Phys Chapter 13: Cardiac Arrhythmias and Their Electrocardiographic Interpretation
Causes of heart arrhythmias:
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Abnormal rhythmicity of the pacemaker
Shift of the pacemaker from the SA node to another place in the heart
Block at some part of the spread of the impulse through the heart
Abnormal pathways of impulse transmission through the heart
Spontaneous generation of impulses at any part of the heart
Tachycardia – fast heart rate, faster than 100 bpm
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Page 143 top pic – sinus tachycardia
o Determined by the time intervals between the QRS complexes
 In the pic, it’s 150 per minute instead of the normal 72 per minute
 On the EKG sheet:
 The vertical axis tells the voltage - 1 mm = 0.1 mV
 The horizontal axis tells the time
o 1 mm = 0.04 s = one little block
o So 5 little blocks = .2 s= one big block
o 5 big blocks = 1 second
 So heart rate = 300 / # of big blocks between beats
o Use top of QRS to top of QRS (called R to R interval)
Causes of tachycardia include increased body temperature, stimulation of the heart by the
symps, or toxic conditions of the heart
o The heart rate increases about 10 beats/min for each degree F the body increases, up to
105 degrees F, after which the heart rate can decrease because the heart stops working
as well
o Simple weakening of the myocardium usually increases the heart rate because the
weakened heart doesn’t pump blood into the arteries enough, triggering symps to
increase the heart rate
Bardycardia – slow heart fate, less than 60 bpm
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Page 143 bottom pic – sinus bradycardia
In athletes, their heart is larger and stronger than a normal persons, which lets them pump a
large stroke volume output per beat
o When the athlete is at rest, excessive amounts of blood pumped into the arteries with
each beat initiate feedback circulatory reflexes to cause bradycardia
o So since they’re so good at pumping it out, they have to slow their HR so they don’t get
too much blood
Any circulatory reflex that stimulates the vagus nerves cause release of acetylcholine in the
heart, causing parasymp effects
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Carotid sinus syndrome – baroreceptor pressure receptors in the carotid sinus of the
carotid artery walls are excessively sensitive
 So even mild external pressure on the neck triggers a strong baroreceptor
reflex, causing intense vagal effects on the heart, like bad bradycardia, or can
even stop the heart for several seconds
Sinus arrhythmia – when circulatory or respiratory conditions change the strengths of symp or
parasymp signals to the SA node
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Respiratory sinus arrhythmia results from spillover of signals from the medullary respiratory
center into the nearby vasomotor center during inspiratory and expiratory cycles of respiration
o The spillover signals cause alternate increase and decrease in the # of impulses
transmitted through the symps and vagus to the heart
Abnormal rhythms from block of heart signals in conduction pathways:
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Sinoatrial block – block of signals from the SA node before they ever enter the atrial muscle
o Page 144 top pic – SA node block with AV nodal rhythm
o Since the atria aren’t getting a signal to contract, there’s no P waves, because there’s no
contraction of the atria
o The ventricles then follow the AV node rhythm, so the rate of the ventricle QRS-T
complex is slowed, but not altered
Atriventricular block:
o The only way the impulses can normally get from the atria into the ventricles is through
the AV bundle aka bundle of His
o Things that can decrease or block the rate of impulse conduction or block it entirely in
the bundle:
 Ischemia of the AV node or AV bundle fibers
 Coronary insufficiency can cause ischemia of the AV node and bundle
 Compression of the AV bundle by scar tissue or calcification
 Inflammation of the AV node or AV bundle
 Extreme stimulation of the heart by the vagus – can block conduction through
the AV node
 This usually happens form strong stimulation of baroreceptors in people
with carotid sinus syndrome
Incomplete atrioventricular (AV) heart block:
o Prolonged P-R (or P-Q) interval (aka first degree heart block)
 Usually, the time between the beginning of the P wave and the beginning of the
QRS complex, is about 0.16 seconds, with the heart beating at a normal rate
 This is the P-R interval, and it usually decreases in length with faster
heartbeat, and increases with slower heartbeat
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When the P-R interval increases to more than 0.2 seconds, the P-R interval is
