Arrhythmia Recognition & Management

OUTLINE
1. Physiology of cardiac conduction
2. Normal sinus rhythm
3. Pathogenesis of arrhythmia
4. Classification of arrhythmias
5. Bradyarrythmias
6. Tachyarrythmias
7. References

ANATOMY OF THE
CONDUCTING SYSTEM

PHYSIOLOGY OF
CARDIAC CONDUCTION

ARRHYTHMIAS
The origin, rate, rhythm, conduct velocity
and sequence of heart activation are
abnormal.

ARRHYTHMIAS
NORMAL SINUS RHYTHM

ARRHYTHMIAS
ELEMENTS OF ECG
 Relationship between P and QRS helps distinguish various cardiac arrhythmias
 Shape and duration of P may indicate atrial enlargement
 Normal duration = 0.12 – 2.0 sec (120 – 200ms) (3 – 4 horizontal boxes
 Represents atria to ventricular conduction time (through His bundle)
 Prolonged PR interval may indicate 1st degree heart block
 Larger than P wave because of greater muscle mass of ventricles
 Normal duration = 0.08 – 0.12 second
 Its duration, amplitude and morphology are useful in diagnosing cardiac
arrhythmias, ventricular hypertrophy, MI, electrolyte derangement, etc.
 Q-wave greater than 1/3 the height of the R-wave, greater than 0.4 sec are
abnormal mad may represent MI.
P-WAVE: DEPOLARIZARION OF BOTH ATRIA
PR INTERVAL: FROM ONSET OF P WAVE TO ONSET OF QRS
QRS COMPLEX: VENTRICULAR DEPOLARIZATION

PATHOGENESIS
AND INDUCEMNET OF ARRHYTHMIA
 Some physical condition
 Pathological heart disease
 Other system disease
 Electrolyte disturbance and acid-base imbalance
 Physical and chemical factors or toxicosis

MECHANISM
OF ARRHYTHMIA
ABNORMAL HEART PULSE FORMATION
ABNORMAL HEART PULSE CONDUCTION
 Sinus pulse
 Ectopic pulse
 Triggered activity
 Reentry
 Conduct block

CLASSIFICATION
OF ARRHYTHMIA
ABNORMAL HEART PULSE FORMATION
1. Sinus arrhythmia
2. Atrial arrhythmia
3. Atrioventricular junctional arrhythmia
4. Ventricular arrhythmia
1. Sinus-atrial block
2. Intra-atrial block
3. Atrio-ventricular block
4. Intra-ventricular block

ARRHYTHMIA
HOW TO RECOGNIZE ARRHYTHMIA?

TREATMENT STRATEGY
HOW TO RECOGNIZE ARRHYTHMIA?
First assess the patient and check their pulse
Are they compromised?
 Low BP, impaired consciousness, heart failure, chest pain
Then assess the ECG
Is there high risk of cardiac arrest?
 VT, complete heart block
If compromised or high risk
Treat with electricity
 DC cardioversion / temporary pacing
If not
Look for reversible causes / treat with drugs

BRADYARRHYTHMIAS
1. Sinus bradycardia
1. Atrioventricular (AV) block
 First degree
 Second degree
Types 1 (Wenkenbach) / Type 2
 Third degree

SINUS BRADYCARDIA
Rate <60 per minute
QRS Complex Normal
Rhythm Regular Sinus
P Wave Present, every P wave followed by QRS complex

HEART BLOCK
 Heart block, AV bundle or bundle branch block affects the
electrical system of the heart.
 It is different from coronary artery disease, which affects
the heart’s blood vessels.
 The heart beats irregularly and more slowly than usual,
potentially stopping for up to 20 seconds at a time.
 A heart block makes it difficult for the heart to pump
blood properly through the circulatory system, so the
muscles and organs do not get enough oxygen to function
properly.
 Heart block itself does not usually need direct treatment,
but related underlying health conditions do.

