Cardiac Arrhythmias
 Abnormal rhythm of the heart
 One or combination in the abnormalities in the rhythmicity-
conduction system of the heart:
1. Abnormal rhythmicity of the pacemaker
2. Shift of the pacemaker from the sinus node to another
place in the heart
3. Blocks at different points in the spread of the impulse
through the heart
4. Abnormal pathways of impulse transmission through the
heart
5. Spontaneous generation of spurious impulses in almost
any part of the heart
ABNORMAL SINUS RHYTHMS
a. Tachycardia
- Fast heart rate; >100 bpm
- 72 bpm normal heart rate
- Causes: increased body temperature, stimulation of the
heart by sympathetic nerves, toxic conditions of the heart
- HR increases by 10 bpm for each degree of Fahrenheit/ 18
beats per degree of Celsius during increased body
temperature but only up to 105 Fah or 40.5 C beyond, HR
decrease due to progressive debility of the heart muscle as
a result of the fever
- Fever causes tachycardia due to increased temperature
increases metabolism of the sinus node increases
excitability and rate of rhythm
- Shock/ semishock  loss of blood  sympathetic reflex
stimulation of the heart  increase HR 150-180bpm
- Weakening of the myocardium  sympathetic reflexes 
increased HR kailangan ni kay weakened myocardium does
not pump blood in the arterial tree to a normal extent
b. Bradycardia
- Slow heart rate <60 bpm
o Bradycardia in athletes
 Athletes heart is larger and stronger
pump large stroke volume output per
beat even in rest
1. At rest
2. Excessive quantities of blood
pumped into arterial tree
3. Each beat initiate feedback
circulatory reflexes
4. Bradycardia
o Vagal stimulation causes bradycardia
 Any circulatory reflex stimulates vagus
nerves  vagus nerves release Ach at
the vagal endingsin the heart 
parasympathetic effect  bradycardia
 Carotid sinus syndrome
baroreceptors (pressure receptors) in
the carotid sinus region in carotid artery
walls very sensitive  mild external
pressure on the neck  strong
baroreceptor reflex  circulatory reflex
stimulates vagus nerves  vagus
nerves release Ach at the vagal endings
in the heart  parasympathetic effect
 bradycardia
c. Sinus Arrhythmia
- Quiet respiration: HR increased and decreased no more
than 5%
- Deep respiration: HR increased and decreased with each
respiratory cycle by 30%
- Can be caused by alterations of sympathetic and
parasympathetic nerve signals to the sinus node
- Respiratory type of sinus arrhythmia:
o Spillover of signals from medullary respiratory
center into the adjacent vasomotor center during
inspiratory and expiratory cycles of respiration
o Spillover causes alternate increase and decrease
in the number of impulses transmitted through
the sympathetic and vagus nerves to the heart
- Cardio tachometer: instrument that records by the height
of successive spikes the duration of the interval between
successive QRS complexes on ECG
ABNORMAL RHYTHMS THAT RESULT FROM BLOCL OF HEART
SIGNALS WITHIN INTRACARDIAC CONDUCTION PATHWAYS
a. Sinoatrial block
- Impulse from the sinus node is blocked before it enters the
atrial muscle
- Cessation of P waves standstill of the atria
- Ventricles pick up a new rhythm  impulse originates in the
AV node  QRS slowed but not altered
b. Atrioventricular block
- Bundle of his
- Impulses travel from atria to the ventricles
- Conditions that decrease the rate of impulse conduction in
the bundle or block the impulse entirely:
o Ischemia of the AV node or Av bundle fibers-
coronary insufficiency causes this and also causes
ischemia of the myocardium
o Compression of the AV bundle by scar tissue or
calcified portions of the heart can depress or
block conduction from the atria to the ventricles
o Inflammation of the AV node or AV bundle
(myocarditis due to diphtheria or rheumatic
fever)
o Extreme stimulation of the heart by vagus nerves
block impulse conduction through the AV node
(carotid sinus syndrome)
c. Incomplete Atrioventricular heart block
o Prolonged PR or PQ interval
 First degree incomplete heart block
(>0.20s)
 First degree heart block means delay of
conduction from the atria to the
ventrivels but not actual blockage of
conduction
 PR interval >0.35-0.45s  conduction
through the AV bundle is depressed 
conduction stops entirely
 Acute rheumatic heart disease 
assess PR interval
 PR interval decrease in tachycardia and
increase in bradycardia
o Second degree block
 There is P wave but no QRST wave with
dropped beats of the ventricles
 AV bundle slowed to increase PR
interval to 0.25-0.45s
 Action potential sometimes passes
through the bundle and sometimes
NOT
 2:1 rhythm  atria beating twice for
ever beat of the ventricles
 Also 3:2 or 3:1
o Third degree block – Complete AV block
 Ventricles establish own signal
originating the AV node or Av bundle
 Ventricles escaped from control of the
atria so beating at their own natural
rate
 P waves dissociated from the QRST
waves
 So no relation between the P wave and
the QRST waves
o Stokes Adams syndrome- Ventricular escape
 Borderline ischemia of conduction
system- impulses from atria to
ventricles for a period of time and
suddenly impulses are not conducted.