said to be prolonged, and the patient is said to have a first-degree incomplete
heart block
 Page 144 bottom pic – prolonged P-R interval
 First degree block – delay of conduction from the atria to the ventricles, but not
actual blockage of conduction
 The P-R interval rarely every increases above 0.35-0.45 seconds, because at that
point the AV bundle has been depressed so much that conduction stops entirely
o Second-degree heart block
 When conduction through the AV bundle is slowed enough to increase the P-R
interval to 0.25-0.45 seconds, the action potential is sometimes strong enough
to pass through the bundle into the ventricles, & sometimes it’s not strong
enough to do this
 When it’s not strong enough, there will be an atrial P wave, but no QRS-T wave,
so you say there’s “dropped beats” of the ventricles
 This is called a second-degree heart block
 Page 145 – bottom left top pic – second degree AV block
 Sometimes, every other beat of the ventricles is dropped, so a “2:1 rhythm”
develops, with the atria beating twice for every single beat of the ventricles
 Other rhythms like 3:2 or 3:1 can happen other times too
Complete A-V block (third degree block)
o When whatever is causing poor conduction in the AV node or bundle gets severe,
there’s a complete block of the impulse from the atria into the ventricles
o The ventricles then spontaneously establish their own signal, usually originating in the
AV node or AV bundle
o This causes the P waves to get dissociated from the QRS-T complexes
 Page 145 bottom left pic – complete AV block
 In the example, atria are beating at 100 bpm, while ventricles at less
than 40 bpm
 There is no relation between the rhythm of the P waves and that of the QRS-T
complexes, because the ventricles have “escaped” from control by the atria,
and are beating at their own natural rate, controlled usually by signals
generated in the AV node or AV bundle
Stoke-Adams syndrome (ventricular escape)
o In some people with A-V block, the total block comes and goes, so there’s periods of
impulses getting from the atria to the ventricles, and then suddenly impulses are not
conducted
o The block can last for seconds to weeks before conduction returns
o Stoke-Adams happens in hearts with borderline ischemia of the conductive system
o Each time the A-V conduction stops, the ventricles often don’t start their own beating
until after a delay of 5-30 seconds
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This happens from overdrive suppression, where the ventricle excitability was
suppressed by the atrial rate, but after a few seconds of loss of the atrial
impulses, a part of the Purkinje system beyond the block, usually in the distal AV
node after the blocked point in the node, or in the AV bundle, starts discharging
at 15-40 times per minute, and acts as the new pacemaker of the ventricles
 This is called ventricular escape
o Since the brain can’t stay active for more than 7 seconds without blood supply, most
patients faint after a few seconds after complete block happens, since the blood doesn’t
pump any blood for up to 30 seconds, until the ventricles escape
o After escape, the slow beating ventricles usually pump enough blood to allow rapid
recovery from the faint, and then to sustain the person
o The periodic fainting spells are called Stoke-Adams syndrome
o Sometimes, the amount of time the ventricles aren’t pumping takes so long that it can
hurt their health or cause death
o Patients at risk for this are given artificial pacemakers, which are small battery-operated
electrical stimulators put beneath the skin, with electrodes usually connected to the
right ventricle
o The pacemaker provides continued rhythmical impulses that control the ventricles
Incomplete intraventricular block (block in the Purkinje system)
o Caused by the same things that cause AV block
o Electrical alternans happens from partial intraventricular block every other heartbeat
o Page 145 – electrical alternans
o Tachycardia can cause electrical alternans, because when the rate of the heart is rapid,
it may be impossible for some parts of the Purkinje system to recover from the previous
refractory period quickly enough to respond during every next heartbeat
o Many things that depress the heart, like ischemia, myocarditis, or digitalis toxicity, can
cause incomplete intraventricular block, resulting in electrical alternans
Premature contraction (aka extrasystole, premature beat, or ectopic beat):
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Most premature contractions are from an ectopic foci in the heart, which emit abnormal
impulses at odd times during the heart rhythm
o Possible causes of ectopic foci are local areas of ischemia, calcified plaques in the heart