FIRST – DEGREE HEART BLOCK
 First degree heart block is actually a delay rather than a block.
 It involves minor heartbeat disruptions, such as skipped beats.
 If each wave of depolarization that originates in the SA node is conducted to
the ventricles, but there is delay somewhere along the conduction pathway, the
the PR interval is prolonged.
 This means than the PR interval will be longer than normal (over 0.20 seconds)
 It does not generally require treatment.
 First degree heart block is not itself important, but it may be a sign of coronary
artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte
disturbances.
TYPES OF HEART BLOCK

SECOND – DEGREE HEART BLOCK
 Sometimes excitation completely fails to pass through the AV node or the
bundle of His. When this occurs intermittently, second degree heart
block is said to exist.
 There are 3 variations of this:
I. Most beats are conducted with a constant PR interval, but
occasionally there is an atrial contraction without a subsequent
ventricular contractions – Mobitz Type II phenomenon
II. There may be progressive lengthening of the PR interval and then
failure of conduction of an atrial beat , followed by a conducted
beat with a shorter PR interval and then a repetition of this cycle –
Wenckebach phenomenon
III. There may be alternate conducted and non-conducted atrial beats
(or one conducted atrial beat and then two non-conducted beats),
giving twice (or three times) as many P waves as QRS complex – 2:1
conduction

SECOND – DEGREE HEART BLOCK TYPE I
 Some impulses are blocked but not all.
 More P waves can be observed vs QRS complexes on a tracing.
 Each successive impulse undergoes a longer delay. After 3 or 4 beats
the next impulse is blocked.
 On a EKG tracing, PR intervals will lengthen progressively with each
beat until a QRS complex is missing.
 After this blocked beat, the cycle of lengthening PR intervals resumes.
 This heart block is also called a Wenckebach block.

SECOND – DEGREE HEART BLOCK TYPE II
 With Mobitz Type II blocks, the impulse is blocked in the bundle of
His
 Every few beats there will be a missing beat but the PR interval will
not lengthen

SECOND – DEGREE HEART BLOCK (2:1 TYPE)

THIRD – DEGREE HEART BLOCK
 With this block, it is said to occur when atrial contraction is normal
but no beats are conducted to the ventricles.
 As a result, the ventricles generate an escape impulse, which is
independent of the atrial beat.
 Complete block is not always immediately obvious in a 12 lead
ECG, where there may be only a few QRS complexes per lead. Ones
need to look at the PR interval in all the leads.
 In most cases the atria will beat at 60 – 100 bpm while the
ventricles asynchronously beat at 30 – 45 bpm
 It is more common in patients with heart disease.
 May occur as an acute phenomenon in patients with MI or it may
be a chronic state, usually due to fibrosis around the bundle of His.
It may also be caused by the block of both bundle branches.

 Sinus rhythm but no P waves are conducted
 Right axis deviation
 Broad QRS complexes (duration 160 ms)
 Right bundle branch block pattern
 The cause of the block could not be determined, though in most patients it results
from fibrosis of bundle of His

BUNDLE BRANCH BLOCK
 If the depolarization wave reaches the interventricular septum
normally, the interval between the beginning of the P wave and the
first deflection in QRS complex will be normal.
 However, if there is abnormal conduction through either the right
of left bundle branches, (‘bundle branch block’) there will be a
delay in the depolarization of part of the ventricular muscle.
 The extra time taken for depolarization of the whole of the
ventricular muscle causes widening of the QRS complex.
 Although a wide QRS complex can indicate BBB, widening also
occurs if depolarization begins within the ventricular muscle itself.
 Remember in the sinus rhythm with bbb, normal P waves are
present with a constant PR interval.

BUNDLE BRANCH BLOCK
 Block of the bundle branches has the same effect as block of His
bundle, and causes complete heart block.
 right bundle branch block (RBBB) often indicates problems in the
right side of heart but RBBB patterns with a QRS complex of normal
duration are quite common in healthy people.
 Left bundle branch block (LBBB) is always an indication of heart
disease, usually of the left side.
 It is important to recognize that bundle branch block is present
because LBBB prevents any further interpretation of the
cardiogram, and RBBB can make interpretation difficult.

