This document discusses various tachyarrhythmias classified by their electrocardiographic features and mechanisms. Broad complex tachycardias include ventricular tachycardia, ventricular flutter, torsades de pointes, and ventricular fibrillation. Narrow complex tachycardias originate from supraventricular structures and include sinus tachycardia, atrial fibrillation, atrial flutter, atrioventricular nodal reentrant tachycardia, and accessory pathway mediated tachycardias. Specific tachycardias like inappropriate sinus tachycardia, multifocal atrial tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation are also described.

1. TACHYARRHYTHMIAS
Presenter: Dr.Muhammad Hashim
Assistant Professor

6. MECHANISMS OF TACHYARRHYTHMIAS
• Classified according to mechanisms involved:
Alterations in Impulse Initiation: Enhanced Automaticity
Afterdepolarizations and Triggered Automaticity
Abnormal Impulse Conduction: Reentry

7. Classification of Tachyarrhythmias
• Tachyarrhythmias are classified based on whether they have broad or narrow QRS
complexes on the ECG.
• Broad is defined as >0.12s (or more than 3 small squares on the standard ECG).
• Narrow is equal to or less than 0.12s.
• Broad QRS complexes are slower ventricular depolarisations that arise from the
ventricles.
• Narrow complexes are ventricular depolarisations initiated from above the
ventricles (known as supraventricular).

8. Classification of Tachyarrhythmias
Broad Complex Tachyarrhythmias
• Premature Ventricular Beats
• Ventricular Tachycardia
• Ventricular flutter
• Torsades de Pointes (PSVT)
• Ventricular Fibrillation
Narrow Complex Tachyarrhythmias
• Sinus Tachycardia (Physiologic)
• Pathologic Supraventricular Tachycardia
1. Atrial origin:
• Inappropriate Sinus Tachycardia
• Focal Atrial Tachycardia
• Multifocal Atrial Tachycardia
• Atrial Flutter
• Atrial Fibrillation
2. AV nodal re-entry Tachycardia
3. Tachycardia asso with accessory AV
pathways
• Orthodromic AV re-entry tachycardia
• Antidromic - Pre-excited Tachycardia

9. Supraventricular tachyarrhythmias
• Originate from or are dependent on conduction through the atrium or atrioventricular
(AV) node to the ventricles.
• Most produce narrow QRS-complex tachycardia (QRS duration <120 ms) characteristic
of ventricular activation over the Purkinje system.

10. Paroxysmal Supraventricular
tachyarrhythmias
• Episodes that occur with sudden onset and termination are referred to as
paroxysmal. (PSVT)

11. Sinus Tachycardia

14. Inappropriate sinus tachycardia
• an uncommon condition in which the sinus rate increases spontaneously at rest or out of
proportion to physiologic stress or exertion.
• Affected individuals are often women in the third or fourth decade of life.
• Fatigue, dizziness, and even syncope may accompany palpitations, which can be disabling.
• Additional symptoms of chest pain, headaches, and gastrointestinal upset are common.
• It must be distinguished from appropriate sinus tachycardia and from focal atrial
tachycardia, as discussed above.

15. Inappropriate sinus tachycardia
• Misdiagnosis of physiologic sinus tachycardia with an anxiety disorder is common
• Careful titration of beta blockers.
• Clonidine and serotonin reuptake inhibitors.
• Ivabradine

16. Focal Atrial Tachycardia

17. Multifocal Atrial Tachycardia (MAT)
• Multifocal AT (MAT) is characterized by at least three distinct P-wave
morphologies.
• Rates are typically between 100 and 150 beats/min.
• Unlike atrial fibrillation, there are clear isoelectric intervals between P waves.
• The mechanism is likely triggered automaticity from multiple atrial foci.
• It is usually encountered in patients with chronic pulmonary disease and acute
illness.

18. Atrioventricular Nodal Re-entry Tachycardia

19. ECG:
🞄Retrograde P wave is inscribed during, slightly before, or slightly after the
QRS and can be difficult to discern.
🞄P wave is seen at the end of the QRS complex as a “pseudo-r” in lead V1
🞄Pseudo Q & pseudo-S waves in leads II, III, and aVF

20. Wolff-Parkinson-White (WPW) syndrome
• Genesis involves the presence of dual conducting pathways between the atria
and the ventricles:
• The natural AV nodal His-Purkinje tract
• One or more AV accessory tract(s) (ie, AV connection or AP
, Kent fibers, Mahaim fibers)

21. • A shortened PR interval (typically <120 ms in a teenager or adult)
• A slurring and slow rise of the initial upstroke of the QRS complex (delta wave)
• A widened QRS complex (total duration >0.12 seconds)
• ST segment–T wave (repolarization) changes, generally directed opposite the major delta
wave and QRS complex, reflecting altered depolarization.

22. Atrial Flutter - Macroreentrant Atrial Tachycardia
• Atrial flutter is a type of supraventricular tachycardia caused by a re-entry circuit within
the right atrium.
• The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a
fairly predictable atrial rate of around 300 bpm (range 200-400).
• Ventricular rate is determined by the AV conduction ratio (“degree of AV block”).
• The commonest AV ratio is 2:1, resulting in a ventricular rate of ~150 bpm.
• Higher-degree AV blocks can occur — usually due to medications or underlying heart
disease — resulting in lower rates of ventricular conduction, e.g. 3:1 or 4:1 block.

23. Atrial Flutter with 2:1 Block
•inverted flutter waves in II, III + aVF at a rate of 300 bpm (one per big square)
•upright flutter waves in V1 simulating P waves
•2:1 AV block resulting in a ventricular rate of 150 bpm
•Note the occasional irregularity, with a 3:1 cycle seen in V1-3

24. ATRIAL FIBRILLATION
• Atrial fibrillation (AF) is characterized by disorganized, rapid, and irregular atrial activation
with loss of atrial contraction and with an irregular ventricular rate that is determined by
AV nodal conduction.
• Atrial Fibrillation (AF) is the most common sustained arrhythmia.

