Arrhythmia

Internal Medicine
FACILITATOR: Jose P. Tirona, MD, FPCP, FPCP DATE: December 14, 2016

"The meaning of life is to find your gift. The purpose of life is to give it away." --Anonymous

OUTLINE
 Cardiac conduction system of the heart  Sudden Cardiac death
 ECG  Genetic basis
 Heart failure
 Arrhythmia
 Treatment
 Automaticity
 Trigger activity LEGEND:
 Reentry  Blue and red – emphasis
 Rhythm abnormalities  Italicized – recordings 2016
 Bradycardia
 Purple – HB108 transcription
 Tachycardia
 Boxed/Green-2018
 Antiarrhythmics
recordings

THE CONDUCTION SYSTEM OF THE HEART

ATRIOVENTRICULAR NODE
 At the base of interatrial septum
 Spindle shape
 Supplied mainly by the right coronary artery
specifically the RIGHT POSTERIOR
DESCENDING CORONARY ARTERY
 Any ischemia in the right coronary artery
results to slowing of conduction or
dysfunction of the AV node, leading to
slow heart rates or bradyarrhythmias
 Usual beat: 60 to 100

CARDIAC PACEMAKERS
 Structures in the heart that generate
impulses producing electrical activity, which
are mechanically converted to contractions
 Sinoatrial node
 Atrioventricular node
 Bundle of His
 Bundle branches
 Distal His-Purkinje system
The conduction system is usually supplied by the
left and right coronary artery.
SINOATRIAL NODE
 PRIMARY PACEMAKER of the heart
 Junction of RA & SVC
 Supplied mainly by the SINUS NODE ARTERY
 Supplied by right coronary artery in 60% of
the time and in the left coronary artery in
the 40% of the time
 Obstruction in these coronary arteries result to
dysfunction of SA node
 Drives the main conduction of the heart
 Usual beat: 80-100
Blood supply is important because if there is impeded
there will be decrease in oxygen leading to
dysfunction & disease.
BUNDLE OF HIS
 Emerges from the AV node
 Courses across the interventricular septum
 DUAL blood supply (AV NODAL ARTERY and
LEFT ANTERIOR DESCENDING ARTERY)
 Supplied mainly by the left coronary artery
 Generates 20 – 40 bpm
BUNDLE BRANCHES
 Left bundle branch
 Right bundle branch
 Also generates 20 – 40 bpm
Summary of the conduction system: SA node 
Interatrial tract AV node His bundle Bundle
branches His-Purkinje system
The right and left side of the heart
contracts simultaneously. Any problem in
structure could lead to arrhythmias.
CARDIAC MYOCYTES
 Intercalated disks are anchoring structures
containing gap junctions.
 Cardiac muscle cells are faintly striated branching
mononucleated cells, which connect by means of
intercalated disks to form functional network.
 The action potential travels through all cells
connected together forming a functional
syncytium in which cells function as a unit.
 Responsible for conduction.
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CARDIAC ACTION POTENTIAL
 Mainly dependent on ions and the transfer of ions
intra and extra-cellularly
 Resting membrane potential: -80 TO -90 MV
 Concentration gradient of potassium
 If its threshold decreases, the heart is prone to
develop arrhythmia such as ventricular
tachyarrhythmia and atrial arrhythmias
FIVE PHASES OF ACTION POTENTIAL

 Sodium and calcium: Primary EXTRAcellular ion

 Potassium: Primary INTRAcellular ion
 Many of the arrhythymias
(tachy/bradyarrhythymias), disorders of impulse
formation, disorders of impulse conduction,
abnormal automaticity, reentrant mechanisms
are the result of the dysfunction of the channels
that are responsible for the passage of these ions
 Anti-arrhythmic drugs can also alter passage of
these ions
 Calcium can cause a lot of arrhythmias especially in
patients with congenital problems
 Resting membrane potential
 -80 to -90 mV and dependent on the
concentration gradient of potassium
 Affected by disease, infection, and some
arrhythmias
 Phase 4: Resting membrane potential
 Phase 0: Rapid depolarization phase
™ Na entry through opening of the fast Na
channels
™ Rapid upstroke
 Phase 1: Closure of Na channels, and partial re-
entry of K
 Phase 2: Plateau phase
™ Entry of Ca in the slow Ca channels
 Phase 3: Refractory Period
™ Ca channels close and K reenters the cell

ELECTROCARDIOGRAM
Clinical Applications THE ECG MACHINE
☤ Rhythm abnormalities In routine clinical electrochocardiography, 12
☤ Chamber enlargement leads are usually recorded:
☤ Ischemia / Infarction  Standard leads: I, II, III
 Augmented Leads: avR, avL, avF
WHAT IS AN ECG?  Precordial Leads: V1,V2,V3,V4, V5, V6 9 The
 Electrocardiogram standard leads and augmented leads
 Valuable record of the heart’s electrical are attached to the extremities, while
activity the precordial leads are attached to
 Easy to understand! the chest
 Attach transthoracically
 Tip: Just recognize the waveforms
 Clinical applications:
 Rhythm abnormalities
 Chamber enlargement
 Ischemia / infarction
 When a patient comes to the
ER with chest pain, the 1st thing thing to do after
the history is to have an ECG

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PRECORDIAL LEADS Again..
x The precordial leads utilize unipolar recording.
The electrodes (or exploring electrode) are
placed on specific areas on the chest wall and the
indifferent electrode is formed by a Wilson’s
central terminal. The placement of the exploring
chest electrode/s on the chest is as follows:
™ V1: 4th ICS, right parasternal border
™ V2: 4th ICS, left parasternal border
™ V3: halfway between V2 and V4
™ V4: Left 5th intercostal space, mid-clavicular
line
™ V5: Horizontal to V4, anterior axillary line
™ V6: Horizontal to V5, mid-axillary line

