Tachyarrhythmia

Presented by Foo Chuan Yi

Definition
Abnormal heart rhythms with a
ventricular rate of 100 or more beats
per minute
Clinical Symptoms of Tachyarrhythmia

1. Breathlessness (dyspnea)
2. Dizziness
3. Syncope (fainting, or
nearly fainting)
4. Fluttering in the chest
5. Chest pain
6. Lightheadedness
7. Sudden weakness
Tachyarrthythmia
Narrow Complex Broad Complex
Tachycardia Tachycardia

● SVT ● Ventricular Tachycardia

● Atrial Fibrillation ● Ventricular Fibrillation

● Atrial Flutter
Narrow Complex
Tachyarrhythmia
● SVT/ PSVT
● Atrial Fibrillation
● Atrial Flutter
Supraventricular
tachycardia
a. arise from the atrium or the atrioventricular
junction. Conduction is via the His–Purkinje
system
b. Types
i. Sinus tachycardia
ii. AV junctional tachycardia
1. AV nodal re-entry tachycardia
(AVNRT)
2. AV reciprocating tachycardia
(AVRT) complexes
iii. Atrial tachyarrhythmia
1. Atrial fibrillation
2. Atrial flutter
3. Atrial tachycardia
4. Multifocal atrial tachycardia
5. Accelerated junctional tachycardia
Sinus tachycardia
i. sinus rhythms with a heart rate > 100 bpm
ii. ECG - P wave morphology similar to sinus
rhythm preceding QRS
iii. Types
1. Inappropriate sinus tachycardia
a. persistent increase in resting
heart rate unrelated to or out of
proportion with the level of
physical or emotional stress.
iv. Causes
1. Acute causes
a. Exercise
b. Emotion
c. Pain
d. Fever
e. Infection
f. Acute heart failure
g. Acute pulmonary embolism
h. Hypovolaemia
2. Chronic causes
a. Pregnancy
b. Anaemia
c. Hyperthyroidism
d. catecholamine excess
i. Management
1. Treat the underlying causes
2. Rate control medication
a. Specific treatment is directed against
the potential causes, together with
rate-slowing drugs such as β-blockers
and calcium channel blockers
3. Catheter ablation
a. Enhanced sinus node automaticity or
sinus node reentry may require
catheter ablation with or without
permanent pacemaker implantation.
Atrioventricular junctional tachycardias
i. Atrioventricular nodal reentry tachycardia (AVNRT)
1. More common in women
2. Tachycardia often strikes suddenly without obvious provocation, but
exertion, coffee, tea and alcohol may aggravate or induce the
arrhythmia
3. Mechanism - AVNRT is caused by a reentry circuit in or around the
AV node.
a. there are two functionally and anatomically different pathways
predominantly within the AV node: one is characterized by a
short effective refractory period and slow conduction, and the
other has a longer effective refractory period and conducts
faster. In sinus rhythm, the atrial impulse that depolarizes the
ventricles usually conducts through the fast pathway. If the
atrial impulse (e.g. an atrial premature beat) occurs early when
the fast pathway is still refractory, the slow pathway takes over
in propagating the atrial impulse to the ventricles. It then
travels back through the fast pathway which has already
recovered its excitability, thus initiating the most common
‘slow-fast’, or typical, AVNRT
ECG
a. normal regular QRS complexes, usually at a rate of 140–
240/minute
b. ECG shows - No visible P-waves (hidden within the QRS
complex) / P-waves immediately before the QRS / P-waves
immediately after the QRS complex
a. Slow- fast AVNRT
i. Accounts for 80-90% of AVNRT
ii. Associated with Slow AV nodal pathway for anterograde conduction and Fast
AV nodal pathway for retrograde conduction.
iii. The retrograde P wave is obscured in the corresponding QRS or occurs at the
end of the QRS complex as pseudo r’ or S waves
iv. ECG:
1. P waves are often hidden – being embedded in the QRS complexes.
2. Pseudo r’ wave may be seen in V1
3. Pseudo S waves may be seen in leads II, III or aVF.
Fast-Slow AVNRT (Uncommon AVNRT)
i. Accounts for 10% of AVNRT
ii. Associated with Fast AV nodal pathway for anterograde conduction and
Slow AV nodal pathway for retrograde conduction.
iii. The retrograde P wave appears after the corresponding QRS / right
before QRS
iv. ECG - QRS -P-T complexes: P waves are visible between the QRS and
T wave