that presses against and irritates heart fibers, and toxic irritation by drugs, nicotine, or
caffeine
Mechanical initiation of premature contractions is also common during heart catheterization
o You get a bunch of premature contractions when the catheter enters the right ventricle
and presses against the endocardium
Page 146 – bottom left pic – premature atrial contraction (beat)
o The P wave of the premature atrial beat happened too soon in the heart cycle
o In the pic, the P-R interval is shortened, indicating that the origin of the ectopic beat is
in the atria near the A-V node
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The interval between the premature contraction and the next contraction is slightly
prolonged, called a compensatory pause
 One reason for this is that the premature contraction originated in the atrium
away from the SA node, and the impulse had to travel through a lot of atrial
muscle before it discharged the SA node
 This made the SA node discharge late in the premature cycle, and made the next
SA node discharge also late
o Premature atrial contractions happen often in otherwise healthy people
 They’re common in athletes whose hearts are very healthy
 Mild toxic conditions from things like smoking, lack of sleep, taking in too much
coffee, alcoholism, and use of drugs, can also initiate premature atrial
contractions
When the heart contracts early, the ventricles didn’t fill with blood normally, and the stroke
volume output for that contraction is decreased
o So the pulse wave into the arteries after a premature contraction may be so weak that
you can’t feel it in the radial artery
 So there’s a decrease in the # of radial pulses felt
Page 146 bottom right pic – AV node premature contraction
o The P wave will be missing, because it is superimposed onto the QRS-T complex,
because the heart impulse traveled backward into the atria at the same time it traveled
forward into the ventricles
 This P wave slightly distorts the QRS-T complex, but you can’t see the P wave
o AV node premature contractions have the same causes and problems as atrial
premature contractions
Premature ventricular contractions (PVCs) – page 147
o The QRS complex is usually pretty prolonged, because the impulse is conducted mainly
through slowly conducting muscle of the ventricles instead of the Purkinje system
o The QRS complex has a high voltage
 When the normal impulse passes through the heart, it passes through both
ventricles nearly simultaneously
 So in the normal heart, the depolarization waves of the 2 sides of the heart,
which are usually opposite polarity to each other, partially neutralize
 When a PVC happens, the impulse goes in only one direction, so there is no
neutralization, and one whole side or end of the ventricles is depolarized ahead
of the other, causing large electrical potentials
o After almost all PVCs, the T wave has an electrical potential polarity opposite the QRS
complex, because the slow conduction of the impulse through the heart muscle causes
the muscle fibers that depolarize first to repolarize first
o Some PVCs don’t really effect heart pumping that much
 Can happen from cigarettes, excessive coffee, lack of sleep, mild toxic states,
and emotions
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Many PVCs result from stray impulses or re-entrant signals that originate around the
borders of infarcted or ischemic areas of the heart
o People with significant #’s of PVCs have a higher than normal chance of developing
spontaneous lethal ventricular fibrillation (vfib)
 Especially a PVC at the end of the T wave when the ventricles are coming out of
refractoriness, which is a very vulnerable period to cause fibrillation
o In the pic, since both leads 2 and 3 are positive, which shows that its origin (the negative
end) is the base of the heart, and its positive end is toward the apex
 So the first part of the heart to be depolarized in the premature contraction is
the base of the ventricles, which is where the ectopic focus is
Long Q-T syndromes:
o Q wave – ventricle depolarization, T wave – ventricle repolarization
o Q-T interval – time from the Q point to the end of the T wave
o Disorders that delay repolarization of ventricles following the action potential, cause
prolonged ventricular action potentials, and therefore excessively long Q-T intervals
 This is called long QT syndrome (LQTS)
o Long QT syndrome is a concern because delayed repolarization of ventricular muscle
increases a person’s susceptibility to develop a ventricular arrhythmia called torsades de
pointes, which means “twisting of the points”
 Torsades de point – page 148
 The shape of the QRS changes over time, usually following a premature
