Arrhythmia

Introduction

Cardiac arrhythmia result from abnormal impulse initiation, abnormal impulse conduction, or
both mechanisms together. Abnormal impulse initiation includes enhanced normal automaticity,
abnormal automaticity, and triggered activity resulting from after depolarization, abnormal
impulse conduction includes conduction block and reentry.

Abnormal impulse initiation

Automaticity

It is the ability of certain cells to spontaneously depolarize and initiate an electrical impulse
without external stimulation. The sinus node (SA node) is the normal pacemaker of the heart
because it has the fastest rate of automaticity. Other cells in the heart also have the property of
automaticity including atria, coronary sinus, pulmonary vein, AV junction, AV valves, and
purkinje system. The rates of these other pacemakers are slower than the rate of the SA node,
therefore they are suppressed by the SA node under normal condition, a phenomenon known as
overdrive suppression. The site of fastest impulse initiation is referred to as the dominant
pacemaker, whereas sites of impulse formation that are suppressed by the dominant site are
called subsidiary or latent pacemakers.

Enhanced normal automaticity

Impulse initiation can be shifted from the SA node to other parts of the heart if the rate of the
SA node drops below that of a subsidiary pacemaker or if the automatic rate of a subsidiary
pacemaker rises above that of the SA node. Increased vagal tone, drugs, electrolyte imbalance, or
disease of the SA node can decrease its rate of automaticity or can cause exit block of its
impulse, thus allowing subsidiary pacemakers to assume control of the heart.

Abnormal automaticity

Atrial and ventricular myocardial cells that do not normally have automaticity can develop
abnormal automaticity when their Transmembrane resting potential (TRP) is reduced and is
referred to as depolarization induced automaticity. Subsidiary pacemaker like those in the
purkinje system that are normally overdrive suppressed by the faster SA node can also develop
abnormal automaticity when their TRP is reduced. This abnormal automaticity is thought to be
mediated by the slow inward current carried mainly by calcium because the normal fast sodium
channels are inactivated at reduced membrane potentials, however both sodium and calcium
channels may play a role in the development of abnormal automaticity.
Abnormal impulse conduction

Conduction block

The electrical impulse can be prevented from propagating through the heart for a variety of
reasons. If the propagating impulse is not strong enough to excite the tissue ahead of it,
conduction will fail. If an impulse arrives at an area where the tissue is still refractory after a
previous depolarization, it will not be able to conduct further. If the impulse reaches tissue that
is abnormally polarized due to ischemia, disease or drugs it may not be able to conduct at all or
will conduct with delay. Scar tissue from previous MI, surgery or catheter ablation also prevents
conduction.

Decremental conduction

It is the progressive decrease in conduction velocity of an impulse as it travels through a region

of myocardium and occurs when an action potential loses its ability to stimulate the tissue ahead
of it. Decremental conduction is a normal function of the AV node, delaying the impulse in the
AV node long enough for atrial contraction to contribute to ventiricular filling. Decremental
conduction normally occurs in areas of the heart where resting potentials are low and action
potentials depend on slow channels, such as AV and SA nodes. It can also occur in areas where
resting potentials are low due to ischemia, disease or drugs. Under such circumstances
conduction velocity is slow because of the slower rate of rise of the action potential that occurs
when cells are stimulated at reduced resting potentials.

Phase 3 block

When a cell is stimulated during phase 3 of the action potential, conduction is impaired because
the membrane has not yet returned to its resting level. Whenever a cell is stimulated at a less
negative membrane potential the rate of rise of the action potential and thus conduction velocity
is slow because most sodium channels are inactive at reduced at reduced membrane potential.

Phase 3 block, also called short cycle aberrancy or tachycardia dependent block, can occur in
normal hearts if impulses are premature enough to reach gibers during their normal refractory
period, resulting in aberrant conduction of premature beats. It is also responsible for rate
dependent bundle branch blocks and for aberration that commonly occurs when cycle lengths are
very irregular, as in arterial fibrillation.

Phase 4 blocks

It is also called long cycle aberrancy or Bradycardia dependent block, occurs late in diastole
when are stimulated at reduced membrane potential secondary to spontaneous phase 4
depolarization. In this case the membrane has begun to depolarize spontaneously during its
normal phase 4. By the time a stimulus arrives, the resting potential has been reduced enough to
cause slow conduction. Again whenever a cell is stimulated at a reduced membrane potential,
only some of the sodium channels are available, and slow conduction results.

Phase 4 block is responsible for abnormal conduction that occurs only at the end of long cycles
or for so called Bradycardia dependent bundle branch block.

