Atrial Impulses Research Articles

Relevance of Anatomical Significance of AV Nodal Structures within Koch's Triangle and Pyramid.

The exploration of the cardiac conduction system evolved over a century, marked by groundbreaking discoveries in atrioventricular (AV) nodal physiology. Atrioventricular nodal re-entrant tachycardia (AVNRT), the most prevalent regular tachycardia in humans, remains enigmatic despite extensive research. Detailed examinations of AV nodal anatomy and histology reveal variations in location and shape, influencing electrophysiological properties. Variability in AV nodal extensions and their embryological origins contribute to the complexity of the conduction system. Physiologically, the AV node plays a crucial role in modulating AV conduction, introducing delays for ventricular filling and filtering atrial impulses. Dual-pathway physiology involving fast and slow pathways further complicates AVNRT circuitry. Integrated approaches combining pre-procedural imaging with electroanatomical mapping enhance our understanding of AV nodal structures and high-definition mapping improves precision in identifying ablation targets. Electrophysiological-anatomical correlations may unveil the specific roles of conduction axis components, aiding in the optimization of ablation strategies. This review traces the historical journey from Tawara's pioneering work to recent integrated approaches aimed at unraveling the intricacies of AV nodal structures while emphasizing the importance of a multidimensional approach, incorporating technological advancements, anatomical understanding, and clinical validation in human mapping studies.

Clinical, electrocardiographic, and diagnostic imaging features and outcomes in cats with electrocardiographic diagnosis of ventricular pre-excitation: a retrospective study of 23 cases (2010–2022)

Introduction/ObjectivesVentricular pre-excitation (VPE) occurs when atrial electrical impulses prematurely excite the ventricles through an aberrant muscle bundle known as an accessory pathway (AP). Orthodromic atrioventricular reciprocating tachycardia is a re-entrant, narrow complex supraventricular tachycardia (SVT), maintained through retrograde conduction over an AP. The study aimed to describe patient signalments, clinical signs, electrocardiographic (ECG) and diagnostic imaging features, treatments, prognostic variables, and outcomes in cats with ECG diagnosis of VPE. AnimalsTwenty-three cats diagnosed with VPE between January 2010 and August 2022 were included in this study. Materials and MethodsThis was a multicenter, retrospective study with twenty-three cats diagnosed with VPE between January 2010 and August 2022. Ventricular pre-excitation diagnosis was based on ECG evidence of shortened PR interval, delta wave, and prolonged QRS duration. The median survival time (MST) was estimated by the Kaplan-Meier curve. Log-rank tests were performed to assess for an association between clinical signs or presence of structural heart disease on the MST. ResultsFourteen (60.8%) cats with VPE also had SVT documented on ECG, with 7 of 14 with ECG confirmation of orthodromic atrioventricular reciprocating tachycardia. Four (17.4%) cats had suspected AP-mediated tachyarrhythmia based on associated clinical signs. Common presenting signs included collapse (15/23; 65.2%) and respiratory distress (14/23; 60.8%). Five (21.7%) cats were asymptomatic. Heart rate during SVT ranged from 310 to 420 bpm (median: 375 bpm). Initial treatment included atenolol (10/18), sotalol (5/18), diltiazem (2/18), and amiodarone (1/18). From the date of diagnosis, MST was 1872 days (5.1 years). ConclusionsThe majority of cats with VPE also had symptomatic SVT. The prognosis for cats with VPE is considered good with an MST of greater than five years.

Pre-excited atrial fibrillation revealed at a very delayed age: case report

BackgroundWolff-Parkinson-White (WPW) syndrome is a condition characterized by the persistence of an accessory pathway responsible for ventricular pre-excitation that can lead to symptomatic and potentially severe arrhythmias. Coexistence with atrial fibrillation is well known and not uncommon, exposing to potential degenerescence into ventricular fibrillation when atrial impulses are transmitted along the accessory pathway. WPW syndrome is most prevalent in younger patients and cases revealed after an advanced age have rarely been described in the literature.Case presentationHere, we report a case of atrial pre-excitation first diagnosed at the age of 72 years that required external electrical cardioversion with a favorable outcome. The diagnosis was based on clinical and electrographic findings.ConclusionsWPW syndrome is a relatively rare cardiac disorder that can be a cause of sudden death, especially when combined with atrial fibrillation. Therefore, cardiologists have to consider this diagnosis in patients presenting clinical signs of arrhythmia with an electrical pattern of WPW.

