Phys Ch 13
Abnormal Sinus Rhythms
 Tachycardia – more than 100 bpm, usually caused by increased body temp, SNS stimulation, and toxic conditions
of heart
o Heart rate increases about 10 bpm for each degree Fahrenheit increase in body temperature (18 bpm
for each degree Celsius) up to a body temperature of 105oF (40.5oC); after that, heart rate may decrease
because of progressive debility of heart muscle as result of fever
o Fever causes tachycardia because increased temp increases rate of metabolism of SA node, which
directly increases its excitability and rate rhythm
o Weakening of myocardium usually increases heart rate because weakened heart does not pump blood
into arterial tree to a normal extent, and this elicits SNS reflexes to increase heart rate
 Bradycardia – less than 60 bpm
o Athlete’s heart is larger and considerably stronger than that of normal person, which allows athlete’s
heart to pump large stroke volume output per beat even during periods of rest; when athlete at rest,
excessive quantities of blood pumped into arterial tree with each beat initiate feedback circulatory
reflexes or other effects to cause bradycardia
o Any circulatory reflex that stimulates vagus nerves causes release of acetylcholine at vagal endings in
heart, giving PNS response
o Patients with carotid sinus syndrome – baroreceptors in carotid sinus excessively sensitive, so even mild
external pressure on neck elicits strong baroreceptor reflex, causing intense vagal-acetylcholine effects
on heart, including extreme bradycardia
 Cardiotachometer – records duration of interval between successive QRS complexes in EKG by height of
successive spikes (flat line means constant heart rate, changes reflect changes in heart rate)
 Sinus arrhythmia – heart rate greatly changes during respiration; can result from circulatory conditions that alter
strengths of SNS and PNS nerve signals to SA node – in respiratory sinus arrhythmia, this results mainly from
spillover of signals from medullary respiratory center into adjacent vasomotor center during inspiratory and
expiratory cycles of respiration (cause alternate increase and decrease in number of impulses transmitted
through sympathetic and vagus nerves to heart)
Abnormal Rhythms That Result from Block of Heart Signals within Intracardiac Conduction Pathways
 Sinoatrial block – impulse from sinus node blocked before it enters atrial muscle; sudden cessation of P waves
with resultant standstill of atria; nodal focus takes over heart rate, so ventricles still depolarize
 AV block – caused by ischemia of AV node or AV bundle fibers, compression of AV bundle by scar tissue or
calcified portions of heart, inflammation of AV node or AV bundle, extreme stimulation of heart by vagus nerves
(as might happen with carotid sinus syndrome)
o PR interval seldom increases above 0.35-0.45 seconds because by that time, conduction through AV
bundle is depressed so much that conduction stops entirely
o Borderline ischemia of conductive system causes total block to come and go
o Can take a few seconds for overdrive suppression to wear off and for lower foci to start beating
o Because brain cannot remain active for more than 4-7 seconds without blood supply, most patients faint
a few seconds after complete block occurs because heart does not pump blood for 5-30 seconds until
ventricles escape
o Stokes-Adams syndrome – periodic fainting spells due to inadequate blood circulation
o Ventricular escape patients need artificial pacemaker (electrodes on right ventricle)
 Electrical alternans – results from partial intraventricular block every other heartbeat (strong beat followed by
weak beat); can be caused by tachycardia because when rate of heart is rapid, it may be impossible for some
portions of Purkinje system to recover from previous refractory period quickly enough to respond during every
succeeding heartbeat
o Many conditions that depress heart rate (ischemia, myocarditis, digitalis toxicity) can cause incomplete
intraventricular block resulting in electrical alternans
Premature Contractions
 Premature contractions also called extrasystole, premature beat, or ectopic beat

Most premature contractions result from ectopic foci in heart caused by local areas of ischemia, small calcified
plaques at different points in heart that press against adjacent cardiac muscle so that some of the fibers are
irritated, or toxic irritation of AV node, Purkinje system, or myocardium caused by drugs, nicotine, or caffeine
 Mechanical initiation of premature contractions frequent during cardiac catheterization: large number of
premature contractions may occur when catheter enters right ventricle and presses against endocardium
 Compensatory pause after premature atrial beat caused because premature contraction originated in atrium
some distance from sinus node and impulse had to travel through a lot of atrial muscle before it discharged SA
node, so SA node discharged late in premature cycle, thus making succeeding SA node discharge late
 Premature atrial beats often happen in athletes whose hearts are in very healthy condition; can also be caused
by smoking, lack of sleep, ingestion of too much coffee, alcoholism, and use of various drugs
 When heart contracts prematurely, ventricles will not have filled with blood normally, and stroke volume output
during that contraction is depressed or almost absent, so pulse wave passing to peripheral arteries after
premature contraction may not be felt in radial artery
