Mechanism of arrhythmias

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor in Chief: Pablo A Quintero, M.D.

## Contents

* 1 Mechanism of Arrhythmias
* 1.1 Disorders of Impulse formation
* 1.1.1 Automaticity Activity
* 1.1.2 Triggered Activity
* 1.2 Disorders of Impulse Conduction
* 1.2.1 Reentry
* 2 References
* 3 Additional Resources

## Mechanism of Arrhythmias

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Mechanism of cardiac arrhytmias are divided into 2 main categories

1. Disorders of Impulse formation
2. Disorders of Impulse conduction

### Disorders of Impulse formation

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There are two major causes of impulse formation that could result in arrythmias

* Automaticity Activity
* Triggered Activity

#### Automaticity Activity

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Automaticity is a characteristic of cardiac cells to undergo spontaneous diastolic depolarization and initiate an electrical impulse in the absence of external electrical stimulation. Normal automaticity makes the sinus node the primary pacemaker of the heart. The sinus nodal discharge rate dominates latent pacemakers because it depolarizes more rapidly. This mechanism has been referred as overdrive supression. Examples of arrhytmias with normal automaticity are sinus tachycardia or bradycardia inappropriate for a particular clinical situation. This arrhythmia is caused by an alteration in the rate of impulse initiation by the normal sinus node pacemaker without shifting the impulse origin to a subsidiary pacemaker at an ectopic site. (Heart)

Abnormal automaticity occurs in cardiac cells when there are abnormal changes in the transmembrane potentials due to disease or interventions. The spontaneous action potentiasl generated by this mechanism may be caused by either Na+ or Ca2+ inward currents and sometimes a mixture of both. Increase cathecolamines, electrolyte abnomalities and medications could all enhance automaticity and lead to arrythmias. An example of abnormal automaticity would be accelerate idioventricular rhythm.

Normal or abnormal automaticity would also initiate arrythmias caused by nonautomatic mechanism. For example, premature beats, caused by automaticity , can lead to reentry.

This arrythmias cannot be stopped or started by pacing.

#### Triggered Activity

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This scenario refers to a pacemaker activity that is initiated secondary to afterdepolarizations from a prior impulse or series of impulses. Afterdepolarizations is an oscillation in membrane potential that occurs after repolarization

Two types of after depolarizations can be identified:

* Early afterdepolarizations (EAD): they arise during the repolarization of the action potential. They can occur with electrolyte abnormalities, acidosis, hypoxemia and increased cathecolamine states. EAD might be responsible for the ventricular arrhytmias of the acquired and congenital forms of long QT syndrome and also in the origen of arrhytmias in heart failure and hyperthrophy. Early depolarizations are supressed by magnesium.

* Delayed Afterdepolarizations (DAD): they occur after repolarization is completed.This activity is seen in conditions that increase intracellular calcium. When these delayed afterdepolarizations reach the threshold potential, it "triggers" an action potential. DAD seems to be responsible for arrhytmias of digitalis toxicity and in the failing heart. Drugs that block calcium influx (betablockers, calcium channel blockers) and drugs that decrease sodium current (lidocaine) supress DAD.

### Disorders of Impulse Conduction

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In normal conditions, the excitation wavefront initiated in the sinus node will activate the cardiac tissue in an organized sequence and then will die out. However, there are cases where the original impulse perpetuates and propagates itself because it always finds excitable myocardial tissue.

#### Reentry

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This is probably the mechanism responsible for the majority of important arrhytmias. It needs two main components so it can occur:

* Two functionally distinct (different in velocity of conduction or refractroy period) conducting pathways
* Unidirectional block in one of the pathways

Of note, the time for conduction within the depressed but unblocked area must exceed the refractroy period of the initially blocked pathway and proximal tissue. If this conditions are achieved, it will allow a repetitive circulation of the impulse over a loop inducing the arrythmia.

Common clinical examples are atrial fibrillation, atrial flutter, AVNRT (AV nodal reentry tachycardia) and WPW (Wolf Parkinson White)

## References

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## Additional Resources

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1\. Fuster, V. Hurst's the Heart. 12th edition. 2008. Chapter 35

2\. Kasper, D. Harrison's Principles of Internal Medicine. 16th edition. 2004. Chapter 214

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Electrocardiography

Overview|

History of the EKG • EKG interpretation basics • Normal sinus rhythm

EKG Complexes|

P wave • QRS complex • ST Segment • T wave • T wave alternans • Tombstone T wave • U wave

Osborn wave • H wave • K wave • Delta wave

NSSTW changes

EKG Intervals|

PR Interval • QRS Interval • ST Interval • QT Interval

Conduction System & Bradycardia|

Cardiac pacemaker • SA node • AV node• Bundle of His • Purkinje fibers • Sinus bradycardia • First Degree AV Block • Second Degree AV Block • Complete or Third-Degree AV Block • Concealed conduction • AV Junctional Rhythms • LBBB • LAHB • LPHB • RBBB • Trifascicular block

Atrial Arrhythmias|

Sinus tachycardia • Premature Atrial Contractions (PACs) • Ectopic Atrial Rhythm • Paroxysmal Atrial Tachycardia (PAT) • Paroxysmal Atrial Tachycardia (PAT) with Block • Multifocal Atrial Tachycardia (MAT) • Atrial Flutter • Atrial Fibrillation • Wandering atrial pacemaker

Ventricular Arrhythmias|

Differential Diagnosis of Tachycardia with a Wide QRS Complex • Accelerated Idioventricular Rhythm • Ventricular Parasystole • Premature Ventricular Contractions (PVCs) • Ventricular tachycardia • Ventricular Fibrillation • Sudden cardiac death

EKG Abnormalities in Disease States|

Hypertrophy & Dilatation • Right atrial enlargement • Left atrial enlargement • Biatrial enlargement • Left Ventricular Hypertrophy • Right Ventricular Hypertrophy • Biventricular Hypertrophy •

Acute myocardial infarction • NSTEMI • STEMI • Tombstone ST elevation • Right ventricular myocardial infarction • Atrial infarction

Pre-excitation Syndromes • Wolff-Parkinson-White Syndrome • Lown Ganong Levine Syndrome • Mahaim Type Preexcitation

Cardiomyopathies • Arrhythmogenic Right Ventricular Dysplasia • Dilated Cardiomyopathy • Hypertrophic Cardiomyopathy

Drug Effects on the EKG • Adenosine • β-blockers • Digitalis • Quinidine • Procainamide • Disopyramide • Lidocaine • Tocainide and Mexiletine • Phenytoin • Encainide, Flecainide and Propafenone • Amiodarone • Bretylium • Ca Channel Blockers • Phenothiazines • Tricyclic Antidepressants • Lithium

Congenital Heart Disease • Dextrocardia • Atrial Septal Defect • Ventricular Septal Defect • Tetralogy of Fallot • Conjoined Twins or Siamese Twins • Congenital heart block

Electrolyte Disturbances • Hyperkalemia • Hypokalemia • Hypercalcemia • Hypocalcemia • Nonspecific Changes

Other Heart Diseases • Pericarditis • Myocarditis • Tamponade • Heart Transplantation • Sick Sinus Syndrome • Long QT Syndrome

Inherited Disease • Brugada Syndrome

Systemic Diseases • CNS Disease • Cardiac Tumors

Heart Transplantation • EKG Changes in patient with Heart Transplantation

Exogenous Effects • Hypothermia • Chest Trauma • Insect Bites • Electric Injuries

Technical Issues and Potential Errors in Interpretation|

Artifacts • Lead Placement Errors • The EKG in a Patient with a Pacemaker • EKG in athletes

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