Pathophysiology of Cardiac Rhytm and conduction disturbances.

PHD. MD.Maria Vrabete

Content. (Examination subjects)

1. Definition of normal electrical activity of heart.

2. Basic mechanims of cardiac rhytm and conduction disturbances
occurrence: reentry
3. Pathophysiology
4. Cardiac rhytm disorders.
5. Cardiac conduction disorders.
6. Preexcitation Syndrome.
7.Criteria BRUGADA to diagnose Ventricular Tachycardia (V.T)

1. Definition of normal electrical activity of heart.

The electrical impulses generated and spread by myocytes with unique
electrical properties trigger a sequence of organized myocardial contractions.
1.1. Rhytm disturbances or arrhythmias and conduction disorders are
caused by abnormalities in the generation or conduction of these electrical
impulses or both.
1.2. Causes of rhytm disturbances genesiss.
-congenital abnormalities of structure (eg, accessory atrioventricular
connection)
-function (eg, hereditary ion channelopathies),
-systemic factors that can cause or contribute to a rhythm disturbance include
-electrolyte abnormalities (particularly low potassium or magnesium),
-hypoxia,
-hormonal imbalances (eg, hypothyroidism, hyperthyroidism),
-drugs

2. Basic mechanims of Cardiac Rhytm and conduction disturbances

occurrence
Reentry
Conduction blocks impaired conduction leads to a phenomenon termed
"reentry."
This mechanism may account for most tachyarrhythmias.
2.1. Mechanism of reentry.
In normal tissue , if a single Purkinje fiber forms two branches (1 & 2), or A,
B) the action potential will travel down each branch. An electrode (*) in a side

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branch off of branch 1 would record single, normal action potentials as they
are conducted down branch 1 and into the side branch. If branches 1 & 2 are
connected together by a common, connecting pathway (branch 3), the action
potentials that travel into branch 3 will cancel each other out.
2.2. Reentry Model.
Reentry can take place within
-a small local region within the heart or
-as global reentry. between the atria and ventricles.

Unidirectional block within a conducting pathway, critical timing the length

of the effective refractory period of the normal tissue.
A model for reentry is shown fig.1.

2.2. Conditions to develop the reentry mechanism (fig 1)

Reentry can occur if one zone, has a unidirectional block (gray zone).
An action potential will travel down the branch 1, into the common distal path
(branch 3), and then travel retrograde through the unidirectional block in

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branch 2 (blue line). (In such a block, impulses cannot travel orthograde, but
retrograde (from branch 3 into branch 2).
-Within the block, the conduction velocity is reduced because of
depolarization.
When the action potential finds the tissue excitable, it will reenter the branch
1 and will continue by traveling down..
-If the action potential exits in branch 2 and finds the tissue unexcitable
(within its effective refractory period), then the action potential will die.
-Timing is critical: action potential must find excitable tissue in order to
continue to propagate.
-If it can re-excite the tissue, a circular (counterclockwise in this case)
pathway of high frequency impulses (i.e., a tachyarrhythmia) will become the
source of action potentials that spread throughout a region of the heart (e.g.,
ventricle) or the entire heart.
2.2.1. Local reentry
-Local sites of reentry may involve a small region within the ventricle or
atrium and can precipitate ventricular or atrial tachyarrhythmias.
Changes in autonomic nerve function can significantly affect reentry
mechanisms, either precipitating or terminating reentry.
Conduction velocity and effective refractory period can
-precipitate reentry
-abolish reentry
2.2.2. Global Reentry
The AV node is normally the only electrical pathway connecting the atria and
ventricles is normally comprised of a bundle of conducting fibers. Some
people have different conduction velocities and refractory periods in these
multiple pathways within the AV node, which can cause reentry within the
AV node. Global reentry between the atria and ventricles may involve
accessory conduction pathways ("bypass tracts") such as the bundle of Kent.
AV nodal reentry is a common cause of
-paroxysmal supraventricular tachycardias, with impulses traveling from the
atria to the ventricles and then from the ventricles back to the atria through
the AV node.
Reentrant impulses, in atria stimulate atrial activity, and they activate the
ventricul so there is still a one-to-one correspondence between the atrial and
ventricular rates, and therefore the rhythm is termed "supraventricular."
The impulse is traveling through the accessory pathway (bundle of Kent),
depolarizing ventricular tissue, then traveling backwards (retrograde) through
the AV node to re-excite the atrial tissue and establishing a counter-clockwise
global reentry