25. Classification of Atrial Fibrillation
• First episode – initial detection of AF regardless of symptoms or duration
• Recurrent AF – More than 2 episodes of AF
• Paroxysmal AF – (Triggered by Ectopic Foci) Self terminating episode < 7 days (
• Persistent AF – (Triggered by electrophysiologic remodelling fibrosis)
Not self terminating, duration > 7 days
• Long-standing persistent AF – (triggered by chronic Substrate fibrosis), > 1 year
• Permanent (Accepted) AF – Duration > 1 yr in which rhythm control interventions
are not pursued or are unsuccessful

26. ECG Features of Atrial Fibrillation
• Irregularly irregular rhythm.
• No P waves.
• Absence of an isoelectric baseline.
• Variable ventricular rate.
• QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory
pathway, or rate related aberrant conduction.
• Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or
coarse (amplitude >0.5mm).
• Fibrillatory waves may mimic P waves leading to misdiagnosis.

28. Ventricular Tachycardia
• Most common cause of wide complex tachycardia.(80%)
• VT arises distal to bifurcation of His bundle or vent muscle or both.
Clinical Presentation
• Haemodynamically stable.
• Haemodynamically unstable — e.g hypotension, chest pain, cardiac failure, decreased
conscious level.
• Prognosis depends on any structural heart diseases

29. Classification of VT
Based on Morphology
1. Monomorphic VT
2. Polymorphic VT
3. Torsades De Pointes (Polymorphic
with QT prolongation)
4. Right Ventricular Outflow Tract
Tachycardia
5. Fascicular Tachycardia
6. Bidirectional VT
7. Ventricular Flutter
8. Ventricular Fibrillation
Based on Duration
• Sustained = Duration > 30
seconds or requiring intervention
due to hemodynamic
compromise.
• Non-sustained = Three or more
consecutive ventricular
complexes terminating
spontaneously in < 30 seconds.

30. Features suggestive of VT
• Very broad complexes (>160ms).
• Absence of typical RBBB or LBBB morphology.
• Extreme axis deviation (“northwest axis”) — QRS is
positive in aVR and negative in I + aVF.
• AV dissociation (P and QRS complexes at different
rates).
• Capture beats — occur when the sinoatrial node
transiently ‘captures’ the ventricles, in the midst of
AV dissociation, to produce a QRS complex of normal
duration.
• Fusion beats — occur when a sinus and ventricular
beat coincide to produce a hybrid complex of
intermediate morphology.

31. Features suggestive of VT
• Positive or negative concordance throughout
the chest leads, i.e. leads V1-6 show entirely
positive (R) or entirely negative (QS)
complexes, with no RS complexes seen.
• Brugada’s sign – The distance from the onset
of the QRS complex to lowest point of the S-
wave is > 100ms.
• Josephson’s sign – Notching near the lowest
point of the S-wave.
• RSR’ complexes with a taller “left rabbit
ear”. This is the most specific finding in
favour of VT. This is in contrast to RBBB,
where the right rabbit ear is taller. Brugada’s sign (red callipers) and Josephson’s sign (blue arrow)

32. Ventricular Tachycardia
Clinical Significance:
• Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required
in all cases of VT.

33. Ventricular Tachycardia
Clinical Features Suggestive of VT
• Age > 35 (positive predictive value of 85%)
• Structural heart disease
• Ischaemic heart disease
• Previous MI
• Congestive heart failure
• Cardiomyopathy
• Family history of sudden cardiac death (suggesting conditions such as HOCM,
congenital long QT syndrome, Brugada syndrome or arrhythmogenic right
ventricular dysplasia that are associated with episodes of VT)

34. Differential Diagnosis of Wide-Complex
Tachycardia
Several arrhythmias can present as a wide-complex tachycardia (QRS > 120 ms)
including:
• Ventricular Tachycardia
• SVT with aberrant conduction due to bundle branch block
• SVT with aberrant conduction due to the Wolff-Parkinson-White syndrome
• Pace-maker mediated tachycardia
• Metabolic derangements e.g. hyperkalaemia
• Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants)

35. Polymorphic VT
• Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which
there are multiple ventricular foci with the resultant QRS complexes varying in amplitude,
axis and duration. The commonest cause of PVT is myocardial ischaemia.
• Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia
occurring in the context of QT prolongation; it has a characteristic morphology in which the
QRS complexes “twist” around the isoelectric line.

36. Polymorphic VT – ECG Features
• During short runs of TdP or single lead recording the characteristic “twisting” morphology
may not be apparent.
• Bigeminy in a patient with a known long QT syndrome may herald imminent TdP.
• TdP with heart rates > 220 beats/min are of longer duration and more likely to degenerate
into VF.
• Presence of abnormal (“giant”) T-U waves may precede TdP

38. Ventricular Fibrillation
• Ventricular fibrillation (VF) is the the most important shockable cardiac arrest
rhythm.
• The ventricles suddenly attempt to contract at rates of up to 500 bpm.
• This rapid and irregular electrical activity renders the ventricles unable to
contract in a synchronised manner, resulting in immediate loss of cardiac output.
• The heart is no longer an effective pump and is reduced to a quivering mess.
• Unless advanced life support is rapidly instituted, this rhythm is invariably fatal.

39. Ventricular Fibrillation
• A chaotic broad complex tachycardia which often occurs as a result of ischaemia and is
immediately life threatening.
• VF is characterized by disordered electrical ventricular activation without identifiable QRS
complexes.