CHAPTER 11: MECHANISMS OF CARDIAC ARRHYTHMIAS

Disorders of heart rhythm result from alterations of:

o Impulse formation
o Impulse conduction
o Both
Normal impulse formation
o Electrical impulse formation in the heart arises from the intrinsic automaticity of specialized
cardiac cells
I.e. the ability of cells to spontaneously depolarize to a threshold voltage and generate
an action potential
o Atrial and ventricular myocytes do not normally have this property.
o Specialized cells of the conducting system do have automaticity:
Pacemaker cells
SA node
AV node
Ventricular conducting system
o Bundle of His
o Bundle branches
o Purkinje fibers
o Ionic basis of automaticity
Ionic basis of automaticity
o Pacemaker cells do not have static resting voltage
Gradual depolarization during phase 4 of the action potential (diastole)
Pacemaker current (If)
If this spontaneous depolarization reaches threshold, AP generated
o If channels open when membrane potential is more negative than ~ -50 mV
Completely different channels than the fast sodium channels responsible for the phase 0
upstroke
Inward flow of sodium through these slow channels is driven by its concentration
gradient
Negative intracellular potential depolarizes
membrane
toward threshold
o In the SA node 3 other currents contribute to phase 4
depolarization
Slow inward calcium L-type Ca2+
channels
that open at the voltages near the end of
phase 4
Progressively declining outward potassium
current
Additional inward sodium current mediated by
activation of electrogenic sodium-calcium exchanger
Activated by calcium release from the
SR
o Once membrane potential reaches threshold, upstroke
happens
Much slower than phase 0 in Purkinje system
Because membrane potential determines proportion of fast sodium channels that
are capable of depolarization
Some may still be in their inactivated state
Less negativeless fast sodium channels available for depolarization
Because resting membrane potential in AV nodal cells is less negative (-50 to -60
mV) than in Purkinje cells (-90 mV), most are still inactivated
Thus, L-type Ca2+ channels mostly generate the phase 0 in pacemaker cells
Native and latent pacemakers

Intrinsic rate of firing depends on 3 variables:

Rate (slope) of phase 4 depolarization
Maximum negative diastolic potential
Threshold potential
o Gap junctions electrically connect myocardial cells
Spread the action potential
Pacemaker cells with the fastest rate of depolarization set the heart rate
o SA node is the native pacemaker
60-100 bpm
o Latent pacemakers have the potential to become pacemaker if necessary
AV node (50-60 bpm)
Bundle of His (50-60 bpm)
Purkinje system (30-40 bpm)
Overdrive suppression
o Na/K ATPase creates hyperpolarizing current
o If current in pacemaker cells is sufficiently large to overcome this effect
o The hyperpolarizing current is increased when cells are caused to fire more rapidly than its
intrinsic pacemaker rate
More sodium enter per unit time
Na/K ATPase is upregulated to restore transmembrane sodium gradient
Electronic interactions
o Decoupling of normally suppressed cells (e.g. AV nodal cells) may reduce inhibitory electronic
influence of gap junction-connected cells and lead to enhanced automaticity
Produces ectopic rhythms by latent pacemaker tissues
Altered impulse formation
o Main abnormalities in impulse initiation leading to arrhythmias are
Altered automaticity
Abnormal automaticity
Triggered activity
o Increased SA node automaticity
Mainly modulated by autonomic nervous
system
Sympathetic stimulation via 1adrenergic receptors
o Increases open probability of
pacemaker channels
through which If can flow
o Leads to steeper phase
4 depolarization
o Increases heart rate
Sympathetic stimulation also
shifts AP
threshold to a more negative
voltage by
increasing the probability that
voltage-sensitive
calcium channels are capable
of opening
o i.e. phase 4
depolarization
reaches threshold
potential earlier
o Decreased SA node automaticity
Parasympathetic nervous system is the main controller of heart rate at rest
Cholinergic stimulation via vagus nerve acts at the SA node
Reduces probability of pacemaker channels opening
Reduces slope of phase 4 depolarization
Slows intrinsic firing rates
Probability of calcium channels being open is decreased
o Increases action potential threshold to a less negative value
Increases the probability of ACh-sensitive potassium channels being open at rest
o Drives diastolic potential more negative
o