BUNDLE BRANCH BLOCK
 The mechanism underlying the ECG patterns of RBBB and LBBB can
be worked out from the first principles.
1. The septum is normally depolarized from left to right
2. The left ventricle, having the greater muscle mass, exerts
more influence on ECG than does the right ventricle
3. Excitation spreading towards a lead causes an upward
deflection within the ECG

RIGHT BUNDLE BRANCH BLOCK
 No conduction occurs down the right bundle branch but the
septum is depolarized from the left side as usual, causing an R
wave in a right ventricular lead (V1) and a small Q wave in a left
ventricular lead (V6)

LEFT BUNDLE BRANCH BLOCK
 If conduction down the left bundle branch fails, the septum
becomes depolarized from right to left, causing a small Q wave in
lead V1 and R wave in lead V6

SINUS RHYTHM WITH RIGHT BUNDLE BRANCH BLOCK

SINUS RHYTHM WITH LEFT BUNDLE BRANCH BLOCK

WHAT TO DO
 Always remember that it is the patient who should be treated , not
the ECG
 Relief the symptoms always comes first
 However, some general points can be made about the action that
might be taken if the ECG shows conduction abnormalities
FIRST DEGREE BLOCK
 Often seen in normal people
 Think about acute myocardial infarction and acute rheumatic fever
as possible causes
 No specific action needed

WHAT TO DO
SECOND DEGREE BLOCK
 Usually indicates heart disease; often seen in acute myocardial
infarction
 Mobitz Type II and Wenckebach block do not need specific
treatment
 2:1 block may indicate a need for temporary or permanent pacing,
especially if the ventricular rate is slow
THIRD DEGREE BLOCK
 Always indicates conducting tissue disease – more often fibrosis
than ischemic
 Consider a temporary or permanent pacemaker

WHAT TO DO
 Think about an atrial septal defect
 No specific treatment
 Think about aortic stenosis and ischemic disease
 If the patient is asymptomatic, no action is needed
 If the patient has recently had severe chest pain, LBBB may
indicate an acute myocardial infarction and thrombolysis should be
considered

Here’s how patients have described their experience:
 “My heart flip-flops, skips beats, and feels like it’s
banging against my chest wall, especially if I’m
carrying stuff up my stairs or bending down.”
 “I was nauseated, light-headed, and weak. I had a
really fast heartbeat and felt like I was gasping for
air.”
 “I had no symptoms at all. I discovered my AF at a
regular check-up. I’m glad we found it early.”
ATRIAL FIBRILLATION

ATRIAL FIBRILLATION
 Atrial fibrillation (also called AFib or AF) is an atrial
tachyarrhythmia characterized by uncoordinated atrial
activation with consequent deterioration of atrial
mechanical function.
 The surface ECG is characterized by ‘absolutely’
irregular RR intervals and the absence of any distinct P
waves. The P waves are replaced by fibrillary waves.
 Atrial fibrillation is the commonest sustained cardiac
arrhythmia and also a major cause of stroke.
 The mortality rate of AF is double that of patient in
sinus rhythm

RISK FACTOR
 Obesity
 Systemic Hypertension
 Pulmonary Hypertension
 Myocardial disease
 Atrial Ischemia
 Coronary Artery disease
 Myocarditis or pericarditis
 Drugs : Alcohol, Caffeine
 Hyperthyroidism
 Pheochromocytoma
 Lone AF
 Familial AF
 Congenital Heart Disease
Some of conditions predisposing
to AF may be reversible such as :
 Acute infections
 Alcohol excess
 Pericarditis
 Myocarditis
 Surgery

SUBTYPES
Atrial fibrillation may be:
 Paroxysmal
 Persistent
 Long Standing Persistent
 Permanent

TERMINOLOGY CLINICAL FEATURES PATTERN
Initial event (first
detected episode)
 Symptomatic
 Asymptomatic
 Onset Unknown
May or may not recur
Paroxysmal  Spontaneous
termination <7 days
and most often <48
hour
Recurrent
Persistent  No self limiting
 Lasting >7 days or
requiring
cardioversion for
termination
Recurrent
Long Standing Persistent  AF that has lasted for
 1 year when it is
decided to adopt
rhythm control
strategy
Recurrent
Permanent  Not terminated
 Terminated but
relapsed
 No cardioversion
attempt
Recurrent

