Lecture 13 abn conduction- Pathology

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Abnormalities in Cardiac Conduction
Lecture 13
Electrophysiology
1) Cardiac cells
2) Depolarization & Repolarization
3) Action Potential
1) Cardiac cells
Two types, electrical and myocardia (working) cells.
1. Electrical cells
 Make up the conduction system of the heart
 Are distributed in an orderly fashion through the heart
 Possess specific properties
o automaticity – the ability to spontaneously generate and discharge an electrical
impulse
o excitability – the ability of the cell to respond to an electrical impulse
o conductivity – the ability to transmit an electrical impulse from one cell to the
next
2. Myocardial cells
 Make up the muscular walls of the atrium and ventricles of the heart
 Possess specific properties
o contractility – the ability of the cell to shorten and lengthen its fibers
o extensibility – the ability of the cell to stretch
2) Depolarization & Repolarization
 Cardiac cells at rest are considered polarized (+ outside, – inside) and impermeable to
sodium, potassium and calcium ions , meaning no electrical activity takes place . This is
called the resting potential.
 Electrical impulses are generated by automaticity of specialized cardiac cells

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 Once an electrical cell generates an electrical impulse, this electrical impulse causes the
opening of sodium, potassium and calcium channels in the cell membrane and the ions
cross it and causes the action potential, also called depolarization
 The movement of ions across the cell membrane through sodium, potassium and calcium
channels, is the drive that causes contraction of the cardiac cells/muscle
 Depolarization with corresponding contraction of myocardial muscle moves as a wave
through the heart
 Repolarization is the return of the ions to their previous resting state, which corresponds
with relaxation of the myocardial muscle
 Depolarization and repolarization are electrical activities which cause muscular activity
 The action potential curve shows the electrical changes in the myocardial cell during the
depolarization – repolarization cycle
 This electrical activity is what is detected on ECG, not the muscular activity

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3) Action potential
Cardiac action potentials are controlled by three types of ion channels—
 the fast sodium channels, which are responsible for the spike like onset of the action
potential;
 the slower calcium-sodium channels, which are responsible for the plateau; and
 the potassium channels, which are responsible for the repolarization phase and return of
the membrane to the resting potential.
(A) Action potential of sinoatrial (SA) and atrioventricular (AV) nodes;
(B) atrial muscle action potential;
(C) Action potential of ventricular muscle and Purkinjefibers.
Action Potential Types
 There are two main types of action potentials in the heart—the slow response and the fast
response.
 The slow response, which is initiated by the slow calcium-sodium channels, is found in
the SA node, and the conduction fibers of the AV node.
 The fast response, which is characterized by opening of the fast sodium channels, occurs
in the normal myocardial cells of the atria, the ventricles, and the Purkinje fibers.
 The fast-response cardiac cells do not normally initiate cardiac action potentials.
Instead, these impulses originate in the specialized slow-response cells of the SA node
and are conducted to the fast-response myocardial cells in the atria and ventricles, where

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they effect a change in membrane potential to the threshold level. On reaching threshold,
the voltage dependent sodium channels open to initiate the rapid upstroke of the phase 1
action potential. The amplitude and the rate of rise of phase 1 are important to the
conduction velocity of the fast response.
Phases of cardiac muscle cell action potential (fast response) Figure A
 Phase 0 – upstroke
 Opening of the fast Na+ channels, rapid depolarization of cell membrane
 is characterized by a sharp, tall upstroke of the action potential
 the cell receives an impulse from a neighboring cell and depolarizes
 during this phase the cell depolarizes and begins to contract
 Phase 1 – spike
 occurs at the peak of the action potential and signifies inactivation of the fast Na+
channels with an abrupt decrease in sodium permeability.
 contraction is in process
 the cell begins an early, rapid, partial repolarization
 Phase 2 – plateau
 It is caused primarily by the slower opening of the calcium-sodium channels,
 Ca2+ enters for actual muscle contraction
 Contraction completes, and the cell begins relaxing
 this is a prolonged phase of slow repolarization
 Phase 3 – downslope
 The slow channels close and the influx of calcium and sodium ceases.
 There is a sharp rise in K+ permeability, contributing to the rapid outward
movement of K+ during this phase and facilitating the reestablishment of the
resting membrane potential (−90 mV).
 this is the final phase of rapid repolarization

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 Phase 4 – rest
 the sodium potassium pump is activated, transporting sodium out of the cell and
moving potassium back into the cell.
 return to the rest period,
 the period between action potentials , the cell is ready to receive an electrical
stimulus
Phases of action potential for cardiac pacemaker cells (Slow response) Figure B
• Cardiac pacemaker cells (SA node) depolarize spontaneously due to a “leakiness
"of their cell membranes that allows Na+ ions to flow slowly inward.
• The slope of Phase 4 (i.e., rate of firing of pacemakers) may be influenced
directly through the actions of Catecholamines (i.e., epinephrine and
norepinephrine) increase the heart rate by increasing the slope or rate of phase 4
depolarization. Acetylcholine, which is released during vagal stimulation of the
heart, slows the heart rate by decreasing the slope of phase 4.