Reentry

It is a type of conduction abnormality that leads to the occurrence of premature beats or sustained
tachycardia rather than to a block. Reentry can occur in areas of the heart where conduction
velocity is abnormally slow because of ischemia, electrolyte abnormalities, drugs, or disease.
Reentry means that an impulse can travel through an area of myocardium, depolarize it and then
reenter the same area to depolarize it again.

For reentry to occur an area of unidirectional block is necessary to allow an impulse to conduct
in one direction and to provide a return pathway by which the original stimulus can reenter a
previously depolarized area. Conduction velocity must be slow enough and the refractory period
short enough to allow time for the previous stimulated area to recover its ability to conduct. If the
refractory period of the previously stimulated tissue is long or conduction velocity is fast, the
impulse dies out because it encounters tissue that is unable to conduct.

When an impulse travels the reentry loop only once, a single premature beat results. If
conduction velocity is slow enough and the refractory period of normal tissue is short enough, a
single impulse could travel the loop numerous times, resulting in a run of premature beats or in a
sustained tachycardia. Reentry that occurs in small loops of tissue such as AV node or purkinje
fibres is called micro reentry. If the reentry loop involves large tracts of tissue such as an AV
bypass tract or bundle branch system in ventricles it is called macro reentry.
Classification of basic arrhythmias and conduction disturbances

A. Rhythm originating in SA node

1. Normal sinus rhythm

2. Sinus Bradycardia
3. Sinus tachycardia
4. Sinus arrhythmia
5. Sinus arrest
6. Sinus exit :- type I, II or complete
7. Sick sinus syndrome

B. Rhythms originating in Atria

1. PAC (Arterial premature depolarization)

2. Wandering arterial pacemaker
3. Multifocal atrial tachycardia(MAT)
4. Atrial tachycardia
5. Arterial flutter
6. Supra ventricular tachycardia:

C. Rhythm originating in AV junction:

1. Premature junctional complexes:

2. Junctional rhythm and junctional tachycardia:

D. Rhythms originating in ventricles

1. Premature ventricular complexes:

2. Accelerated idioventricular rhythm:
3. Ventricular tachycardia: types Monomorphic, Polymorphic
4. Ventricular flutter
5. Ventricular asystole
E. Conduction abnormalities

1. First degree AV block

2. Second degree AV block
a. Type I (Wenckebach) or (Mobitz I)
b. Type II (Mobitz II)
3. 2:1 conduction (either Type I or Type II)
4. High grade AV block
5. Third degree AV block

F. Complex arrhythmias and conduction disturbances

1. Pre excitation syndrome:

2. Wolf Parkinson White syndrome:
3. Short QT syndrome:
4. Torsades de Pointes:
Rhythm originating in SA node

The SA node is the normal pacemaker of the heart because it has the highest rate of automaticity
of all potential pacemaker sites. The arrhythmias that originate in the SA node are sinus
Bradycardia, sinus tachycardia, sinus arrhythmia, sinus arrest, sinus exit block, and sinus
syndrome.

Normal sinus rhythm

The SA node normally fires at a regular rate of 60 to 100 beats per minute. The impulse spreads
from the SA node through the atria and to the AV node, where it encounters a slight delay before
it travels through the bundle of His, right and left bundle branch, and purkinje fibers into the
ventricles.

Rate: 60-100 beats per min

Rhythm: regular

P wave: precede every QRS complex and are consistent in shape

PR interval: 0.12-0.20 sec

QRS complex: 0.04-0.10 sec

Sinus Bradycardia

It is discharge of SA node at a rate slower than 60 beats per sec. It can be a normal variant,
especially in athletes and during sleep. Sinus Bradycardia may be a response to vagal stimulation
such as carotid siunus massage, ocular pressure, coughing or vomiting. Pathological sinus
Bradycardia can occur with inferior wall MI, hypothyroidism, hypothermia, sleep apnea,
increased intracranial pressure, glaucoma, myxedema, hypoxia, infection, and sick sinus
syndrome.

Rate: less than 60 beats per min

Rhythm: regular

P wave: precede every QRS consistent shape

PR interval: usually normal (0.12-0.20sec)

QRS complex: usually normal (0.04-0.10sec)

Sinus tachycardia

It is a sinus rhythm at a rate faster than 100 beats per min. it is a normal response to anything that
stimulates the sympathetic nervous system, including sympathomimetic drugs, exercise, and
emotion. Sinus tachycardia that persists at rest usually indicates some underlying problem, such
as fever, blood loss, anxiety, pain, heart failure, hypemetabolic states, or anaemia. Sinus
tachycardia is a normal physiological response to a decreased cardiac output. Drugs that can
cause sinus tachycardia include, atropine, isoprpterenol, epinephrine, dopamine, dobutamine,
nitroprusside, and caffine.