NORMAL VALUES
 P WAVE (0.08 to 0.10 seconds) – Atrial
depolarization
 P-R interval (0.12 to 0.20 seconds) - Conduction
from Atria to AV node
 QRS (0.06 to 0.10 seconds) - Ventricular
depolarization, normally narrow
 S-T segment – Ventricular repolarization
 U WAVE – seen in some people
 Q –Tc interval (< 0.44 seconds) – Ventricular
ECG INTERVALS depolarization and repolarization
™ Very important because a lot of ventricular
arrhythmias happen in this interval
™ Life threatening arrhythmias happen because
of changes in Q-T interval
™ Any disease or drug that prolong the Q-T
interval can render individuals prone to
sudden cardiac death secondary to
ventricular arrhythmias
™ QTc = QT divided by the Square root of RR
 Any alteration or prolongation of these values can
reflect
™ Ifslowing of conduction
your P wave is prolonged = it can signify
™ Alterations in P-R interval = defects in the AV
node like the use of calcium channel blockers,
beta blockers, which affect the conduction of
the AV node
™ Widened QRS complex = Patients with large
hearts, MI, dilated cardiomyopathies or with
Any slowing in conduction cause prolongation in ventricular premature beats
the interval. So if there’s a large atrium, AV node
conduction will slow down and it will reflect as
prolongation of PR interval.
QRS complex defect – whether there’s
enlargement or delay in conduction in the
ventricles causing prolongation of conduction will
WIDEN the QRS complex
ST segment defect- any disease or defect that can
happen in ST segment will prolong it and it will
predispose it to a lot of arrhythmias

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 ECG INTERVALS NORMAL VALUE DESCRIPTION
P WAVE 0.08 to 0.10 seconds Atrial depolarization Enlargement of the atria
P-R INTERVAL 0.12 to 0.20 seconds Conduction from Atria to Defects in the AV node like
AV node the use of calcium channel
blockers, beta blockers,
which affect the conduction
of the AV node
QRS 0.06 to 0.10 seconds Ventricular depolarization Normally narrow
If widened: Patients with
large hearts, MI, dilated
cardiomyopathies or with
ventricular premature beats
ST SEGMENT Ventricular repolarization
QTC INTERVAL < 0.44 seconds

ST segment:
 Primarily used to determine if the patient has an acute injury pattern/acute myocardial infarction (MI) or just an
ischemia; the ST segment is isoelectric meaning there is no electrical activity (kaya straight line lang sya sa ECG,
that’s the baseline voltage). We use the isoelectric point as basis to determine whether there is an ST elevation or
depression.
™ ST depression – means patient is having an ongoing ischemia or a non-ST elevation MI
™ ST elevation – patient is having an acute injury pattern or an ST elevation MI

ECG MEASUREMENTS
 As you can see in the ECG, there several boxes.
The dark lines are the big boxes. The big boxes
are further divided into smaller boxes which
measure 1 mm each. For each big box, there are 5
smaller boxes horizontally and vertically for a
total of 25 small boxes in one big box.
 These boxes represent seconds.
™ One small box is 0.04 sec (40 msec).
™ Hence, each big box is 0.2 sec (0.04 x 5).
 The ECG paper speed is 25 mm/second.
Therefore, the smallest (1mm) horizontal
division corresponds to 0.04 second. (1mm
divided by 25 mm/second is 0.04 second)

RULE OF THUMB
 Smallest square is 0.04
seconds x 5 large box is 1
second
 1 large box is 0.2 seconds
 10 mm/1 mV Reference

X axis - time
Y axis - amplitude

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EXAMPLE OF READING AN ECG (FROM PAST TRANX
NG PAST TRANX LOL)
 PR interval
™ 4 small boxes = 4 x .04 = 0.16 seconds for
the impulse from the SA node reach the AV
node
 QRS interval
™ 2 ½ small boxes = 2.5 x 0.04 = 0.1 seconds
for the depolarization of the ventricle to
occur (remember that it is not the actual
contraction that takes 0.1 s to occur since
there is a very slight delay between the
electrical activity and the mechanical
activity of the heart).
 QT interval
 11 small boxes = 11 x 0.04 = 0.44
seconds duration for the electrical
excitation/depolarization until electrical
relaxation
x There are actual normal interval durations for
which you interpret your ECG.
 a. P wave = 0.08 – 0.10 (around 2 to 2.5 small
boxes)
 b. PR interval = 0.12 – 0.2 (3-5 small boxes)
 c. QRS interval = 0.06 - 0.10; sometimes it’s as
small as 0.04 (around 1 to 2.5 small boxes)
 d. QT interval = less than 0.44 for males. For
females, it’s up to 0.46.
 e. QTc interval/corrected QT = actual QT
divided by the squareroot of RR (distance
between two QRS complexes)

GUIDE IN READING ECG

 Standardization and technique  QRS complex morphology and duration
 Rate: Atrial and Ventricular  ST Segment
 Rhythm and axis  T-wave
 P wave morphology and duration  U-wave
 P-R Interval  Q-T interval

1. STANDARDIZATION AND TECHNIQUE

 There’s a standardization button on the ECG. When you press it, an impulse will come out. If the impulse covers
2 big boxes vertically (10 mm), then that means the ECG is standardized.
 10 mm standardization
 Usual paper speed: 25mm/s
 At 25 mm/s, each small box is 0.04 and the big box is 0.20.

The paper speed will tell you whether you’re recording correctly or not. The normal paper speed is 25 mm/s. Whenever you look at the
ECG, it’s important to check the paper speed. If the speed is very fast (e.g. 50 mm/s), an actual heart rate of 70 beats may appear as 35
beats only on the ECG. So you might mistakenly interpret it as sinus bradycardia

2. RATE: ATRIAL AND VENTRICULAR

 A measurement of number of beats per minute; in the ECG, it is recorded by looking at two R-R intervals.

Measurement of Rate:

 Count how many small squares are there from the tip of the QRS to the tip of the next QRS (this is your RR
interval)
 Bakit 1500? Kasi there are 1500 small boxes per minute:
 1 small box = 0.04 sec
 5 small boxes = 1 large box = 0.2 sec
 25 small boxes = 5 large boxes = 1 sec
 25 small boxes x 60 sec = 1500 small boxes = 1 min
 So if you are using the big squares, use the 300 as numerator.