beat, a pause, and then another beat with a long Q-T interval, which
may trigger arrhythmias, tachycardia, and possible vfib
 When ventricle muscle fiber action potential is prolonged from delayed
repolarization, a premature depolarization can happen before complete
repolarization
 Repetitive premature depolarizations can lead to multiple
depolarizations
 In torsades de pointes, premature ventricular beats lead to pauses,
postpause prolonged QT interval, and arrhythmias
o Disorders of heart repolarization that lead to LQTS can be inherited or acquired
 Congenital forms are rare mutations to sodium or potassium channel genes
 More common are the acquired forms of LQTS, which are associated with
plasma electrolyte changes like low magnesium, potassium, or calcium, or
giving them excess antiarrhythmic drugs like quinidine, or some antibiotics like
fluoroquinolones or erythromycin that prolong the QT interval
o Some people with LQTS have no symptoms other than the prolonged QT interval
o Others show fainting and ventricular arrhythmias that can be precipitated by exercise,
intense emotions, or being startled
 The ventricular arrhythmias can deteriorate into vfib and sudden death
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Treatment for LQTS includes magnesium sulfate for acute LQTS, and antiarrhthmic
durgs for long term LQTS, like β-blockers, or surgical implant of a heart defibrillator
Some abnormalities in different parts of the heart can sometimes cause rapid rhythmic discharge of
impulses that spread in all directions throughout the heart
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This is caused most often by re-entrant circus movement feedback pathways that set up local
repeated self re-excitation
Since it’s rapid, this focus becomes the new pacemaker
Paroxysmal tachycardia – the heart rate becomes rapid in paroxysms (episodes), where it starts
suddenly, lasts for seconds to hours, and then ends suddenly
Paroxysmal tachycardia can often be stopped by triggering a vagal reflex
o You can press on the neck at the carotid sinus
o Drugs like quinidine and lidocaine both decrease sodium permeability of the heart
muscle membrane, blocking discharge at the ectopic foci
Atrial paroxysmal tachycardia – page 148 middle pic
o You’ll see an abnormal P wave before each QRS, that’s sometimes inverted, or
superimposed onto the normal T wave
 This indicates that the origin of the tachycardia is in the atrium, but not near the
SA node because of the abnormal P wave
AV nodal paroxysmal tachycardia often results from an abnormal rhythm of the AV node
o This causes normal QRS, but missing or hidden P waves
Atrial and AV node paroxysmal tachycardia are called supraventricular tachycardias, because
the foci is before the ventricles
o They usually happen in young, otherwise healthy people, who then grow out of them
as they grow up
o Usually, supraventricular tachycardia frightens the person, and may cause weakness
during the episode, but rarely does permanent harm to them
Ventricular paroxysmal tachycardia – page 149 to pic
o It’s EKG looks like a series of ventricular premature beats, without any normal beats
between them
o Ventricular paroxysmal tachycardia is a serious problem
 It usually doesn’t happen unless there is a lot of ischemic damage to ventricles
 Ventricular tachycardia often triggers ventricular fibrillation, because of rapid
repeated stimulation of the ventricular muscle
o Sometimes intoxication from the heart drug digitalis causes irritable foci that lead to
ventricular tachycardia
o Quinidine can be used to block irritable foci causing ventricular tachycardia, because it
increases the refractory period and threshold for excitation of heart muscle
The most serious heart arrhythmia is ventricular fibrillation (vfib), which if not stopped within 1-3
minutes, is almost always fatal
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Vfib happens from heart impulses that have gone berserk in the ventricular muscle, stimulating
first one part of the ventricle, then another, and another, eventually feeding back onto itself to
re-excite the same ventricular muscle over and over, never stopping
When this happens, many small parts of the ventricular muscle will be contracting at the same
time, while other parts of the ventricle will be relaxing
So there is never a coordinated contraction of the whole ventricle at once, which is something
that is needed for the heart to pump
The ventricle chambers neither enlarge or contract, and instead remain in a state of partial
contraction, and pump no blood, or only tiny amounts
So after vfib starts, they become unconscious within 4-5 seconds from lack of blood to the brain
After a few minutes, irreversible death of the body tissues starts to happen
