Tachyarrhythmias are classified based on the mechanisms of electrical impulse generation and conduction abnormalities. They can exhibit either broad or narrow QRS complexes on ECG and are categorized further into various types such as atrial flutter, atrial fibrillation, and different forms of supraventricular tachycardia. Treatment may include techniques like vagal maneuvers, medications, and radiofrequency ablation, depending on the specific type of tachyarrhythmia present.

1. TACHYARRHYTHMIAS
Presenter: Dr.Arun Vasireddy
28th March 2016

2. Descriptive Physiology
• The normal cardiac impulse is generated by pacemaker cells
in the SA node situated at the junction of the right atrium and
the superior vena cava .
• This impulse is transmitted slowly through nodal tissue to the
anatomically complex atria, where it is conducted more
rapidly to the AV node, inscribing the P wave.
• The time needed for activation of the atria and the AVN delay
is represented as the PR interval.
• The AVN is the only electrical connection between the atria
and the ventricles in the normal heart.
• The electrical impulse emerges from the AVN and is
transmitted to the His-Purkinje system, facilitating activation
of ventricular muscle.

3. Descriptive Physiology
• the ventricles are activated rapidly through the Purkinje
network, inscribing the QRS complex.
• Recovery of electrical excitability occurs more slowly and is
governed by the time of activation and duration of
regional action potentials.
• The relative brevity of epicardial action potentials in the
ventricle results in repolarization that occurs first on the
epicardial surface and then proceeds to the endocardium,
which inscribes a T wave normally of the same polarity as
the QRS complex.
• The duration of ventricular activation and recovery is
determined by the action potential duration and is
represented on the body surface ECG by the QT interval.

4. • Cardiac myocytes exhibit a characteristically long action potential (200–
400 ms) compared with neurons and skeletal muscle cells (1–5 ms).
• The action potential profile is sculpted by the orchestrated activity of
multiple distinctive time- and voltage-dependent ionic currents.
• The currents are carried by transmembrane proteins that passively
conduct ions down their electrochemical gradients through selective pores
(ion channels), actively transport ions against their electrochemical
gradient (pumps, transporters), or electrogenically exchange ionic species
(exchangers).
• Action potentials in the heart are regionally distinct. The regional
variability in cardiac action potentials is a result of differences in the
number and types of ion channel proteins expressed by different cell types
in the heart.
• Further, unique sets of ionic currents are active in pacemaking and muscle
cells, and the relative contributions of these currents may vary in the same
cell type in different regions of the heart

5. MECHANISMS OF TACHYARRHYTHMIAS
• Cardiac arrhythmias result from abnormalities of electrical impulse
generation, conduction, or both.
• Classified according to mechanisms involved:
Alterations in Impulse Initiation: Enhanced Automaticity
Afterdepolarizations and Triggered Automaticity
Abnormal Impulse Conduction: Reentry

6. Automaticity
• Heart cells other than those of the SA node depolarize
faster than SA node cells, and take control as the cardiac
pacemaker.
(spontaneous depolarization of atrial, junctional, or ventricular
pacemakers)
• Factors that enhance automaticity include:
SANS,  PANS,  CO2,  O2,  H+,  stretch, hypokalemia and
hypocalcaemia.
Examples: Ectopic atrial tachycardia or multifocal tachycardia
in patients with chronic lung disease OR ventricular ectopy
after MI

7. Triggered Automaticity
• Triggered activity is like a domino effect where the arrhythmia is due to the
preceding beat.
• It is initiated by Early after-depolarizations arise during the plateau phase or
the repolarization phase of the last beat
(EAD of the phase 3,LAD of phase 4 of action potential.)
• Attributed to an increase in intracellular calcium accumulation.
• It is due to the increased catecholamines or adrenergic drive.
• Subsides on removal of the stimulus or cause.