ATRIAL FIBRILLATION
The term lone AF applies to young individuals
(<60 years of age) or echocardiography evidence
of cardiopulmonary disease, including
hypertension. These patient has favorable
prognosis with respect to thromboembolism and
mortality.
‘Silent AF’ being asymptomatic is detected by an
opportunistic ECG or may present as an AF-
related complication such as ischemic stroke.

INITIAL MANAGEMENT
Clinical Management of AF patients should
concentrate on:
 Relief of symptoms
 Assessment of AF-associated risk
 Determination of EHRA score
 Estimation of stroke risk
 Search for conditions that predispose to AF
 Search for complications of the arrhythmia

EHRA SCORING SYSTEM
The EHRA symptom score provides a simple clinical tool for
assessing symtoms during AF. The score only considers
symptoms that are attributable to AF and reverse or reduce
upon restoration of sinus rhythm or with effective rate
control.

CHADS2-VASc
Estimation of stroke risk
Maximum total score = 9
Score:
0 – No need therapy preferred
1 – Aspirin or Oral anti-coagulation
≥2 – Oral anti-coagulation

DETECTION
Those with undiagnosed AF can receive treatment sooner if an
opportunistic case finding is undertaken. Routine palpation of the
radial pulse (not less than 20 seconds) during screening of blood
pressure will be a good opportunity to pick up undiagnosed atrial
fibrillation.
In patients presenting with any of the following:
 Breathlessness
 Palpitations
 Syncope/dizziness
 Chest discomfort or stroke/TIA
Manual pulse palpation should be performed to assess for the
presence of an irregular pulse that may indicate AF.

DETECTION
The diagnosis of AF requires confirmation by ECG,
sometimes in the form of bedside telemetry,
ambulatory Holter recordings and event loop
recordings.
If AF is presented at the time of recording, a
standard 12-lead ECG is sufficient to confirm the
diagnosis.
In paroxysmal AF, 7 days Holter ECG recording or
daily and symptom-activated event recordings
may document the arrhythmia in 70% of AF
patients.

ECG
Rate Wide range of ventricle response
(irregular)
QRS Complex Present
Rhythm Irregular
P Wave Chaotic atrial fibrillatory waves

MANAGEMENT
General Principles
AIM
1. Relief symptoms
2. Prevention of serious complications
3. Optimal management of concomitant
cardiovascular disease
4. Rate control
5. Correction of rhythm disturbance

COMPLICATIONS
 Stroke.
In atrial fibrillation, the chaotic rhythm may cause blood to pool in the
atrium and form clots. If a blood clot forms, it could dislodge from the
heart and travel to the brain. There it might block blood flow, causing a
stroke.
The risk of a stroke in atrial fibrillation depends on the age (you have a
higher risk as you age) and on whether they have high blood pressure,
diabetes, a history of heart failure or previous stroke, and other
factors.
Certain medications, such as blood thinners, can greatly lower the risk
of a stroke or the damage to other organs caused by blood clots.
 Heart failure. Atrial fibrillation, especially if not controlled, may
weaken the heart and lead to heart failure.

SUMMARY
 An ECG should be performed in all patients, whether
symptomatic or not, in whom AF is suspected because
an irregular pulse has been detected.
 The stroke risk stratification algorythms, CHADS2 and
CHA2DS2-VASC, should be used in patients with AF to
assess their risk of stroke and thromboembolism, while
the HAS-BLED score should be assess their risk of
bleeding.
 Antithrombotic therapy should be based upon the
absolute risks of stroke/thromboembolism and
bleeding, and the relative risk and benefit for a given
patient

SUMMARY
 In patient with permanent AF, who need
treatment for rate control, beta blockers or
rate limiting calcium antagonist should be the
preferred initial monotherapy in all patients
while digoxin should only be considered as
monotherapy in predominantly sedentary
patients.