An atrioventricular node model incorporating autonomic tone.

The response to atrial fibrillation (AF) treatment is differing widely among patients, and a better understanding of the factors that contribute to these differences is needed. One important factor may be differences in the autonomic nervous system (ANS) activity. The atrioventricular (AV) node plays an important role during AF in modulating heart rate. To study the effect of the ANS-induced activity on the AV nodal function in AF, mathematical modelling is a valuable tool. In this study, we present an extended AV node model that incorporates changes in autonomic tone. The extension was guided by a distribution-based sensitivity analysis and incorporates the ANS-induced changes in the refractoriness and conduction delay. Simulated RR series from the extended model driven by atrial impulse series obtained from clinical tilt test data were qualitatively evaluated against clinical RR series in terms of heart rate, RR series variability and RR series irregularity. The changes to the RR series characteristics during head-down tilt were replicated by a 10% decrease in conduction delay, while the changes during head-up tilt were replicated by a 5% decrease in the refractory period and a 10% decrease in the conduction delay. We demonstrate that the model extension is needed to replicate ANS-induced changes during tilt, indicating that the changes in RR series characteristics could not be explained by changes in atrial activity alone.

Value of a 12-Lead Electrocardiogram for Assessing P Waves.

Scenario: The rhythm strip below was printed from the bedside monitor of a 71-year-old man admitted to the intensive care unit for hypoxemic respiratory failure, fluid overload, and septic shock. The patient’s history includes coronary artery disease, hypertension, diabetes, paroxysmal atrial fibrillation after successful cardioversion (prescribed at-home apixaban), alcoholic cirrhosis, heart failure (ejection fraction, 50%), and chronic obstructive pulmonary disease (COPD). When this electrocardiogram (ECG) was generated, his blood pressure was 119/63 mm Hg, heart rate was 95/min, and oxygen saturation was 97% while receiving mechanical ventilation with a fraction of inspired oxygen of 0.8. The nurse noted that the rhythm looked like either a heart block or multifocal atrial tachycardia (MAT) and decided to record a 12-lead ECG (see next page). What is your interpretation?Atrial flutter (AFL) with 3:1 conduction with a ventricular rate of ~100/min and right bundle branch block (RBBB).Atrial flutter is common in patients with hypertension, diabetes, COPD, alcohol misuse, and atrial fibrillation (risk factors in this scenario) and is typically initiated or terminated by a premature complex (atrial or ventricular) or rapid atrial pacing. When a premature stimulus excites an area in the atrium, it travels in a single stable reentry circuit (either clockwise or counterclockwise) that is long enough to allow initially depolarized myocardial tissue to recover and then be capable of depolarizing again owing to the reentered stimulus. This mechanism can be seen in this example, particularly in leads III and aVF, as regular, uniform flutter waves (or F waves). The typical atrial rate for AFL is 200-350/min and is characterized by the absence of an atrial diastolic interval, as is seen in sinus rhythm.The rhythm strip displayed only leads II and V1 and showed upright P waves in V1 with various PR intervals, which could be confused with third-degree heart block. In lead II, the P wave is negative, suggesting a junctional rhythm with retrograde conduction of the atria. However, the sharp negative P wave in lead II raises the suspicion of AFL, which was confirmed on the 12-lead ECG. The unique feature of F waves (ie, “sawtooth” pattern) associated with AFL can be seen clearly in leads III and aVF. The F waves that are negative in the inferior leads but positive in V1 indicate the AFL is moving in a counterclockwise direction, which is most common (~75% of cases). The flutter waves should not be confused with MAT, which typically exhibits at least 3 different P-wave morphologies and is irregular because of multiple focal sites of atrial impulse formation. In contrast, AFL is a self-sustaining macroreentrant atrial arrhythmia without focal sites of impulse formation. The ventricular rate in AFL is usually a multiple of the FF interval. In this case, the F waves occur at a rate of 300/min and result in a ventricular rate of ~100/min and can be slightly irregular.Left ventricular hypertrophy in the presence of RBBB can be examined by using an S wave >2 mm in V1 or an R wave >15 mm in V5 or V6, both of which are absent on this ECG.Clinical management is focused on converting AFL to normal sinus rhythm, which will reduce the heart rate and prevent embolic stroke. In this case, the cardiology service was consulted, and ibutilide, an antiarrhythmic, was prescribed with a return to normal sinus rhythm. The patient’s anticoagulant was changed to clopidogrel, an antiplatelet. Given this patient’s underlying risk factors and the risk of prolonging QT with ibutilide, the QT interval should be closely monitored to prevent torsades de pointes. The patient's hospital course was complicated by continued respiratory distress and acute alcohol withdrawal. He was later transferred to the step-down unit.