8. Re-entry
• defined as the circulation of an activation wave around an inexcitable
obstacle.
• It is the most common arrhythmia mechanism,resulting from abnormal
electrical impulse conduction.
• 2 distinct pathways that come together at beginning and end to form a loop.
• Slow conduction in the unblocked pathway.
• The fast conducting pathway is blocked because of its long refractory period so the beat
can only go down the slow conducting pathway

9. Re-entry Mechanism
• An arrhythmia is triggered by a
premature beat
• The wave of excitation from the
premature beat arrives at the distal
end of the fast conducting pathway,
which has now recovered and
therefore travels retrogradely
(backwards) up the fast pathway.
• On arriving at the top of the fast
pathway it finds the slow pathway
has recovered and therefore the
wave of excitation ‘re-enters’ the
pathway and continues in a ‘circular’
movement. This creates the re-
entry circuit

10. Re-entry Mechanism (continued)
• Sustained reentry utilizing such a
circuit, a gap (excitable gap) exists
between the activating head of
the wave and the recovering tail.
• One mechanism of termination of
reentry occurs when the
conduction and recovery
characteristics of the circuit
change and the activating head of
the wave collides with the tail,
extinguishing the tachycardia

11. 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).

12. 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

13. 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.
• Conduction block in the left or right bundle branch or activation of the ventricles from
an accessory pathway produces a wide QRS complex during SVT that must be
distinguished from VT.
• SVT can be of brief duration, non-sustained, or can be sustained such that an
intervention, such as cardioversion or drug administration, is required for
termination.

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

15. Sinus Tachycardia
• Sinus tachycardia (>100 beats/min) is considered physiologic when it is an appropriate
response to exercise, stress, or illness.
• Sinus tachycardia can be difficult to distinguish from focal atrial tachycardia (see below)
that originates from a focus near the sinus node.
• A causative factor (such as exertion) and a gradual increase and decrease in rate favors
sinus tachycardia, whereas an abrupt onset and offset favor atrial tachycardia.
• The distinction can be difficult and occasionally requires extended ECG monitoring or even
invasive electrophysiology study.

18. 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.

19. Inappropriate sinus tachycardia
• Misdiagnosis of physiologic sinus tachycardia with an anxiety disorder is common. Therapy
is often ineffective or poorly tolerated.
• Careful titration of beta blockers and or calcium channel blockers may reduce symptoms.
• Clonidine and serotonin reuptake inhibitors have also been used.
• Ivabradine, a drug that causes sinus node depolarization, is promising.
• Catheter ablation of the sinus node has been used, but long-term control of symptoms is
usually poor, and it often leaves young individuals with a permanent pacemaker.

20. Focal Atrial Tachycardia
• Focal atrial tachycardia (AT) can be due to abnormal automaticity, triggered
automaticity, or a small reentry circuit confined to the atrium or atrial tissue extending
into a pulmonary vein, the coronary sinus, or vena cava. It can be sustained,
nonsustained, paroxysmal, or incessant.
• Because impulses are spread from an ectopic atrial focus, instead of the SA node, the
p waves tend to look abnormal.
• The ectopic rate can be as fast as 250bpm, but the AV node will be electrically
refractive to some of these impulses.
• Thus, the ventricular rate is often lower than the atrial rate and sometimes irregular.

21. Focal Atrial Tachycardia
• AT typically presents as an SVT either with 1:1 AV conduction or with AV block
that can be Wenckebach type conduction or fixed (e.g., 2:1 or 3:1) block.
• When 1:1 conduction to the ventricles is present, the arrhythmia can
resemble sinus tachycardia typically with a P-R interval shorter than the R-P
interval

22.  Depending on the atrial rate, the P wave may fall on top of the t wave or,
during 2:1 conduction, may fall coincident with the QRS.
 Maneuvers that increase AV block, such as carotid sinus massage, Valsalva
maneuver, or administration of AV nodal–blocking agents, such as
adenosine, are useful to create AV block that will expose the p wave.
 Associated with significant structural heart disease such as CAD, Cor pulmonale
 Rx
 Digitalis, BB or CCB to slow ventricular rates
 If refractory Class 1A, 1C, III drugs can be added
 In digitalis toxicity the drug should be stopped and digitalis antibodies and
potassium be added.

23. 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.