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Under certain conditions, typically precipitated by a premature beat, reentry
can cause continuous circulation of an activation wavefront, causing a
tachyarrhythmia (see Figure: Initiation of an atrioventricular nodal reentry
tachycardia.). Normally, reentry is prevented by tissue refractoriness
following stimulation. However, 3 conditions favor reentry: shortening of
tissue refractoriness (eg, by sympathetic stimulation), lengthening of the
conduction pathway (eg, by hypertrophy or abnormal conduction pathways),
and slowing of impulse conduction (eg, by ischemia).
2.2.3. The reentry rhytm
-supraventricular tachyarrhythmias
-Wolff-Parkinson
-AV nodal reentry tachycardia.
These types of tachyarrhythmias are often paroxysmal in nature (sudden onset
and disappearance) because the conditions necessary to establish and maintain
reentry are altered by normal variations in conduction velocity and
refractoriness.
Drugs that depress AV nodal conduction: adenosine, beta-blockers and
calcium channel blockers, are very effective in terminating these reentry
supraventricular tachycardias.

3. Pathophysiology
Rhythm disturbances result from abnormalities of impulse formation, impulse
conduction, or both.
3.1. Symptoms and Signs
Arrhythmia and conduction disturbances may be asymptomatic or cause
palpitations (sensation of skipped beats or rapid or forceful beats), symptoms
of hemodynamic compromise (eg, dyspnea, chest discomfort, presyncope,
syncope), or cardiac arrest. Occasionally, polyuria results from release of
atrial natriuretic peptide during prolonged supraventricular tachycardias
(SVTs).
Palpation of pulse and cardiac auscultation can determine ventricular rate and
its regularity or irregularity. Examination of the jugular venous pulse waves
may help in the diagnosis of AV blocks and tachyarrhythmias. For example,
in complete AV block, the atria intermittently contract when the AV valves
are closed, producing large a (cannon) waves in the jugular venous pulse.
Other physical findings of arrhythmias are few.
3.2. ECG
Requires a 12-lead ECG to establish the relationship between symptoms and
rhythm.

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The key diagnostic features are rate of atrial activation, rate and regularity of
ventricular activation, and the relationship between the two. irregular
activation signals are classified as
3.2.1. Regularly irregular
Regular irregularity is intermittent irregularity: regular rhythm (
-premature beats or
-recurrent relationships between groups of beats: bigeminism, trigeminism.
3.2.1.1. A narrow QRS complex (< 0.12 sec) indicates a supraventricular
origin (above the His bundle bifurcation).
3.2.1.2. A wide QRS complex (≥ 0.12 sec) indicates a ventricular origin
(below the His bundle bifurcation) or a supraventricular rhythm conducted
with an intraventricular conduction defect or with ventricular preexcitation in
the Wolff-Parkinson-White syndrome.
3.2.2.Irregularly irregular (no detectable pattern).
When the QRS rhythm is irregular, P waves usually outnumber QRS
complexes; some P waves produce QRS complexes, but some do not
(indicating 2nd-degree AV block. An irregular QRS rhythm with a 1:1
relationship between P waves and the following QRS complexes usually
indicates sinus arrhythmia with gradual acceleration and deceleration of the
sinus rate (if P waves are normal).
Pauses in an otherwise regular QRS rhythm may be caused by blocked P
waves (an abnormal P wave can usually be discerned just after the preceding
T wave or distorting the morphology of the preceding T wave), sinus arrest,
or sinus exit block, as well as by 2nd-degree AV block.

From A practical approach!!! Scann

4. Cardiac rhytm disorders.

4.1. NSA: Sinus tachycardia, S.bradicardia, arrhytmia sinoatrila block,

sinus arrest,sick sinus syndrome.
4.2. Atria: Atrial arrhytmias: premature atrial beat , paroxismal atrial
tachycardia, atrial flutter, atrila fibrilation.
4.3. NAV (Jonction) Junctional arrhytmias: junctional escape beats and
thytm, accelarated junctional rhytm, nonparoxysmal junctional
tachycardia.
4.4.Ventricular arrhytmias: premature contractions, venbtricular
tachycardia, ventricular fibtilation
5. Cardiac conduction disorders.