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FAST METHOD: GRID METHOD (SHORTCUT METHOD)
 Look at the QRS (specifically the peak of the R) that coincides with the beginning of a one big box. This is
designated as 300
 Then Count how many big squares there are from that point to the next QRS. Each succeeding big square is
designated as 150, 75, 60, 50, 43, 37
 Can only be used for patients with a normal rhythm of the heart. If patient has irregular rhythm, you make use of
the 6 –second strip and count the number of QRS complexes. Then multiply by 10 (since 1 min = 60 sec) to get the
number of beats per minute.
 If hindi sakto sa big box ung next QRS, then you compute. Example, tumama ung second QRS in between box 75
and 60. Diba in one big box, there are 5 smaller boxes. So 75 minus 60, that’s 15. Hence, each small box between
those two is equivalent to 3 (15/5). So pag nag-compute ka ng heart rate, that will be 63, 66, 69, 72, then 75. If for
example naman between ng box 100 and 75 tumama ung second QRS, then 100-75 = 25. There are 5 small boxes in
1 big box. So each small box will be 25/5 = 5. So ang count mo is 75, 80, 85, 90, 95, 100.

 Take note of the R-R interval

 Basic Eyeballing on ECG
 Used in a regular rhythm
 REMEMBER: start with 300 – 150 –
100 – 75 – 60 –50 (if ever he gives an
ECG)

RHYTHM
 The heart rhythm can be assessed while the axis can also be assessed. The axis is just the vector of the conduction, the
direction of the conduction.
 Normal direction: The Sinus Node can go downwards and laterally, but axis can also change from the normal
cephalocaudal it could be reversed
 Determine whether patient is in sinus beat or not. Sinus beat: the impulse is coming from the sinus node.
 How to know if it’s a sinus beat?
 a. It should always have a P wave preceeding each QRST
 b. P wave should be normal looking
 c. P waves should have the same contour in one lead. It is always upright in leads I, II and avF. If it’s negative in
I, II, and AVF, that impulse did not originate from the sinus node. Hindi rin pwede na in one lead, one impulse
is upright, and one is negative, or one impulse is mataba, the next is medyo mapayat. Same dapat lahat in one
lead.

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 AXIS
 Direction of the electrical activity
 Summary of different vectors.
 Determine if normal axis, left axis, right axis or
extreme axis
 Normal: electrical contraction should be downward
and to the left (This is because the strongest muscle
in the heart is the left ventricle).
 In determining the axis, you focus only on:
 Lead I which is positive going to the left, and
 Lead avF which is positive going downwards.
 A wave of depolarization is recorded with a
positive (upright) deflection if it spreads towards
the positive pole of that lead. Hence, if a wave of
depolarization is going to the left, then that
means it is spreading towards the direction of the
positive pole of lead I, and a positive deflection
will be recorded on lead I.
 If a wave of depolarization is going downwards,
then, it is going towards the positive pole of
lead avF and it will also have a positive upright
deflection on lead avF.  Normal is 0 degrees to 90 degrees. +90 to ---­­180 in
the direction of impulse is a right axis deviation, 0
to
---­­90 is a left axis deviation. Remember, sinus node
to ventricle. If the ventricle is the predominant
impulse, we have a VA (ventriculo---­­atrial)
conduction, hence, we have an axis deviation.

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 ARRYTHMIAS
 Any group of conditions in which the electrical activity of the heart is irregular or is faster/slower than normal
 Normal heart rate is 60-100 bpm so anything less than 60 is bradyarrythmia and anything more than 100 is
tachyarrythmia.

MECHANISMS OF ARRHYTHMIA
 Automaticity
 Triggered Activity
 Reentry
 Please take note that this mechanisms can overlap. Meaning at one point one mechanism has triggered an arrhythmia and
another mechanism has perpetuated that particular arrhythmia. So pwedeng two mechanisms at the same time is
happening in one patient for example, one arrythmia is triggered by automaticity just like premature beat and then it is
being sustained and perpetuated by another mechanism such as re-entry and one particular example is one patient with
normal sinus rhythm and then being triggered by a premature beat and then develops atrial fibrillation.

1. AUTOMATICITY
 Property of cardiac cells to undergo spontaneous depolarization and initiate an electrical impulse in the absence of
external electrical stimulation.
 Result of net inward ionic current during phase 4 of the action potential
 Inward current of sodium and calcium plus slow outward potassium current mainly pertaining to your action
potential.

SA Node – 60 -100 bpm

AV Node – 40-60 bpm
Purkinjie Fiber – 20 – 40bpm

A. NORMAL AUTOMATICITY
 Depolarization is due to ionic currents involved in
impulse generation during physiological conditions.
 Drugs, adrenergic and cholinergic stimulation and
hormones can affect normal automaticity (e.g. drugs
that could make heart beat faster (tachycardia) like
drugs used in treatment of asthma like terbutalin,
salbutamol, duolin nebulisations. On the other side,
drugs can also decrease the normal automaticity or
make the patient (bradycardia) such as those
hypertensive patients being given beta blockers or
calcium channel blockers that can slow down heart rate
that could affect your normal automaticity. Adrenergic,
cholinergic in the clinics in the hospital we give
epinephrine, norepinephrine that can accelerate heart
rate.
B. ABNORMAL AUTOMATICITY
 Due to ionic currents not normally involved in the
initiation of spontaneous impulses and may become
pacemaker currents
 This can be exhibited by cells other than the sinus node.
Predominant pacemaker is the SA node.
 The atrial tissue can also exhibit abnormal
automaticity such as in patients with premature
atrial depolarization or supraventricular
premature beat.
 The bundle of His or the junction and the
ventricular tissue can also exhibit abnormal
automaticity.
 So as side from the normal sinus beat, these
particular sites can also trigger an action
potential assuming that they have fired outside
the refractory period of that myocardium.

