C ARDIAC ARRHYTHMIA
I. INTRODUC TION
o Arrhythmia is loss of cardiac rhythm, especially
irregularity of heartbeat
o Arrhythmia is referred to as any change from the
normal sequence of natural impulses. The impulses
may happen too fast, too slowly, or erratically -
causing the heart to beat too fast, too slowly, or
erratically. - American Heart Association
II. EPIDEMIOLOGY
• Atrial Fibrillation, bradyarrhythmias, and conduction
system diseases account for most rhythm conditions
• Abnormalities of cardiac rhythm are prevalent in
community-dwelling adults, affecting >2% of
individuals
• Risk of incident rhythm abnormalities is increased in
the setting of older age, male sex, traditional
cardiac risk factors, chronic kidney disease and
heart failure
• In 2016, atrial Fibrillation occurs in 2% of Filipinos
above 70 years of age based on a national survey
conducted by Department of Health and the Food
and Nutrition Research Institute
III. PATHOPHYSIOLOGY
PATHOPHYSIOLOGY: Electrical system of the heart
o The normal electrical sequence begins in the
sinoatrial node - known as the natural pacemaker
o The SA node initiates cardiac rhythm by releasing
electrical impulses and spreads throughout the atria
to the atrioventricular node causing them (the atria) to
contract.
o AV node serves as a circuit breaker that slows down
or blocks impulses that are too closely spaced to give
blood some time to enter the ventricles.
o From the AV node, electrical impulses then travel to a
group of specialized fibers called the His-Purkinje
system to the ventricles causing them to contract and
produce a heart beat.
o After a group of cells within the heart is electrically
stimulated, a brief period of time follows in which
these cells cannot be excited is called the refractory
period.
How impulses travel:
= heart beat
PATHOPHYSIOLOGY: Cardiac action potential
o When neurons are at rest and not receiving electrical
signal, their internal charge is negative.
o Ion channels allow many charged ions to pass across
a cell membrane.
o When all these gates to ion channels are closed, a
neuron is at rest. But when a neuron is struck by a
stimuli, it triggers an ion channel to open.
o As ions pass into the cell, they alter the membrane
charge. As charged particles rapidly diffuse across the
membrane, they depolarize it, thus changing its
charge.
o As the sodium enters, the white line rises as voltage
approaches a very important threshold: -55 mV.
o At this threshold, thousands of voltage gated sodium
channels open. Sodium gates let forth a flood of
positive sodium ions into the neuron, resulting in
depolarization.
o A flood of positively charged sodium ions enter the
cell and it becomes rapidly positively charged or
depolarized.
o As a neuron reaches an internal charge of around +30
mV, a conformational shape change happens in the
sodium channels - they close and voltage gated
potassium channels open, allowing positively charged
potassium ions to leave the cell.
o As for membrane repolarization, sodium channels
(light purple) close. Potassium channels (dark purple)
open and diffuse positively charged ions out of the
cell.
o This entire process lasts in 1-2 ms.
2 CARDIAC ARRHYTHMIA

PATHOPHYSIOLOGY: Electrical activity of the heart

The default resting state

o Action potentials propagating down neuron branches

as chain reactions, causing a wave of depolarizations
and repolarizations.
o Action potentials only travel in one direction