Slow-Slow AVNRT
v. 1-5% AVNRT
vi. Associated with Slow AV nodal pathway for anterograde conduction
and Slow left atrial fibres approaching the AV node as the pathway for
retrograde conduction.
vii. ECG: Tachaycardia with a P-wave seen in mid-diastole… effectively
appearing ‘before the QRS complex’
Atrioventricular reciprocating
tachycardia (AVRT)
1. Presence of an abnormal connection of myocardial fibres
from the ventricle back to the atrium
a. It is called an accessory pathway or bypass tract and
results from an incomplete separation of the atria
and the ventricles during fetal development
1. In contrast to AVNRT, this tachycardia is due to a macroreentry circuit and each part of the
circuit is activated sequentially. As a result atrial activation occurs after ventricular activation
and the P wave is usually clearly seen between the QRS and T wave
a. Accessory pathway (Accessory pathways are most commonly situated on the left but
may occur anywhere around the AV groove)
i. Kent bundle
1. in the free wall or septum
ii. Mahaim fibres
1. atrio-fascicular or nodofascicular fibres entering the ventricular
myocardium in the region of the right bundle branch
b. Accessory pathways that conduct bidirectionally usually are manifest on the surface
ECG
i. If the accessory pathway conducts from the atrium to the ventricle during
sinus rhythm, the electrical impulse can conduct quickly over this abnormal
connection to depolarize part of the ventricles abnormally (pre-excitation). A
pre-excited ECG is characterized by a short PR interval and a wide QRS
complex that begins as a slurred part known as the δ wave
c. Patients with a history of palpitations and a pre-excited ECG have a syndrome known
as Wolff–Parkinson–White (WPW) syndrome.
i. Delta wave
ii. Short PR interval
a. orthodromic AVRT
i. During AVRT the AV node and ventricles are activated normally,
ii. resulting usually in a narrow QRS complex
b. antidromic AVRT
i. tachycardia circuit can be reversed, with activation of the ventricles via the
accessory pathway and atrial activation via retrograde conduction through the
AV node
ii. This results in a broad complex tachycardia. These patients are also prone to
atrial fibrillation.
c. DO NOT treat with Verapamil and digoxin
i. may allow a higher rate of conduction over the abnormal pathway and
precipitate ventricular fibrillation. Therefore, neither verapamil nor digoxin
should be used to treat atrial fibrillation associated with the WPW syndrome
i. Management for both AVNRT & AVRT （ as both respond to same treatment)
1. Acute management
a. Hemodynamic stable
i. Vagal manoeuvres
1. Right carotid massage
2. Valsalva manoeuvre
a. In supine position
i. (thus avoiding elevated background sympathetic tone)
b. Valsalva manoeuvre is an abrupt voluntary increase in intrathoracic and intra-abdominal
pressures by straining.
c. Patient is in supine position. Patient should not take deep inspiration before straining.
Ideally, the patient blows into the mouthpiece of a manometer against a pressure of 30–40
mmHg for 15 s.
d. Alternatively, the patient strains for 15 s while breath-holding.
e. Transient acceleration of tachycardia usually occurs during the strain phase as a result of
sympathetic excess.
f. On release of strain, the rate of tachycardia slows because of the compensatory increase in
vagal tone (baroreceptor reflex), and it may be terminated in about 50% of patients.
g. Termination of tachycardia may be followed by pauses and transient ventricular ectopics.
ii. tion of the slow pathway
 i. IV adenosine (if not useful)
1. 6mg bolus, 12, 12
2. Side effect
a. Bronchospasm
i. Contraindicated in patient with asthma
b. Flushing
c. Chest pain
d. Heaviness of limbs
e. Sense of impending doom
3. Alternative medication
a. IV Verapamil 5 - 10mg over 5-10 mins
b. IV diltiazem
c. Beta-blockers
i. Esmolol
ii. Propranolol
iii. Metoprolol
a. Patient with hemodynamic instability
i. Emergency cardioversion
1. Long term management
a. Patients with suspected cardiac arrhythmias should always be
referred to the cardiologist for electrophysiological evaluation
and long-term management
b. Pharmacological
i. Verapamil, diltiazem
ii. Beta-blockers
iii. Sodium-channel blockers
1. Flecainide
2. Propafenone
iv. potassium repolarization current blocker
1. Sotalol
2. Dofetilide
3. Azimilide
v. multichannel blocker
1. amiodarone
c. Non-pharmacological
i. Ablation of an accessory pathway
a. Atrial tachyarrhythmia
i. Atrial fibrillation
ii. Atrial flutter
1. Causes similar to A fib
2. Atrial flutter is often associated with atrial fibrillation and often requires a similar initial
therapeutic approach
3. Atrial flutter is usually an organized atrial rhythm with an atrial rate typically between 250
and 350 b.p.m
4. involves a macro re-entrant right atrial circuit around the tricuspid annulus. The wavefront
circulates down the lateral wall of the right atrium, through the Eustachian ridge between
the tricuspid annulus and the inferior vena cava, and up the interatrial septum, giving rise
to the most frequent pattern, referred to as counter-clockwise flutter. Re-entry can also
occur in the opposite direction (clockwise or reverse flutter).
5. ECG
a. regular sawtooth-like atrial flutter waves (F waves) between QRS complexes. In
typical counter-clockwise atrial flutter, the F waves are negative in the inferior
leads and positive in leads V1 and V2. In clockwise atrial flutter, the deflection of
the F waves is the opposite
b. If F waves are not clearly visible, it is worth trying to reveal them by slowing AV
conduction by carotid sinus massage or by the administration of AV nodal blocking
drugs such as adenosine or verapamil
6. Symptoms are largely related to the degree of AV block. Most often, every second flutter
beat conducts, giving a ventricular rate of 150 b.p.m. Occasionally, every beat conducts,
producing a heart rate of 300 b.p.m. More often, especially when patients are receiving
treatment, AV conduction block reduces the heart rate to approximately 75 b.p.m
1. Management
a. Similar to A fib
b. symptomatic acute paroxysm or Patient with acute onset
(< 1 - 2 days)
i. Urgent cardioversion
c. Patient with acute onset (> 1 - 2 days)
i. Cardioversion with anticoagulant prior
d. Recurrent paroxysms may be prevented by class III
antiarrhythmic agents
e. Recurrent atrial flutter
i. catheter ablation
1. which permanently interrupts re-entry by
creating a line of conduction block
within the isthmus between the inferior
vena cava and the tricuspid valve ring
1. Atrial fibrillation is
a. A type of atrial tachyarrhythmia
i. Due to multiple foci in atria firing continuously,
causing irregularly irregular heart beat (atrial
quiver continuously)
ii. Mechanism
1. Atrial ectopic (locating within the
pulmonary vein), depolarize rapidly
2. + activation of atrium by multiple reentry-
wave
a. the tachycardia causes atrial
structural and electrophysiological
remodelling changes that further
promote AFib; the longer the
patient is in AFib the more difficult
it is to convert back to sinus
rhythm
b. Rate
i. Atrial
1. 300 - 600
ii. Ventricle
1. 75 - 175 (150 - 200)
a. Caused by
i. Ischemic Heart Disease
ii. Thyrotoxicosis
iii. Mitral stenosis
iv. Others
1. Cardiac causes
a. Heart failure
b. Valvular heart disease
c. Cardiomyopathy: dilated, hypertrophic
d. Myocarditis
e. Pericarditis
f. Familial tachyarrhythmia (e.g. lone atrial fibrillation)
g. Genetic predisposition
2. Non-cardiac causes
a. Phaeochromocytoma
b. Pulmonary disease
i. Acute and chronic pulmonary disease
1. Pneumonia
2. chronic obstructive pulmonary disease
ii. Pulmonary vascular disease (pulmonary embolism)
c. Electrolyte disturbances
i. hypokalaemia
d. Alcohol misuse (‘holiday heart’ and long-term use)
e. Stimulant
i. Caffeine
ii. Smoking
iii. recreational drug use, e.g. cannabi
 Clinical classification of atrial
fibrillation includes
i. first detected
ii. paroxysmal (stops
spontaneously within 7
days)
iii. persistent (requires
cardioversion to stop)
iv. Permanent (no spontaneous
or induced cardioversion)