24. MAT - Rx
• Therapy for MAT is directed at treating the underlying disease and correcting
any metabolic abnormalities.
• Electrical cardioversion has no effect.
• The calcium channel blockers verapamil or diltiazem may slow the atrial and
ventricular rate.
• Patients with severe pulmonary disease often do not tolerate beta blocker
therapy.
• MAT may respond to amiodarone, but long-term therapy with this agent is
usually avoided due to its toxicities, particularly pulmonary fibrosis.

25. Atrioventricular Nodal Re-entry Tachycardia
• AV nodal re-entry tachycardia (AVNRT) is the most common form of PSVT, representing
approximately 60% of cases referred for catheter ablation.
• It most commonly manifests in the second to fourth decades of life, often in women.
• It is often well tolerated, but rapid tachycardia, particularly in the elderly, may cause
angina, pulmonary oedema, hypotension, or syncope.
• It is not usually associated with structural heart disease.
• AVNRT occurs due the presence of a second conduction pathway in (or near) the AV
node. One pathway conducts quickly and repolarises slowly, whilst the other conducts
slowly and repolarises quickly.

26.  AVNRT is triggered by an ectopic (early) atrial
beat.
 The ectopic beat is forced to use the slower
conducting pathway because the fast one is still
repolarising.
 The impulse reenters the AV node, in the
opposite direction, through the fast conducting
pathway which has by this time recovered.
 This cycling continues as, essentially, a short
circuit loop has been established within the AV
node.
• This short circuit sends out normal ventricular depolarisations
and retrograde atrial depolarisations.
• This results in a regular, narrow complex tachycardia with a rate of 140-
240bpm.

27. 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

28. Wolff-Parkinson-White (WPW) syndrome
• It is an AVRT defined as a preexcited QRS during sinus rhythm and episodes of PSVT
• 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)
• Types of AVRT include :
Antidromic AV re-entryOrthodromic AV re-entry

29. WPW (contd..)
Presentation of AVRT
• Chest pain
• Palpitations (often sudden)
• Breathing difficulty
• Pulse that is regular and “too
rapid to count”
• Typically, a concomitant
reduction in their tolerance
for activity
Clinical features of
associated cardiac defects
may be present, such as
the following:
• Cardiomyopathy
• Ebstein anomaly
• Hypertrophic cardiomyopathy
( AMPK mutation)

30. • 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.

31. Termination of acute episodes (AVRT & AVNRT)
is done by blocking AV node conduction with the following:
• Vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage, splashing cold water or ice water
on the face)
• Adults: IV adenosine 6-12 mg via a large-bore line (the drug has a very short half-life)
• Adults: IV verapamil 5-10 mg or diltiazem 10 mg
Atrial flutter/fibrillation or wide-complex tachycardia is treated as follows:
• IV procainamide or amiodarone if wide-complex tachycardia is present, ventricular tachycardia
(VT) cannot be excluded, and the patient is stable hemodynamically
The initial treatment of choice for hemodynamically unstable tachycardia is direct-
current synchronized electrical cardioversion, biphasic, as follows:
• A level of 100 J (monophasic or lower biphasic) initially
• If necessary, a second shock with higher energy (200 J or 360 J)

32. Radiofrequency ablation
• Radiofrequency ablation is indicated in the following patients:
• Patients with symptomatic AVRT
• Patients with AF or other atrial tachyarrhythmias that have rapid ventricular response via an
accessory pathway (preexcited AF)
• Patients with AVRT or AF with rapid ventricular rates found incidentally during EPS for
unrelated dysrhythmia, if the shortest preexcited RR interval during AF is less than 250 ms
• Asymptomatic patients with ventricular preexcitation whose livelihood, profession, insurability,
or mental well-being may be influenced by unpredictable tachyarrhythmias or in whom such
tachyarrhythmias would endanger the public safety
• Patients with WPW and a family history of sudden cardiac death

33. 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.