Atrial Fibrillation with Ventricular Pre-Excitation: A Diagnosis That Must Not Be Missed

Wolff-Parkinson-White (WPW) syndrome is caused by an accessory pathway that communicates between the atria and ventricles known as the Bundle of Kent. The development of atrial fibrillation, can result in the atrial impulses all being conducted via the accessory pathway and result in a sinister, board complex, irregular tachycardia, with varying QRS morphology (known as pre-excited atrial fibrillation) Adenosine is a potent atrioventricular node blocker, which can be used in the treatment of supraventricular tachycardias, but also has diagnostic utility, particularly in differentiating between supraventricular tachycardia with aberrant conduction (which would often terminate) and a ventricular tachycardia (which would not respond to adenosine). However, the administration of adenosine in pre-excited atrial fibrillation can precipitate 1:1 atrial to ventricular conduction, which can degenerate into life-threatening ventricular arrythmias. This case describes a patient who presented with pre-excited atrial fibrillation and received intravenous adenosine that resulted in development of broad complex tachycardia with haemodynamic compromise. In patients with pre-exited atrial fibrillation, AV nodal blocking agents should be avoided and direct current cardioversion should be utilised.

3rd-Degree Atrioventricular Block.

3rd-Degree Atrioventricular Block.

Complete AVB Initially Complicating STEMI in Post Percutaneous Revascularization: Case Report

Complete or third degree atrioventricular block (cAVB), defined by the complete and permanent interruption of the transmission of atrial impulses to the ventricles...

Arrhythmias and diabetes: atrial fibrillation

Arrhythmias and diabetes: atrial fibrillation

Insulin sensitization causes accelerated sinus nodal dysfunction through autophagic dysregulation in hypertensive mice.

Insulin sensitizers, while effective in glucose-lowering for diabetes control, are linked to an increased risk of heart disease through mechanisms that are not well understood. In this study, we investigated the molecular mechanisms underlying the effects of insulin sensitization on cardiac sinus node dysfunction. We used pharmacologic or genetic approaches to enhance insulin sensitivity, by treating with pioglitazone or rosiglitazone, or through phosphatase and tensin homolog (PTEN) deletion in cardiomyocytes respectively. We employed an angiotensin II (Ang II)-induced hypertensive animal model which causes sinus node dysfunction and accumulation of oxidized calcium/calmodulin-dependent protein kinase II (CaMKII), which also serves as a biomarker for this defect. While neither PTEN deficiency nor insulin sensitizers caused sinus node dysfunction in normotensive mice, both accelerated the onset of sinus node dysfunction and CaMKII oxidation in hypertensive mice. These abnormalities were accompanied by a significant defect in autophagy as revealed by unc-51 like autophagy activating kinase 1 (ULK1) signaling. Indeed, mice deficient in ulk1 in cardiomyocytes and the sinus node also showed early onset of slow atrial impulse conduction with frequent sinus pauses and upregulated CaMKII oxidation following Ang II infusion similar to that seen with PTEN deficiency, or treatment with insulin sensitizers. To further elucidate the role of autophagy in sinus node dysfunction, we treated mice with a peptide D-Tat-beclin1 that enhanced autophagy, which significantly abrogated the frequent sinus pauses and accumulation of oxidized CaMKII induced by insulin sensitizers treatment, or PTEN deficiency in hypertensive animals. Together, these findings provide clear evidence of the detrimental cardiac effects of insulin sensitization that occurs through failure of autophagy-mediated proteolytic clearance.