Escape rhythms
Impulse initiated by a latent pacemaker because the SA node rate has slowed is called
an escape beat
Persistent impairment of SA nodeseries of escape beats called escape rhythm
o Enhanced automaticity of latent pacemakers
Latent pacemakers can assume control of impulse formation if its intrinsic rate is higher
than that of the SA node
Ectopic beatectopic rhythm
o Abnormal automaticity
Cardiac tissue injury leads to cells outside the conduction system acquiring automaticity
If the pace outruns the SA node, these cells become the source of an abnormal ectopic
rhythm
o Triggered activity
Action potentials can trigger
abnormal depolarizations that
lead
to extra heart beats or
tachyarrhythmias
First action potential
leads to oscillations of
membrane voltage
called
afterdepolarizations
Two types of
afterdepolarization
Early: during repolarization phase of inciting beat
o Can occur during phase 2 or 3.
Phase 2: mostly inward calcium current
Phase 3: mostly sodium channels
o More likely in conditions that prolong QT interval
o Could be the initiating mechanism of torsade de pointes
Delayed: after repolarization has
completed
o Develop in states of high
intracellular calcium
Digitalis
intoxication
Catecholamine
stimulation
o Intracellular calcium
accumulation activates
chloride currents or Na/Ca
exchanger
Altered impulse conduction
o Conduction block
Propagating impulse is blocked when It encounters a region of the heart that is
electrically unexcitable
Can be:
Transient
Permanent
Unidirectional
Bidirectional
Conditions that cause this:
o

Ischemia
Fibrosis
Inflammation
Certain drugs
Functional blocks occur when a propagating impulse encounters cardiac cells that are
still refractory
Fixed blocks occur when a block is caused by a barrier imposed by fibrosis or scarring
that replaces myocytes
AV block removes normal overdrive suppression
Unidirectional block and reentry
o Electric impulse circulates repeatedly around a reentry path, recurrently depolarizing a region of
cardiac tissue
o Normally, refractory period of each
cell prevents immediate reexcitation
from adjacent cells
o Conduction block that prevents rapid
depolarization of parts of the
myocardium can create an
environment for continued
propagation and reentry
o action potential can conduct in a
retrograde direction, but not an
anterograde direction
o 2 conditions required:
unidirectional block
slowed conduction through
reentry path
usually appears as monomorphic tachycardia on ECG
polymorphic tachycardia is where the QRS shape varies
Bad news bears if you go polymorphic VTVF
Accessory pathways and Wolff-Parkinson-White Syndrome
o Affects 1 in 1,500 people
o Additional accessory pathway between ventricle
and atrium
Bypasses the AV node
Bundle of Kent
Spans the AV groove somewhere along the
mitral or tricuspid annuli
Accessory tissue conducts impulses faster
than the AV node
Leads to pre-excitation
o Signs on EKG
Shortened PR
Delta wave
Widened QRS
Physiologic basis of Antiarrhythmic therapy
o Bradyarrhythmias
Doesnt always require treatment
Transient pharmacotherapy
Anticholinergic drugs
1-blockers
Implanted pacemakers for sustained therapy
o Tachyarrhythmias

Goals:
Protect the patient from consequences of arrhythmia
Correct mechanism responsible for abnormality
Pharmacologic agents
To eliminate rhythms from increased automaticity:
o Reduce slope of phase 4 spontaneous depolarization
o Make the diastolic potential more negative (hyperpolarize)
o Make threshold potential less negative
To interrupt reentrant circuits:
o Inhibit conduction o reentry circuit to the point that conduction fails
o Increase refractory period within reentrant circuit
o Suppress premature beats
To eliminate triggered activity:
o Shorten AP duration
Prevent EAD
o Correct conditions of calcium overload
Prevent DAD
Vagotonic maneuvers
Carotid sinus massage
Rub firmly for a few seconds over the carotid sinus
parasympathetic
sympathetic
due to stretching of carotid baroreceptors
o i.e. the carotid body thinks the pressure is too high and baroreflex adjusts
autonomics accordingly
Electric cardioversion and defibrillation
Cardioversionterminate SVT or VT
Sedate the patient
Defibrillationterminate VF
CLEAR!!
Implantable cardioverter-defibrillators
Device continually monitors cardiac activity
Applies therapeutic countershock when needed