34. Atrial Flutter - Macroreentrant Atrial Tachycardia
• Atrial flutter with 1:1 conduction can occur due to sympathetic stimulation or in the
presence of an accessory pathway — especially if AV-nodal blocking agents are
administered to a patient with WPW.
• Atrial flutter with 1:1 conduction is associated with severe haemodynamic instability and
progression to ventricular fibrillation.

35. Atrial Flutter – Classification
Atypical Atrial Flutter (Common, or Type I Atrial Flutter)
• Involves the IVC & tricuspid isthmus in the reentry
circuit. Can be further classified based on the direction of
the circuit:
• Anticlockwise Reentry. This is the commonest form of
atrial flutter (90% of cases). Retrograde atrial conduction
produces:
• Inverted flutter waves in leads II,III, aVF
• Positive flutter waves in V1 – may resemble upright P waves
• Clockwise Reentry. This uncommon variant produces the
opposite pattern:
• Positive flutter waves in leads II, III, aVF
• Broad, inverted flutter waves in V1

36. Atrial Flutter – Classification
Atypical Atrial flutter (Uncommon, or Type II Atrial Flutter)
• Does not fulfil criteria for typical atrial flutter.
• Often associated with higher atrial rates and rhythm instability.
• Less amenable to treatment with ablation.
General Features
• Narrow complex tachycardia
• Regular atrial activity at ~300 bpm
• Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF — may be
more easily spotted by turning the ECG upside down!
• Flutter waves in V1 may resemble P waves
• Loss of the isoelectric baseline

37. Atrial Flutter with 2:1 Block (anticlockwise flutter)
•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

38. Management of Atrial Flutter
• Electrical cardioversion is warranted for hemodynamic instability or severe
symptoms.
• Otherwise, rate control can be achieved with administration of AV nodal–
blocking agents, but this is often more difficult than for atrial fibrillation.
• The risk of thromboembolic events is felt to be similar to that associated
with atrial fibrillation.

39. • Anticoagulation is warranted prior to conversion for episodes more than 48 h
in duration and chronically for patients at increased risk of thromboembolic
stroke based on the CHA2DS2-VASc scoring system

40. Management of Atrial Flutter
• For a first episode of atrial flutter, conversion to sinus rhythm with no
antiarrhythmic drug therapy is reasonable.
• For recurrent episodes, antiarrhythmic drug therapy with sotalol, dofetilide,
disopyramide, and amiodarone may be considered, but more than 70% of
patients experience recurrences.
• For recurrent episodes of common atrial flutter, catheter ablation of the
cavotricuspid isthmus abolishes the arrhythmia in over 90% of patients with a
low risk of complications that are largely related to vascular access and
infrequent heart block.
• Approximately 50% of patients presenting with atrial flutter develop atrial
fibrillation within the next 5 years

41. 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.
• Lifetime risk over the age of 40 years is ~25%.
• Clinical consequences are related to rapid ventricular rates, loss of atrial contribution to
ventricular filling, and predisposition to thrombus formation in the left atrial appendage
with potential embolization.
• Complications of AF include haemodynamic instability, cardiomyopathy, cardiac failure,
and embolic events such as stroke.

42. 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

43. Features of AF
• Ashman’s Phenomenon – presences of aberrantly conducted beats, usually of RBBB
morphology, due a long refractory period as determined by the preceding R-R
interval.
• The ventricular response and thus ventricular rate in AF is dependent on several
factors including vagal tone, other pacemaker foci, AV node function, refractory
period, and medications.
• Commonly AF is associated with a ventricular rate ~ 110 – 160.
• AF is often described as having ‘rapid ventricular response’ once the ventricular rate
is > 100 bpm.
• ‘Slow’ AF is a term often used to describe AF with a ventricular rate < 60 bpm.
• Causes of ‘slow’ AF include hypothermia, digoxin toxicity, medications, and sinus
node dysfunction.

