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