Arrhythmia power point

ARRHYTMIA

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 output

Terminology 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 widely

Terminology and Basics

Supraventricular: origin is above the ventricle, i.e., SA, atrial muscle, AV or HIS origin

Ventricular: origin is in ventricle

Arrhythmia 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 potential

Mechanisms of Arrhythmias

• Altered automaticity

• Normal, enhanced normal, abnormal

• Triggered activity

• Reentry

Mechanisms

From: Berne and Levy, “Physiology”, Mosby, 1983.

Change slope, change rate. 1o sympathetic mechanism;

PNS dec phase 4 slope and hyperpolarize

1. Altered Automaticity

Change 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 Activity• Afterdepolarization reaches threshold

– Early: interrupt repolarization• Congenital or acquired long QT syndrome: altered K+ and Na+

currents during phase 2 can produce dangerous V-tach

– Delayed: after completion of AP

3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)

• Anatomic: nodal tissue, Purkinje, BB, accessory path– Example: WPW

• Functional– Local differences in conduction velocity and membrane characteristics

3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)

• Anisotropic:– circuit determined by difference in conduction velocity through length of fiber

• Reflection– Parallel pathways with depressed segments

• Requires: available circuit, unidirectional block, and different conduction speed in limbs of circuit– Conditions that depress conduction velocity or shorten refractory period promote functional block– Exp: WPW reciprocating tachycardia, AV-nodal reentry, V-tach due to bundle branch reentry, infarcted area.

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Electrical Impulse

Cardiac Conduction

Tissue

Tissues 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



Premature Beat Impulse

Cardiac Conduction

Tissue

1. 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)


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



Cardiac Conduction

Tissue


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



Cardiac Conduction

Tissue


Atrial Re-entry• atrial tachycardia• atrial fibrillation• atrial flutter

Atrio-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)

ARRHYTHMIA THERAPIES

1. Pharmacological Treatment • Accordingly, drugs which may reduce

ventricular rate by reducing AV nodal conduction include: – calcium channel blockers (verapamil

(Isoptin, Calan), diltiazem (Cardiazem))

– beta-adrenergic receptor blockers (propranolol (Inderal)), and

– digitalis glycosides.

1. Pharmacological Treatment

• Treatment of atrial fibrillation: Verapamil (Isoptin, Calan) & Diltiazem (Cardiazem) – Blocks cardiac calcium channels in slow response

tissues, such as the sinus and AV nodes. • Useful in treating AV reentrant tachyarrhythmias and in

management of high ventricular rates secondary to atrial flutter or fibrillation.

– Major adverse effect (i.v. administration) is hypotension. Heart block or sinus bradycardia can also occur.

2. Implantable Cardioverter Defibrillators

• implantable cardioverter defibrillators (ICDs) attempt to terminate tachyarrhythmias once they have been initiated by altering the electrophysiological substrate of the heart through electrical stimulation

3. Ablation Therapy

4. Gene and Cell Therapy

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