Cardiac Arrhythmias

All three major components (inward Na+ and Ca2+ and outward K+) are
voltage gated
Resting membrane potential is determined primarily by 3
factors
o The concentration of ions on the inside and outside of the cell
o The activity of electrogenic pumps (e.g., Na+/K+-ATPase and Ca2+
transport pumps)
o The permeability of the cell membrane to K+
 Gap junction
channels are made of connexions
o Each channel is made of two connexons, one in the plasma membrane
of each of the cells linked
Conduction velocity in cardiac tissue
o Velocity of spread of activation along tissue dependent on:
Action potential upstroke speed (ie amount of depolarizing
current)
Coupling of cells (gap junction function)
o Slow conduction
Blocking sodium channels in working myocardium
Blocking calcium channels in nodal tissue
Affecting gap junction function
Difference between normal physiology of nodal and working myocardial tissue
o Nodal
Action potential dependent primarily on Ca2+ ions
AP has slow upstroke therefore conduction velocity is slow
As rate of stimulation is increased, conduction velocity slows,
refractory period increases
Behaviour influenced profoundly by autonomic tone
Automaticity
o Property of cardiac cells to depolarize spontaneously
o Normally only cells of the SA node, AV node and Hi-Purkinje system
possess automaticity
o SA Node Ca2+
o Purkinje Fibre Na2+
Mechanisms of Bradyarrhythmia
o Failure of impulse formation (e.g sinus bradycardia)
o Failure of impulse propagation (e.g. Mobitz II AV Block)
Mechanisms of Tachyarrhythmia
o Automaticity
Normal (sinus tachycardia)
Abnormal (reperfusion arrhythmias)
o Triggered activity
Early afterdepolarizations associated with AP prolongation
(torsades de pointes)
 Delayed afterdepolarisations associated with Ca2+ overload and
depolarization (e.g. digoxin)
o Re-Entry
Favoured by slow conduction
Favoured by cellular heterogeneity
Characteristics of Arrhythmias
o Automaticity
Morphology of the initiating P or QRS is the same as subsequent
complexes
Exhibit progressive warm-up (acceleration in rate)
Automatic tachycardias cannot be initiated by programmed
electrical stimulation (PES) or pacing
o Triggered activity
Early afterdepolarisations
Seen with bradycardia and prolonged action potentials
Thought to be secondary to L-type Ca2+ channel recovery

Delayed afterdepolarizations
Seen with tachycardia and cell Ca2+ overload
Thought to be secondary to a Ca2+-dependent transient
inward current or sodium calcium exchange
o Re-entry tachycardia

~95% of clinical arrhythmias

Absolute requirement
Unidirectional conduction block
Favouring conditions
Slow conduction such as occurs with fibrosis
 Normally the QT is the RR interval

Atrial Fibrillation and Flutter

o Disorganized electrical pulses in the atria cause the rhythm of the
lower chambers to be fast and irregular
 Normally, the top chambers (atria) contract and push blood into the bottom
chambers (ventricles). In atrial fibrillation, the atria beat irregularly. In atrial
flutter, the atria beat regularly, but faster than usual and more often than the
ventricles, so you may have four atrial beats to every one ventricular beat.
o Catheter ablation is usually considered the best treatment for atrial
flutter, whereas medication is often the first treatment for atrial
fibrillation. Catheter ablation is a procedure that is done under local
anaesthetic, where radiofrequency energy is used to destroy the area
inside your heart thats causing the abnormal heart rhythm.
o Atrial fibrillation linked to males
Ventricular Tachycardia and Fibrillation
o
 Pac
emaker Indication
o Sinus Node Dysfunction
o AV Block
o Iatrogenic
o Neurocardiogenic Syncope
o Long QT
o Heart Failure and Resynchronization

Class I Na+ Blockers

Class II Beta Blockers
 Class III K+ Blockers
Class IV Ca2+ Blockers
Getting rid of Re-Entry
o K+ Channel Prolong refractory period
o Na+ Channel Critically slow conduction
Proarrhythmia is a new or more frequent occurrence of pre-existing
arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which
means it is a side effect associated with the administration of some existing
antiarrhythmic drugs, as well as drugs for other indications.
o Class I Brugada Syndrome
Brugada syndrome is a rare inherited heart rhythm disturbance
that restricts the flow of sodium ions into the heart cells.
The symptoms of Brugada syndrome can include blackouts
caused by a disturbance in the hearts rhythm (ventricular
arrhythmia) or palpitations. However, you may experience no
symptoms at all.
Brugada Syndrome can be difficult to diagnose. You will have to
have an ECG. The differences in the ECG waveform that are
characteristic of Brugada Syndrome may appear on your results
continuously, intermittently, or they may not show at all.
o Class III Long QT
The maze procedure is a surgical treatment for atrial fibrillation. It
can also be called a surgical ablation. The surgeon can use small incisions,
radio waves, freezing, or microwave or ultrasound energy to create scar
tissue.
 Class I: Fast sodium (Na) channel blockers
o Ia - Quinidine, procainamide, disopyramide (depress phase 0,
prolonging repolarization)
o Ib - Lidocaine, phenytoin, mexiletine (depress phase 0 selectively in
abnormal/ischemic tissue, shorten repolarization)
o Ic - Flecainide, propafenone, moricizine (markedly depress phase 0,
minimal effect on repolarization)
Class II: Beta blockers (partial list)
o Propranolol (decreases slope of phase 4)
o Esmolol (decreases slope of phase 4)
o Timolol (decreases slope of phase 4)
o Metoprolol (decreases slope of phase 4)
o Atenolol (decreases slope of phase 4)
Class III: Potassium (K) channel blockers
o Amiodarone (prolongs phase 3; also acts on phases 1, 2, and 4)
o Sotalol (prolongs phase 3, decreases slope of phase 4)
o Ibutilide (prolongs phase 3)
o Dofetilide (prolongs phase 3)