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 TACHYARRHYTHMIAS
 Enhanced automaticity
 Enhanced activity of the sinus node, specialized atrial fibers, AV node fibers, His-Purkinje fibers
 Causes:
 Increased endogenous/exogenous catecholamines
 Electrolyte imbalances- hypo/hypernatremia, hypo/hyperkalemia
 Hypoxia or ischemia- coronary artery dse/MI – may hamper the conduction system that can create abnormal
physiologic mileu  flow of ion will be hamper and resting membrane potential/phase 3 will be prolonged
 Mechanical effects (stretch) affect chamber or valves
 Drugs (digoxin, quinidine, theophylline)

REGULARLY IRREGULAR. Regular beats 1-3 (sinus, sinus, sinus) followed by premature beat.
Let’s say this is a narrow complex, so this is a premature beat definitely this is not sinus, it doesn’t have a P wave, must be
coming from a, let’s say QRS complex, a ventricular premature beat and an atrial premature beat. But definitely this is a
premature beat, the question now is whether it is coming from the atria or the ventricle. We have criteria differentiating
which is atrial premature beat which is ventricular premature beat.
If you’re claiming it is ventricular premature beat because QRS complex is wide, BUT you can have a bundle branch in here
which can give rise to a wide QRS complex. The T wave gives us a clincher that this is a supraventricular premature beat
because the T wave is upright also your QRS complex. Normally kasi kapag ventricular premature beat negative yung T
wave and the axis is the same as the premature beats, doesn’t change kasi kapag ventricular nag-iiba yung axis nya
nagiging negative yung QRS complex mo.

Now this is a patient with atrial flutter, which is saw-toothed T-wave. If this particular arrhythmia is sustained, this is an
example of a re-entry mechanism, ito yung sinasabi natin na one mechanism can perpetuate another. This is triggered by an
abnormal automaticity and maintained by a re-entrant mechanism. So basically atrial flutter as we have seen here is a re-entry
mechanism. But the most common trigger is a premature beat, atrial or ventricular, mostly atrial.

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 2. TRIGGERED ACTIVITY
 Impulse initiation in cardiac fibers that is dependent on afterdepolarizations.
 Has something to do with the alteration with the Resting Membrane Potential (RMP)
 RMP is around -70 to -90 mV
 Premature beats can alter the RMP
 Alterations of the RMP drop about initial depolarizations, so kung marami kang premature beat s that can make
the threshold lower, and predispose patients to develop arrhythmias, eto yung nangyayari mostly sa ventricular
tachyarrythmias
 Impulse initiation in cardiac fibers that is dependent on after depolarizations

From Harrison’s: Triggered activity is related to cellular afterdepolarizations that occur at the end of the action
potential, during phase3, and are referred to as early afterdepolarizations; when they occur after the action potential,
during phase 4, they are referred to as late afterdepolarizations. Afterdepolarizations are attributable to an increase
in intracellular calcium accumulation. If sufficient afterdepolarization amplitude is achieved, repeated myocardial
depolarization and a tachycardic response can occur

AFTERDEPOLARIZATIONS
 Oscillations in the membrane potential that follow the upstroke of an action potential.
 So nag-iiba iba yung membrane potential. The problem here are still channels, they either open up longer or
close faster due to a disease process. This happens during the repolarization stage.
 Harbingers of fatal depolarization, destruction or fatal arrhythmias
 Normally the resting membrane potential is -80-80 mV when this oscillations happen it become more positive or
negative then depolarization can happen that can upstroke action potential that can predispose you to fatal
arrhythmias.

 Early Afterdepolarization
 Sudden change in time course of repolarization of an action potential
 Membrane potential does not follow the trajectory of normal repolarization but suddenly shifts in a
depolarizing direction
 Can lead to second upstrokes or action potentials that occur before complete repolarization
 Occurs during PHASE 2 or 3 of the action potential

Abnormal situation: defects in Na, K,

Ca channels, congenital long QT,
brugada, MI, drugs, catecholamine –
this can all create oscillations in the
resting membrane potential that can
develop to after depolarization that
can predispose pt. to a lot of
arrhythmias

*Label retyped: (A) monophasic action potential with a late phase-2 EAD synchronous U wave, causing prolongation of the
QT interval. (B) or left image, EAD of SUFFICIENT amplitude can trigger PVC or premature ventricular contraction, which
in turn can initiate torsades de pointes if preceded by a pause associated with hypokalemia or hypomagnesemia.

 In this ECG: this shows as a premature ventricular contractions which usually happens in the ST segment
 There are also problems in the repolarization, due to an alteration in K+ channels wherein the QT lengthens, hence,
early after depolarization usually occurs in phase 3.
 You have an action potential, then all of a sudden you have a wave there, (as shown by the triggered beat label). Note
in Picture B that in the ECG, the wave was strong enough to be able to produce a QRS complex.
 From Harisson’s: With increasing amplitude of afterdepolarizations, threshold can be reached and repetitive activity
produced). The danger is if you have an afterdepolarization that produces a QRS complex, this may cause
ventricular arrhythmia.

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TRIGGERED ACTIVITY
HEHEHE

Delayed afterdepolarizations
 Occur in conditions where there is INCREASE in CA 2+ in the myoplasm and the sarcoplasmic
reticulum above normal levels (CA OVERLOAD)
 Digitalis, catecholamines
 After phase 3 of the action potential
 This is where ventricular arrythimias happens, Vtach or fibrillations

REFRACTORINESS
 The phase in which any amount of stimulation the heart is relatively refractory,
cannot trigger a response! afterdepolarizations can produce a lot
 Absolute refractory period (seen as the 0 in the of new arrhythms and patient can go
graph below.) into arrhythmia).
 Portion of action potential during which no
stimulus can evoke response
 Equivalent to Phase 0 (rapid influx of
sodium)
 Coincides with the QRS. When you have QRS,
you cannot produce another QRS no matter
how much you stimulate it because the
ventricle has just depolarized

 Effective refractory period (number 1 in the

graph below)
 Stimulus can evoke a local, nonpropagated
response because the muscles are still
refractory and some of the muscles are
starting to relax already.
 Phase 1-2
 The conduction will not progress to an actual
contraction.
 Relative refractory period (number 2 in the graph
below)
 End of ERP (Phase 3) to the time the tissue is
fully recovered (Phase 4)
 The heart is relatively well relaxed that the
heart may contract when a stimulus is applied
 Afterdepolarizations may be enough to ARP – when
produce new complexes, hence arrhythmia. ventricles are
actively
This is why the repolarization phase is called
depolarizing
the vulnerable phase. (At this phase when