 PVCs have wide QRS complex because impulse conducted mainly through slowly conducting muscle of ventricles
instead of through Purkinje system
o QRS complex has high voltage because when normal impulse passes through heart, it passes through
both ventricles simultaneously, so depolarization waves partially neutralize each other – when PVC
occurs, impulse almost always travels in only one direction, so there is no neutralization effect, and one
entire side or end of ventricles is depolarized ahead of the other
o After almost all PVCs, T wave has electrical potential polarity exactly opposite that of QRS complex
because slow conduction of impulse through cardiac muscle causes muscle fibers that depolarize first to
also repolarize first
o Presence of PVCs is not to be taken lightly, even though some PVCs are relatively benign and can be
caused by excessive caffeine intake or lack of sleep; however, significant numbers of PVCs have a much
higher than normal chance of developing spontaneous V fib, presumably initiated by one of the PVCs
 Occurs easily with R on T phenomenon (vulnerable period)
 Can locate origin of ectopic PVCs with vector analysis (take mean of two vectors)
 Long QT syndrome (LQTS) – disorders that delay repolarization of ventricular muscle following AP (prolonged QT intervals); delayed repolarization of ventricles increases person’s susceptibility to develop torsade de pointes
o Shape of QRS complex may change over time with onset of arrhythmia usually following a premature
beat, a pause, and then another beat with a long Q-T interval, which may trigger arrhythmias,
tachycardia, and sometimes V fib
o Congenital forms of LQTS are rare disorders caused by mutations of Na or K channel genes
o Most common LQTS are acquired forms associated with plasma electrolyte disturbances, such as
hypomagnesemia, hypokalemia, or hypocalcemia
o Can be caused by administration of excess amounts of antiarrhythmic drugs such as quinidine or some
antibiotics such as fluoroquinolones or erythromycin that prolong Q-T interval
o Some people show no symptoms, some exhibit fainting and ventricular arrhythmias that may be
precipitated by physical exercise, intense emotions such as fright or anger, or when startled by noise
o Treatment for LQTS includes magnesium sulfate for acute LQTS and antiarrhythmic medications such as
beta-adrenergic blockers for long term LQTS (can have artificial pacemaker installed)
Paroxysmal Tachycardia
 Some abnormalities in various foci can cause rapid rhythmical discharge of impulses that spread in all directions
throughout heart, most frequently caused by re-entrant circus movement feedback pathways – because of rapid
rhythm in irritable focus, this becomes pacemaker of heart
 Paroxysmal tachycardia – heart rate becomes rapid in paroxysms (sudden onset, continues for a while, then
rhythm goes back to normal); often stopped by eliciting a vagal reflex (press on carotid sinus) or can use
quinidine or lidocaine, either of which depresses normal increase in sodium permeability of cardiac muscle
membrane during generation of AP, blocking rhythmical discharge of focal point causing paroxysm
 Supraventricular tachycardias usually occur in young, otherwise healthy people who generally grow out of
predisposition to tachycardia after adolescence – very scary to person at time and may cause weakness during
paroxysm, but seldom does it cause permanent harm

Ventricular paroxysmal tachycardia serious because it usually does not occur unless considerable ischemic
damage is present in ventricles and it frequently initiates V fib because of rapid repeated stimulation of
ventricular muscle
o Sometimes intoxication from digitalis can cause irritable foci that lead to V tach
o Quinidine, which increases refractory period and threshold for excitation of cardiac muscle, may be used
to block irritable foci causing V tach
Ventricular Fibrillation
 If not stopped in 1-3 minutes, it is almost invariably fatal
 Results from cardiac impulses that have gone berserk in ventricular muscle mass, stimulating different portions
of ventricular muscle and eventually feeding back onto itself to re-excite the first ventricular focus
 Ventricles remain in an indeterminate stage of partial contraction, pumping little to no blood
 Most common causes of fibrillation include sudden electrical shock of heart or ischemia of heart muscle,
conduction system, or both
 Circus movements – when normal cardiac impulse has traveled through extent of ventricles, it has nowhere to
go because all ventricular muscle is refractory and cannot conduct impulse farther, so impulse dies; three
different conditions can cause circus movement (re-entry of impulse into muscle that has already been excited)
o Pathway is too long, such that by time impulse returns to original position, the muscle there will no
longer be refractory and impulse will continue around another time (as would occur in dilated hearts)
o If velocity of conduction is decreased, an increased interval of time will elapse before impulse returns to
position of origin, and originally stimulated muscle may be out of refractory state, so impulse would go
around again (as would occur from blockage of Purkinje system, ischemia of heart, high blood K+ levels,
or many other factors)
o Refractory period of muscle becomes shortened, such that impulse can continue around again (as would
occur in response to epinephrine or after repetitive electrical stimulation)