Both sudden electrical shock of the heart, and ischemia of the heart muscle or conducting
system, can trigger vfib
When the normal heart impulse in the normal heart has gone through the extent of the
ventricles, it has no place to go because all the ventricular muscle is refractory and can’t
conduct the impulse any farther
o So the impulse dies, and the heart doesn’t move until a new action potential starts at
the SA node
“circus movement” – when the impulse re-enters muscle that has already been excited
o If the pathway is too long, by the time the impulse returns to its starting point, the
originally stimulated muscle is no longer refractory, and the impulse will continue
around its pathway again – page 149 bottom pics
 Long pathways usually happen in dilated hearts
o If the velocity of conduction decreases enough, it takes more time to get back to the
starting point, so when it gets there the muscle is no longer refractory, and the impulse
cycles through its pathway again
 Decreased rate of conduction often happens from blockage of the Purkinje
system, ischemia of the muscle, or high blood potassium
o If the refractory period of the muscle is made shorter, then when the impulse gets back
to this muscle it’s no longer refractory and the impulse continues
 A shortened refractory period often happens in response to drugs like
epinephrine, or after repetitive electrical stimulation
o So re-enetry can cause abnormal patterns of heart contraction or abnormal heart
rhythms that ignore the SA node
In vfib, you see many separate and small contractile waves spreading at the same time in
different directions over the heart muscle
o The re-entrant impulses aren’t just one impulse moving in a circle, they instead have
degenerated into a series of many waves that work like a chain rxn
o Fibrillation by giving them electrical shock:
 An electrical stimulus is applied to a central point in the ventricles through an
electrode
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The first cycle of electrical stimulus causes a depolarization wave to spread in
all directions, leaving all the muscle beneath the electrode in a refractory state
 After about 0.25 seconds, part of the muscle starts to come out of the refractory
state
 Some parts stop being refractory before others
 Page 150 – pic of this, dark red is refractory, light is tissue that can be excited
 Continuing stimuli from the electrode can cause impulses to travel only certain
directions now through the heart, not all directions
 Next several things happen at once:
 Block of impulses in some directions, but not in other directions, allows
movement of some depolarization waves in only some directions
around the heart, but not others
 The rapid stimulation of the heart causes 2 things that predispose to
circus movement
o Velocity of conduction through the heart muscle decreases,
making it take longer for impulses to travel around the heart
o The refractory period of the heart muscle is shortened
 When a depolarization wave reaches a refractory area, it travels to both
sides around the area, by splitting the impulse into 2 impulses
o Then each split impulse meets a new refractory area, causing
both impulses to split again
o These chain rxns form many small depolarization waves
traveling in many directions at the same time
o This creates many routes for impulses to travel, greatly
lengthening the conductive pathway, which can allow circus
movements
 So more and more impulses are formed, causing more and more patches of
refractory muscle, which cause more and more division of the impulses
 So any time a part of the heart muscle stops being refractory, an
impulse is coming in to re-enter the area
In vfib, the EKG shows no regular rhythm – page 151 top left pic
o During the first few seconds of vfib, large areas of muscle contract simultaneously,
causing coarse irregular waves in the EKG
o After another few seconds, these coarse contraction of the ventricles disappear, and the
EKG changes into a pattern of low-voltage irregular waves
o There is no repetitive pattern in vfib
o The voltages seen are usually very small after 20-30 seconds
Electroshock defibrillation of the ventricles – page 151 top right pic
o Although a moderate alternating current voltage applied directly to the ventricles
usually throws the ventricles into fibrillation, a strong high voltage alternating electrical
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current passed through the ventricles for a fraction of a second can stop fibrillation by
throwing all the ventricular muscle in refractoriness at the same time
o This is done by passing intense current through large electrodes placed on 2 sides of the
heart