SINUS TACHYCARDIA
The normal adult heart rate, arising from the sinoatrial (SA) node,
range from 60 to 100 bpm.
Sinus tachycardia = a sinus rhythm with a rate exceeding 100 bpm
 Sinus tachycardia is a rhythm in which the rate of impulses arising from
the sinoatrial (SA) node is elevated.
 It is one of the most commonly encountered, and often overlooked,
rhythm disturbances that may portend an adverse prognosis, particularly
in patients with cardiovascular disease.
 Rapid rates, though they may be compensating for ischemia elsewhere,
increase myocardial oxygen demand and reduce coronary blood flow,
thus precipitating an ischemic heart or valvular disease.
 Sinus tachycardia accompanying a myocardial infarction may be
indicative of cardiogenic shock.

SINUS TACHYCARDIA
PHARMACOLOGICAL PHARMACOLOGICAL
Exercise Beta Agonist : adrenaline, isoprenaline,
salbutamol, dobutamine
Pain Sympathomimetics: amphetamines,
cocaine, methylphenidate
Hypoxia Antimuscarinics: antihistamines,
carbamazepine, atropine
Anxiety Other stimulants: caffeine, nicotine,
amphetamines
Hyperthyroidism
Acute coronary ischemia and myocardial
infarction
Sinus tachycardia is a normal physiologic response to exercise and conditions in
which catecholamine release is physiologically enhanced or, less commonly, in
situations where the parasympathetic nervous system is withdrawn. A long list of
other factors may be responsible in selected cases, including:

SINUS TACHYCARDIA
Sinus tachycardia as a Physiologic
Response
 In the majority of patients, sinus tachycardia is a physiologic response
to a demand for greater cardiac output, increased sympathomimetic
state, or vagal/parasympathetic withdrawal.
 Important mechanism for increasing cardiac output in the setting of
infection or volume depletion.
 Because of this, most patients do not have symptoms directly
attributable to the tachycardia itself but present with signs or
symptoms related to the associated condition (eg, pain, fever,
shortness of breath, etc).

SINUS TACHYCARDIA
Sinus tachycardia as a Physiologic
Response
 Sinus tachycardia can indirectly lead to other symptoms due to the impact of
the tachycardia on other underlying organic heart disease. Tachycardia may
result in:
I. Decreased cardiac output due to shortened ventricular filling time
II. Increased myocardial oxygen consumption
III. Reduced coronary blood flow
 The above physiologic changes induced by tachycardia may result in symptoms
of angina or dyspnea, the severity of which will depend upon how rapidly the
heart is beating and the extent of the underlying cardiac comorbidities.

SINUS TACHYCARDIA
Postural Orthostatic Tachycardia Syndrome
 Postural orthostatic tachycardia syndrome (POTS) is a condition that occurs
predominantly in young women in the absence of structural heart disease.
 It is the most common syndrome of young people seen in autonomic
dysfunction clinics. Patients present at a relatively young age (14 to 45 years).
 Characteristically, patients develop symptoms upon assuming the standing
position.
 Symptoms may include palpitations, fatigue, lightheadedness, or exercise
intolerance.
 The 2015 Heart Rhythm Consensus statement defined POTS as a heart rate rise
of ≥30 beats per minute (≥40 beats per minute in individuals 12 to 19 years of
age) in the absence of orthostatic hypotension (≥20 mmHg systolic blood
pressure drop).
 Sinus tachycardia is only one component of this condition, which is a disorder
of autonomic dysregulation

SINUS TACHYCARDIA
Inappropriate sinus tachycardia
Inappropriate sinus tachycardia, also called chronic non-paroxysmal sinus tachycardia,
is an unusual condition that occurs in individuals without apparent heart disease or
other cause for sinus tachycardia, such as hyperthyroidism or fever, and is generally
considered a diagnosis of exclusion.
Inappropriate sinus tachycardia is defined as a resting heart rate >100 beats per minute
(with a mean heart rate >90 beats per minute over 24 hours) associated with highly
symptomatic palpitations.
Commonly used criteria to define inappropriate sinus tachycardia include:
 P wave axis and morphology similar or identical to sinus rhythm.
 Resting heart rate of 100 beats per minute or greater (with a mean heart rate >90
beats per minute over 24 hours) or with activity heart rates of 100 beats per
minute or greater but in excess of what one would expect for the amount of
exertion.