 60-cycle electrical stimulus to heart – first cycle of stimulus causes depolarization wave to spread in all
directions, leaving all muscle beneath in refractory state; after 0.25 seconds, part of muscle begins to come out
of refractory state before others, so stimuli can cause impulses to travel in certain directions through heart, but
not all directions, as stimuli travel between refractory areas and stimulate receptive parts
o Block of impulses in some directions but successful transmission in other directions creates condition for
re-entrant signal to develop
o Rapid stimulation of heart causes 2 more changes that predispose to circus movement
 Velocity of conduction through heart decreases
 Refractory period of muscle is shortened
o Division of impulses – when depolarization wave reaches refractory area in heart, it travels to both sides
around refractory area (single impulse becomes 2 impulses), and new wave fronts continually being
formed cause chain reaction until there are many small depolarization waves traveling in many
directions at once
o Irregular pattern of impulse travel causes many circuitous routes for impulses to travel, greatly
lengthening conductive pathway, which is one of conditions that sustains fibrillation (causes continual
irregular pattern of patchy refractory areas in heart)
 Ventricular muscle contracts as many as 30-50 small patches of muscle at a time, and potentials change
constantly and spasmodically (large irregular waves followed by smaller waves followed by larger waves on EKG
with no rhyme or reason or periodicity to size of waves)
 Strong high-voltage alternating electrical current passed through ventricles for fraction of a second can stop
fibrillation by throwing all ventricular muscle into refractoriness simultaneously; all APs stop and heart remains
quiescent for 3-5 seconds, then it begins to beat again, usually with SA node but sometimes another focus can
become pacemaker; sometimes, same re-entrant focus that had originally caused fibrillation is still present and
can cause fibrillation again almost immediately
o Defibrillator usually uses 110 volts of 60-cycle AC applied for 0.1 second (can also use 1000 volts of DC
for a few thousandths of a second)
 Unless defibrillated within 1 minute after fibrillation begins, heart usually too weak to be revived by
defibrillation because of lack of nutrition from coronary blood flow, but performing manual CPR and
defibrillating later can be successful
o
o
Small quantities of blood delivered into aorta and renewed coronary blood supply develops with CPR
Fibrillating hearts have been kept alive by CPR for as long as 90 minutes followed by successful
defibrillation
o Lack of blood flow to brain for more than 5-8 minutes usually causes permanent mental impairment or
destruction of brain tissue, so even if heart is revived, person may die from effects of brain damage or
live with permanent mental impairement
Atrial Fibrillation
 Identical mechanism to V fib except that process occurs only in atrial muscle mass instead of ventricles
 Frequent cause is atrial enlargement resulting from heart valve lesions that prevent atria from emptying
adequately into ventricles or from ventricular failure with excess damming of blood in atria
 Dilated atrial walls provide ideal conditions of long conductive pathway, as well as slow conduction, both of
which predispose to A fib
 When A fib occurs, impulses arrive from atrial muscle at AV node rapidly and irregularly; because AV node will
not pass a second impulse for about 0.35 seconds after previous one, at least 0.35 seconds must elapse between
one ventricular contraction and next
o Additional variable interval of 0-0.6 seconds occurs before one of irregular atrial fibrillatory impulses
happens to arrive at AV node, so interval between successive ventricular contractions varies from
minimum of 0.35 seconds to maximum of 0.95 seconds, causing very irregular heartbeat
 Because of rapid rate of fibrillatory impulses in atria, ventricular contraction rate is usually 120-150
 Can also be treated by electroshock same as V fib, but heart can only resume normal rhythm if it is capable of
sustaining normal rhythm
Atrial Flutter
 Caused by circus movement in atria, but electrical signal travels as single large wave in one direction and
continues re-entry style (signal never splits as with A fib)
 Causes rapid rate of contraction of atria (200-350 bpm), but because one side of atria is contracting while other
side is relaxing, amount of blood pumped by atria is slight
 Signals reach AV node too rapidly for all of them to be passed into ventricles, so there are usually 2-3 beats of
atria for every single beat of ventricles
Cardiac Arrest
 Results from cessation of all electrical control signals in heart (no spontaneous rhythm remains)
 May occur during deep anesthesia when patients develop severe hypoxia because of inadequate respiration
 Hypoxia prevents muscle fibers and condu tive fibers from maintaining normal electrolyte concentration
differentials across membranes, and excitability may be so affected that automatic rhythmicity disappears
 In most instances of cardiac arrest from anesthesia, prolonged CPR (many minutes to hours) is quite successful
in reestablishing normal heart rhythm
 In some patients, severe myocardial disease can cause permanent or semipermanent cardiac arrest, which can
cause death
 Condition treated with implanted artificial pacemaker