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Cardiac conduction Key Terms
 Heart muscle is a unique tissue in that it has the capability of both generating and
conducting electrical impulses.
 Specialized cells of the heart called pacemaker cells have the property of automaticity,
which means they can spontaneously depolarize to generate an action potential without
the need for exogenous commands.
 Threshold potential — The minimum depolarization required to initiate an action
potential.
 Conduction velocity — Rate at which electrical impulses are carried through the
myocardium; directly affected by the speed of the action potential in various cells.
Cardiac conduction system components
1. Sinoatrial (SA) node
 Located in the right atrial wall, just inferior to the entrance of the superior vena cava.
 Primary pacemaker of the heart that sets normal rate and rhythm
 Depolarizes spontaneously 60 to 100 times per minute to set the resting heart rate
 Transmits depolarization impulses to AV node via conduction bundles
2. Atrioventricular (AV) node
 Located in the posterior wall of the septum
 Receives impulses from the SA node and transmits them via the bundle of His
 through the ventricular septum
 The AV junction "surrounds" the AV node may take over as primary pacemaker if the
SA node is defective, but at a slower rate of depolarization
3. Left and right bundle branch
 Conducts electrical impulses from the AV node and bundle of His
 down the ventricular septum to the apex of the ventricles
4. Purkinje fibers
 Highly branched fibers that carry electrical impulses up through the muscle mass of the
ventricles
 May act as a tertiary pacemaker in the event of SA and AV node failure but have a very low
rate of depolarization that yields a very low cardiac output if pacing the heart.

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Electrical Signal Flow - Conduction Pathway
 Cardiac impulse originates at SA node
 Action potential spreads throughout right and left atria
 Impulse passes from atria into ventricles through AV node (only point of electrical
contact between chambers)
 Action potential briefly delayed at AV node (ensures atrial contraction precedes
ventricular contraction to allow complete ventricular filling)
 Impulse travels rapidly down interventricular septum by means of bundle of His
 Impulse rapidly disperses throughout myocardium by means of Purkinje fibers
 Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions

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Cardiac Conduction (Pacemakers)
 An impulse (action potential) that originates from the SA node at a rate of 60 - 90
beats/minute (bpm) is known as normal sinus rhythm.
 If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known as sinus
bradycardia.
 If SA nodal impulses occur at a rate exceeding 100 bpm, the consequent rapid heart rate
is sinus tachycardia. These conditions are not necessarily bad symptoms, however ,
trained athletes, for example, usually show heart rates slower than 60 bpm when not
exercising.
 If the SA node fails to initialize, the AV junction can take over as the main pacemaker of
the heart.
 The AV junction "surrounds" the AV node (the AV node is not able to initialize its own
impulses) and has a regular rate of 40 to 60 bpm.
 These "junctional" rhythms are characterized by a missing or inverted P-Wave.
 If both the SA node and the AV junction fail to initialize the electrical impulse, the
ventricles can fire the electrical impulses themselves at a rate of 15 to 40 bpm and will
have a QRS complex of greater than 120 ms.

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Refractory period
 Refractory period in excitable cells mean: Inability of the cell to respond to any stimulus
(abolishing of excitability) during a period of time.
 In cardiac muscle cells, there are absolute and relative refractory periods.
1) Absolute refractory period (ARP):or ( effective refractory period (ERP) is a period during
which the cardiac excitability is totally cancelled (cardiac muscle will not respond to any
stimulus).
 It prologs from the beginning of the depolarization phase till the end of plateau phase;
Begins from the onset of phase 0 and extends midway through phase 3(about 250-
300ms).
 This period coincides with the systole (contraction) of the cardiac muscle, so: thankful to
this absolute period another contraction would never occur except after completion of the
systole, which enables the heart to pump blood and then to relax to be filled with blood in
cardiac cycle.
2) Relative refractory period:
 is a period that follows the absolute period, and the excitability begins to recover
gradually until it reaches its normal value.
 during which a greater-than-normal stimuli can start another action potential.
 It coincides with the period of rapid repolarization following the plateau ( which occurs
in the 2nd half of phase 3)

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AV node Facts
 The AV node has 2 basic pathways which are running parallel.
 The nodal tissue itself has no pacemaker cells; the tissue surrounding it (called the
junctional tissue) contains pacemaker cells that can fire at an inherent rate of 40 – 60
beats per minute.
 One of these conducts "fast“(has a longer refractory period ) - and the other "slower“ (
has a shorter refractory period) .
 A special characteristic of the A-V bundle is the inability, except in abnormal states, of
action potentials to travel backward from the ventricles to the atria; this means the (One-
Way Conduction Through the A-V Bundle).
 This prevents re-entry of cardiac impulses by this route from the ventricles to the atria,
allowing only forward conduction (anterograde conduction) from the atria to the
ventricles.
 Conduction preferentially goes down the "fast" pathway (thereby 'blocking' and
preventing conduction down the slow pathway).
 An important property that is unique to the AV node is decremental conduction, in which
the more frequently the node is stimulated the slower it conducts. This is the property of
the AV node that prevents rapid conduction to the ventricle in cases of rapid atrial
rhythms, such as atrial fibrillation or atrial flutter.

