Pathophysiology of Arrhythmias

Re-entry homogenous myocardium

When right and left sides excite similarly

What is the most common type of ventricular preexcitation syndrome?

Wo lff-Parkinson-White(WPW) syndrome

Supraventricular arrhythmias: Is there normal QRS?

Yes (narrow)

Long-QT Syndrome risk

sudden cardiac death (SCD) due to torsades de pointes (TDP)

atrial fibrillation most often initiated (triggered) by

rapid firing from the pulmonary veins -triggers (ectopic foci, abnormal automaticity, TA) and -substrate (remodeled atria supporting multiple reentries).

What is the most common cause of a tachy-arrhythmias?

re-entry

Wolff-Parkinson-White Syndrome may result in

reentry circuit --> supraventricular tachycardia.

If automaticity is increased (too fast) this result in

sinus tachycardia - usually secondary, could be physiological (e.g., exercise), also seen in disease states (fever, thyrotoxicosis, etc.) - Inappropriate sinus tachycardia

Early afterdepolarization (EAD): Risk increases at

slower HR (bradycardia --> prolongs AP) - due to re-opening of L-type Ca channel

RyR2 dysfunction is usually worsened by what? tx?

sympathetic excitation like exercise or acute emotion tx: beta blocker

Describe re-entry of the heart?

this occurs if the same impulse re-excites the heart again

Long QT interval predisposes to

torsades de pointes - caused by drugs, hypokalemia, hypomagnesium

Ventricular arrhythmias: Where does it originate?

below his bundle

How can reentry be terminated?

by pacing capturing the excitable gap

Ventricular tachycardia (VT) polymorphic VT-TDP causes

cadiac channelopathies 1. long-QT syndrome 2. brugada syndrome 3. short QT syndrome 4. CPVT

AED (automated external defibrillator) mechanism

coverts back to sinus rhythm

Wavelength and excitable gap: How do you increase the reentry risk?

decrease WL

Wolff-Parkinson-White Syndrome: Describe the QRS complex and shortened PR interval

delta wave w/ widened QRS complex and shorted PR interval

Brugada syndrome

diminished inward sodium current, particularly in RVOT - epicardium-epicardial dispersion of repolarizations

Delayed afterdepolarizaion (DAD) causes

due to calcium overload - digitalis toxicity, reperfusion- induced arrhythmias, CPVT (catecholaminergic polymorphic VT)

Early afterdepolarization (EAD) cause

due to prolonged action potential - long QT syndrome, hypokalemia

Atrioventricular junction tachycardia causes

enhanced normal automaticity, abnormal automaticity or TA (digitalis toxicity)

Delayed afterdepolarizaion (DAD): Risk increases at

faster HR - Na/Ca exchanger current --> most positive charge --> repolarizes membrane potential

Wavelength and excitable gap: How do you decrease the reentry risk?

for a given reentry circuit - increasing WL reduces risk - increase ERP/CV or both

Supraventricular arrhythmias: Where do they originate?

from a site at his bundle or above

Conduction sequence of the heart

SN-Atria-AVN-His bundle (supraventricular)- Bundle branches-Purkinje system-Ventricles

Abnormal impulse conduction: Conduction block causes

SN-atrial, AV, His bundle, and bundle branches --> causes bradyarrhythmias

AVNRT cure

SP ablation

Abnormal impulse initiation: Two Types

- Abnormal automaticity - Triggered activity

Romano-Ward syndrome

-Congenital long QT syndrome -Autosomal dominant, pure cardiac phenotype (no deafness).

Jervell and Lange-Nielsen syndrome

-Congenital long QT syndrome -Autosomal recessive, sensorineural deafness

ventricular fibrillation could be initiated by any of the 3 mechanisms

-automaticity, TA and reentry, maintained by multiple wavelets, as in AF.

tachy-arrhythmias mechanism

1 or more of these 3 basic mechanisms: abnormal automaticity, TA, or reentry

Two arrhythmia mechanisms

1. Abnormal impulse initiation 2. Abnormal Impulse Conduction

brady-arrhythmias: mechanism (2)

1. Failure of impulse generation (decreased automaticity) -sinus bradycardia or arrest Sick Sinus Syndrome (SSS) 2. Failure of impulse propagation (conduction block) -Sino-atrial block -AV block

Ventricular tachycardia (VT) monomorphic VT

1. Structural heart disease ischemic, non-ischemic cardiomyopathy arrhythmogenic RV dysplasia predominantly reentry 2. Structurally normal hearts-idiopathic VT a. Outflow tract tachycardia-TA b. Fascicular ventricular tachycardia-reentry

Ventricular tachyarrhythmias (abnormal, widen-QRS): Causes (2)

1. Ventricular premature beat abnormal automaticity, TA or reentry 2. Accelerated idioventricular rhythm abnormal automaticity

Two causes of abnormal impulse conduction of the heart?