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 3. REENTRY
 Quite common in patients with atrial flutter, atrial fibrillation, ventricular fibrillation, AV node reentrant tachycardia,
atrial tachycardia, junctional tachycardia, and most of the supra ventricular tachyarrythmias are being sustained by
the reentrant mechanism
 DISORDER OF IMPULSE PROPAGATION
 There is a circuit that is normally dapat sana pag sinus dadaan sa av node to the his bundle to the purkinje fibers then fades
away na siya diba so wala na yon. Then another sinus impulse comes, propagates then fades away.
 Dapat ganon lang un, but this one: impulses coming from the sinus is being conducted all throughout the conduction
system but somewhere along the middle, there is a circuit. But the impulse does not just go downwards and die there
or fade away.
 The impulse is being CIRCUITED BACK TOWARDS THE PARTICULAR REENTRANT PORTION. So that
can explain the reentrant mechanism. This is clearly a disorder of impulse propagation.
 Produced by premature complexes or rapid stimulation

 Properties / Conditions that can bring about reentry:

 ELECTROPHYSIOLOGIC INHOMOGENUITY
 Ano ba yun? So again isipin nalang natin, IONS  Meron kang electrolyte prob  Increase in calcium
 Calcium overload, this process can bring about physiologic inhomogenuity.
 Also, kung meron kang problema dun sa TISSUE, particularly the myocardium, (scarred tissue
that was brought about by coronary artery disease for example, post myocardial infarction) can
bring about the physiologic inhomogenuity
 This inhomogenuity can make individuals prone to develop reentrant arrhythmias such as
ventricular fibrillation
 Also seen patients with CONGENITAL PROBLEMS like Brugada syndrome which causes defects in
channels
 Unidirectional block in one pathway
 Slow conduction over an alternative pathway
 Reexcitation of the initially blocked pathway to complete loop of activation

DISCLAIMER (From batch 2016): This large amount of text that you are about to read was briefly discussed. According to
the previous trans, Doc Tirona does not expect us to master this part at our current level (which frustrated the past-trans’
transcriber, as I am now), BUT STILL, NGUNIT SUBALI’T DATAPWAT, here’s the explanation. (correct me if I’m wrong na
lang).
 The impulse conduction of the heart is normally uni-directional, it comes from the sinus node to the AV node to
the His-bundle. It usually just goes down.
 But sometimes, in the area of the AV node, there are 2 pathways that may be present, one fast and slow.
The normal pathway conducts fast but recovers slow (longer refractory period). The other pathway conducts
slow but recovers fast.
 Game! For example, you have an impulse, conduction will proceed normally one pathway (usually the
fast conduction slower recovery pathway). This pathway is then considered BLOCKED (or
UNIDIRECTIONALLY
BLOCKED PROPERTY).

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  If a second impulse is generated, it thus can’t pass through the fast pathway, kasi nga since that’s still refractory
(remember it recovers slow) , it then passes instead through the alternative slow pathway (ALTERNATE PATHWAY
WITH SLOW CONDUCTION PROPERTY).
 By the time the second impulse finishes traversing its slow pathway, the fast pathway has already recovered, and
di na sya blocked (REEXCITATION OF THE BLOCKED PATHWAY). The second impulse then, instead of just
going downwards in its unidirectional flow, may REENTER the fast pathway, so that the impulse goes around and
around and around.
 Hence, the term REENTRY, producing the Arrhythmia.
 This can happen in the atria – [atrial fibrillation, atrial flutter, atrial tachycardia], ventricles – [ventricular tachycardia,
ventricular fibrillation], and av node – [av node reentrant, junctional tachycardia].

Typical example of reentry. You have a PQRST, then all of a sudden, you have a premature atrial beat/P wave (small
bump). Also notice that the PR interval is prolonged, compared to the others, so you know that the impulse actually
passed through the slow pathway and this caused the rhythm to go very fast = arrhythmia. This particular arrhythmia
is called AV nodal reentrant tachycardia.

Pre-excitation Wolff Parkinson White ECG

(Wolff ‘yan haaa)
 Supraventricular rhythm with wide QRS complex because of pre-excitation
 Short or no PR segment followed by a delta wave (slurred upstroke of QRS)

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 RHYTHM ABNORMALITIES
 Bradyarrhythmias Tachyarrhthmias
 Abnormal of automaticity  Enhanced automaticity
 Abnormal of conduction  Reentrant activity
 HR: <60 bpm  Triggered activity
 HR: > 100 bpm

1. BRADYARRHYTHMIAS
 Sinus node dysfunction – abnormal automaticity AVnode dysfunction – abnormal conduction
 Sinus bradycardia (slowing of conduction in the AV node.)
 Sinoatrial block  1st degree AV block
 Bradycardia – Tachycardia syndrome  2nd degree AV block
 3rd degree AV block

A. SINUS BRADYCARDIA
 Regularly occurring PQRST
 Rate < 60 / min (If you’ll zoom in and measure the HR, 48 beats per minute. It is slow and therefore is sinus bradycardia.)
™ The QRS and T waves are all normal.

Sinus Bradycardia.

B. FIRST DEGREE AV BLOCK

 Focus on the PR interval. Normally it should be <0.2 sec. Here, it is around 0.3 seconds. But here, the impulse is still
being conducted from atria to the ventricle. So longer PR interval.
 Benign condition.

PR interval of greater than 0.2 seconds. First degree AV block.

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C. SECOND DEGREE AV BLOCK TYPE I (WENKEBACH)
 PR interval is gradually prolonging until the atrial impulse can no longer be conducted to the ventricle.
 Prolonging PR interval before dropped beat.

The PR interval is prolonging (21, 31, 35), until hindi na ma-conduct ang Atrial impulse. Second degree AV block (Type I).