Diagnosis
1. ECG findings:
a. Irregularly irregular rhythm
i. irregular RR intervals and excessively
rapid series of tiny, erratic spikes on
ECG with a wavy baseline and no
identifiable P waves
ii. QRS rhythm is rapid and irregular
iii. the ventricular rate is usually 120–
180/minute
b. fibrillation or f waves
i. fine oscillations of the baseline
c. no clear P waves
Acute AFib in a hemodynamically stable patient
a. Rate control
i. Determine the pulse in a patient with AFib. If it
is too rapid, it must be treated. Target rate is 60
to 100 bpm.
ii. β-Blockers are preferred. Calcium channel
blockers are an alternative
iii. If left ventricular systolic dysfunction is present,
consider digoxin or amiodarone (useful for
rhythm control).
b. Cardioversion to sinus rhythm (after rate control is
achieved) - rhythm control
i. Candidates for cardioversion include those who
are hemodynamically unstable, those with
worsening symptoms, and those who are having
their first ever case of AFib.
ii. Electrical cardioversion is preferred over
pharmacologic cardioversion. Attempts should
be made to control ventricular rate before
attempting DC cardioversion.
iii. Use pharmacologic cardioversion only if
electrical cardioversion fails or is not feasible:
Parenteral ibutilide, procainamide, flecainide,
sotalol, or amiodarone are choices.
Anticoagulation to prevent embolic cerebrovascular accident (CVA)
i. If AFib present >48 hours (or unknown period of time), risk
of embolization during cardioversion is significant (2% to
5%).
ii. Anticoagulate patients for 3 weeks before and 4 weeks after
cardioversion.
iii. An INR of 2 to 3 is the anticoagulation goal range. • To avoid
waiting 3 weeks for anticoagulation, obtain a transesophageal
echocardiogram (TEE) to image the left atrium (LA). If no
thrombus is present, start IV heparin and perform
cardioversion within 24 hours. Patients still require 4 weeks
of anticoagulation after cardioversion.