Rate: greater than 100 beats per min

Rhythm: regular

P wave: precede every QRS, have consistent shape, may be buried in the preceding T wave

PR interval: usually normal, may be difficult to measuer if P wave are buried in T waves

QRS complex: usually normal

Conduction: normal through atria, AV node, Bundle branches and ventricles

Sinus arrhythmia

Sinus arrhythmia occurs when the SA node discharges irregularly. It occurs as a normal
phenomenon, especially in the young, and decreases with age. Sinus arrhythmia is commonly
associated with the phases of respiration, during inspiration, the SA node fires faster, during
expiration it slows, other than this phasic increase and decresase in rate, sinus arrhythmia looks
like normal sinus rhythm and it does not require treatment.

Rate : 60-100 beats per min

Rhythm: irregular, phasic increase and decrease in rate, which may be related to respiration

P wave: Precede every QRS, have consistent shape

PR interval: usually normal

QRS complex: usually normal

Conduction: normal through atria, AV node, bundle branches, ventricles

Sinus arrest

It occurs when the SA node automaticity is depressed and impulse are not formed when
expected. This delay results in the absence of a P wave at the time it is expected to occur and
unless there is escape of a junctional or ventricular pacemaker, the QRS complex is also missing.

If only one sinus impulse fails to form the term sinus pause is usually used, whereas if more than
one sinus impulse in a row fails to form, sinus arrest has occurred.

Rate: atrial- usually within normal range but may be in bradycardic range if several sinus
impulses fail to form.

Ventricular- usually within normal range but may be in bradycardic range if several sinus
impulses fail to form and there are no junctional or ventricular escape beats.

Rhythm: irregular due to the absence of SA node discharge

P wave: present when SA node is firing and absent during periods of sinus arrest. When present,
they precede every QRS complex and are consistent in shape. If junctional escape beats occur, P
waves may be inverted either before or after the junctional QRS

PR interval: usually normal when P wave are present. If junctional escape beats occur, the PR
interval is short when the P wave precedes the QRS

QRS complex: usually normal when SA node is functioning and absent during periods of sinus
arrest unless escape beats occur. If ventricular escape beats occur, QRS complex is wide.

Conduction: normal through atria, AV node, bundle branches, and ventricles when SA node is
firing. When the SA node fails to form impulses, there is no conduction through the atria. If a
junctional escape beats occurs, ventricular conduction is usually normal, whereas if a ventricular
escape beats occurs, conduction through the ventricle is abnormally slow.
Sinus exit

It occurs when the impulse is formed in the SA node normally but fails to exit the node to excite
atrial tissue. Sinus exit block can be type I, II or complete.

Type I (Wenckebach)

Type II looks exactly like sinus arrest except for the P P interval which are multiples of the basic
sinus cycle length.

Complete sinus exit block exists when no impulses reach the atria from the SA node and no P
wave occurs

Rate: atrial- usually within normal range but may be in bradycardic range if several sinus
impulses fail to exit the SA node.

Ventricualr- ususlly is normal range but may be in bradycardic range if no junctional or

ventricular escape beats occurs during periods of sinus exit block

Rhythm: irregular due to pauses caused by sinus exit block

P wave: present except when impulse fails to exit SA node. When present, they precede every
QRS and are consistent in shape. The P P interval is an exact multiple of the sinus cycle because
impulses are formed regularly but occasionally fail to exit the SA node

PR interval: ususlly normal when P waves are present but may be prolonged if AV node
conduction is slow

QRS complex: usually normal when sinus impulses conducts and absent when exit block occurs.
If ventricular escape beats occur, QRS is wide

Conduction: normal through atria, AV node, bundle branches, and ventricles when impulse exits
SA node normally.
Sick sinus syndrome

The term is used to describe rhythms in which there is marked sinus Bradycardia, sinus pauses,
or periods of sinus arrest alternating with paroxysms of rapid atrial arrhythmias, especially atrial
flutter of AF.

The term brady tachy syndrome is commonly used to describe the same arrhythmias. Sinus
Bradycardia or arrest, juctional escape rhythms commonly occur.

Rate: Bradycardia or tachycardia

Rhythm: irregular, pause of 3 sec or more

P wave:usually normal. Absent during arrest of AF

PR interval: normal or prolonged

QRS complex: Normal unless Bundle branch block

Conduction: abnormal through atria during periods of arterial tachycardia. Conduction through
ventricles is normal unless bundle branch block present.
Rhythms originating in Atria

PAC (Arterial premature depolarization)

Occurs when an irritable focus in the atria fires before the next sinus impulse is due, can be
caused by caffeine, alcohol, nicotine.

