Rubery: Arrhythmias 2

Front 1

Tachyarrhythmias: abnormal automaticity

Back 1

Ischemia, metabolic derangement, or ion channel abnormality transforms phase 4 activity of atrial or ventricular myocyte

Front 2

Tachyarrhythmias: triggered activity

Back 2

Afterdepolarizations
-Following the usual depolarization sequence, spontaneous depolarization occurs during or just after the previous action potential
-Afterdepolarization amplitude must reach threshold in order to generate a new action potential

Front 3

Early afterdepolarization

Back 3

Phase 3 repolarization is interrupted by a depolarizing current
Usually caused by reactivation of Ca++ channels
Can be self-perpetuating: dangerous arrhythmias
Torsades de Pointes: initiates with Early Afterdepolarizations (EADs)
More likely to occur in presence of drugs or conditions that prolong phase 3
- i.e. things that prolong the QT interval

Front 4

Acquired Long QT syndromes

Back 4

Acquired
-Usually caused by metabolic (electrolyte) abnormality, or effect of a drug
--Doesn’t have to be a cardiac drug – lots of antibiotics, antipsychotics, even SSRIs can cause prolonged QT

Front 5

Congenital long QT syndromes

Back 5

Congenital
-Can be sporadic or inherited
-Lot of genetic terms come into play:
--Penetrance, expressivity, all that stuff – affects whether or not the genotype causes the phenotype, and if so, how severe it is…
-Caused by mutations in ion channels
-Currently seven types are known:
--Most involve loss of function of potassium channels (↓IK)
--Some involve gain of function of sodium channels (↑INa)
-Regardless of exact mechanism, the result is prolongation of the QT interval
--Predisposes to polymorphic VT (aka Torsades de Pointes)
Can be relatively benign, or very dangerous
One source of danger = the doctor
-Many drugs can affect the QT interval
-Cardiac drugs (obviously)
-Antibiotics
-Antipsychotics
-Don’t give a QT-prolonging drug to a patient with Long QT syndrome!
--And be very careful with their “unaffected” family members, too!

Front 6

Jervell and Lange-Nielsen syndrome

Back 6

Congenital long QT syndromes
Autosomal recessive
Associated with sensorineural deafness present at birth
A very long QT on EKG
A very malignant form of the disease – high risk of fatal arrhythmias

Front 7

Romano Ward syndrome, Andersen-Tawil syndrome, Sudden Infant Death Syndrome

Back 7

Congenital Long QT syndromes

Romano Ward
-Autosomal dominant

Andersen-Tawil
-Autosomal dominant
-Hypokalemic periodic paralysis

SIDS
-Multifactorial
-Long QT is probably one of the causes

Front 8

Delayed afterdepolarization

Back 8

Afterdepolarization occurs during phase 4
Occurs in setting of intracellular Ca++ overload
-Most commonly assoc. with digoxin toxicity, but other arrhythmias also have this mechanism

Front 9

Tachyarrhythmias: Reentry

Back 9

The most common mechanism of cardiac tachyarrythmias

Normal AV Node reentry
-Wave of depolarization
-Can either take slow or fast pathway
-At some point they rejoin and hit each other head on in refractory periods extinguishing conduction

Abnormal AV Node reentry
-Wave of depolarization
-Fast pathway blocks. Cells below this point are not depolarized, will not be refractory when slow current arrives from below.
-Wave takes slow pathway and works its way around to fast pathway block point
-Impulse arrives from below. If the signal arrives too quickly, this area will still be refractory, and the wavefront will be extinguished.
-If the slow pathway is “slow enough”, the signal will be delayed until this area has had time to recover, and is no longer refractory. Cells are activated, wavefront passes through and initiates reentry circuit.
--This is called unidirectional block because initially, block occurred antegrade, but after recovery it was able to conduct retrograde.

Reentry in the reverse direction
-Block in the slow pathway
-This is the mechanism for "atypical" AV node reentry
-Reentrant loop uses the slow pathway as the retrograde limb

Reentry using two slow pathways
-Another "atypical"

Reentry is possible when:
- at least two pathways are available for impulse conduction
-unidirectional block is possible
- slow (i.e. relatively slower) conduction is possible in at least one of the available pathways

Front 10

What causes unidirectional block?

Back 10

Almost always due to a premature beat
Premature beat comes in very soon after the preceding beat
In this case, the Fast pathway is still refractory from the previous beat, cannot be activated by the premature beat
The ERP of the cells, not the “speed” of the pathway, determines whether unidirectional block will occur.

Front 11

Wolff-Parkinson-White syndrome (WPW)

Back 11

Accessory pathway as the "fast pathway"
AV Node: slow conduction

If there is an extra beat, there is a block in the accessory pathway
-Causes Atrioventricular reciprocating tachycardia (AVRT)
-Reentry

Front 12

Ventricular tachycardia after myocardial infarction

Back 12

Is usually due to reentry, through the “mostly dead” scar zones
All VT is bad, but VT due to reentry caused by myocardial infarction scar is the most dangerous, because it can be incessant
-(well, it stops eventually but not necessarily in a good way...)

Front 13

Idiopathic Ventricular Tachycardia

Back 13

This is just one example of idiopathic VT, and this one is caused by reentry
-There are also forms of idiopathic VT caused by abnormal automaticity and also some caused by triggered activity
Even though this VT is caused by reentry, this is less dangerous than reentrant VT due to myocardial infarction
-Mainly because the heart function is otherwise normal, so it can maintain cardiac output despite the arrhythmia

Front 14

Reentry overview

Back 14

Reentry is a very common mechanism for tachyarrhythmias
Reentry is the mechanism for
-AVNRT (AV nodal reentry tachycardia)
-AVRT (atrioventricular reciprocating tachycardia)
--the arrhythmia associated with WPW (Wolff-Parkinson-White)
-Typical atrial flutter
-The worst kind of VT after a myocardial infarction
--The kind that kills people
--The kind that needs to be treated with a defibrillator
-Atrial fibrillation and ventricular fibrillation

Front 15

Non-pharmacologic treatment of tachyarrhythmias

Back 15

Implantable cardioverter defibrillators
-all ICDs are also pacemakers
Catheter ablation