SINUS TACHYCARDIA
 Palpitations, presyncope, or both related to the
tachycardia. Very rarely do patients experience
syncope.
 Exclusion of identifiable causes of sinus tachycardia.
 Exclusion of atrial tachycardia.
Most of these patients are young and female.
Affected patients have an elevated resting heart rate
and/or an exaggerated heart rate response to exercise
that is out of proportion to the body's physiological
needs; many patients have both.

SINUS TACHYCARDIA
 Patients with inappropriate sinus tachycardia are usually
symptomatic and have resting heart rates of greater than
100 beats per minute and average heart rates on a 24-
hour Holter greater than 90 beats per minute with no
clear physiologic, pathologic, or pharmacologic trigger.
 The pathophysiologic mechanism behind this disease is
poorly understood and is thought to consist of intrinsic
sinus node hyperactivity coupled with autonomic
disturbance modulated by neurohormonal influences.
 One study suggested that this tachycardia is related to a
primary sinus node abnormality, characterized by a high
intrinsic heart rate, depressed efferent cardiovagal
reflex, and beta-adrenergic hypersensitivity.

With very fast heart rates the P waves may be hidden in the preceding T wave, producing a ‘camel
hump’ appearance.
Life In the Fastlane

SUPRAVENTRICULAR
TACHYCARDIA
Any tachyarrhythmia arising from above the level of the Bundle of His.
ATRIAL TACHYARRHYTHMIA
JUNCTIONAL ARRHYTHMIA
1. Atrial tachycardia
2. Atrial flutters
3. Atrial fibrillation
1. AV nodal reentrant tachycardia
2. AV nodal reciprocating tachycardia – Wolff-
Parkinson-White syndrome

BILIARY ATRESIA
REGULAR IRREGULAR
ATRIAL
 Sinus tachycardia
 Atrial tachycardia
 Atrial flutter
 Atrial fibrillation
ATRIOVENTRICULAR (AV)
 Atroventricular re-entry
tachycardia (AVRT)
 AV nodal re-entry
tachycardia (AVNRT)
SUPRAVENTRICULAR
TACHYCARDIA
Classification by site and regularity

ATRIAL FLUTTER
Atrial flutter is a common abnormal heart rhythm,
similar to atrial fibrillation, the most common
abnormal heart rhythm. Both conditions are types of
supraventricular (above the ventricles) tachycardia
(rapid heart beat).
In atrial flutter, the upper chambers (atria) of the heart
beat too fast (re-entrant mechanism), which results in
atrial muscle contractions that are faster than and out
of sync with the lower chambers (ventricles).

ATRIAL FLUTTER
QRS Complex Present
Rhythm Regular
Ventricular rhythm often regular
Set ratio atrial rhythm e.g. 2 to 1
P Wave No true P waves
Flutter waves in “sawtooth” pattern

ATRIAL FLUTTER
General treatment goals for symptomatic atrial flutter are
similar to those for atrial fibrillation and include the
following:
1. Control of the rate
2. Restoration of sinus rhythm
3. Prevention of recurrent episodes or reduction of their
frequency or duration
4. Prevention of thromboembolic complications
5. Minimization of adverse effects from therapy

AVRT
ATRIOVENTRICULAR RE-ENTRANT
TACHYCARDIA
Most associated with Wolff-Parkinson-White syndrome
in which as accessory pathway allows electrical signals
from the heart’s ventricles to enter the atria and cause
earlier then normal contraction, which leads to
repeated stimulation of the AV node

AVRT
TACHYCARDIA
Wolff-Parkinson-White Syndrome
 First described in 1930 by Louis Wolff, John Parkinson and Paul
Dudley White.
 Wolff-Parkinson-White (WPW) Syndrome is a combination of the
presence of a congenital accessory pathway and episodes of
tachyarrhythmia.
 Incidence 0.1 – 3.0 per 1000.
 Associated with a small risk of sudden cardiac death.