Rate: usually within normal range

Rhythm: PAC have non compensatory pause (interval between complex before and that after the
PAC is less than two normal RR waves) because premature depolarization of atria by the PAC
also causes premature depolarization of the SA node, thus causing the SA node to ‘reset’ itself.

P wave: P waves impulse originates in a different part of atria and depolarizes them in a different
way.

PR interval: May be long depending on the prematurity of the beat. Very early PACs may find
AV junction still partially refractory and unable to conduct at a normal rate, resulting in
prolonged PR interval

QRS complex: maybe normal, aberrant (wide), or absent. If PAC occurs during refractory period
of the bundle branch or ventricle, the QRS wide. If PAC occurs early in refractory period, then
QRS absent.

Conduction: PAC travel through atria differently from sinus impulses because they originate
from a different spot. Conduction through the AV node, bundle branch, and ventricles is usually
normal unless the PAC is very early.
Wandering arterial pacemaker

WAP refers to rhythms that exhibit varying P wave morphology as the site of impulse formation
shifts from the SA node to various sites in the atria to the AV junction and back. Arrhythmias
occurs when 2 or more supraventricular pacemakers compete with each other for control of the
heart.

Rate:60-100 beats per min

Rhythm: irregular

P wave: Exhibit varying shapes (upright, flat , inverted, notched) as impulses originate
indifferent parts of the atria or junction and as atrial fusion occurs.

PR interval: May vary depending on proximity of the pacemaker to the AV node

QRS: normal

Conduction: conduction through the bundle branches and ventricles is usually normal

Multifocal atrial tachycardia(MAT)

MAT is rapid firing of several ectopic atrial foci at a rate faster than 100 beats per min. Most
commonly seen in elderly patients.

Rate: 100-130 beats per min

Rhythm: irregular

P wave: at least 3 different P waves are seen. They usually precede each QRS complex, but some
may be blocked in the AV node.

PR interval: depending on proximity of each ectopic atrial focus to the AV node and prematurity
of atrial impulses

QRS compelx: normal

Conduction: Usually normal through AV node and ventricles. Aberrant ventricular conduction
may occur if an impulse is conducted into the ventricles while they are partially refractory.
Atrial tachycardia

It is a rapid atrial rhythm at a rate of 100-250 beats per min, that arises from a single site within
the right or left atrium. It may be due to rapid firing ectopic focus(automaticity), atrial micro
reentry circuit that allows an impulse to travel rapidly and repeatedly around a pathway in the
atria, or after load depolarization resulting in triggered atrial tachycardia.

Rate: atrial rate 100-250 beats per min

Rhythm: regular unless block at AV node

P wave: ectopid P wave. Occurs in second half of tachycardia (RR interval).

PR interval: difficult to measure because of hidden P waves

QRS complex: may be wide if aberrant conduction is present

Conduction: in atrial tachycardia with block, some atrial impulses do not conduct into the
ventricles. Aberrant ventricular conduction may occur.
Arterial flutter

It is an organized atrial rhythm in which the atria are depolarized at rates of 250-440 tiems
permin. Classic or typical atrial flutter (type I) is due to fixed re entry circuit in the right atrium
around which the impules circulates in a counter clockwise direction. Occasionally, the impulse
reverses direction and circulates in a clockwise direction, resulting in positive flutter wave in
Lead II and III, is called atypical flutter.

Rate: atrial rate varies between 250-450 beats per min.

Rhythm: atrial rhythm is regular. Ventricular rhythm may be regular or irregular because of
varying AV block.

P wave: flutter waves are seen, characterized by regular, biphasic sawtooth pattern with no
isoelectric segment between waves.

PR interval: May vary in Wenckebach type pattern.

QRS complex: aberration may be present

Conduction: Normal through AV node and ventricles.

Atrial fibrillation

It is extremely rapid and disorganized pattern of depolarization in atria. Mechanisms include:

1.Rapid firing of ectopic impulses in atria.

2.single reentry circuit with variable rate and conduction in atria or pulmonary veins

3. multiple reentry circuits within the atria

Rate: 400-600 beats per min. ventricular rate varies with amount of block at the AV node.

Rhythm: irregular. Arterial fibrillation is the marked irregularity of the ventricular response
because of concealed conduction in the AV junction.

P wave: Not present. Atrial activity is chaotic, with no formed atrial impulses visible.

PR interval: No P wave

QRS complex: Aberration is common, especially faster ventricular rates

Conduction: intra arterial conduction is disorganized and irregular. Most of the impulses are
blocked in AV junction. If atrial impulse reaches bundle branch system during its refractory
period, aberrant intraventricular conduction can occur.