CHAPTER 12: CLINICAL ASPECTS OF CARDIAC ARRHYTHMIAS

Bradyarrhythmias
o Sinus bradycardiarate <60 bpm

Sick sinus syndrome

Periods of inappropriate bradycardia
Dizziness, confusion, syncope
Elderly people
Commonly with AFSVT
Bradycardia-tachycardia syndrome

Escape rhythms
o SA node activity is impaired or a block
o AV node or His-Purkinje system takes overlatent pacemakers
o Junctional escape rhythms arise form AV node or proximal bundle of His
Normal, narrow QRS complex
40-60 bpm
no P waves because impulse originates below the atrium
retrograde P waves may be observed after QRS

Ventricular escape rhythms

Slower rate (30-40 bpm)
Widened QRSventricles not depolarized by normal rapid conduction over bundle
branches

Atrioventricular conduction system

o First-degree AV block
Signs on EKG
PR interval lengthened (>0.2 sec)
1:1 ratio P to QRS maintained
reversible causes:

Second-degree AV block
Mobitz type 1 (Wenckebach) block
Degree of AV delay (i.e. PR interval) increases gradually until a QRS gets
dropped

vagal tone
ischemia of AV node
-blockers
CCBs
Digitalis
Structural causes:
MI
Chronic degeneration

Mobitz type 2 block

More dangerous than type 1
Sudden intermittent loss of AV conduction without preceding lengthening of PR
interval
If it persists for 2 or more beats, its called high-grade AV block

Third-degree AV block
Complete heart blockcomplete failure of AV conduction
Complete dissociation of P wave from QRS

Tachyarrhythmias

Supraventricular arrhythmias
Sinus tachycardia

Atrial premature beats

Common in health and disease
Automaticity or reentry in atrial focus outside the SA node
Exacerbated by SNS stimulation
Earlier than expected P wave with abnormal shape

Atrial flutter
Rapid regular atrial activity
180-350 bpm
many impulses reach the AV node during refractory period and dont conduct
o slower ventricular rate
Sawtooth appearance on EKG
To fix it:
o Electrical cardioversion
o Rapid atrial stimulation
o Pharmacologic intervention
-blockers
CCBs (verapamil, diltiazem)
Digoxin
Atrial fibrillation
Very fast atrial rate (350-600 /min)
Distinct P wave not discernible on EKG
Average ventricular rate in untreated AF is ~140-160 bpm
Mechanism is probably multiple wandering reentrant circuits within the atria
Things to worry about:
o Rapid ventricular rates could compromise cardiac output
LV hypertrophy
Pulmonary edema
o Stasis of blood within the atria
Formation of thrombusstroke

Treatment:
o Ventricular rate control
-blockers
CCBs (diltiazem, verapamil)
Digitalis is NOT effective unless ventricular contractile function is
concomitantly impaired
o Try to restore sinus rhythm
Chemical or electrical cardioversion
Maze procedure
Multiple incisions to prevent formation of reentry circuits
Percutaneous catheter ablation
Cauterize left atrium around pulmonary veins
Last resort is catheter ablation of AV node
o Prevention of thromboembolism

Paroxysmal supraventricular tachycardia (PSVT)

Manifested by
o Sudden onset and termination
o Atrial rates between 140-250 bpm
o Narrow (normal) QRS complexes
Reentry involving AV node, atrium, or accessory pathway

AV nodal reentrant tachycardia (AVNRT)

o Most common PSVT in adults
o In normal hearts, AV node has atrial extensions
Some fast-conducting, some slow-conducting
Allows for setup of reentrant loop when slow-conducting gets to
the bundle of His after repolarization from fast-conducting
impulses
Travels from slow-conducting, retrograde up the fast-conducting,
and back down
o EKG:
Normal QRS
P waves may not be apparent
Retrograde depolarization happens simultaneously with
ventricular depolarization
May be superimposed on the late portion of QRS and
inverted
o Treatment:
Acute:

