Arrhythmias:Terminology, Definitions, and Mechanisms

Ectopic Beats or Rhythms beats or rhythms that originate in places other than the SA node the ectopic focus may cause single beats or take over and pace the heart, dictating its entire rhythm they may or may not be dangerous depending on how they affect the cardiac outputTerminology and Basics Causes of Ectopic Beats or Rhythms hypoxic myocardium - chronic pulmonary disease, pulmonary embolus ischemic myocardium - acute MI, expanding MI, angina sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia, imbalances of calcium and magnesium bradycardia - a slow HR predisposes one to arrhythmias enlargement of the atria or ventricles producing stretch in pacemaker cells

Arrhythmia or Dysrhythmia? dysrhythmia accurate, but arrhythmia most widelyTerminology and BasicsSupraventricular: origin is above the ventricle, i.e., SA, atrial muscle, AV or HIS originVentricular: origin is in ventricleArrhythmia is generally named for anatomical site or chamber of origin

Automaticity: Spontaneous Phase 4 Depolarization (SA, AV, Purkinje tissue) rate dependent on: Threshold potential slope of phase 4 depolarization resting membrane potentialMechanisms of Arrhythmias Altered automaticity Normal, enhanced normal, abnormal Triggered activity ReentryMechanisms

From: Berne and Levy, Physiology, Mosby, 1983.Change slope, change rate. 1o sympathetic mechanism; PNS dec phase 4 slope and hyperpolarize1. Altered AutomaticityChange threshold, change rate.Change RMP, change rate

From: Berne and Levy, Physiology, Mosby, 1983. hypothermia decrease, hyperthermia increase phase 4 slope hypoxia & hypercapnia both increase phase 4 slope cardiac dilation increases phase 4 slope local areas of ischemia or necrosis increases automaticity of neighboring cells hypokalemia increases phase 4 slope, increases ectopics, prolongs repolarization hyperkalemia decreases phase 4 slope; slow conduction, blocks

2. Triggered ActivityAfterdepolarization reaches thresholdEarly: interrupt repolarizationCongenital or acquired long QT syndrome: altered K+ and Na+ currents during phase 2 can produce dangerous V-tachDelayed: after completion of AP.3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)Anatomic: nodal tissue, Purkinje, BB, accessory pathExample: WPWFunctionalLocal differences in conduction velocity and membrane characteristicsAnisotropic:circuit determined by difference in conduction velocity through length of fiberReflectionParallel pathways with depressed segments

3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)Requires: available circuit, unidirectional block, and different conduction speed in limbs of circuitConditions that depress conduction velocity or shorten refractory period promote functional blockExp: WPW reciprocating tachycardia, AV-nodal reentry, V-tach due to bundle branch reentry, infarcted area.

Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryThe Re-Entry Mechanism of Ectopic Beats & RhythmsElectrical ImpulseCardiac Conduction TissueTissues with these type of circuits may exist: in microscopic size in the SA node, AV node, or any type of heart tissue in a macroscopic structure such as an accessory pathway in WPW

Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryPremature Beat ImpulseCardiac Conduction Tissue1. An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only Repolarizing Tissue (long refractory period)The Re-Entry Mechanism of Ectopic Beats & Rhythms

3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueThe Re-Entry Mechanism of Ectopic Beats & Rhythms

4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation re-enters the pathway and continues in a circular movement. This creates the re-entry circuit

Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueThe Re-Entry Mechanism of Ectopic Beats & Rhythms

Atrial Re-entry atrial tachycardia atrial fibrillation atrial flutterAtrio-Ventricular Re-entry Wolf Parkinson White supraventricular tachycardia

Ventricular Re-entry ventricular tachycardia

Atrio-Ventricular Nodal Re-entry supraventricular tachycardia

Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

Clinical Manifestations of Arrhythmias many go unnoticed and produce no symptoms palpitations ranging from noticing or being aware of ones heart beat to a sensation of the heart beating out of the chest if Q is affected (HR > 300) lightheadedness and syncope, fainting drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia, imbalances of calcium and magnesium very rapid arrhythmias u myocardial oxygen demand r ischemia and angina sudden death especially in the case of an acute MI mechanism differentiation from ECG very difficult to impossible

Clinical Application No rhythms precisely regular Incidence: common (PVC, PAC), increase with age ECG differentiation may be impossible Monitor leads V1 or MCL1: L&R ventricular ectopy, RBBB & LBBB, good P-waves Where to look for clues P-wave morphology PR interval QRS morphology QTc interval Matching atrial rate with ventricular Look for gaps in the rhythm

Clinical Application Eight basic rhythm disturbances early beats (extrasystole) unexpected pauses (nonconducted atrial extrasystole) bradycardia (sinus bradycardia) tachycardia (ventricular or atrial) bigeminal rhythm (ventricular or supraventricular extrasystolic) group beating (2nd degree heart block) total irregularity (atrial fibrillation) regular non-sinus rhythm at normal rate (accelerated AV rhythm)