D. MOBITZ TYPE II SECOND DEGREE AV BLOCK

 Constant PR interval before dropped beat.
 Signify a worse prognosis than av wenkebach. No prolongation of the PR interval.
 Bigla na lang nag ba-block.
 Then you have a wide QRS complex. Area of block is farther than the AV node
 Most commonly in the bundle of His. Most patients become symptomatic with dizziness, light headedness and
syncopal episodes.)

Constant PR interval followed by dropped beat. Second degree AV block (Type II).

E. HIGH-GRADE AV BLOCK
 3 or more “p” waves for every 1 QRS.
 Most impulses not conducted.

3 or more “p-waves” for every 1 QRS. High grade AV block.

F. THIRD-DEGREE AV BLOCK
 No more impulse from atrium reaches the ventricle.
 QRS is not from atria or sinus but is coming from ventricle already.
 If no more conduction from the atria, you have backup generators. What happens is that when there is no more
impulse, it is sensed by the junction or ventricles then these latent pacemakers would fire. Clue is that if you have
a narrow QRS (junctional galing). If wide, it is from the ventricle.

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 Pag wala nang conduction from the atria, may backup generators (the secondary pacemakers) would fire. (If may
generator kayo sa bahay, may generator din tayo sa puso.) Here, the P-waves are non-conducting, but the QRS is. Hindi
sya galing sa atria, kundi sa ventricles. Again, Sinus node is 60 to 90 beats per minute, AV Node 40 to 60 bpm, Bundle of
His 20 to 40 bpm. Eto yung mga pag asa natin sa mabuhay.
Heart rate of this ECG is about 53 bpm. This is still coming from the junction (AV Node). Another clue that this is coming
from the junction is the narrow QRS.
If wide na yan, it’s from the ventricular contraction (Bundle of His).

TREATMENT OF BRADYARRHYTHMIAS:
 Drugs/pharmacologic
 Device therapy: Pacemaker

2. TACHYARRHYTHMIAS
 Supraventricular Arrhythmias  Ventricular Arrhythmias
 Sinus tachycardia  Ventricular tachycardia
 Atrial tachycardia  Ventricular fibrillation
 Atrial flutter/fibrillation
 Junctional tachycardia
 AV nodal reentrant tachycardia
 AV reentrant tachycardia

1. SUPRAVENTRICULAR ARRHYTMIA

A. SINUS TACHYCARDIA
 Regularly occurring PQRST
 Rate: > 100 / min

Heart Rate of more than 100 bpm. Sinus Tachycardia. Sinus kasi regular yung PQRST sequence.

Normal axis, narrow QRS, HR > 100.

B. PREMATURE ATRIAL COMPLEX

 The P wave changes in morphology, with a shortened PR interval.
 From the book: Most common arrhythmia identified during extended ECG monitoring

Sinus, sinus, and another sinus, tapos may premature contraction bigla!

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You have a PQRS, then all of a sudden, you have an abnormal looking P wave which occurred early, and produced a normal
looking QRS. This is a premature atrial beat. This did not come from the sinus node since it’s abnormal looking.

C. SINUS ARRHYTHMIA
 Normal in young individuals. All of them are coming from the sinus.
 Identical but irregularly occurring PQRST
 Longest PP or RR > the shortest by 0.16 seconds or more
 From the book: The P wave is upright in leads II, III, and aVF and negative in lead aVR. The P---­­wave morphology
in lead V1 characteristically has a biphasic, positive/negative contour.

The longest RR interval is 94, the shortest is 60. 94 – 60 is 34. If more than 16, Sinus Arrhythmia.

D. MULTIFOCAL ATRIAL TACHYCARDIA

It is common in patients with chronic lung problems such as COPD, emphysema. Sa atria nang-gagaling ung P wave but the
P waves are different. (Refer to the blue circles: Eto si juan, eto si pedro, eto si juancho.) Iba-iba yung itsura nila di ba?
Different morphologies of the P wave. This is because iba iba yung pinanggagalingan niya. PR interval also is different.
Irregularly irregular heart rhythm.

E.
ATRIAL FLUTTER (MACRO REENTRANT AT)
 Atrial rate: 220 – 300 /min (P as flutter waves)
 Variable degree of AV block (irregular RR interval)

Take note of the saw-­­toothed appearance of the P waves in ECG leads II, III, and aVF. ECG in AF is
characterized by the lack of organized atrial activity and the irregularly irregular ventricular response
Usually, flutter waves conduct in an even number. Example, atrial flutter with 4: 1 conduction or 4 flutter waves for 1
QRS. Or atrial flutter with 6:1 conduction. But sometimes, you may have an atrial flutter with varying conduction.
But always remember the sawtooth or picket fence appearance. Do not mistake this for an atrial fibrillation
because the rhythm is still organized. You can still see a normal P wave
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F. AV NODAL REENTRANT TACHYCARDIA
 P waves are embedded within or after QRS complexes

Typical example of reentry. You have a PQRST, then all of a sudden, you have a premature atrial beat/P wave (small
bump). Also notice that the PR interval is prolonged, compared to the others, so you know that the impulse actually
passed through the slow pathway and this caused the rhythm to go very fast = arrhythmia. This particular arrhythmia
is called AV nodal reentrant tachycardia

G. ATRIAL FIBRILLATION
 MOST COMMON SUPRAVENTRICULAR
ARRHYTHMIA IN CLINICS
 No discernible P waves
 Irregular RR interval
 Irregularly irregular
 There is a multiple foci of re-entry and the AV
node conducts slower
 A problem of reentry: there are impulses
coming from several parts of the atrium. So
instead of having a synchronized atrial
contraction, the atrium is quivering. This is why
there is no discernible P wave. Also, some
impulses are getting into the ventricle, some are
not, which is why the rhythm is irregular.
 Some impulses can still conduct to the ventricles
because there is no AV block. However, some
impulses can’t pass, kasi otherwise pag
pumasok lahat ng impulse, your patient will die
of tachycardia.
 Note that atrial fib can have a rate as high as 300,
so pag pumasok lahat yan, mamamatay ka
talaga. But remember the AV node beats at only
60-100, so despite the fast rhythm from the
atrium, AV node will try to block it, so di lahat ng
impulse pumapasok.
 From the book: Although typically the rate will
vary between 120 and 160 beats per minute, in
some patients it can be >200 beats per minute.
Occasionally, AF appears to have a well--­­-­­defined
etiology, such as acute hyperthyroidism, an acute
vagotonic episode, or acute alcohol intoxication.
Acute AF is particularly common during the
acute or early recovery phase of major vascular,
abdominal, and thoracic surgery, in which case
autonomic fluxes and/or direct mechanical
irritation potentiate the arrhythmia.AF also may
be triggered by other supraventricular
tachycardias.