Terminate reentry
o Valsalva
o Carotid sinus massage
o IV adenosine
o IV CCBs
o IV -blockers
Preventative:
Oral -blockers, CCBs or digoxin
Catheter ablation if those dont work

AV reentrant tachycardias (AVRTs)

o Similar to AVNRTs, but theres actually an accessary tract that facilitates
the reentry loop
o Two things could happen:
Pre-excitation syndrome (WPW)
EKG:
o Short PR interval (<0.12 sec)
o Slurred QRSdelta wave
o Widened QRS complex
Most common is orthodromic AVRT
o Impulse travels anterogradely down the AV node to
ventricles, then retrogradely back up the accessory
tract back to the atria
o No delta wave since normal pathway of AV
nodebundle of His is utilized
o Retrograde P waves often visible
~10% patients with AVRT have antidromic AVRT
o Anterogradely down the accessory path
o Retrogradely back up the AV node
o Difficult to distinguish from VT on EKG alone

Treatment:
o Greater caution is needed than with AVNRT
o Same drugs block conduction in normal AV node,
but often do not work on accessory pathways
Sometimes they even shorten refractory
period on accessory pathway and lead to
even faster rates of ventricular tachycardia
o Preferred drugs:
Sodium channel blockers (Class IA and IC
antiarrhythmics)
Class III antiarrhythmics
These slow conduction in the accessory
pathway
o If accompanied by hemodynamic collapse, wide
QRS tachycardia must be cardioverted

If hemodynamically stable:
IV procainamide (class IA)
Ibutilide (class III)
Lown-Ganong-Levine syndrome
o Short PR, but normal, narrow QRS
No delta wave
PSVT from concealed accessory pathway
Can result in orthodromic AVRT under the right conditions
Management is the same as for patients with AVNRT
Focal atrial tachycardia
Results from automaticity of atrial ectopic site or reentry
Looks like sinus tachycardia, but P wave has a different morphology
o Suggests atopic depolarization
Can be caused by digitalis toxicity
Can be exaggerated during sympathetic elevation
Vagal maneuvers have no effect on these
Treatment:
o -blockers
o CCBs
o Class IA, IC, III antiarrhythmics
o Catheter ablation as last resort
Multifocal atrial tachycardia
EKG shows irregular rhythm with multiple (>3) P wave morphologies
Average atrial rate is >100 bpm
o

Treat with verapamil

Ventricular arrhythmias
Ventricular premature beats
AP from ectopic ventricular focus
EKG:
o Widened QRS not related to P wave
Can occur in:
o Bigeminyevery 2 beats
o Trigeminyevery 3 beats
o Quadrigeminyevery 4 beats
o Couplets2 in sequence
o Triplets3 in sequence

No treatment necessary unless advanced structural disease predisposes patient

to life-threatening ventricular arrhythmias

Ventricular tachycardia
Series of 3 or more VPBs
2 flavors:
o Sustained VT
> 30 seconds
produces syncope
requires cardioversion or drugs
o Non-sustained VT
Self-terminating
Both commonly found in patients with structural heart disease
EKG:
o Wide QRS (>0.12 sec)
o 100-200 bpm or faster
Can be categorized by QRS
o Monomorphictheyre all the same
Structural abnormality that supports reentry circuit
Maybe from old infarction/scar
o Polymorphictheyre not the same
Multiple ectopic foci
Most commonly caused by
Acute myocardial ischemia/infarction
Torsades de pointes
Management
o Cardioversion
o Antiarrhythmic drugs
Torsades de Pointes
Polymorphic VT
Varying amplitudes of QRS
Causes:
o EAD with QT prolongation
Can result from hypokalemia or hypomagnesemia
Can result from persistent bradycardia
Can result from drugs that block potassium currents
o

Many noncardiac medications

Erythromycin
Phenothiazines
Haloperidol
Methadone

Ventricular fibrillation
Immediately life-threatening arrhythmia
Disordered, rapid stimulation of ventricles with no coordinated contractions
Must cardiovert, or patient dies

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