional, may increase their vulnerability to AF in the absence of a large atrium.15

In models of AF associated with elevated vagal tone, class I drugs slow the atrial activation frequency and increase the organization of the arrhythmia prior to termination.16 The exact mechanisms of action of these agents, and more specifically lidocaine, remain uncertain. Most experiments suggest that vagally induced AF is a reentrant mechanism and that the wavelength (wavelength = conduction velocity X refractory period) of the reentrant circuit is the major determinant for maintenance of the arrhythmia.17 Class I drug blockage of sodium channels causes a use-dependant prolongation of the post-repolarization refractoriness. This results in an increase in the reentrant wavelength thatcan- not be sustained by the atrial tissue and terminates the arrhythmia.18 Other experimental and mathematical models do not support this theory, but suggest that an increase in the excitable gap of the reentrant wave is the mechanism for conver- sion.19,20 Most recently, mathematical modeling of vagotonic atrial fibrillation (AF) suggests that pure sodium blockade can decrease the dominant frequency and decrease the generation of secondary wavelets by wave- break.21 Finally, conversion of vagally induced AF with the local anesthetic lidocaine might result from a direct blockage of the cardiac muscarinic receptors, opposing the parasympathetic stimulation. Some studies showed the effects of lidocaine on various types of muscarinic receptors in different tissues.22,23 It is this explanation that might be the most plausible in the clinical setting described in these two dogs.

In both dogs the sinus rhythm was initially slow after the conversion. This could be due to the pervasive elevation in vagal tone slowing sinus node automaticity or the effects of the AF. Sinus node recovery time was prolonged in dogs with experimentally induced AF due to electrophysiological remodeling, although this would explain only a transient pause in the sinus rhythm.24 Such electrophysiological alterations have been documented in the dog to occur after as little as 2 weeks of atrial fibrillation (AF); however, in the dogs of this report, AF duration was less than an hour.

In conclusion, we report that lidocaine administered within 1 h of the onset of AF associated with elevation in vagal tone can pharmacologically cardiovert dogs back to sinus rhythm. For a subset of dogs with AF such immediate treatment might preclude persistent AF with its detrimental effects. To evaluate whether these initial findings are as consistent as our experimental results, evaluation of a larger number of dogs is required.


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