Duration of block is dependent on when
mubalik jud ang normal conduction
 Complete AV block comes and goes
 Ventricles start own beating when
there is 5-30s delay from atria 
overdrive suppression
  Overdrive suppression- ventricles stop
contracting for 5-30s  ventricles
excitability is first suppressed because
ventricles have been driven by the atria
at a greater rate than natural
 Ventricular escape- overdrive
suppression then purkinje fibers begins
discharging 15-40bpm and acts as the
pacemaker of the ventricles
1. Brain cannot remain active without blood
in 4-7s nya delay bya ug 5-30s so mu faint
ang patient
2. Ventricular escape allow enough blood
to allow rapid recovery
 Interval of ventricular standstill and
onset of complete block is long that
causes death
 Artificial pacemaker- small battery
operated electrical stimulator planted
beneath the skin; electrodes connected
at the right ventricle ; provides
continued rhythmical impulses to take
control of the ventricles
d. Incomplete intraventricular block- electrical alternans
- Partial intraventricular block every other heartbeat
- Tachycardia  some portion of purkinje fibers do not
recover from previous refractory period quickly to respond
to every heartbeat
- Depresses the heart (ischemia, myocarditis, digitalis
toxicity) incomplete intraventricular block  electrical
alternans
PREMATURE CONTRACTIONS
- Contraction of the heart before the time that normal
contraction would have been expected
- Extrasystole, premature beat, ectopic beat
- Most premature contraction result from ectopic foci ( emit/
produce abnormal impulses at odd times during the cardiac
rhythm)
- Ectopic beat- beats arise from fibers outside the region of
the heart muscle
- Atrial ectopic focus- atrial cell outside the SA nodes initiate
depolarization; part of conduction system or from cardiac
muscle cell
- Causes of ectopic foci:
o Local areas of ischemia
o Small calcified plaques at different points in the
heart press against the adjacent cardiac muscle so
the fibers are irritated
o Toxic irritation of the AV node (drugs, alcohol,
caffeine)
o Mechanical initiation during cardiac
catheterization ( large numbers of premature
contractions often occur when the catheter
enters the right ventricle and presses against the
endocardium)
a. Premature atrial contraction
- Atria contractions earlier than normal
- Atrial ectopic focus- atrial cell outside the SA nodes initiate
depolarization; part of conduction system or from cardiac
muscle cell
- Can be caused by reentrant loop  do not depolarize right
 scar tissue na mu depolarize around the adjacent cells
mao makacontract
- Ectopic focus depolarizes the SA node causing the SA node
to skip a cycle
- Location of the ectopic focus:
o Bottom of the atrium then upside down kay
opposite to the direction of the depolarization
o Close to AV node then short PR interval kay dali ra
maabot sa AV node since duol ra sya
o Tachycardia- P wave and T wave is one, making a
camel lump
- Compensatory pause- interval between the premature
contraction and next contraction is slightly prolonged (mas
layu ang ectopic focus sa sinus node)
- Mild toxic conditions like smoking, lack of sleep, coffee,
alcoholism; healthy people and athletes
- Pulse deficit: heart contracts ahead ventricles not
completely filled  stroke volume output depressed or
absent  pulse wave to radial artery so weak cannot be felt
 deficit of radial impulses compared to contractions of
the heart
b. AV nodal or AV bundle premature contraction
- Premature contraction originated in the AV bundle or Av
node
- No P wave kay na superimposed in the QRST complex
because the cardiac impulse traveled backward into the
atria at the same time it travelled forward into the
ventricles
c. Premature ventricular contraction
- Abnormal t waves since the timing and direction of
repolarization is abnormal
- Cigarette, coffee, lack of sleep, mild toxic states, emotional
irritability, stray impulses, reentrant signals that originate
around the borders of the infarcted or ischemic areas of the
heart
- Increased PVC higher chance of developing lethal
ventricular fibrillation that can be initiated by this PVC