Dulaglutide inhibited perilipin 2-induced atrial fibrillation through the improvement of atrial impulse conduction slowing in transgenic mice

Dulaglutide inhibited perilipin 2-induced atrial fibrillation through the improvement of atrial impulse conduction slowing in transgenic mice

P wave dispersion over two decades after its discovery. What the cardiologist should know

For years, there has been an increase in cases of atrial fibrillation, reaching alarming levels. This is why intense work is done to find predictors of this arrhythmia. The electrocardiogram has shown to be useful for this purpose, and multiple indices derived from the P wave have been developed. Among the most notable is the P wave dispersion (PWD). It has been verified that PWD can predict the occurrence of paroxysmal atrial fibrillation in the absence of diseases as well as in the context of multiple cardiovascular pathologies or other systems. PWD is considered by most researchers to be the result of inhomogeneous conduction of the atrial electrical impulse, but a vector explanation may play a role in its genesis. The large body of evidence surrounding PWD supports its use in clinical practice.

Visual representations of canine cardiac arrhythmias with Lorenz (Poincaré) plots.

To characterize the patterns associated with Lorenz plots (LPs) or Poincaré plots derived from the Holter recordings of dogs with various cardiac rhythms. 77 dogs with 24-hour Holter recordings. A 1-hour period from the Holter recordings from each of 20 dogs without arrhythmias and from each of 57 dogs with arrhythmias (10 each with supraventricular premature complexes, complex supraventricular ectopy, ventricular premature complexes, complex ventricular ectopy, and atrial fibrillation, and 7 with high-grade second-degree atrioventricular block) were used to generate the LPs. Patterns depicted in the LPs were described. Arrhythmia-free Holter recordings yielded LPs with a Y-shaped pattern and variable silent zones. Recordings with single premature complexes yielded LPs with double side and triple side lobes. Complex ectopy was denoted by dots clustered in the lower left corner of the LPs. The LPs of recordings with atrial fibrillation had fan patterns consistent with a nonlinear relationship between atrial electrical impulses and atrioventricular nodal conduction. The recordings with atrioventricular block yielded LPs with island patterns consistent with variable atrioventricular nodal conduction. Distinct LP patterns were identified for common cardiac rhythms of dogs, supportive of nonrandom mechanisms as the cause of most rhythms. Visual interpretation of an LP generated from a Holter recording may aid in determining the arrhythmia type and understanding the arrhythmia's mechanism in dogs and other species.

UNCOMMON CAUSE OF COMPLETE ATRIOVENTRICULAR BLOCK PRESENTING WITH DYSPNEA

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Myxedema coma is defined as severe hypothyroidism leading to decreased mental status, hypothermia, hypotension, bradycardia, hyponatremia, hypoglycemia, hypoventilation and other symptoms related to slowing of function in multiple organs. Severe hypothyroidism is associated with bradycardia, decreased myocardial contractility, a low cardiac output, hypotension however, ventricular function is rarely compromised. Atrioventricular (AV) block is defined as a delay or interruption in the transmission of an impulse from the atria to the ventricles due to an anatomical or functional impairment in the conduction system. The conduction disturbance can be transient or permanent, with conduction that is delayed, intermittent, or absent. In the third degree, complete AV block, no atrial impulses reach the ventricle. We present a case with the uncommon manifestation of complete AV block secondary to myxedema coma. CASE PRESENTATION: A 66-year-old man with no past medical history and no medical follow up presented to our urgency room complaining of dyspnea at rest, lightheadedness, reduced exercise tolerance that was getting worse since 1 moth prior to seek for medical help. On physical examination he had altered mental status with vital sign with BP in 92/56mmHg, heart rate of 35 beats per minute, temperature of 35 Celsius degrees, respiratory rate of 12 per minute. He is obese, bald and dry skin. His electrocardiogram (ECG) showed evidence of complete heart block. Labs remarkable for a thyroid stimulating hormone of greater than 100 mIU/L. No other apparent cause for AV block. DISCUSSION: Due to hypoventilation patient developed a hypercapnic respiratory failure that required endotracheal intubation ad mechanical ventilation. He was admitted to intensive care unit and placed on a transvenous pacemaker. After the treatment with intravenous levothyroxine for 6 days patient was successfully extubated, and the ECG returned to normal sinus rhythm without any other treatment. The transvenous pacemaker was discontinued and transitioned to oral levothyroxine. He was successfully treated and discharged home with complete resolution of symptoms. CONCLUSIONS: This case showed an uncommon and reversible cause of complete AV block secondary to severe hypothyroidism. With adequate recognition and treatment, we successfully treat this condition with high morbidity and mortality if not treated. The AV block was completely resolved with the thyroid hormone replacement. Reference #1: Kwaku MP, Burman KD. Myxedema coma. J Intensive Care Med 2007; 22:224. DISCLOSURES: No relevant relationships by Marlene Farinacci Vilaro, source=Web Response No relevant relationships by Ricardo Fernandez, source=Web Response No relevant relationships by Luis Gerena Montano, source=Web Response