Supra ventricular tachycardia:

SVT can be applied to any rhythm at rate faster than 100 beats per min. SVT is an umbrella term
for rhythm that originates above ventricle (resulting in narrow QRS complex)

Rate: greater than 100-280 beats per min

Rhythm: regular

P wave: not visible

PR interval: no measurable P

QRS complex: narrow, may be wide if aberrant ventricular conduction occurs.

Conduction: conduction through atria varies depending on mechanism of tachycardia.

Conduction is normal unless bundle branch block present.
Rhythm originating in AV junction:

Premature junctional complexes:

It is due to irritable focus in AV junction. It can be due to MI, CAD disrupting blood flow to the
AV junction.

Rates: 60-100 beats per min

Rhythm: irregular because of early beats

P wave: occur before, during or after the QRS complex and are inverted in inferior leads
(II,III,aVF)

PR interval: short, 0.10 sec or less when P wave precede the QRS complex

QRS complex: usually normal but may be aberrant if PJC occurs early and conducts into the
ventricle during the refractory period of bundle branch

Conduction: retrograde through the atria, usually normal through ventricles

Junctional rhythm and junctional tachycardia:

It can occur if the SA node rate falls below the automatic rate of an AV junctional pacemaker or
in presence of digitalis toxicity. Junctional rhythms commonly occur after inferior wall MI
because the blood supply to the SA node and the AV junction is disrupted, and junctional
tachycardia is common in children undergoing surgical repair of congenital defects.

Rate: usually 40-60 beats per min. accelerated junctional rhythm 60-100 beats per min,
junctional tachycardia 100-250 beats per min

Rhythm: regular

P wave: may precede or follow QRS

PR interval: short 0.10 sec or less

QRS complex: normal

Conduction: retrograde through atria, normal through ventricles.

Rhythms originating in ventricles

Premature ventricular complexes:

PVC are caused by pre mature depolarization of cells in the ventricular myocardium or Purkinje
system due to enhanced normal automaticity or abnormal automaticity, reentry in ventricles, or
after depolarization. It can be caused by hypoxia, MI, hypokalemia, acidosis, digitalis toxicity,
caffeine, alcohol, etc

Rate: 60-100 beats per min

Rhythm: irregular because of early beats

P wave: it may follow PVC because of retrograde conduction from the ventricle backward
through the atria.

PR interval: If P wave happens, by coincidence, to precede a PVC, the PR interval is short

QRS complex: wide and bizarre, usually greater than 0.12 sec. May vary in morphology if PVC
originates from more than 2 focus in ventricles.

Conduction: impulses originating in the ventricles conduct through ventricular myocardium from
muscle cell to muscle cell rather than through purkinje fibre, resulting in wide QRS complex.
Some PVC may conduct retrograde into the atria, resulting in inverted P wave that follows the
PVC.

Accelerated idioventricular rhythm:

It occurs when an ectopic focus in ventricles fires at a rate of 50-100 beats per min. It commonly
occurs in the presence of inferior MI and during reperfusion with thrombolytic therapy, when the
rate of SA node slows below rate of the latent ventricular pacemaker.

Rate: 50-100 beats per min

Rhythm: regular

P wave: may be seen but dissociated from QRS. If retrograde conduction from ventricles to the
atria occurs, P waves follows the QRS complex

PR interval: not present

QRS complex: wide and Bizarre

Conduction: if sinus rhythm is the basic rhythm, atrial conduction is normal. Impulses
originating in the ventricles conduct through the ventricular myocardium by cell to cell
conduction resulting in wide QRS complex.
Ventricular tachycardia:

VT is rapid ventricular rhythm due to reentry in ventricle, although automaticity of an ectopic

focus and after depoloarization may also be its mechanism. It can be classified according to,

1.duration: non sustained lasts less than 30 sec and , sustained : last more than 30 sec

2. Morphology: ECG appearance of QRS complex-

Monomorphic: QRS complex have the same shape during tachycardia

Polymorphic: QRS complex vary randomly in shape

Bidirectional: alternating upright and negative QRS complexes during tachycardia.

The most common cause of VT is CHD, including acute ischemia and MI, prior MI, chronic
coronary disease, cardiomyopathy, valvular heart disease, right ventricular dysplasia, cardiac
surgery.

Rate: ventricular rate 100-220 beats per min

Rhythm: regular or slightly irregular

P wave: often dissociated from QRS complex. If sinus rhythm is the underlying basic rhythm,
regular P wave may be seen but are not related to QRS complex. P wave is usually buried in
QRS complex and T wave.