AF is quite rapid, it can reach 500 bpm. BUT NGUNIT SUBALIT DATAPWAT, the AV node can only accommodate only one at
a time. (Di gaya ng iba, 2 or more (dapat isa lang! :P)). There is thus a physiologic slowing, as a protective mechanism for this
kind of arrhythmia.

2.VENTRICULAR ARRHYTHMIAS
 In general, these have WIDENED QRS complexes due to the duration of the conduction across the ventricles is
slower.
A. PREMATURE VENTRICULAR CONTRACTION
 Among the most common arrhythmias; occur in persons with or without heart disease
 No P wave
 Bizaare looking QRS
 The impulse is coming from the ventricles, either left or right, such that one ventricle is depolarized before the
other, producing a wide QRS. (*usually narrow ang QRS because the right and left ventricles are contracting at
the same time.
 Thus, the contraction you are predominantly seeing is actually that of the left ventricle because it’s the bigger
muscle. However, if right ventricle is stimulated earlier, contractions will separate. The right will contract earlier
and will block the left producing a left bundle branch block morphology. Kung mauna naman ung left, you have
right bundle branch block)
 PVCs are associated with a "fully compensatory pause" = i.e., the duration between the last QRS before the PVC and
the next QRS complex equal to twice the sinus rate.

Narrow QRS,
Wide QRS,
Tas narrow ulit. PVC

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VARIATIONS OF PVC PATTERNS
1. Bigeminy
 Premature contraction after every normal beat (wide QRS after every normal QRS). Second beat is always
abnormal.
 Every sinus beat is followed by a PVC, alternate pattern.

Normal then abnormal. Bigeminy type of PVC.

2. Trigeminy
 Every 3rd beat is a PVC; two normal beats, then an abnormal beat
 Two sinus beats are followed by a VPC or every third beat is PVC

Normal normal then abnormal. Trigemny!

3. Couplets
 2 Consecutive PVCs
 Sinus rhythm then 2 PVC’s in succession

Abnormal tas abnormal PVC ulit! Couplet!

4. Triplets
 3 consecutive PVCs
 3 or more consecutive PVC’s are also called a Non-sustained Ventricular tachycardia when the rate exceeds
100 beats/min

Abnormal abnormal abnormal PVC. Naglolokohan na tayo dito! Triplets!

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B. VENTRICULAR FIBRILLATION
x There is no effective contraction anymore; the heart is only quivering
x No cardiac output anymore; no more circulation
x Onset of ventricular flutter/fibrillation is rapidly followed by loss of consciousness, and if untreated, death
x Defibrillator is indicated.

Very chaotic rhythm, no recognizable P wave, no organized QRS contraction. All Chaos.

TREATMENT OF TACHYARRHYTHMIAS
 Medical
 Electrical
 Ablative procedures

ANTI-ARRHYTHMICS
x Vaughan-williams classification table

SUBCLASS MECHANISM PROTOTYPE

IA Mod. block Ph.0; slow Quinidine
conduction, increase APD Procainamide
IB Min. block Ph 0; slow Lidocaine
conduction; shorten Ph. 3; Phenytoin
repolarization
IC Marked block Ph.0; slow Flecainide
conduction; no change APD Encanide
or repolarization.; increased
suppression of NA channels
CLASS II Beta Blockers; decrease Propanolol
adrenergic input; no effect Others
APD; suppress Ph. 4
depolarization
CLASS III Prolong Bretylium
repolarization/refractory Amiodarone
period other means than
exclusively INA block (mainly
K channel blockade)
CLASS IV Ca channel blockers. Slow Verapamil
conduction and increase Diltiaze
effective refractory period in
normal tissue (A-V node) and
Ca dependent slow
responses of depolarized
tissue (atria, ventricle,
Purkinje)