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SA node & Ectopic pacemaker
 An ectopic pacemaker is an excitable focus outside the normally functioning SA node. It
gives rise for ectopic heartbeats.( Ectopic : out of place)
 Ectopic beats can originate in the atria, the AV junction, or the ventricles, and are named
according to their point of origin
 Ectopic heartbeats come in two general classes:
1) Premature beats: occurring before the next sinus beat is due :
a) impulses occur prematurely before the sinus node recovers enough to initiate another
beat
b) premature beats are produced by either increased automaticity, or by reentry
It may be:
 Premature ventricular contractions (PVC) or ventricular extrasystole (VES) :
 The heartbeat is initiated by Purkinje fibres in the ventricles rather than by the
sinoatrial node, the normal heartbeat initiator.
 Premature atrial contractions (PAC)
2) Escape beats: may come after an abnormally long pause or delay.
a) ectopic beats resulting from sinus node failure serve as a protective function by
initiating a cardiac impulse before prolonged cardiac standstill can occur.
b) if the sinus node fails to resume normal function, the ectopic site will assume the role
of pacemaker and sustain a cardiac rhythm; this is referred to as an escape rhythm
c) after the sinus node resumes normal function, the escape focus is suppressed
Dysrhythmias and Conduction Disorders
 A cardiac arrhythmia or dysrhythmia means abnormal rate or rhythm of the heartbeats.
 Cardiac dysrhythmias are commonly divided into two categories: supraventricular and
ventricular dysrhythmias.
 The supraventricular dysrhythmias (Above the ventricles) include those that are generated
in the SA node, atria, AV node, and junctional tissues.
 The ventricular dysrhythmias include those that are generated in the ventricular
conduction system and the ventricular muscle.
 Because the ventricles are the pumping chambers of the heart, ventricular dysrhythmias
(e.g., ventricular tachycardia and fibrillation) are the most serious in terms of immediate
life-threatening events.

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Mechanism of Bradyarrhythmias
 Abnormal impulse formation
o decrease impulse formation (Sinus bradycardia is a result of abnormally slow
automaticity)
 Abnormal impulse conduction
o conduction block (Bradycardia due to AV block is caused by abnormal
conduction within the AV node or the distal AV conduction system.
Mechanism of Tachyarrhythmia
Mechanisms generating Tachycardias include:
1) Abnormal impulse formation
1) Accelerated automaticity.
2) Triggered activity
2) Abnormal impulse conduction
 Re-entry (or circus movements) is the most common cause of Arrhythmias
1) Accelerated automaticity
 Enhanced cardiac automaticity refers to the accelerated generation of an action
potential by either normal pacemaker tissue (enhanced normal automaticity) or by
abnormal tissue within the myocardium (abnormal automaticity).
 The discharge rate of normal or abnormal pacemakers may be accelerated by drugs,
various forms of cardiac disease, or alterations of autonomic nervous system tone, 
CO2,  O2,, hypokalemia and hypocalcemia

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 Enhanced normal automaticity accounts for the occurrence of sinus tachycardia,
 while abnormal automaticity may result in various atrial or ventricular
arrhythmias, for example, an accelerated idioventricular rhythm or an ectopic atrial
tachycardia.
A) Normally, the SA node drives the heart.
B) If another potential pacemaker (e.g. the AV junction) is accelerated, it can take over
the heart and overdrive the SA node.
2) Triggered activity
 Triggered arrhythmias are a relatively rare cause of tachycardias, usually drug-
induced.
 Triggered arrhythmias are due to early or delayed after depolarizations eg,
depolarizations which occur before the next action potential of the cell.
 If the after depolarization occurs before phase 4 of the cardiac action potential, it
is called an early after depolarization (EAD). Early after depolarizations are
believed to be responsible for the ventricular tachycardia known as torsade de
pointes.
 If the after depolarization occurs during phase 4 of the cardiac action potential, it
is called a delayed after depolarization (DAD). Delayed after depolarizations
appear to precipitate the arrhythmias secondary to ischemic injury, digitalis
toxicity, hypokalemia, hypercalcemia, and catecholamines.

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Concept of Reentry
 During normal electrical activity, the cardiac cycle begins in the sinoatrial node and
continues to propagate until the entire heart is activated.
 When the normal cardiac impulse reaches the ventricles it has no place to go because all
the ventricle muscle fibers have been excited and are refractory and cannot conduct the
impulse further. Therefore the impulse dies and the heart awaits a new potential action to
begin in the AS node.
 For this self-propagating pattern to occur, three conditions must be met:
1. the two pathways must be connected proximally and distally by conducting tissue
forming a potential circuit,
2. one pathway must have a long refractory period relative to the other pathway,&
3. the pathway with the shorter refractory period must conduct slower than the other
pathway.
 However, if a transient block occurs at one side, one impulse is blocked and dies off, the
other one goes on around the ring.
 By the time it reaches the block area, the block would have finished and the impulse
passes this area and continues to circulate.
 Such a process is commonly denoted as reentry, reentrant excitation, circus movement.
Mechanism of Reentry

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Reentry Requires
1) 2 distinct pathways that come together at beginning and end to form a loop.
2) A unidirectional block in one of those pathways.
3) Slow conduction in the unblocked pathway.
 Large reentry circuits, like a-flutter, involve the atrium.
 Reentry in WPW involves atrium, AV node, ventricle and accessory pathways.
 During sinus rhythm, electrical impulses travel down both pathways simultaneously.
 The impulse transmitted down the fast pathway enters the distal end of the slow pathway
and the two impulses cancel each other out.
 tissues with these type of circuits may exist:
o in the SA node, AV node, or any type of heart tissue
o in a “macroscopic” structure such as an accessory pathway in WPW

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1. An arrhythmia is triggered by a premature beat
2. The fast conducting pathway is blocked because of its long refractory period so the
beat can only go down the slow conducting pathway
3. The wave of excitation from the premature beat arrives at the distal end of the fast
conducting pathway, which has now recovered and therefore travels retrogradely
(backwards) up the fast pathway