PR interval: not measurable because of dissociation of P wave form QRS complex

Conduction: impulse originating in one ventricle and spreads by muscle cell to cell conduction
through both ventricles. There may be retrograde conduction through the atria, but oftenr the SA
node continue to fire regularly and depolarizes the atria normally.
Ventricular flutter

It is similar to ventricular tachycardia but is faster. Hemodynamically, it is more dangerous

because there is no cardiac output.

Rate: ventricular rate 220-400 beats per min

Rhythm: regular

P wave: not seen

PR interval: none measurable

QRS complex: very wide, regular, sine wave type pattern

Conduction: originates in ventricle and spreads through muscle cell to cell conduction, resulting
in very wide, bizarre complexes.

Ventricular asystole

It is the absence of any ventricular rhythm, no QRS complex, no pulse, no cardiac output. It is
also called ventricular standstill, arterial activity still present but no ventricular activity

Rate: none

Rhythm: none

P wave: may be present if SA node is functioning

PR interval: none

QRS complex: none

Conduction: if SA node functioning atrial function normal, but no ventricular activity

CONDUCTION ABNORMALITIES

One of the main function of AV node is to block rapid atrial impulses to prevent dangerously fast
ventricular rates in response to rapid atrial rhythms such as rapid atrial tachycardia, atrial flutter
or atrial fibrillation.

Classification:

First degree AV block

Second degree AV block

Type I

Type II

2:1 conduction (either Type I or Type II)

High grade AV block

Third degree AV block

First degree AV block:

It is prolonged AV conduction time of supraventricular impulses into ventricles. This delay

occurs in AV node, and all impulses conduct to ventricles, but with delayed conduction time.

Rate: can occur at any sinus rate, usually 60-100 beats per min

Rhythm: regular

P wave: Normal, precedes QRS

PR interval: greater than 0.20 sec

QRS complex: normal unless bundle branch block exists

Conduction: normal through atria, delayed through AV node, normal through ventricles.
Second degree AV block:

It occurs when one atrial impulse at a time fails to be conducted to the ventricles. It is divided in
to 2 catagories:

Type I: occurs in AV node

Type II: occurs below AV node in bundle of His or bundle branch system
Type I (Wenckebach) or (Mobitz I):

It is a progressive increase in conduction times of consecutive atrial impulses into the ventricles
until one impulse fails to conduct or is ‘dropped’. On ECG it appears as gradual lengthening PR
interval until one P wave fails to conduct and is not followed by QRS complex, resulting in a
pause after which the cycle repeats itself.

Rate: can occur at any sinus or atrial rate

Rhythm: irregular unless 2:1 conduction present. Overall appearance of rhythm demonstrates
group beating.

P wave: normal. Some P waves may not be conducted, but only one at a time fails to conduct

PR interval: Gradually lengthens in consecutive beat. The PR interval preveding the pause is
longer than that following the pause.

QRS complex: normal unless there is associated bundle branch block

Conduction: normal through atria. Progressively delayed through AV node until impulse fails to
conduct. Venticular conduction is normal. 6:5 conduction means, every sixth P wave resulted in
five QRS complex, or every 6th P wave was blocked.

Type II (Mobitz II)

It is sudden failure of conduction of an atrial impulse to ventricles without progressive increase

in conduction time of consecutive P wave. It occurs below AV node and usually associated with
bundle branch block, therefore the dropped beats are usually a manifestation of bilateral bundle
branch block. In this form of block, there is no progressive increase in PR interval before the
blocked P wave.

Rate: can occur at any basic rate

Rhythm: irregular due to blocked beats unless 2:1 conduction is present

P wave: regular and precede each QRS. Periodically , P wave is not followed by QRS complex

PR interval: constant before all conducted beats. PR interval preceding the pause is the sameas
that after the pause.

QRS complex: almost always wide because of associated bundle branch block

Conduction: normal through atria and AV node but intermittently blocked at bundle branch
system and fails to reach ventricles. Conduction through ventricle is abnormally slow because of
associated bundle branch block.
2:1 conduction:

It is a failure of conduction of every other atrial impulse. Because only one P wave at a time is
blocked it is by definition a second degree block. If the lesion causing conduction failure is in the
AV node, it is type I block and if it is below AV node it is type II block.

PR interval: often longer than normal more than 0.20 sec in type I and normal type II. Also, the
PR in type I is normal on conduction beats because the blocked P wave allows enough time for
the AV node to recover so that it is able to conduct every other P wave with a normal PR
interval.

QRS complex: narrow in type I and almost wide in type II. Exception can occur in type I when
there is a coincidental bundle branch block that widens the QRS and in type II when the block is
in the bundle, resulting in narrow QRS.