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 SUDDEN CARDIAC DEATH
DEFINITION
 Natural death due to cardiac causes heralded by
abrupt loss of consciousness within one hour of
the onset of acute symptoms, in an individual who
may have a pre-existing heart disease but in
whom the time and mode of death are
unexpected
 Usually occurs during sleep
 A direct consequence of cardiac arrest
EPIDEMIOLOGY
 SCD due to Coronary Artery disease: single most
important cause of death in adult population
™ Even in the young, but the incidence of CAD
as cause of sudden cardiac death increases
as a function of advancing age (the older
you are, the more likely that the cause of
sudden cardiac death is a coronary artery
problem – you probably had an MI. Other
possible cardiac causes of sudden death
include cardiomyopathies – 15%, other
causes make up 5%
 Incidence increases as a function of advancing age
 Account for 80% of incidence
 Ventricular fibrillation: 75 – 80%
 Bradyarrhythmias; asystole & PEA: 20 – 30%
ACUTE MYOCARDIAL INFARCTION
 15% risk of VF within the first 24 to 48 hours
 Incidence falls to 3% within the next several days
SCD INCIDENCE BY AGE
 <30 years old: 1:100,000
 >35 years old: 1:1000
 2 peak incidences
 Between birth & 6 months of age
 Between 45 to 75 years of age: 1-
2/1000/year
SCD ETIOLOGY
 1-13 years old: 1 out of 5
 14 to 21 years old: 30%
 Middle age to elderly: 88%
SCD INCIDENCE BY GENDER
 Preponderance in males during young adult to
early middle age
 7:1 before the age of 65
 2:1 beyond 65
GENETIC BASIS
 Long QT syndrome
 Brugada syndrome
™ Genetic abnormality in one of the channels
of the heart; predisposes a patient to
develop ventricular tachycardia and
fibrillation theorized cause of bangungot
™ Pancreatitis is not the cause of bangungot,
it’s actually a sequelae of the bangungot
 Hypertrophic cardiomyopathy
 Arrhythmogenic Right Ventricular
cardiomyopathy
 Catecholaminergic polymorphic ventricular
tachycardia
 Family history is a strong independent predictor
of susceptibility to SCD
RISK FACTORS FOR SUDDEN CARDIAC ARREST
 Previous Sudden Cardiac Arrest (SCA) Event
 Prior episode of Ventricular Tachyarrhythmia (VT)
 Previous Myocardial Infarction (MI)
 Coronary Artery Disease (CAD)
 Heart failure
 Hypertrophic Cardiomyopathy (HCM)
 Long QT Syndrome
 A combination of these risk factors further
increases the risk of SCA
SCD RATES IN POST MI PATIENTS WITH LV
DYSFUNCTION
 Total Mortality: 20-30%
 SCD accounts for 50% of the total deaths.
Lumalaki ang left ventricle  humihina heart
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 TREATMENT OPTIONS FOR SCA
TREATMENTS TO REDUCE SCD
 Defibrillation is the only effective treatment for
SCA
CORRECTING ISCHEMIA IMPROVING PUMP
 Irreversible organ damage within 4 minutes of VF
FUNCTION
Revascularization ACE inhibitor  VF tends to rapidly deteriorate into asystole
Beta-blocker Beta-blocker  Asystole cannot be successfully treated with
PREVENTING PLAQUE PREVENTION OF defibrillation
RUPTURE ARRHYTHMIAS
Statin Beta-blocker
ACE inhibitor Amiodarone
Aspirin
STABILIZING AUTONOMIC TERMINATING
BALANCE ARRYTHMIAS
Beta-blocker Implantable Cardioverter
ACE inhibitor Defibrillators (ICDs)
Automatic External
Defibrillators (AEDs)
PREVENT VENTRICULAR REMODELING AND COLLAGEN
FORMATION
Aldosterone receptor blockade

 Implantable Cardioverter Defibrillator .

 First line therapy for patients at risk for
SCA
 Defibrillation is the only effective treatment
for sudden cardiac arrest
 Irreversible organ damage within 4 minutes
of VF
 VF tend to rapidly deteriorate into asystole
 Asystole cannot be successfully treated with
defibrillation
SUDDEN CARDIAC ARREST SURVIVORS
 Highest risk factor for sudden cardiac arrest is a
previous SCA event
 30 to 50% of SCA survivors will experience
another SCA event within one year
 First degree relatives of SCA patients have a 50%
higher risk of MI or primary cardiac arrest.
CONCLUSIONS
 The key to SCD prevention is to identify high risk
patients BEFORE they have SCA event. The
majority of cases are in patients with:
 Coronary artery disease, previous MI
 Low left ventricular ejection fraction
 Dilated cardiomyopathy and heart failure

----------------end -------------------------

When the toxicity of being med school is really taking its toll
Think about the ones who did not make it to med school
The ones who were not lucky to be there
Your folks, who are scrounging up every centavo they have to keep you there
Think about the future patients who will benefit from the hell you’re going through
And think about the fact that you are aiming for the noblest profession of all
Noblest then, noblest now, and noblest forever will be. 
-Anonymous

Laban lang Batch 2018!!!

“Ang sumusuko ay hindi nagwawagi!!”

Notes:
 Basically a mash up of 2016 and 2018 transes! HEHE remix
 Removed parts of the ECG if you want to read about it see the 2016 tranx.  Doc removed a lot of slides that’s why it’s shorter.


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 PAST E Batch 2015

11. A 28--­­-­­year--­­-­­old male school teacher

presented with cardiac arrest during sleep. His brother
died of a similar Illness a year ago at age 30. At the ER, 16. In the cardiac action potential, the fast Na channels
his heart rhythm revealed ventricular fibrillation. What is are responsible for this phase:
your diagnosis? a.) Brugada Syndrome a.) Phase 0
b.) Vasovagal syncope b.) Phase 1
c.) Asystole c.) Phase 2
d.) None of the business d.) Phase 3

12. A 20--­­-­­year--­­-­­old male consulted because of 17. A phenylalkylamine calcium channel blocker that
palpitations. You did an ECG, which revealed sinus causes significant delay in AV nodal conduction:
rhythm with wide QRS complex and the presence of a.) Nifedipine
the delta wave. This finding is consistent with which of b.) Diltiazem
the following? c.) Amlodipine
a.) Ventricular Tachycardia d.) Felodipine
b.) Wolff--­­-­­Parkinson White syndrome
c.) Long QT syndrome (ventricular 18. Antiarrhythmic drug used in patients with accessory
arrhythmias) d.) None of the above pathway And could trigger hypo/hyperthyroidism
a.) Amiodarone
13. The most common supraventricular tachyarrhythmia b.) Sotalol
seen in clinical Practice is which of the following? c.) Verapamil
a.) Atrial fibrillation d.) Flecainide
b.) Sinus arrest
c.) Junctional tachycardia 19. A 25--­­-­­year--­­-­­old female, known case of toxic goiter
d.) Ventricular tachycardia presented to the ER with palpitations. Her ECG showed
rapid heart rate with irregularly irregular rhythm and
14. Exhibits automaticity and regarded as the absent P waves. What is your ECG diagnosis?
predominant pacemaker of the heart a.) Atrial fibrillation
a.) Sinus node b.) AV node reentrant
b.) AV node c.) tachycardia c.) Sinus tachycardia
HIS bundle d.) d.) Sinus arrhythmia
Left bundle
20. A 28--­­-­­year old male, asymptomatic consulted
15. Which of the following is primarily a disorder of for work clearance as a chief in a hotel. His ECG
impulse conduction? showed constant PR interval from beat to beat of 0.26
a.) Sick sinus syndrome b.) seconds. What is your ECG diagnosis?
Complete heart block c.) a.) First degree AV block b.)
Junctional tachycardia d.) AV Wenkebach block c.)
AV reentrant tachycardia Mobitz Type II AV block d.)
Complete heart block

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