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4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and
therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement.
This creates the re-entry circuit

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Classification of arrhythmia (according to the site)
1) Atrial
 Premature Atrial Contractions (PACs)
 Wandering Atrial Pacemaker
 Multifocal atrial tachycardia
 Atrial flutter
 Atrial fibrillation (Afib)
2) Junctional arrhythmias
 Supraventricular tachycardia (SVT)
 AV nodal reentrant tachycardia is the most common cause of Paroxysmal Supra-
ventricular Tachycardia (PSVT)
o Junctional rhythm
o Junctional tachycardia
o Premature junctional contraction
3) Ventricular
 Premature Ventricular Contractions (PVC) sometimes called Ventricular Extra Beats
(VEBs) bigeminy“ trigeminy“ ventricular tachycardia
 Accelerated idioventricular rhythm
o Monomorphic Ventricular tachycardia
o Polymorphic ventricular tachycardia
o Ventricular fibrillation

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4) Heart blocks
 First degree heart block,
 Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
 Type 2 Second degree heart block, also known as Mobitz II
 Third degree heart block, also known as complete heart block.
5) SADS, or sudden arrhythmic death syndrome, is a term (as part of, Sudden unexpected
death syndrome) used to describe sudden death due to cardiac arrest brought on by an
arrhythmia in the absence of any structural heart disease on autopsy. The most common
cause of sudden death in the US is coronary artery disease
Causes of Tachyarrhythmia
1) Intra-cardiac causes
 Ischemic heart disease
 Valvular heart disease
 Heart failure
 Cardiomyopathy
 Congenital heart disease
2) Extra-cardiac causes
 Drugs
 Alcohol
 Stimulants e.g. caffeine
 Stress
 Hyperthyroidism
 Infection/Sepsis
 Metabolic e.g. hyperkalemia
Signs and Symptoms of Tachyarrhythmias
Symptoms
 Asymptomatic
 Palpitations
 Shortness of breath
 Chest pain (due to rate related ischemia)
 Syncope or pre-syncope
Signs
 Fast pulse
 Irregular pulse
 Low blood pressure
 Signs of acute heart failure including: tachypnea, desaturation, respiratory crackles on
auscultation, raised JVP, peripheral edema

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Classification of Tachyarrhythmias
 Tachyarrhythmias are classified based on whether they have broad or narrow QRS
complexes on the ECG.
 Broad is defined as >0.12s (or more than 3 small squares on the standard ECG).
 Narrow is equal to or less than 0.12s.
 Broad QRS complexes are slower ventricular depolarization that arise from the
ventricles.
 Narrow complexes are ventricular depolarizations initiated from above the ventricles
(known as supraventricular).
 One important exception is when there is a supraventricular depolarization conducted
through a diseased AV node. This will produce wide QRS complexes despite the rhythm
being supraventricular in origin.
 most wide-complex (broad-complex) tachycardias are ventricular in origin.
Classification of Tachyarrhythmias
1) Narrow QRS complex
 Sinus tachycardia
 Atrial fibrillation
 Atrial flutter
 AV nodal reentrant tachycardia
 Accessory pathway mediated tachycardia
 Atrial tachycardia
 Multifocal atrial tachycardia (MAT)
 Junctional tachycardia
2) Wide QRS-complex tachycardias
 Ventricular tachycardia (VT)
 Torsades de Pointes
 Ventricular fibrillation (VF)

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 SVT with aberrancy (a narrow complex tachycardia combined with a problem
with the conduction system)
 SVT with Pre-excitation (WPW) (A narrow complex tachycardia with an
accessory conduction pathway)
 Pacemaker-mediated tachycardia
Normal Sinus Rhythm
Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via
the AV node and His-Purkinje system.
EKG Characteristics:
 Regular narrow-complex rhythm
 Rate 60-100 bpm
 Each QRS complex is proceeded by a P wave
 P wave is upright in lead II & downgoing in lead aVR
Abnormal impulse formation
1) Decreased Automaticity (Sinus Bradycardia)

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2) Accelerated automaticity
Classification of Arrhythmias (for studying)
I. Arrhythmias That Are Of Sinus Origin
A. Sinus Arrhythmia
B. Sinus Arrest
C. Wandering Pacemaker
D. Sick Sinus Syndrome (Brady-Tachy Syndrome)
II. Unsustained Ectopic Supraventricular Dysrhythmias
A. Premature Atrial Contractions or Atrial Premature Beats (PAC's or APB's)
B. Premature Junctional Beat (PJB's
III. Sustained Supraventricular Dysrhythmias
A. Paroxysmal Supraventricular Tachycardia (PSVT)
B. Atrial Flutter
C. Atrial Fibrillation
IV. Ectopic Ventricular Dysrhythmias
A. Premature Ventricular Contractions (PVC's)
B. Ventricular Tachycardia
C. Ventricular Fibrillation

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V. AV Blocks
A. First Degree AV Block
B. Second Degree AV Block - Mobitz Type I and a Mobitz Type II
C. Third Degree AV Block
VI. Bundle Branch Blocks
Right Bundle Branch Block
Left Bundle Branch Block
VII. U Waves
I. Arrhythmias That Are Of Sinus Origin
A. Sinus Arrhythmia
B. Sinus Arrest
A. Sinus arrhythmia
 A condition in which the heart rate varies with breathing.
 inhalation causes the heart rate to be higher and exhalation results in a reduction in
heart rate.
 This is usually a benign condition