during the end of the T wave when ventricles is out from
refractoriness
o QRS is prolonged kay ang impulse from the slowly
conducting muscle of the ventricles and not from
the purkinje system
o QRS has voltage because:
 Impulse travels in one bundle branch to
another  not together
 One side of the ventricles is depolarized
ahead of the other
o The cardiac muscle that depolarize first will
repolarize first  T wave has an electrical
potential polarity opposite to the QRS complex
PAROXYSMAL TACHYCARDIA
- Can be stopped by producing a vagal reflex to press the
neck in the regions of the carotid sinuses to cause vagal
reflex to stop the paroxysm
- Quinidine, lidocaine depress normal increase in Na
permeability of the cardiac muscle during action potential
blocking rhythmical discharge of the focal point causing
paroxysmal attack
- Reentrant loops for depolarization in all directions through
the heart
- Ectopic focus becomes the pacemaker of the heart
- Paroxysmal- means that the HR becomes rapid in
paroxysms with the paroxysm beginning suddenly and
lasting on few secs, mins or hours then ends suddenly with
the pacemaker of the heart shifting back to the sinus node
Atrial paroxysmal tachycardia
- Inverted P wave before QRST complex
- P wave superimposed in T wave
- Origin of the paroxysmal tachycardia is in the atrium but
abnormal in shape so not near the sinus node
AV nodal paroxysmal tachycardia
- Missing or obscured P waves; almost normal QRST waves
!!!! Supraventricular tachycardias- Atrial and AV nodal
paroxysmal tachycardia; grows out to predisposition to
tachycardia after adolescence; frightens a person tremendously
causes weakness during paroxysm seldom permanent harm
from the attack
Ventricular Paroxysmal tachycardia
- Series of ventricular premature beats occurring one to the
other without any normal beats interspersed
- Serious condition:
o Occur only in considerable ischemic damage in
ventricles
o Initiate lethal condition of ventricular fibrillation
- Drug digitalis causes irritable foci leading to ventricular
tachycardia
 - Quinidine increases refractory period and threshold for
excitation of cardiac muscle to block irritable foci
VENTRICULAR FIBRILLATION
- Quivering from uncoordinated muscle contraction
- Not contracting at the same time
- Tissue heterogeneity  signal radiates out  PVS  >3 PVS
in a row is called ventricular tachycardia that can progress
to VF
- Functional reentry- spiraling of signals in focus to initiate
another depolarization  fibrillation
- Anatomical reentry- scar tissue spiraling signals
- Electrical stimulation on upslope of the T wave to induce
fibrillation so some cells are ready for depolarization and
some not so some contract and some don’t kay still
refractory phase  abnormal conduction  reentry
- Fib waves
- Defibrillation- high energy shock to depolarize everything at
once
- When ventricular fibrillation is not stopped within 1-3mins
 invariably fatal
- No coordinate contraction of ventricular muscle at once
- Ventricles neither enlarge or contract but remain
indeterminate stage of partial contraction pumping no
blood or negligible amounts
- Fibrillation begins  unconsciousness within 4-5s lack of
blood in brain  death in tissues
- Initiate fibrillation:
1. Sudden electrical shock of the heart
2. Ischemia of the heart muscle, conducting
system or both
Re entry
- Circus movements as the basis for ventricular fibrillation
o Pathway along the circle is too long by the time
the impulse returns to the 12 o’clock position, the
originally stimulated muscle is no longer
refractory and the impulse will continue around
the circle again
o Decreased velocity of the conduction so hinay
mutuyok igo mahuman ang refractory period
o Shortened refractory period
- Long pathway occurs in dilated hearts
- Decreased rate of conduction due to blockage of purkinje
system, ischemia of the muscle, high blood K level
- Shortened refractory in response to EP, after repetitive
electrical stimulation
- Abnormal patterns of contraction that ignore the pace
setting effects of the sinus node
CHAIN REACTION MECHANISM OF FIBRILLATION
- Not a single impulse moving in circle but degenerated into