44. Mechanism of AF
The mechanisms underlying AF are not fully understood but it requires an initiating
event (focal atrial activity / PACs) and substrate for maintenance (i.e. dilated left atrium).
• Focal activation – In which AF originates from an area of focal activity. This activity may be
triggered, due to increased automaticity, or from micro re-entry. Often located in the
pulmonary veins.
• Multiple wavelet mechanism – In which multiple small wandering wavelets are formed.
The fibrillation is maintained by re-entry circuits formed by some of the wavelets. This
process is potentiated in the presence of a dilated LA — the larger surface area facilitates
continuous waveform propagation.

45. 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.

47. Management of AF
• The cornerstones of AF management are rate control and anticoagulation, as
well as rhythm control for those symptomatically limited by AF.
• New-onset AF that produces severe hypotension, pulmonary edema, or angina
should be electrically cardioverted starting with a QRS synchronous shock of
200J, ideally after sedation or anesthesia is achieved.
• If AF terminates and reinitiates, administration of an antiarrhythmic drug, such
as ibutilide, and repeat cardioversion may be considered.
• If the patient is stable, immediate management involves rate control to
alleviate or prevent symptoms & anticoagulation if appropriate.

48. AF - Cardioversion
• Cardioversion (both electrical and pharmacological) doesn't come without significant
risks, and should be undertaken cautiously in stable patients.
• Given that most AF is paroxysmal and 2/3rds of those self-terminate within 24 hours, it is
prudent to wait and see (in stable patients) if it resolves on its own initially.
• In cases that persist, cardioversion can, for some, permanently restore sinus rhythm.
• It is useful to know the exact time of onset because many methods of pharmacological
cardioversion have only shown to be beneficial within 48 hours of onset.
• Pharmacological options include Flecainide and Amiodarone.
• There is a lower rate of successful cardioversion compared with electrical cardioversion,
but it may be preferable because patients don't require conscious sedation or
anaesthesia.

49. AF - Cardioversion
• Electrical cardioversion can be attempted up to 12 months after
onset.
• Cardioversion requires prior anticoagulation as the procedure
increases the risk of thromboembolism.
• The longer the atria have been fibrillating the greater the risk of
thromboembolism, hence:
• 4 weeks of oral anticoagulation (INR >2.0) required in those presenting >48
hours of onset(or uncertain timing). or,
• Stat dose of heparin required in those presenting <48 hours since onset.
• All patients must remain anticoagulated for 4 weeks following cardioversion
therapy.

50. AF - Longterm Management
• Long-term, AF can be managed using rate or rhythm control drugs, or a combination of
both.
• The more recent the onset of AF, the more likely rhythm control will be considered.
Rate Control
• Beta-Blockers and rate limiting calcium channel blockers (Verapamil and Diltiazem) are first
line choices to lower the ventricular rate in AF.
• These are used first line in those with permanent AF, those over 65, those with ischaemic
heart disease and those who can't tolerate antiarrhythmic drugs.
• They are used with caution in congestive heart failure, as they can make it worse.
• Digoxin is preferable in this situation, due to it's concomitant inotropic action on the heart.

51. AF - Longterm Management
Rhythm Control
• Drug therapy can be instituted once sinus rhythm has been established or in anticipation of
cardioversion.
• β-Adrenergic blockers and calcium channel blockers help control ventricular rate, improve
symptoms, and possess a low-risk profile, but have low efficacy for preventing AF episodes.
• Class I sodium channel–blocking agents (e.g., flecainide, propafenone, disopyramide) are options
for subjects without significant structural heart disease, but they have negative inotropic and
proarrhythmic effects that warrant avoidance in patients with coronary artery disease or heart
failure.
• The class III agents sotalol and dofetilide can be administered to patients with coronary artery
disease or structural heart disease but have approximately a 3% risk of inducing excessive QT
prolongation and torsades des pointes.

52. AF - Longterm Management
Rhythm Control
• Dofetilide should be initiated only in a hospital with ECG monitoring, and many
physicians take this approach with sotalol as well.
• Dronedarone increases mortality in patients with heart failure.
• All of these agents have modest efficacy in patients with paroxysmal AF, of whom
approximately 30–50% will benefit.
• Amiodarone is more effective, maintaining sinus rhythm in approximately two-thirds of
patients. It can be administered to patients with heart failure and coronary artery
disease.