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B. Sinus Arrest
 Sinus arrest =(sinus pause or sinus block).
 Sinus arrest occurs when the sinoatrial node stops firing.
 If nothing else were to happen, the patient would die. However, the heart does have other
pacemakers that are usually dominated, overdriven or blocked.
 During sinus arrest, there will be a short time lag before a secondary pacemaker is
activated and begins the work of stimulating the heart to rhythmically beat.
 The appearance of these secondary pacemakers rescue us from death.
 These rescuing beats produced by these secondary pacemakers are called escape beats or
rescue beats.
 Causes:
 cardiovascular disease
 increased vagal tone
 infection
 drugs such as digitalis, quinidine, salicylates

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 Two or more pacemakers competing with each other for control of the heart's rhythm.
 Consequently the P waves have different shapes.
 The PR intervals vary in duration within the upper and lower limits of normal.
 The QRS complex and the T wave are normal because the AV node and the lower
conduction system of the heart are both functioning normally
 Caused by ischemia due to poor perfusion in the area of the SA node.

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Causes:
 idiopathic
 Sick sinus syndrome usually develops slowly over many years,
 It occurs more often in people over 50,
 but children may develop the condition after having open heart surgery.
Manifestations:
 Fainting (syncope)
 Dizziness or lightheadedness
 Confusion that comes and goes
 Heart palpitations (the feeling that the heart has skipped a beat)
 Chest pain
 Angina
 Shortness of breath
 Fatigue
 Muscle aches
 Chronic symptomatic sick sinus syndrome requires permanent pacing (AAI), with
additional antiarrhythmic drugs (or ablation therapy) to manage any tachycardia element.
 Thromboembolism is common in tachy-brady syndrome and patients should be
anticoagulated unless there is a contraindication.

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II. Unsustained Ectopic Supraventricular Dysrhythmias
A. Premature Atrial Contractions or Atrial Premature Beats (PAC's or APB's)
B. Premature Junctional Beat (PJB's)
A. Premature Atrial Contractions
 A condition in which an atrial pacemaker site above the ventricles sends out an electrical
signal early.
 The ventricles are usually able to respond to this signal, but the result is an irregular heart
rhythm.
 PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol,
cigarettes, or medications.
 Treatment is rarely necessary.

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B. Premature Junctional Beat (PJB's)
Is characterized by:
 The P wave is absent.
 The single beat is premature.
 The QRS complex is normal
III. Sustained Supraventricular Dysrhythmias
B. Atrial Flutter

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 PSVT is also known as paroxysmal atrial tachycardia (PAT).
 Atrioventricular nodal re-entry tachycardia (AVNRT)
 It usually begins and ends rapidly, occurring in repeated periods. This condition can
cause symptoms such as weakness, fatigue, dizziness, fainting, or palpitations if the heart
rate becomes too fast.
 PSVT has a very high rate of between 150 - 250 bpm.
 The cause of PSVT is usually a re-entrance phenomenon usually near the AV node.
 Re-entry is a phenomenon typically seen in an ischemic heart. Ischemic hearts are
electrically irritable.
 In AVNRT, there are two functionally and anatomically different pathways 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.
 P waves are usually absent. They are frequently hidden behind the T waves of this
dysrhythmia.
 If a P wave is present, then it is often a retrograde P wave or an upside down P wave.
 Stress, certain drugs and ischemia make this dysrhythmia more likely to occur.
 Carotid massage can be used to bring a patient out of PSVT. Carotid massage causes
baroreceptors to send signals through the vagus nerve to the heart. These signals are
responsible for slowing the conduction through the AV node with the net effect of
slowing the heart rate. Carotid massage has the effect of interrupting the re-entry circuitry
and terminates the tachycardia.

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PSVT Acute Management
 Patients presenting with SVTs and haemodynamic instability require emergency
cardioversion.
 If the patient is haemodynamically stable, vagal manoeuvres, including right carotid
massage, Valsalva manoeuvre and facial immersion in cold water can be successfully
employed.
 If not successful, intravenous adenosine (up to 0.25 mg/kg) , verapamil 5-10 mg i.v.
over 5-10 minutes, i.v. diltiazem, or beta-blockers should be tried.
 Long-term management : It includes ablation of an accessory pathway. Also,
verapamil, diltiazem & β-blockers; are effective in 60-80% of patients.
B. Atrial Flutter
 Atrial flutter has a regular rhythm with P waves appearing at a rate of between 220-
300/minute.
 The characteristics of atrial flutter are :
 A QRS complex followed by a definite and regular sequence of P waves called a
block.
 If there is one QRS followed by 4 P waves, this is called a 4:1 block. If the QRS
complex is followed by 2 P waves, it is called a 2:1 block.
 There are no visible T waves
 There is no PR interval and no ST segment
 Atrial flutter is a serious supraventricular tachydysrhythmia.
 Treatment of the symptomatic acute paroxysm is electrical cardioversion.
 Before a patient is cardioverted (DC shock) out of atrial flutter into a normal rhythm
either using electrical or pharmacological conversion, the patient must be given
Anticoagulants.
 It is a condition in which the electrical signals come from the atria at a fast but even rate,
often causing the ventricles to contract faster and increase the heart rate.
 When the signals from the atria are coming at a faster rate than the ventricles can respond
to, the ECG pattern develops a signature "sawtooth" pattern (instead of P waves),showing
two or more flutter waves between each QRS complex.
The causes for atrial flutter can be:
 Premature atrial contractions (PAC's)
 Ischemic heart disease
 Re-Entry Phenomenon
 Pulmonary emboli
 Unknown etiology

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Anticoagulation for Atrial Flutter
 Anytime a patient has been having runs of PSVT, atrial flutter or atrial fibrillation, they
may have had the risk of thrombus formation in the auricles of their atria.
 Thrombus are formed their because pooled blood is so mechanically beaten up that it
forms clots.
 Unless the Thrombus are dissolved, prior to the patient being successfully converted (DC
shock) to a normal rhythm, the clots can be pumped out to downstream sites with the
patient auto-embolizing themselves.