a series of multiple wave fronts that have the appearance
of chain reaction
Fibrillation caused by 60 cycle alternating current
o Alternating current is BAD kay mu cause
fibrillation
o Block of impulses in some directions then
successful transmission in other directions
creates one of the necessary re entrant signal to
develop
o Rapid stimulation of the heart causes two
changes in the cardiac muscle itself both of Cardiac Arrest
predisposes (making susceptible) to circus
movement
 Decreased velocity of the conduction
 Shortened refractory period
o Division of impulses- progressive chain reactions
with many wave fronts ready to depolarize;
irregular patterns of impulse travel causes many
circuits routes for the impulses to travel greatly
lengthening the conductive pathway that sustains
fibrillation
ECG in VF
1. Coarse irregular waves
2. Corse contractions disappear
3. Low voltage very irregular waves
4. No repetitive ECG pattern
- Ventricular muscle contracts 30-50 small patches of muscle
at a time; ECG potentials change constantly and
spasmodically kay all directions ang electric currents sa
heart
- ECG voltages in VF 0.5mv then decay after 20-30s then 0.2-
0.3mv. 0.1mv recorder after 10 mins na nagstart ang VF
Electroshock defibrillation of the ventricles:
- Strong high voltage alternating electrical current 
together mu depolarize together ang refractory
- 2 large electrodes in 2 sides of the heart
- All action potentials stop and remains quiescent for 3-5s
then beats again with the sinus node however if focus is
present then fibrillation occurs again
- Fibrillation stopped by 100 mv of 60 cycle alternating
current applied for 0.1s or 1000 volts applied for few
thousandths of a second
- Dog defibrillated 130x through the chest wall
HAND PUMPING OF THE HEART (CARDIOPULMONARY
RESUSCITATION): AID TO DEFIBRILLATION
- Kung imo i-defibrillate after 1 minute nag fibrillation 
heart is weal to be revived kay lack of nutrition from
coronary blood flow so revive the heart by pumping the
heart by hand (intermittent hand squeezing) for 90 mins
along with artificial respiration is called CPR and defibrillate
the heart later
- So small blood is delivered into the aorta and renewed
coronary blood flow develops
- Lack of blood flow to the brain for 5-8 mins causes
permanent mental impairment/ brain tissue destruction
ATRIAL FIBRILLATION
- Caused by atrial enlargement resulting from heart valve
lesions that prevent atria from emptying into ventricles or
damming of blood in the atria
- Dilated atrial walls slow conduction for atrial fibrillation
- Blood flows passively from atria to the ventricles
- Decreased 20-30% ventricular pumping
- A person can live for months or years with atrial fibrillation
but reduced overall heart pumping
- AV node will not pass a second impulse for about 0.35
second after the precious one so at least 0.35s must elapse
between 1 ventricular contraction and the next
- Interval of 0-0.60s occurs before one of the irregular atrial
fibrillatory impulses happens to arrive at the AV node
- 0.35-0.95s interval between successive ventricular
contractions  irregular heartbeat
- HR 125-150 bpm
ATRIAL FLUTTER
- Circus movement of the atria where electrical signal travels
as a single large wave in one direction around and around
the atrial muscle mass
- 200-350 bpm in the atria
- One side of atria contracting and one side relaxing 
amount of blood pumped by the atria is slight
- Signals reach the AV node to rapidly for it to be passed to
the ventricles kay AV node and AV bundle has high
refractory period mao dili ma pass
- 2 or 3 beats of the atria per beat of the ventricles 2:1 3:1
- P waves very strong due to semicoordinate masses of
muscle
- Final serious abnormality of the cardiac rhythmicity
conduction system
- Cessation of all electrical signals in the heart
- Likely to occur during deep anesthesia where many
patients develop severe hypoxia due to inadequate
respiration
- Hypoxia  no normal electrolyte con in muscle fibers
across membrane  excitability affected that automatic
rhythmicity disappears
- Myocardial disease causes cardiac arrest
- Implanted electronic cardiac pacemaker to maintain
impulses in the heart