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5.1.Atrioventricular blocks.
5.2.Intraventricular blocks
5.2.1. Right Bundle Brench block (RBBB)
5.2.2. Left Bundle Brench (LBBB)
5.2.3 Left anterior hemiblock (antero-superior fascicular block)
5.2.4. Left posterior hemiblock (postero-inferior fascicular block)
5.2.5. Bifascicular block.
6. Preexcitation Syndrome.
6.1. Wolf-Parkinson White syndrome (accessory pathway Kent bundle).
6.2. Lown-Ganong Levine (LGL) syndrome accessory bundle James.
6.3.Preexicitation syndrome determined by presence of Mahaim fibers.

7.Criteria BRUGADA to diagnose Ventricular Tachycardia (V.T)

I. Presence of dissociation atrio-ventricular (AV)

That means:
Independent P waves / QRS.
Capture beats
Fusion beats
YES NO.
Dg. VT. Is there a RS in any precordial lead?
II. NO YES
Dg. VT Is QRS onset to nadir
QS wave 100 msec. in
any precordial lead.
III. YES NO
Dg.VT Are there
morphologic for
VT criteria in
both V1,V6.
IV. YES NO.
VT No
supraventricular
tachycardia.

Treatment
Treatment of cause
Sometimes antiarrhythmic drugs, pacemakers, cardioversion-defibrillation,
catheter ablation, or electrosurgery

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The treatment varies and is guided by symptoms and risks of the arrhythmia.
-Asymptomatic arrhythmias without serious risks do not require treatment
even if they worsen.
-Symptomatic arrhythmias may require treatment to improve quality of life.
Potentially life-threatening arrhythmias require treatment.
Treatment with
-antiarrhythmic therapy, including antiarrhythmic drugs,
-cardioversion-defibrillation,implantable
-cardioverter-defibrillators (ICDs),
-pacemakers (and a special form of pacing, cardiac resynchronization
therapy), or a combination, is used.
Patients with arrhythmias that have caused or are likely to cause symptoms of
hemodynamic compromise may have to be restricted from driving until
response to treatment has been assessed.
Surgery for cardiac arrhythmias
Surgery to remove a focus of a tachyarrhythmia is becoming less necessary
most commonly when patients with AF require valve replacement or repair or
when patients with VT require revascularization or resection of a left
ventricular aneurysm.

Desen de mână, la mine

Re entry. (Alt desen)

I Two Pathways connect the same points.
Pathway A has a slow conduction and a short refractory period.
Pathway B conducts normally and has a longer refractory period

II A premature impulse finds pathways B refractory and is blocked but it

can be conducted on pathway A because its refractory period is shorter. On
arriving at 2, the impăulse continues forward and retropgrade up pathway B
where isi is blocked by refractory tissue at 3. A premature suăraventricular
beat will an increased PR interval results.

III.If conduction over pathway A is sufficiently slow, a premature impulse

may continue impulse way continue retrograde all the way up pathway B
which is noe past its refractory period. If pathway A is also past its
refractory period the impulse may reenter pathway A and continue to circle
sending an impulse each cycle to the ventricle (4) and retrograde to the
atrium (5) producing a sustained reentrant tachycardia.

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Recapitulation..
Anatomy of the Cardiac Conduction System
At the junction of the superior vena cava and high lateral right atrium is a cluster of cells that generates the
initial electrical impulse of each normal heart beat, called the sinoatrial (SA) or sinus node. Electrical
discharge of these pacemaker cells stimulates adjacent cells, leading to stimulation of successive regions of
the heart in an orderly sequence. Impulses are transmitted through the atria to the atrioventricular (AV) node
via preferentially conducting internodal tracts and unspecialized atrial myocytes. The AV node is located on
the right side of the interatrial septum. It has a slow conduction velocity and thus delays impulse transmission.
AV nodal transmission time is heart-rate–dependent and is modulated by autonomic tone and circulating
catecholamines to maximize cardiac output at any given atrial rate.
The atria are electrically insulated from the ventricles by the annulus fibrosus except in the anteroseptal
region. There, the bundle of His, the continuation of the AV node, enters the top of the interventricular
septum, where it bifurcates into the left and right bundle branches, which terminate in Purkinje fibers. The
right bundle branch conducts impulses to the anterior and apical endocardial regions of the right ventricle.
The left bundle branch fans out over the left side of the interventricular septum. Its anterior portion (left
anterior hemifascicle) and its posterior portion (left posterior hemifascicle) stimulate the left side of the
interventricular septum, which is the first part of the ventricles to be electrically activated. Thus, the
interventricular septum depolarizes left to right, followed by near-simultaneous activation of both ventricles
from the endocardial surface through the ventricular walls to the epicardial surface.
Cardiac Physiology
An understanding of normal cardiac physiology is essential before rhythm disturbances can be understood.
Electrophysiology
The passage of ions across the myocyte cell membrane is regulated through specific ion channels that cause
cyclical depolarization and repolarization of the cell, called an action potential. The action potential of a