Third degree AV block:

It is complete failure of conduction of all atria impulses to the ventricles. There is complete AV
dissociation, the atria are usually under the control of the SA node, although complete block can
occur with any atrial arrhythmia and either a junctional or ventricular pacemaker controls the
ventricles. The ventricular rate is usually less than 45 beats per min, a faster rate could indicate
an accelerated junctional or ventricular rhythm that interferes with conduction from the atria into
the ventricles by causing physiologic refractoriness in the conduction system, thus causing a
physiologic failure of conduction system function of complete AV block.

Rate: atrial rate is normal when sinus rhythm is present, a ventricular rate is usually less than 45
beats per min

Rhythm: regular

P wave: normal but dissociated form QRS complex

PR interval: NO consistency in PR interval because there is no relationship between P wave and

QRS

QRS complex: normal if ventricles controlled by a junctional pacemaker, wide if controlled by a

ventricular pacemaker.

Conduction: normal through the atria. All impulses are blocked at the AV node or in the bundle
branches so there is no conduction to the ventricles. Conduction through the ventricles is slow is
ventricular escape rhythm occurs
Complex arrhythmias and conduction disturbances

Pre excitation syndrome:

It refers to early activation of the ventricular myocardium by supraventricular impulses entering

the ventricles through the accessory pathway. These pathways are capable of carrying the
impulse directly into the ventricles, bypassing all or part of the normal AV conduction system.
the most common pathway is an AV bypass tract, the bundle of Kent, which originates in the
atrium and inserts in the ventricle, bypassing the entire conduction system. Other accessory
pathway include AV nodal bypass tract which carry the impulse form the atrium into the distal or
compact AV node or from the atrium to the bundle of HIS, and nodo ventricular connections
which originate in or below the AV node and carry the impulse directly into the ventricular
myocardium.

Wolf Parkinson White syndrome:

During sinus rhythm, the ventricle is stimulated prematurely through the Kent bundle while the
impulse is simultaneously conducted through the normal His-Purkinje conduction system.
impulses travel faster down the accessory pathway because they bypass the normal AV node
delay. Part of the ventricle receives the impulse early through the accessory pathway and begins
to depolarize before the rest of the ventricle is deactivated through the His purkinje system.
Premature ventricular stimulation forms a characteristic slurring of the initial portion of the QRS
complex called the delta wave. The remainder of the QRS is normal through the Purkinje system.

A supraventricular impulse conducts to the ventricle through the normal AV conduction system
and through the accessory pathway simultaneously. The impulse reaches the ventricle first
through the accessory pathway and pre excites it, causing a delta wave and short PR interval on
ECG.

The degree of pre-excitation can vary depending on the relative rate of conduction through the
bypass connection and AV node, and it determines the length of the PR interval and the size of
the delta wave.

Mechanism of pre-excitation:

a. Pre excitation
b. Maximal pre excitation
c. Concealed accessory pathway.

Maximal pre excitation occurs when the ventricles are activated totally by the accessory
pathway, resulting in an extremely short PR interval and uniformly wide QRS complex.
A concealed pathway is present when the ventricles are depolarized exclusively through the
normal conduction system even though a bypass tract exists, thus the PR interval and QRS
complex are normal because the accessory pathway is not being used for ante retrograde
conduction.

WPW is clinically significant because the presence of two pathways provide the opportunity for
reentry of the impulse and may result in rapid reentrant tachycardia.

ECG characteristics of AF with ante retrograde conduction through accessory pathway is:

Rate: ventricular rates up to 300 beats per min

Rhythm: irregular. Often appears a group of very short RR intervals alternating with groups of
longer RR intervals. The longest RR intervals are often more than twice the shortest RR interval

P wave: none, because atria are fibrillating

PR interval: none

QRS complex: wide, bizarre due to abnormal depolarization of ventricles through accessory
pathway

Conduction: disorganized and chaotic through atria. Atrial impulses conduct into ventricles
through accessory pathway, resulting in muscle cell to cell conduction through ventricles.
Short QT syndrome:

It is a genetic disorder in which patients have a corrected QT interval <340 milliseconds,

sometimes with a measured QT interval as short as 210 milliseconds. The most common
prensetation is cardiac arrest, which can be seen as early as first year of life. Syncope is also a
presenting symptom due to self terminating runs of Polymorphic ventricular tachycardia. SQTS
is also due to very short refractory period in atria.

Torsades de Pointes:

It means ‘twisting of points’ and describes a special type of Polymorphic ventricular tachycardia
in which the QRS complex displayrs continuously changing morphologies and seems to twist
around an imaginary line, often resembling a VT. The underlying cause of this type of VT is
delayed ventricular repolarization, which manifests on ECG as abnormal prolonged QT interval,
large U wave after T or merging with T wave, wide notched, or biphasic T wave and often
associated with T wave alterans.