53. CATHETER AND SURGICAL ABLATION FOR
ATRIAL FIBRILLATION
• For patients with previously untreated but recurrent
paroxysmal AF, catheter ablation has similar efficacy to
antiarrhythmic drug therapy and is superior to
antiarrhythmic drugs for patients who have recurrent
AF despite drug treatment.
• The procedure involves cardiac catheterization,
transatrial septal puncture, and radiofrequency ablation
or cryoablation to electrically isolate the regions around
the pulmonary veins, abolishing the effect of triggering
foci to interact with the left atrial AF substrate.
• A permanent pacemaker may be indicated for those
who undergo ablation, but have significant left
ventricular dysfunction. Pacemakers also have some
benefit in terminating paroxysmal AF.

54. Ventricular Tachycardia
• Most common cause of wide complex tachycardia.(80%)
• VT arises distal to bifurcation of His bundle or vent muscle or both.
• Mechanism of impulse formation
1. Triggerd activity
2. Enhanced automaticity
3. Conduction – Reentry
Clinical Presentation
• Haemodynamically stable.
• Haemodynamically unstable — e.g hypotension, chest pain, cardiac failure, decreased
conscious level.
• Prognosis depends on any structural heart diseases

55. 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.

56. 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.

57. 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)

58. Ventricular Tachycardia
Clinical Significance:
• Ventricular tachycardia may impair cardiac output with consequent hypotension,
collapse, and acute cardiac failure. This is due to extreme heart rates and lack of
coordinated atrial contraction (loss of “atrial kick”).
• The presence of pre-existing poor ventricular function is strongly associated with
cardiovascular compromise.
• Decreased cardiac output may result in decreased myocardial perfusion with
degeneration to VF.
• Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required
in all cases of VT.

59. 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)

60. 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)

61. Premature ventricular beats
• also referred to as premature ventricular contractions [PVCs]are single ventricular beats
that fall earlier than the next anticipated supraventricular beat.
• PVCs that originate from the same focus will have the same QRS morphology and are
referred to as unifocal.
• PVCs that originate from different ventricular sites have different QRS morphologies and
are referred to as multifocal.
• Two consecutive ventricular beats are ventricular couplets.

62. Monomorphic Ventricular Tachycardia (VT)
• Monomorphic VT has the same QRS complex from
beat to beat, indicating that the activation sequence
is the same from beat to beat and that each beat
likely originates from the same source.
• The initial site of ventricular activation largely
determines the sequence of ventricular activation.
Therefore, the QRS morphology of PVCs and
monomorphic VT provides an indication of the site of
origin within the ventricles.
• VT arises due to mini electrical circuits around edges
of infarcted myocardium. VT may arise as an escape
rhythm due to bradycardia.

63. Monomorphic Ventricular Tachycardia (VT)
• Arrhythmias that originate from the right ventricle or septum result in late activation of
much of the left ventricle, thereby producing a prominent S wave in V1 referred to as a
left bundle branch block–like configuration.
• Arrhythmias that originate from the free wall of the left ventricle have a prominent
positive deflection in V1, thereby producing a right bundle branch block–like morphology
in V1.

64. Monomorphic Ventricular Tachycardia (VT)
• An axis that is directed inferiorly, as indicated by dominant R waves in leads II, III, and
AVF, suggests initial activation of the cranial portion of the ventricle, whereas a frontal
plane axis that is directed superiorly (dominant S waves in II, III, and AVF) suggests
initial activation at the inferior wall.

65. 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.
• For TdP to be diagnosed, the patient has to have evidence of both PVT and QT
prolongation.
• Bidirectional VT is another type of polymorphic VT, most commonly associated with digoxin
toxicity.

66. Pathophysiology of PVT (Tdp)
• A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction.
• This prolonged repolarisation period also gives rise to early after-depolarisations (EADs).
• EADs may manifest on the ECG as tall U waves; if these reach threshold amplitude they may
manifest as premature ventricular contractions (PVCs).
• TdP is initiated when a PVC occurs during the preceeding T wave, known as ‘R on T’
phenomenon.
• The onset of TdP is often preceded by a sequence of short-long-short R-R intervals, so
called “pause dependent” TDP, with longer pauses associated with faster runs of TdP.