Chronic AFib
iv. Rate control with a β-blocker or calcium channel blocker
v. Anticoagulation
1. Patients with “lone” AFib (i.e., AFib in the absence of
underlying heart disease or other cardiovascular risk
factors) under age 60 do not require anticoagulation
because they are at low risk for embolization (aspirin
may be appropriate)
2. Treat all other patients with chronic anticoagulation
(warfarin).
Ventricular tachycardia
a. Types
i. Life-threatening ventricular tachyarrhythmias
ii. Torsades de pointes
iii. Normal heart ventricular tachycardia
iv. Non-sustained ventricular tachycardia
v. Ventricular premature beats.
b. Life-threatening ventricular tachyarrhythmias
i. Sustained ventricular tachycardia
1. >30 s
2. Clinical features
a. pre-syncope (dizziness)
b. Syncope
c. Hypotension
d. cardiac arrest
3. pulse rate typically between 120 and 220 b.p.m.
1. clinical signs of atrioventricular dissociation (i.e. intermittent cannon ‘a’ waves in the neck)
2. ECG
a. rapid ventricular rhythm with broad (often ≥0.14 s), abnormal QRS complexes
b. AV dissociation may result in visible P waves which appear to march through the tachycardia
c. capture beats (intermittent narrow QRS complex owing to normal ventricular activation via
the AV node and conducting system)
d. fusion beats (intermediate between ventricular tachycardia beat and capture beat
3. Supraventricular tachycardia with bundle branch block may resemble ventricular tachycardia on the
ECG. However, if a broad complex tachycardia is due to SVT with either right or left bundle branch
block, then the QRS morphology should resemble a typical RBBB or LBBB pattern
a. VT is more likely than SVT with bundle branch block where there is:
i. a very broad QRS (>0.14 s)
ii. atrioventricular dissociation
iii. bifid, upright QRS with a taller first peak in V1
iv. deep S wave in V6
v. concordant (same polarity) QRS direction in all chest leads (V1–V6)
1. All wave will be one side
vi. Got captured beats & fusion beats
vii. In VT - 2 ears - first ear higher than second ear
viii. In RBBB - second ear higher than first ear
1. Management
a. Patient with haemodynamically compromised (e.g. hypotensive or
pulmonary oedema)
i. emergency DC cardioversion
b. Patient with stable haemodynamic
i. IV therapy with class I drugs
1. Lidocaine
a. 50– 100 mg i.v. over 5 minutes followed by a
lidocaine infusion (2–4 mg i.v. per minute)
ii. Amiodarone
1. dilute intravenous infusion
a. 5 mg/kg over 1 hour (loading dose) followed by a
maintenance infusion of 1200 mg over 24 hours.
i. Ventricular fibrillation
1. very rapid and irregular ventricular activation with no mechanical effect.
2. Clinical features
a. pulseless and becomes rapidly unconscious, and respiration ceases (cardiac
arrest)
b. ECG
i. shapeless, rapid oscillations
1. there is no hint of organized complexe
2. It is usually provoked by a ventricular ectopic beat
c. Management
i. All patient
1. Electrical defibrillation
a. 200J
ii. Patient with in the absence of an identifiable reversible cause (e.g. acute
myocardial infarction, severe metabolic disturbance), at high risk of
sudden death
1. Implantable cardioverter-defibrillators (ICDs) are first-line
therapy