ECG findings of Torsades de Pointes:

1. Markedly prolonged QT intervals with wide T-U waves

2. Initiation of the arrhythmia by an R on T PVC with a long coupling interval
3. Wide, bizarre, multi form QRS complex that change direction frequently, appearing to
twist around the isoelectric line.

.
Medical Management:

Management of atrial fibrillation and atrial flutter:

Class I: 1. Control of rate using either beta blocker (metaprolol, propranolol) or

nondihydropyridine (verapamil, diltiazem)

2. Administration of AV nodal blocking agents for rate control in post operative AF

3. In absence of preexcitation, IV beta blockers, or nondihydropyridine to slow

ventricular response

4. IV digoxin or amiodarone for those patients with absent accessory pathway

5. Oral digoxin to control heart rate at rest

Class IIa: 1. Combination of digoxin and either beta blocker or nondihydropyridine to control
heart rate at rest/ exercise. Caution for Bradycardia

2. Ablation therapy (Cardiac ablation is a procedure to scar or destroy tissue in

your heart that's allowing incorrect electrical signals to cause an abnormal heart rhythm
by a catheter), when pharmacological intervention insufficient.

3. IV amiodarone

4.IV procainamide in patients with accessory pathway and when cardioversion is not
necessary.

5. IV digitalis to improve LV function in MI or Heart Failure

Class IIb: 1. Oral amiodarone when ventricular rate cannot be adequately controlled
using beta blocker, nondihydropyridine, digoxin

2.Ablation of the AV node when rate cannot be controlled with pharmacological therapy.

Prevention of thrombus formation:

Risk factors of thrombus formation include (age>75 years, HTN, HF, impaired LV Function,
LVEF<30%, DM)

1. Antithrombotic therapy for all patients with AF

2. For patients without mechanical heart valve, oral anticoagulants with Vit K antagonist
3. Therapeutic target of INR is 2.0-3.0, should be determined weekly
4. For pharmacological cardioversion administer flecainide, dofetilide, prepafenone or
ibutilide
5. Immediate electric (direct current
Management for monomorphic VT: Electric cardioversion, calcium channel blockers, IV
procainamide, IV amiodarone, IV lidocaine.

Management for polymorphic VT: Electric cardioversion, IV beta blockers, IV amiodarone, IV

lidocaine

Acute management of tachycardia:

For narrow SVT with BBB: vagal maneuver(valsalva), adenosis, verapamil, beta blockers,
digoxin

For pre excited SVT: procainamide, electric cardioversion

Wide QRS tachycardia: amiodarone, sotalol, procainamide, lidocaine, adenosine

Accessory pathway mediated arrhythmia (Wolf Parkinson white syndrome): catheter ablation,
vagal maneuver, pill in pocket (verapramil, diltiazem, beta blockers), sotalol, amiodarone.

Management for Torsades de Pointes: withdrawal of any offending drugs and correction of
electrolyte abnormalities, IV magnesium, long term pacing in combination with beta blockers,
potassium repletion therapy, IV lidocaine.
Nursing interventions:

Monitoring and managing dysrhythmias:

The nurse regularly evaluates the patients BP, pulse rate and rhythm, rate and depth of
respiration and breath sounds to determine dysrhythmias hemodynamic effect. The nurse also
asks the patient about episodes of lightheadedness, dizziness, or fainting as part of the ongoing
assessment. If patient is hospitalized then ECG is taken, continuous cardiac monitoring is done.

Control over occurrence of dysrhythmias is achieved with anti arrhythmic medications.

The nurse also conducts a 6 min walk test to identify patients ventricular rate and response to
exercise and physical activity.

The nurse assesses factors contributing to dysrhythmias such as oxygen deficit, acid base and
electrolyte imbalance, caffeine, non adherence to medication regimen.

Minimizing anxiety:

When the patient experiences an episode of dysrhythmias, the nurse stays with the client and
provides assurance of safety and security while maintaining a calm and reassuring attitude. This
assists in reducing anxiety and fosters a trusting relationship. The nurse also encourages
verbalization of fears and feeling, providing positive and empathetic statements, assisting the
patient to recognize feelings of anxiety, anger, or sadness.

Promoting home and community based care

Teaching patient self care:

The nurse provides client information and health education regarding the disease condition, its
specific manifestations in terms that are understandable and in a manner that is not frightening or
threatening.

The nurse teaches about self monitoring of counting heart rate, blood pressure.

The nurse informs patient to notify the health care provider about any development of
complications if they occur.