Normally, the action potential impulse will spread through the heart quickly enough that each cell will respond only once. However, if there is some essential heterogeneity of refractory period or if conduction is abnormally slow in some areas (for example in heart damage) so the myocardial cells are unable to activate the fast sodium channel, part of the impulse will arrive late and potentially be treated as a new impulse. Depending on the timing, this can produce a sustained abnormal circuit rhythm. As a sort of re-entry, vortices of excitation in the myocardium (autowave vortices) are considered to be the main mechanism of life-threatening cardiac arrhythmias. In particular, the autowave reverberator is common in the thin walls of the atria, sometimes resulting in atrial flutter. Re-entry is also responsible for most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia. These types of re-entry circuits are different from WPW syndromes, which utilize abnormal conduction pathways. Although omega-3 fatty acids from fish oil can be protective against arrhythmias, they can facilitate re-entrant arrhythmias. Fibrillation
When an entire chamber of the heart is involved in multiple micro-reentry circuits and is, therefore, quivering with chaotic electrical impulses, it is said to be in fibrillation. Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation): ventricular fibrillation is imminently life-threatening. Atrial fibrillation affects the upper chambers of the heart, known as the atria. Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by a physician. It is not typically a medical emergency.
Classification
Arrhythmia may be classified by rate (tachycardia, bradycardia), mechanism (automaticity, re-entry, triggered) or duration (isolated premature beats; couplets; runs, that is 3 or more beats;  non-sustained = less than 30 seconds or sustained= over 30 seconds).Arrhythmias are also classified by site of origin:

Atrial arrhythmia
Sinus bradycardia
Sinus arrhythmia
Sinus tachycardia
Premature atrial contractions (PACs)
Wandering atrial pacemaker
Atrial tachycardia
Multifocal atrial tachycardia
Supraventricular tachycardia (SVT)
Atrial flutter
Atrial fibrillation (Afib)
AV nodal reentrant tachycardia

Junctional arrhythmia
AV nodal reentrant tachycardia
Junctional rhythm
Junctional tachycardia
Premature junctional contraction

Ventricular arrhythmia
Premature ventricular contractions (PVCs), sometimes called ventricular extra beats (VEBs)
Premature ventricular beats occurring after every normal beat are termed ventricular bigeminy
PVCs that occur at intervals of 2 normal beats to 1 PVC, or 1 normal beat to 2 PVCs, are termed "PVCs in trigeminy"
Groups of three premature ventricular beats are called triplets and are considered a brief run of non-sustained ventricular tachycardia (NSVT); if the grouping lasts for more than 30 seconds, it is considered sustained ventricular tachycardia (VT). Accelerated idioventricular rhythm
Monomorphic ventricular tachycardia
Polymorphic ventricular tachycardia
Ventricular fibrillation
Torsades de pointes
Arrhythmogenic right ventricular dysplasia
Re-entry ventricular arrhythmia

Heart blocks
These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They are the most common causes of bradycardia:
First-degree heart block, which manifests as PR prolongation
Second-degree heart block
Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
Type 2 Second degree heart block, also known as Mobitz II
Third-degree heart block, also known as complete heart blockFirst, second, and third-degree blocks also can occur at the level of the sinoatrial junction.