AVRT
TACHYCARDIA

TREATMENT
TACHYCARDIA
The aim is to interrupt the circuit.
1. Inhibition of AV node – vagal maneuvre to slow
down heart rate
2. IV adenosine – complete electrival blockade at AV
node and interrupt the reentrant electrical circuit.
3. Radiofrequency ablation of accessory pathway

AVNRT
ATRIOVENTRICULAR NODAL RE-ENTRANT
TACHYCARDIA
 Atrioventricular Nodal Reentrant Tachycardia is a type of
supraventricular tachycardia (i.e it originates above the level
of the Bundle of His) and is the commonest cause of
palpitations in patients with hearts exhibiting no structurally
abnormality.
 AV nodal reentrant tachycardia is the most common regular
supraventricular tachycardia.
 It is more common in women than men (approximately 75%
of cases occur in females).

AVNRT
TACHYCARDIA
 Atrioventricular Nodal Reentrant Tachycardia is a type of
supraventricular tachycardia (i.e it originates above the level of the
Bundle of His) and is the commonest cause of palpitations in patients with
hearts exhibiting no structurally abnormality.
 AV nodal reentrant tachycardia is the most common regular
supraventricular tachycardia.
 It is more common in women than men (approximately 75% of cases
occur in females).
 The circuit usually involves two anatomical pathways: the fast pathway
and the slow pathway, which are both in the right atrium. The slow
pathway is located inferior and slightly posterior to the AV node.

AVNRT
TACHYCARDIA

AVNRT
TACHYCARDIA
 Absent P waves, or inverted P waves after the QRS complex
 Narrow (<120 ms) QRS complex
 Heart rate 140-250 bpm, with a regular rhythm
 Can occur in the young and healthy
 Three quarters of patients are female

TREATMENT
TACHYCARDIA
1. Vagal maneuvers
2. Medication
Adenosine, beta blockers or calcium channel blockers
3. Cardioversion
In very rare instances, cardioversion (the electrical restoration of a normal heart
rhythm) is needed in the treatment of AVNRT. This would normally only happen if all
other treatments have been ineffective, or if the fast heart rate is poorly tolerated
(e.g. the development of heart failure symptoms, low blood pressure or coma).
4. Electrophysiology
After being diagnosed with AVNRT, patients can also undergo an Electrophysiology
(EP) study to confirm the diagnosis. Catheter ablation of the slow pathway, if
successfully carried out, can potentially cure the patient of AVNRT.

VENTRICULAR TACHYCARDIA
 Can be defined as three or more premature ventricular contraction in a row
 The impulse is iniatiated from the ventricle itself.
 Rate is 150-250, regular rhythm and wide QRS
 a/w coronary artery disease, myocardial infarction, electrolyte imbalace,
myocardiopathy
 Manage depends on severity- if stable (keep on ecg monitoring), if unstable
unconcious no pulse ( immediate defibrillationt, iv amiodarone)

VENTRICULAR FIBRILLATION
 Rapid disorganized ventricular rhythm that results of inactive
activities of the ventricles, absence of audible heartbeat and
no palpable pulse.
 No atrial activity seen ,rate and rhythm cannot be determined
 a/w acute MI, untreated ventricular tachycardia, electrical
shock, drug overdose
 Manage with immediate defibrillation, CPR, iv amiodarone

TORSADE DE POINTES
 Polymorphic ventricular tachycardia with long QT interval, rapid
irregular QRS complex.
 Caused by a medication such as sotalol, procanamaide, quinidine,
hypokalemia, bradycardia after MI
 If acute, remove offending medication, shorten QT interval with
magnesium sulphate, isoprterenol.
 If chronic, pacemaker, amiodarone and beta blocker.

Arrhythmia Recognition & Management

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