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 A condition in which the electrical signals come from the atria at a very fast and erratic
rate. The ventricles contract in an irregular manner because of the erratic signals coming
from the atria.
 The ECG shows normal but irregular QRS complexes, fine oscillations of the baseline
(so-called fibrillation or f waves) and no P waves.
 Atrial fibrillation occurs as a consequence of re-entry phenomenon, rheumatic disease,
pericarditis, atherosclerotic disease, hyperthyroidism, HTN, cardiomyopathy, sick sinus,
WPW, and Alcohol (ETOH) . It may also occur in healthy subjects as a result of strong
sympathetic activation.
 Atrial fibrillation is serious because individuals who have been in atrial fibrillation may
have formed thrombus. This predisposes the patient to embolic events such as myocardial
infarctions, infarctions of organ systems - i.e. - strokes.
Irregularly irregular ventricular response
Atrioventricular reciprocating tachycardia (AVRT)
 Atrioventricular reciprocating tachycardia (AVRT) occurs when there is an extra
electrical pathway linking the atria and ventricles of the heart.
 Normally, the AV node is the only tissue that conducts electrical impulses between the
atria and ventricles of the heart : all electrical impulses must go through the AV node to
reach the lower chambers .

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 In an atrioventricular reciprocating tachycardia, electrical impulses travel one direction in
the normal manner, down the AV node to the ventricles, but they then travel back up to
the atria through an abnormal, extra electrical pathway (accessory pathway) located
outside the AV node.
 Atrial activation occurs after ventricular activation and the P wave is usually clearly seen
between the QRS and T complexes
 Illustration of orthodromic atrioventricular reciprocating tachycardia (AVRT) with a
reentrant circuit consisting of 2 limbs.
 The forward or antegrade limb involves the normal AV nodal system,
 and the reverse, or retrograde, limb involves the accessory pathway.
 This type of SVT leads to a narrow-complex rhythm on the EKG as seen below..
Wolff-Parkinson-White Syndrome (WPW)
 WPW is a congenital defect caused by the presence of an abnormal extra electrical
connection (also called a Kent Bundle) between the atria and ventricles .
 Patients with the WPW Syndrome are often without symptoms, but some can exhibit a
variety of supraventricular tachycardias, e.g. AVRT and atrial fibrillation.
 Incidence: 4/ 100,000 births.

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 Image of preexcitation of the EKG with a manifest accessory pathway leading to the
EKG findings of WPW pattern. As seen here, electrical conduction from the atria to the
ventricles can occur via the normal AV nodal system and the accessory pathway
simultaneously.
 This leads to the creation of the slurred upstroke, or delta wave, seen on the surface EKG
lead and denoted by arrows in the tracing seen.
 ECG shows:
 Short PR interval
 Delta wave on the upstroke of the QRS complex
 Drug treatment includes
 flecainamide, amiodarone or disopyramide.
 Digoxin and verapamil are contraindicated.
 Transvenous catheter radiofrequency ablation is the treatment of choice.

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Accessory Pathway: Bundle of Kent

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Multifocal Atrial Tachycardia (MAT)
 Automatic atrial rhythm from various different foci
 Seen in hypoxia, COPD, atrial stretch and local metabolic imbalance.
 Three or more types of p waves and a rate > 100
 Digoxin worsens it, so treat with oxygen and slow channel blocker like verapamil or
diltiazem.
(Summary)Reentrant Rhythms
1) AV nodal reentrant tachycardia (AVNRT)
2) Supraventricular tachycardia
3) AV reentrant tachycardia (AVRT)
4) Wolf – Parkinson – White syndrome
5) Atrial flutter
6) Ventricular tachycardia
7) Atrial fibrillation
8) Ventricular fibrillation

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IV. Ectopic Ventricular Dysrhythmias
B. Ventricular Tachycardia
C. Ventricular Fibrillation
Etiology:
 May occur in normal person
 Myocarditis, CAD,
 valve heart disease, hyperthyroidism,
 Drug toxicity (digoxin, quinidine and anti-anxiety drug)
 electrolyte disturbance,
 anxiety, drinking, coffee
 If each normal contraction is followed by a single PVC, we call this bigeminy. If two
normal contractions are followed by a single PVC, we have trigeminy
Manifestation:
 palpitation
 dizziness
 syncope
 loss of the second heart sound
ECG features:
 The P wave is absent
 The QRS complex is wide and bizarre because ventricular depolarization does not
follow the normal pathway
 The wave is premature
 There is a compensatory pause before the next normal wave