An integrated overview of AV node physiology

The atrioventricular (AV) node generates half of the AV delay needed for blood pumping and filters atrial impulses that could otherwise induce life-threatening ventricular arrhythmias. It is also a pacemaker and a key target in the treatment of cardiac arrhythmias. The special roles of the AV node primarily arise from its slow conduction, long refractory period, and cellular automaticity. However, efforts to establish the dynamics of these properties and their interaction led to many controversies. In fact, the AV node's behavior is so complex that it seems to escape broadly applicable rules. This review summarizes progresses made in resolving these issues and in integrating the multiple roles of the AV node within a common functional model. Presented evidence shows that the rate-dependent conduction and refractory properties of the AV node can be reliably characterized and reconciled from nodal responses to S1 S2 S3 protocols. It also supports the concept that dual pathways constitute a feature of the normal AV node and account for its overall conduction and refractory properties. In this model, the posterior extension and compact node provide the core of the slow and fast pathway, respectively. The transitional tissues and lower nodal bundle provide a common proximal and distal pathway, respectively. These pathways would also support bidirectional conduction. The dual pathway involvement can also be extended to widely variable AV nodal responses, such as Wenckebach cycles, hysteresis, and ventricular response to atrial fibrillation. In brief, the intricate AV nodal behavior may obey a limited set of accessible and definable rules.

IRON ISOMALTOSIDE DIMINISHES ATRIAL ELECTRICAL INHOMOGENEITY IN CHRONIC HEART FAILURE WITHOUT ALTERING ATRIAL SIZE: A FERRIC-HF II SUBSTUDY

Atrial sinus impulse propagation is critically dependent on atrial energetics. Enhanced atrial electrical inhomogeneity, as reflected by a prolonged P wave dispersion (Pd), can result from impaired energetics and heralds atrial fibrillation and worsening chronic heart failure (CHF). Because iron

P wave dispersion in obese dogs with and without mitral valve disease

ABSTRACT: Pwave dispersion (Pd) is an electrocardiographic index defined as the difference between the minimum and maximum Pwave duration in multiple leads. The augmentation of Pd reflects the discontinuous and inhomogeneous atrial depolarization resulting from cardiac and non-cardiac conditions. In humans, an increased Pd is associated with the development of cardiac arrhythmias, particularly atrial fibrillation. To investigate Pd in obese dogs, we enrolled 76 dogs, which were classified in four distinct categories according to body condition and the existance of valve insufficiency: obese dogs (O), dogs with both obesity and cardiac disease (O+CD), lean dogs with cardiac disease (CD) and healthy controls (H). To be included in the study, all dogs underwent an electrocardiographic and echocardiographic assessment. We reported significantly higher Pd in the animals included in categories O, O+CD and CD (18.0±7.6ms, 16.1±4.4ms, 12.1±4.3ms, respectively) as compared to the healthy subjects (7.3±2.2ms). Also, significant correlations between Pd and both the body mass index and body fat percentage were documented for the obese dogs. However, no association between Pd and LA/Ao could be identified in patients belonging to the O, O+CD and H categories. Thus, we have demonstrated that obese dogs, regardless of their valvular competency status, present high Pd values, suggesting an impaired propagation of atrial electrical impulse.

Overexpression of Perilipin 2 Induces Cardiac Steatosis and Atrial Fibrillation via Connexin 43 Remodeling