1. conduction block 2. re-entry

What are the two major causes of brady-arrhythmias? (<60 bpm)

1. conduction block 2. reduced automaticity

What are the two major causes of tachy-arrhythmias? (>100 bpm)

1. increased automaticity 2. triggered activity 2. re-entry (most common)

Supraventricular arrhythmias: causes (3)

1. sinus tachycardia - enhanced normal automaticity 2. Atrial premature beat or atrial tachycardia - automaticity, TA, or reentry 3. Atrial flutter: macroeentry

AED (automated external defibrillator)

A portable device that checks the heart rhythm and if needed, can send an electric shock to try to restore a normal rhythm. - monophasic (360-400 joules) or biphasic (120-200 joules) DC current

AVNRT

AV nodal reentrant tachycardia - dual pathway AVN electrophysiology - micro-reentry

Wolff-Parkinson-White Syndrome

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node → ventricles begin to partially depolarize earlier →characteristic delta wave with widened QRS complex and shortened PR interval

Wavelength and excitable gap: Formula for Wavelength (distance)

CV (speed) * ERP (time)

Re-entry inhomogenous myocardium: Compare CV and ERP of fast and slow pathways

CV: fast --> ERP: long CV: short --> ERP: short

AVRT

Atrioventricular reentrant tachycardia - pre-excitation syndrome or WPW

Abnormal impulse initiation: Triggered activity causes (2)

Both triggered by the previous AP: a. Early afterdepolarization (EAD) b. Delayed afterdepolarizaion (DAD)

Cardioversion vs Defibrillation

Cardioversion: in sync with QRS (R wave not T wave), used in AFib, PSVT, or VT; requires lower energy Defibrillation: not in sync with QRS, used in VFib, requires higher energy - deliver immediately require higher energy

Common medications that may lead to long QT

Class IA, IC, III antiarrhythmics Abx (erythromycin)

Early Afterdepolarization (EAD): What phases are involved?

Late phase 2 and phase 3

Macro-reentry vs. Micro-reentry

Macro- involves atria and ventricles (two pathways linking the two --> form reentry Micro - occurs in small region

Wavelength and excitable gap: reentry circuit =

WL + excitable gap - WL < reentry circuit

Where does the normal heart beat originate from?

SA node

Conditions to form reentry (3)

When all are met --> reentry occurs 1. unidirectional block 2. slow conduction 3. recovery of previously excited proximal tissue

Brugada syndrome ECG

Coved-type (pseudo-right bundle branch block) with ST Elevation in V1-V3

Acquired LQT Syndrome: ABCDE

Drug-induced long QT (ABCDE): AntiArrhythmics (class IA, III) AntiBiotics (e.g., macrolides) Anti"C"ychotics (e.g., haloperidol) AntiDepressants (e.g., TCAs) AntiEmetics (e.g., ondansetron)

AV nodal reentrant tachycardia: AV conduction through

FP fast CV

Describe the normal heart beat and how it propagates a signal throughout the heart?

Normally a heart beat generated inside the sinus node will propagate throughout the whole heart and die out. - When this doesn't occur --> reentry occurs

Delayed afterdepolarizaion (DAD): What channels are involved?

Phase 4

Long-QT Syndrome: two types

Prolonged AP; inherited disorder of myocardial repol. --> typically due to ion channel defects inherited (congenital) LQT syndrome: reduced outward K+ currents and increased inward Na+ or Ca++ currents - LQT1-3 acquired LQT syndrome: meds

If automaticity is decreased (too slow) this result in

Sinus bradycardia-could be physiological (at rest), also seen in disease (sick sinus syndrome, SSS)

What is the major mechanism involved in Long-QT?

TA (EAD) - sympathetic excitation increases inward currents, prolongs QT-B-blocker treatment

Abnormal impulse initiation: Abnormal automaticity causes (2)

a . Altered normal automaticity - sinus tachycardia or bradycardia b. Abnormal automaticity - non-pacemaker cell (atrial and ventricular) - premature beat or tachycardia of either atrial or ventricular in origin

Abnormal impulse conduction: Re-entry causes

a. Anatomic reentry b. Functional reentry

Atrioventricular reentrant tachycardia (AVRT): macro-reentry causes

a. narrow versus wide-QRS tachycardia b. concealed accessory pathway c. multiple pathways

Atrial flutter-reentry in RA: tx and where?

ablation - Cavotricuspid isthmus: between the IVC and the TV

Atrioventricular reentrant tachycardia (AVRT) cure

ablation of accessory pathway

atrial fibrillation cure

ablation of pulmonary veins

Ventricular arrhythmias: Is there normal activation of the ventricles?

abnormal ventricular activation

Atrioventricular reentrant tachycardia (AVRT) causes?

accessory pathway - bundle of kent - macro-reentry

AV nodal reentrant tachycardia: form reentry

antegrade SP retrograde FP

Brugada syndrome most common in

asian males

What is the most common clinically significant arrhythmia?

atrial fibrillation

What are common causes of abnormal automaticity of the heart?

hypoxia, ischemia, inflammation --> cause cell injury --> membrane potential increases (more positive) --> inactiv. Na+ channels --> could become slow response cells (excites by ICa-L) - once injured, cannot maintain membrane potential

Brugada syndrome: prevent SCD w/

implantable cardioverter-defibrillator (ICD)

shortened QT syndrome: what is the ERP and WL?

increased IK+, QT<0.3s - short ERP, WL - multiple reentry

Catecholaminergic polymorphic VT: due to

leaky cardiac ryanodine receptor (RyR2)-DAD - genetic disorders of Ca++ release channels (RyR2) and their controlling proteins (ryanodine receptor and calquestrin)

AV nodal reentrant tachycardia: FP blocked due to

long ERP

tx of torsades de pointes

magnesium sulfate

Arrhythmia

not normal sinus rhythm

Why should you not use cardioversion on a T-wave?

ventricle vulnerable period - any shock can trigger ventricular fibrillation

polyventricular tachycardia is characterized by shifting sinusoidal waveforms on ECG and can progress to

ventricular fibrillation

Brugada syndrome have risk of

ventricular tachyarrhythmias and SCD

Ventricular arrhythmias: Is there normal QRS?

wide QRS

Supraventricular arrhythmias: Is there normal activation of the ventricles?

yes