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working myocyte begins when the cell is depolarized from its diastolic −90 mV transmembrane potential to
a potential of about −50 mV. At this threshold potential, voltage-dependent fast sodium channels open,
causing rapid depolarization mediated by sodium influx down its steep concentration gradient. The fast
sodium channel is rapidly inactivated and sodium influx stops, but other time- and voltage-dependent ion
channels open, allowing calcium to enter through slow calcium channels (a depolarizing event) and potassium
to leave through potassium channels (a repolarizing event).
At first, these 2 processes are balanced, maintaining a positive transmembrane potential and prolonging the
plateau phase of the action potential. During this phase, calcium entering the cell is responsible for
electromechanical coupling and myocyte contraction. Eventually, calcium influx ceases, and potassium
efflux increases, causing rapid repolarization of the cell back to the −90 mV resting transmembrane potential.
While depolarized, the cell is resistant (refractory) to a subsequent depolarizing event. Initially, a subsequent
depolarization is not possible (absolute refractory period), and after partial but incomplete repolarization, a
subsequent depolarization is possible but occurs slowly (relative refractory period).
There are 2 general types of cardiac tissue:
Fast-channel tissues
Working atrial and ventricular myocytes, His-Purkinje system) have a high density of fast sodium channels
and action potentials characterized by little or no spontaneous diastolic depolarization (and thus very slow
rates of pacemaker activity), very rapid initial depolarization rates (and thus rapid conduction velocity), and
loss of refractoriness coincident with repolarization (and thus short refractory periods and the ability to
conduct repetitive impulses at high frequencies).
Slow-channel tissues (SA and AV nodes) have a low density of fast sodium channels and action potentials
characterized by more rapid spontaneous diastolic depolarization (and thus more rapid rates of pacemaker
activity), slow initial depolarization rates (and thus slow conduction velocity), and loss of refractoriness that
is delayed after repolarization (and thus long refractory periods and the inability to conduct repetitive
impulses at high frequencies).
Normally, the SA node has the most rapid rate of spontaneous diastolic depolarization, so its cells produce
spontaneous action potentials at a higher frequency than other tissues. Thus, the SA node is the dominant
automatic tissue (pacemaker) in a normal heart. If the SA node does not produce impulses, tissue with
the next highest automaticity rate, typically the AV node, functions as the pacemaker. Sympathetic
stimulation increases the discharge frequency of pacemaker tissue, and parasympathetic stimulation
decreases it.

Normal cardiac rhythm

The resting sinus heart rate in adults is usually 60 to 100 beats/min. Slower rates (sinus bradycardia)
occur in young people, particularly athletes, and during sleep. Faster rates (sinus tachycardia) occur with
exercise, illness, or emotion through sympathetic neural and circulating catecholamine drive. Normally, a
marked diurnal variation in heart rate occurs, with lowest rates just before early morning awakening. A slight
increase in rate during inspiration with a decrease in rate during expiration (respiratory sinus arrhythmia) is
also normal; it is mediated by oscillations in vagal tone and is particularly common among healthy young
people. The oscillations lessen but do not entirely disappear with age. Absolute regularity of the sinus rhythm
rate is pathologic and occurs in patients with autonomic denervation (eg, in advanced diabetes) or with severe
heart failure.

Most cardiac electrical activity is represented on the ECG (see Figure: Diagram of the cardiac cycle,
showing pressure curves of the cardiac chambers, heart sounds, jugular pulse wave, and the ECG.), although
SA node, AV node, and His-Purkinje depolarization does not involve enough tissue to be detected. The P
wave represents atrial depolarization. The QRS complex represents ventricular depolarization, and the T
wave represents ventricular repolarization.

The PR interval (from the beginning of the P wave to the beginning of the QRS complex) is the time from
the beginning of atrial activation to the beginning of ventricular activation. Much of this interval reflects
slowing of impulse transmission in the AV node. The R-R interval (time between 2 QRS complexes)
represents the ventricular rate. The QT interval (from the beginning of the QRS complex to the end of the T
wave) represents the duration of ventricular depolarization. Normal values for the QT interval are slightly
longer in women; they are also longer with a slower heart rate. The QT interval is corrected (QTc) for
influence of heart rate. The most common formula (all intervals in sec) is

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