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B. Ventricular Tachycardia (VT)
 Ventricular tachycardia is defined as a run of three or more consecutive PVCs. The rate is
usually between 100 - 200 bpm.
 In normal patients, short runs of ventricular tachycardia cause the patient to feel
palpitations in the chest and feel faint.
 If they are sustained for longer periods of time, then unconsciousness will probably
result.This is due to poor cardiac output and poor perfusion of the brain and heart.
 It can develop as an early or late complication of a of a myocardial infarction unless the
patient has immediate help.
 Ventricular tachycardia quickly degenerates into ventricular fibrillation.
 Ventricular tachycardia can be caused by : Ischemic heart disease, myocardial
infarctions, Cardiomyopathy, Heart failure, Heart surgery, Myocarditis, Valvular heart
disease, drug toxicity, and re-entry phenomenon. It can occur without heart disease.
 In VT an electrical signal is sent from the ventricles at a very fast but often regular rate.
 The ECG shows a rapid ventricular rhythm with broad (often 0.14 s or more), abnormal
QRS complexes.
Ventricular fibrillation (VF)
 A condition in which many electrical signals are sent from the ventricles at a very fast
and erratic rate. As a result, the ventricles are unable to fill with blood and pump.
 This rhythm is life-threatening because there is no pulse and complete loss of
consciousness.
 The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes
 A person in VF requires prompt defibrillation to restore the normal rhythm and function
of the heart. It may cause sudden cardiac death. Basic and advanced cardiac life support
is needed
 Survivors of these ventricular tachyarrhythmias are, in the absence of an identifiable
reversible cause (e.g. acute myocardial infarction, severe metabolic disturbance), at high

341

risk of sudden death. Implantable cardioverter-defibrillators (ICDs) are first-line therapy
in the management of these patients
Torsades de pointes
 It is a French term means Twisting of the points)
 This is a type of short duration tachycardia that reverts to sinus rhythm spontaneously. It
may be due to:
 Congenital
 Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia.
 Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics.
 It may present with syncopal attacks and occasionally ventricular fibrillation.
 QRS complexes are irregular and rapid that twist around the baseline. In between the
spells of tachycardia the ECG show prolonged QT interval.
 Treatment includes; correction of any electrolyte disturbances, stopping of causative
drug, atrial or ventricular pacing, Magnesium sulphate 8 mmol (mg2+) over 10-15 min
for acquired long QT, IV isoprenaline in acquired cases and B blockers in congenital
types
 Long-term management of acquired long QT syndrome involves avoidance of all drugs
known to prolong the QT interval. Congenital long QT syndrome is generally treated by
beta-blockade, left cardiac sympathetic denervation, and pacemaker therapy.
 Patients who remain symptomatic despite conventional therapy and those with a strong
family history of sudden death usually need ICD therapy.

342

Pacer rhythm
 A ventricular rhythm originating from a cardiac pacemaker is associated with wide QRS-
complexes because the pacing electrode is (usually) located in the right ventricle and
activation does not involve the conduction system.
 In pacer rhythm the ventricular contraction is usually preceded by a clearly visible pacer
impulse spike. The pacer rhythm is usually set to 72/min..
Sinus Tachycardia
 A condition in which the heart rate is 100-160/min
 Symptoms may occur with rapid heart rates including; weakness, fatigue, dizziness, or
palpitations.
 Sinus tachycardia is often temporary, occurring under stresses from exercise, strong
emotions, fever, dehydration, thyrotoxicosis, anemia and heart failure.
 If necessary, beta-blockers may be used to slow the sinus rate, e.g. in hyperthyroidism

343

Sinus Tachycardia converted to NSR
Sinus Bradycardia
 Physiological variant due to strong vagal tone or atheletic training.
 Rate as low as 50 at rest and 40 during sleep.
 Common causes of sinus bradycardia include:
o Extrinsic causes; Hypothermia, hypothyroidism, cholestatic jaundice and raised
intracranial pressure.
o Drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs.
o Intrinsic causes; Acute ischemia and infarction of the sinus node (as a
complication of acute myocardial infarction). Chronic degenerative changes such
as fibrosis of the atrium and sinus node (sick sinus syndrome).

344

Cardiac conduction block
 Heart block means failure of conduction of impulses from the S-A node down to the
ventricles.
 Block position:
o Sinoatrial; intra-atrial; atrioventricular; intra-ventricular
 Block degree
o 1st
Degree AV Block : prolong the conductive time
o 2nd
Degree AV Block : partial block
o 3rd
Degree AV Block: complete block
1st
Degree AV Block
 Seldom of clinical significance, and unlikely to progress.
 ECG shows prolonged PR interval.
 May be associated with acute rheumatic fever, diphtheria, myocardial infarction or drugs
as digoxin

345

2nd
Degree AV Block
 Acute myocardial infarction may produce second-degree heart block.
 In inferior myocardial infarction, close monitoring and transcutaneous temporary back-up
pacing are all that is required.
 In anterior myocardial infarction, second-degree heart block is associated with a high risk
of progression to complete heart block, and temporary pacing followed by permanent
pacemaker implantation is usually indicated.
2nd Degree AV Block Mobitz type I (Wenchebach phenomenon):
 The conduction defect is located below the AV node.
 It is characterized by the following :
o With each success atrial impulse, the PR interval becomes progressively longer.
o As the PR interval gets progressively longer, suddenly a QRS complex is dropped
- called a dropped beat.
o The normal rhythm is re-established and the process starts all over again - i.e. -
the PR interval starts to lengthen, eventually you have a dropped beat, and a
return to a normal rhythm.
o When isolated, usually physiological and due to increased vagal tone and
abolished by exercise and atropine.