67. 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

69. 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.
• Prolonged ventricular fibrillation results in decreasing waveform amplitude, from
initial coarse VF to fine VF and ultimately degenerating into asystole due to
progressive depletion of myocardial energy stores.

70. Ventricular Fibrillation
• Ventricular fibrillation (VF) is the the most important shockable cardiac arrest
rhythm.
• A chaotic broad complex tachycardia which often occurs as a result of ischaemia and is
immediately life threatening.
• 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.

71. 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.

72. VF Management
• Treatment follows ACLS guidelines with
defibrillation to restore sinus rhythm.
• If resuscitation is successful, further evaluation
is performed to identify and treat underlying
heart disease and potential causes of the
arrhythmia, including the possibility that
monomorphic or polymorphic VT could have
initiated VF.
• If a transient reversible cause such as acute MI
is not identified, therapy to reduce the risk of
sudden death with an ICD is often warranted.
Chronic amiodarone therapy may be considered
for individuals who are not ICD candidates.

73. Incessant VT and Electrical Storm
• VT is incessant when it continues to recur shortly after electrical, pharmacologic,
or spontaneous conversion to sinus rhythm.
• “VT storm” or “electrical storm” refers to three or more separate episodes of VT
within 24 h, most commonly encountered in patients with ICDs.
• Slow incessant VT is sometimes asymptomatic, but can cause heart failure or
tachycardia-induced cardiomyopathy.
• Measures to reduce sympathetic tone, including β-adrenergic blockade,
sedation, and general anesthesia, have been used effectively.
• Intravenous administration of amiodarone and lidocaine can be effective for
suppression. Urgent catheter ablation can be lifesaving.

74. Ventricular arrhythmias associated with
Heart Disease
I. Idiopathic VT without structural heart
disease
A. Outflow tract origin
1. RV outflow tract: left bundle branch block
pattern with inferior axis (tall QRS in inferior
leads) and late transition in the precordial
leads
2. LV outflow tract: prominent R in V1 with
inferior axis
B. Left posterior fascicular VT
1. Right bundle branch block pattern with left
axis deviation
II. Ischemic cardiomyopathy
A. Monomorphic VT is common with prior
large myocardial infarction
B. Polymorphic VT and VF should prompt
ischemia evaluation
III. Nonischemic cardiomyopathy
A. Polymorphic VT and VF more common but
fibrotic scars can cause monomorphic VT
especially with sarcoidosis and Chagas’
disease
IV. Arrhythmogenic right ventricular
cardiomyopathy
A. Monomorphic VT usually of right ventricular
origin (left bundle branch morphology)
B. Polymorphic VT and VF can occur
independently or through degeneration of
monomorphic VT
V. Repaired tetralogy of Fallot
A. Monomorphic VT of right ventricular origin
(usually left bundle branch morphology)
VI. Hypertrophic cardiomyopathy
A. Polymorphic VT or ventricular fibrillation
B. Less commonly, monomorphic VT associated
with myocardial scars

77. IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS
• ICDs are highly effective for termination of VT and VF and also provide
bradycardia pacing.
• ICDs decrease mortality in patients at risk for sudden death due to structural
heart diseases.
• In all cases, ICDs are recommended only if there is also expectation for survival
of at least a year with acceptable functional capacity.

78. IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS
• ICDs can often terminate monomorphic VT by a burst of rapid pacing faster
than the VT, known as antitachycardia pacing (ATP).
• If ATP fails or is not a programmed treatment, as is often the case for rapid VT
or VF, a shock is delivered.
• The most common ICD complication is the delivery of unnecessary therapy in
response to a rapid SVT or electrical noise due to ICD lead failure.

79. References
 Harrison’s principles of Internal Medicine 19th Ed.
 Washington manual of critical care 2nd Ed.
 CMDT 2016
 Online Sources – Medscape & Life in the Fast Lane