A premature ventricular contraction originates in the ventricle, and this must be differentiated from an impulse that originates above the ventricle (i.e. it is supraventricular in origin) and conducts with a delay (i.e. a wide complex, it is aberrantly conducted).

Aberrant ventricular conduction is:

• A transient form of abnormal intraventricular conduction delay (#IVCD) and occurs when there is unequal refractoriness of the two bundles.
• The right bundle has a longer action potential duration, and is more vulnerable to conduction delay or failure.
• The refractory period is affected by the preceding cycle length.
• The refractory period is longer when there is a long preceding RR interval.
• Aberrant ventricular conduction is favored when a premature supraventricular impulse comes after a long preceding RR interval (Ashman phenomenon).
• If the underlying rhythm is sinus in origin, and if the abnormal QRS is preceded by a premature P wave, then the ectopic beat is likely to be supraventricular in origin.
• The absence of a fully compensatory pause further supports this diagnosis.
• If a retrograde P wave is identifiable after the QRS complex and the RP interval is less than 0.11 second, the premature beat is likely to have originated from the AV junction, since the RP interval is too short for VA conduction (unless an accessory pathway is present).
• A long RP interval of 0.20 seconds or longer is suggestive but not diagnostic of a PVC, since the retrograde conduction time of a junctional beat is less likely to exceed this duration.
• The beat is more likely to be due to aberrancy if the initial forces are similar to those of the sinus beat and if it has an RSR’ configuration in lead V1.
• If the QRS complexes in all the precordial leads are positive or all negative, then a PVC is more likely.
• Diagnosis of PVCs in the presence of atrial fibrillation:

  • Absence of P waves and the irregularity of the rhythm are the handicaps
  • A constant coupling time is suggestive of PVCs
  • Ashman phenomenon. Keep in mind that a long cycle length also favors the precipitation of a PVC, therefore this sign is helpful but not diagnostic of aberrancy.
  • PVC is favored if the abnormal complex terminates a short-long cycle.

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

OR

[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

OR

[Disease name] must be differentiated from [differential dx1], [differential dx2], and [differential dx3].

OR

As [disease name] manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. [Subtype name 1] must be differentiated from other diseases that cause [clinical feature 1], such as [differential dx1] and [differential dx2]. In contrast, [subtype name 2] must be differentiated from other diseases that cause [clinical feature 2], such as [differential dx3] and [differential dx4].

On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].

The table below provides information on the differential diagnosis of ventricular tachycardia in terms of ECG appearance:

Disease Name	Causes	ECG Characteristics	ECG view
Ventricular tachycardia [19][20][21][22][23]	Ischemic heart disease Illicit drug use such as cocaine and methamphetamine Structural heart diseases Electrolyte disturbances Congestive heart failure Myocarditis Obstructive sleep apnea Pulmonary artery catheter Long QT syndrome	Ventricular tachycardia originates from a ventricular focus. Lasts more than 30 seconds. Broad QRS complexes: rate of >90 BPM.	[24]
Ventricular fibrillation [17][25][26][27]	Acute coronary ischemia Cardiomyopathies Congenital heart disease Myocardial infarction Heart surgery Electrolyte abnormalities	Poorly identifiable QRS complexes and absent P waves The heart rate is >300 BPM Rhythm is irregular	[28]
Ventricular flutter [29][30][31]	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm	[32]
Asystole [33][34]	Hypovolemia Hypoxia Acidosis Hypothermia Hyperkalemia or Hypokalemia Hypoglycemia Cardiac Tamponade Tension pneumothorax Thrombosis Myocardial infarction Thrombosis Pulmonary embolism Cardiogenic shock Degeneration of the sinoatrial or atrioventricular nodes Ischemic stroke	There is no electrical activity in the asystole	[35]
Pulseless electrical activity [36][37]	Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hypothermia Electrolyte disturbances Hypoglycemia Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers Tamponade Tension pneumothorax Thrombosis (Myocardial infarction) Thrombosis (Pulmonary embolism) Trauma (Hypovolemia from blood loss)	Several pattern are possible including: Normal sinus rhythm Sinus tachycardia, with discernible P waves and QRS complexes Bradycardia, with or without P waves	[38]
Torsade de Pointes [39][40][41]	*Electrolyte disturbances Medications such as: Amiodarone Azithromycin Clozapine Famotidine Flecainide Foscarnet Levofloxacin Lithium Mirtazipine Quetiapine Risperidone Tacrolimus Tamoxifen Ziprasidone	Paroxysms of VT with irregular RR intervals. A ventricular rate between 200 and 250 beats per minute. Two or more cycles of QRS complexes with alternating polarity. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion. Prolongation of the QT interval. Is often initiated by a PVC with a long coupling interval, R on T phenomenon. There are usually 5 to 20 complexes in each cycle.	[42]