347

2nd
Degree AV Block Mobitz type II
 Block is located high up in the Bundle of His.
 The characteristics of the Mobitz Type II second degree AV block are :
 There are a series of normal beats with normal PR intervals
 Suddenly a P wave appears without a QRS complex following it - a dropped beat
 There is a resumption of a normal rhythm and the cycle begins to repeat itself
 A Mobitz Type II second degree AV block is a dangerous dysrhythmia. It is dangerous
because it will absolutely degenerate into a third degree AV block. A third degree AV
block is a medical emergency requiring the implantation of a pacemaker.

348

 The PR interval is consistent (whether it is normal or longer than normal)
 Periodically a P wave is not followed by a QRS complex
 This contrasts with Mobitz Type 1 block where the PR interval becomes progressively
longer before an atrial beat is not conducted to the ventricles

349

3rd
Degree AV Block
 In third degree AV block, there is a complete lack of atrial impulses making it through to
the AV node and on through the conduction system of the ventricles.
 For this reason it is called complete heart block.
 The ventricles respond to this lack of signaling by developing a rescue or escape rhythm
from a ventricular focus.
 The rate of a ventricular pacemaker is quite low - around 30-45 bpm. It is so low, that in
most cases, the patient must undergo a pacemaker implant procedure.
 The atria and the ventricles are functioning completely independent of one another and
the atria beat faster than ventricles. The P waves that appear on the rhythm strip are not
associated with the QRS complexes that appear on the rhythm strip.
 This dissociation of the atria and the ventricles affects cardiac output and in most cases,
the patient will loose consciousness.
 Caused by;
 Common in elderly age groups due to idiopathic bundle branch fibrosis.
 myocardial ischemia (inferior wall infarction can permanently damage the AV
node, requiring the implantation of a pacemaker)
 Congenital lupus (antibodies from the patients mother may destroy the AV node
during gestation)
 Lyme disease

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 Complete heart block with a junctional escape rhythm & RBBB
 There is complete uncoupling of the atrial and ventricular rhythms
 The P to P interval will be much shorter than the R to R interval
 This is because the SA node has a higher level of automaticity compared to either the
AV node or Purkinje fibers that pace the ventricle under these conditions
 The RR interval is typically constant
VI. Bundle Branch Blocks
 Bundle branch blocks are dysrhythmias that occur because of ischemic regions of either
the right or the left bundle branch in the heart's conduction system.
 Since the bundle branchs carry the depolarization wave to their respective ventricular
muscle, the changes in the EKG that we look for are in the QRS complexes.
 Right Bundle Branch Block (RBBB)
 Left Bundle Branch Block (LBBB)
Right Bundle Branch Block (RBBB)
 In right bundle branch block, there is a delay of the conduction potential through the right
bundle resulting in a delay in right ventricular depolarization.
 The right ventricle, therefore, does not start to depolarize until nearly all of the left
ventricular muscle mass has depolarized.

351

 The following characteristics are typical of right bundle branch block:
 A wide QRS complex greater than 3 mm in duration - this is because the two
ventricles have not synchronously depolarized
 RSR1 waves - this occurs because the two ventricles are dysynchronous in their
depolarization - looks like "Rabbit Ears"
 Loss of the R wave progression seen only in the precordial chest leads
 ST segment depression and T wave inversion frequently seen in V1 and V2
 Large R waves in V1-V2
 Depolarization spreads from the left ventricle to the right ventricle.
 This creates a second R-wave (R’) in V1, and a slurred S-wave in V5 - V6.
 The T wave should be deflected opposite the terminal deflection of the QRS complex.
This is known as appropriate T wave discordance with bundle branch block. A
concordant T wave may suggest ischemia or myocardial infarction.

352

Left Bundle Branch Block(LBBB)
 In LBBB, there is a conduction delay in the conduction potential through the heart's
conduction system serving the left ventricle.
 Unlike RBBB, LBBB is always associated with an underlying heart disease.
 The characteristics of LBBB are as follows :
 The QRS complexes will be wider than 3 mm in duration
 loss of the R wave progression
 Huge S waves in V1-V3
 ST segment depression and T wave inversion are frequently seen in
V5-V6.
 Depolarization enters the right side of the right ventricle first and simultaneously
depolarizes the septum from right to left.
 This creates a QS or rS complex in lead V1 and a monophasic or notched R wave in
lead V6.
 The T wave should be deflected opposite the terminal deflection of the QRS complex.
This is known as appropriate T wave discordance with bundle branch block. A
concordant T wave may suggest ischemia or myocardial infarction.

354

Bundle Branch Block (BBB)
Hemiblock
 Delay or block in the divisions of the left bundle branch produces a swing in the direction
of depolarization (electrical axis) of the heart.
 When the anterior division is blocked (left anterior hemiblock), there is left axis
deviation. Delay or block in the postero-inferior division causes(right axis deviation).
Bifascicular block
 This is a combination of a block of any two of the following: the right bundle branch, the
left antero-superior division and the left postero-inferior division.
 Block of the remaining fascicle will result in complete AV block.
Management of arrhythmias
 Pharmacological therapy.
 Cardioversion.
 Pacemaker therapy.
 Surgical therapy e.g. aneurysmal excision.
 Interventional therapy “ablation”.

356

Action of Antiarrhythmic drugs on Conduction system
Mechanism of action of Antiarrhythmic drugs

Lecture 13 abn conduction- Pathology

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Lecture 13 abn conduction- Pathology