o The current penetrates most of the fibers of the ventricles at the same time, stimulating
all parts of the ventricles simultaneously, and causing them all to become refractory
o All action potentials stop, and the heart remains quiescent (inactive) for 3-5 seconds,
after which it starts to beat again, usually with SA node pace
o However, the same re-entrant focus that originally caused vfib is often still there, and
can cause fibrillation again immediately
Hand pumping of the heart (cardiopulmonary resuscitation) to help defibrillation:
o Unless defibrillated within a minute after fibrillation starts, the heart is usually too weak
to be revived by defibrillation, cause of the lack of nutrition from coronary blood flow
o You can still revive the heart by pumping the heart by hand, and then defibrillating the
heart after
o This causes small amounts of blood to get into the aorta, bringing in new coronary
blood supply
o After a few minutes of hand pumping, electrical defibrillation becomes possible
o Cardiopulmonary resuscitation (CPR) – intermittent thrusts of pressure on the chest wall
along with artificial respiration
o After 5-8 minutes of no blood to the brain, you get permanent mental impairment or
death of brain tissue
 So even if the heart is revived, the person may die from brain damage, or live
permanently impaired
Since the atria and ventricles are separated by fibrous tissue, fibrillation in each often happen separately
Atrial fibrillation (afib):
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Works just like the vfib, just in the atria instead
A common cause of afib is atrial enlargement from heart valve lesions that prevent the atria
from emptying enough into the ventricles, or from ventricle failure with excess damming of
blood in the atria
Dilated atrial walls provide ideal conditions of a long conductive pathway, as well as slow
conduction, predisposing to afib
The atria don’t pump blood in afib
o So blood can only flow passively from the atria into the ventricles, decreasing
ventricular pumping by 20-30%
o So unlike vfib, afib is not lethal and they can live for months to years with afib
Page 152 – bottom left pic - EKG of afib
o You see no P waves or only a high frequency, low voltage wavy record, with normal
looking QRS complexes that have irregular timing
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Many small depolarization waves spread in all directions through the atria in
afib, that are weak and have opposite polarity, so they neutralize each other
During afib, impulses go from the atrial muscle to the AV node rapidly and irregularly
o Because the AV node will not pass a second impulse for about 0.35 seconds after a
previous one, at least 0.35 seconds have to go by between one ventricular contraction
to the next
o Then an additional interval of 0 to 0.6 seconds happens before one of the irregular atrial
impulses gets to the AV node
o So the interval between each ventricular contraction can be anywhere from 0.35 to 0.95
seconds each time, causing a very irregular heartbeat
 This is a clinical finding used to diagnose afib, and is called an irregularly
irregular rate
o Also, because of the rapid rate of the fibrillatory impulses in the atria, the ventricle is
driven at a fast heart rate, usually between 125 to 150 bpm
You can also shock the atria to fix afib just like vfib, but only works if the heart is capable
Atrial flutter – another thing caused by circus movements that differs from afib in that the electrical
signal travels as a single large wave in one direction around and around the atrial muscle
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Page 152 – right pic – difference between afib and atrial flutter
Atrial flutter causes a rapid rate of contraction of the atria, usually between 200-350 bpm
Since one side of the atria is contracting though while the other is relaxing, the amount of blood
pumped by the atria is slight
Also, the signals reach the AV node too fast for all of them to be passed into the ventricles, due
to the refractory period of the AV node and AV bundle
o So there are usually 2-3 beats of the atria for every beat of the ventricles
Page 153 – atrial flutter EKG
o The P waves are strong, and there is 2-3 P waves before each QRS
Cardiac arrest – stop of all electrical signals in the heart, with no spontaneous rhythm happening
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Cardiac arrest can happen during deep anesthesia, when many patients develop severe hypoxia
because of inadequate respiration
o The hypoxia prevents muscle fibers and conductive fibers from maintain normal
electrolyte concentrations across their membranes, changing their excitability so that
automatic rhythmicity disappears
o CPR is good at fixing heart rhythm in this case