Atrial fibrillation (AF) is prevalent among diabetic patients. Diabetes is also associated with myocardial lipid droplet accumulation (steatosis), which is thought to be a source of intracellular lipotoxicity. Since the relative contribution of cardiac steatosis per se to AF has not been elucidated, the current study was designed to clarify the causal effect of cardiac steatosis on AF using an aged mouse model of cardiac steatosis. Cardiac-specific perilipin (PLIN) 2-overexpressing mice (PLIN2-Tg) were created and maintained on a chow diet for >12 months. Cardiac steatosis was assessed by electron microscopy and triacylglycerol (TAG) content. AF was induced by transesophageal electrical burst pacing, and the duration of AF was measured. Atrial impulse conduction patterns were analyzed in Langendorff-perfused hearts using optical mapping technique. Myocardial localization of a gap junction protein, connexin (Cx) 43, was analyzed by confocal microscopy. Electron microscopy of the atrium of PLIN2-Tg revealed accumulation of small lipid droplets around clusters of mitochondria, and the atrial TAG content in PLIN2-Tg was 4- to 8-fold higher than that in wild type (Wt) atrium. Electrocardiograms showed significantly longer RR intervals in PLIN2-Tg compared to Wt mice. The prevalence of sustained (>5min) AF was significantly greater in PLIN2-Tg compared with Wt mice (69% vs. 24%). Confocal microscopy revealed that Cx43 was distributed at the intercalated discs in Wt atria, whereas it was heterogeneously redistributed to the lateral side of the cardiomyocytes in PLIN2-Tg atria. Isochrone mapping showed slow and heterogeneous impulse propagation in PLIN2-Tg atria compared with Wt atria. These results indicate that PLIN2-induced steatosis causes Cx43 remodeling, impaired conduction propagation, and a higher incidence of AF. Controlling cardiac steatosis might be an important target for inhibiting AF in patients with cardiac steatosis. Disclosure S. Sato: None. J. Suzuki: None. M. Hirose: None. T. Nakaya: None. M. Yamada: None. M. Ichikawa: None. M. Imagawa: None. Y. Zenimaru: None. S. Takahashi: None. F.B. Kraemer: None. T. Konoshita: None. T. Ishizuka: None.

Dual atrioventricular nodal pathways: physiology, arrhythmic findings, and electrocardiographic manifestations

The atrioventricular (AV) node is an anatomically well-defined structure, conveniently housed in the triangle of Koch. There are two distinct atrial impulse approaches to the AV node, one of which (in the anterior portion of triangle of Koch) has a faster conduction, while the other one (in the posterior portion) has a slower conduction. However, it is not said that such a conductive duality translates into any arrhythmic phenomena. Actually, these arrhythmias are due to an imbalance of the two pathways electrophysiological properties, which does not always exist. In the presence of such an imbalance, the dual AV nodal physiology is, however, the substrate for various arrhythmias and curious electrocardiographic behaviors. Often the fast pathway is characterized by a relatively long refractory period. In contrast, the slow approach is often characterized by shorter refractoriness.The unbalanced refractoriness of the two nodal pathways constitutes the prerequisite for the most common form of paroxysmal supraventricular tachycardia: the AV nodal reentrant tachycardia (AVNRT). In subjects prone to this type of arrhythmia, during sinus rhythm, nodal conduction usually occurs from the anterior approach (fast pathway). However, a premature atrial beat may find this pathway refractory and cross the AV node through the posterior approach (slow pathway), resulting in a sudden prolongation of the AV conduction time ("jump"). This allows the impulse, once it reaches the common end, to excitate the fast pathway in a retrograde direction and to return backwards to the atrium, thus triggering a circus movement that can result in a "slow-fast" AVNRT. More rarely, an AVNRT can take place in an opposite direction of the reentrant impulse ("fast-slow" variety of AVNRT). A paroxysmal supraventricular tachycardia may seldom occur with a regularly alternating RR cycle, if the reentrant mechanism involves retrogradely an accessory AV pathway and, in anterograde direction, a fast and a slow AV nodal pathway, alternately. Among the mechanisms underlying the total RR irregularity during atrial fibrillation, there is probably also the possibility that the AV node may offer to the atrial impulses two distinct pathways to reach the His bundle. Not too rarely, a dual AV nodal physiology can occur during sinus rhythm, through unexpected and sudden changes in the AV conduction time, so that two distinct PR families can be observed. It is likely that the presence of dual AV nodal pathways can facilitate or promote a Wenckebach conduction mechanism at nodal site.

PAROXYSMAL AV BLOCK: A RARE CAUSE OF CARDIAC ARREST

Paroxysmal AV block is an abrupt, unexpected, repetitive block of atrial impulses as they propagate to the ventricles and is a rare cause of cardiac arrest. A 66-year old man with a history of hyperlipidemia and left bundle branch block was admitted to the hospital for an esophagectomy for