Each normal heart beat should follow the same sequence of

electrical events:
■ The P wave represents depolarization of the atria in
response to signalling from the sinoatrial node (i.e.
atrial contraction)
■ The QRS complex represents depolarization of the
ventricles (i.e. ventricular contraction), triggered by
signals from the AV node
o Electrical stimulation (or depolarization) will result in
■ The T wave represents repolarization of the ventricles
membrane potential over time or a characteristic action
(i.e. ventricular relaxation) and the completion of a
potential curve.
standard heart beat
o The action potential curve results from the
■ Between these periods of electrical activity are
transmembrane movement of specific ions and is divided
intervals allowing for blood flow (PR interval and ST
into different phases:
segment)
- Phase 0: Depolarization - Na channels open and Na
rapidly enters the cell and calcium slowly into cell
PATHOPHYSIOLOGY: Types of Arrhythmias
causing rapid depolarization of atrial tissues
Tachyarrhythmia - heart rate with more than 100 bpm
- This rapid depolarization more than equilibrates the
○ Supraventricular Arrhythmias
electrical potential, resulting in brief initial
■ Atrial Flutter
repolarization or Phase 1 caused by Na channels
■ Atrial Fibrillation
closing
■ Paroxysmal Supraventricular
- Calcium influx continues through Phase 2: Plateau
Tachycardia
Phase and balanced by K+ going out the cell thus
○ Ventricular Arrhythmias
plateau or flat
■ Premature Ventricular Complexes
- The membrane remains permeable to potassium
■ Ventricular Tachycardia
efflux during Phase 3: Rapid repolarization - Ca
■ Ventricular Proarrhythmia
channels close and K rapidly goes out of the cell
■ Ventricular Fibrillation
- Phase 4: Resting potential and is related to
Bradyarrhythmia - heart rate with less than 60 bpm
constant sodium leak into the the intracellular space
○ Sinus block
balanced by a decreasing efflux of potassium
○ Atrioventricular block
 C ARDIAC ARRHYTHMIA 3

A. Tachyarrhythmia ● Ventricular Proarrhythmia
Supraventricular Arrhythmias ○ The development of a significant new
arrhythmia
AFl Contraction: Rapid but Acute AF - onset within 48h § Ventricular Tachycardia
regular and organized Paroxysmal - terminates § Ventricular Fibrillation
atrial activation spontaneously in <7d § Torsade de Pointes (TdP)
Atrial Rate: 270-330 bpm Recurrent - >2 episodes
○ or worsening of an existent arrhythmia
Persistent - >7 days and
§ Longer, faster, or more frequent episodes
does not terminate
spontaneously
○ Incessant Monomorphic Ventricular
Permanent - does not tachycardia
terminate with attempts at § Prototypical form of proarrhythmia
pharmacologic or electrical caused by class IC AADs
cardioversion § Results from excessive sodium channel
AF Contraction: Irregularly Disordered heartbeat results blockade and slowed conduction
irregular rhythm and to not pumping blood out of
disorganized atrial the heart efficiently
activation All Antia r rhyt hmic Dr ugs have the potential to
Atrial Rate: 400-600 bpm aggravate existing arrhythmias or cause new
Loss of atrial contraction arrhythmias.
PSVT Rapid heartbeats that Caused by re-entry: AV
start in parts of the heart nodal, SA nodal, intraatrial re-
above the ventricles entries and AV re-entry Torsade de Pointes
Can be transient incorporating an anomalous ● rapid form of polymorphic VT associated with
AV pathway
evidence of delayed ventricular depolarization
due to blockade of K+ conductance (long QT
Ventricular Arrhythmias interval)
● Premature Ventricular C omplexes ● Potential Causes of Torsade de Pointes:
○ Can occur in patients with or without ○ Genetics
structural heart disease ○ Drugs - Delay ventricular repolarization by
○ Occurs early and the ventricle contracts when it influencing ion movement usually blocking
is incompletely filled thus PVCs are usually potassium efflux which triggers TdP
asymptomatic and non-life-threatening ■ Antiarrhythmics, Cancer chemotherapy,
● Ventricular tachycardia and Antibiotics,
○ Defined by 3 or more repetitive Premature ○ Diseases
Ventricular Complexes (PVCs) occurring at more ■ HF, MI, hypokalemia, severe bradycardia
than 100 beats/minute and severe hypothermia
○ May result from severe electrolyte abnormalities,
drug toxicity or during an acute Myocardial B. Bradyarrhythmia
Infarction or Ischemia complicated by Heart Sinus bradyarrhythmia
Failure ● Common especially in young, athletically active
○ Non- sustained VT - may last for a few individuals
seconds ● Asymptomatic and does not require intervention
○ Sustained VT - last for many minutes or even ● However, some patients (elderly) have sinus
hours and if left untreated, may progress to node dysfunction:
ventricular fibrillation. ○ attenuates SA nodal function
● Ventricular Fibrillation ○ Usually cause by underlying structural
○ An electrical anarchy of ventricle resulting in no heart disease
cardiac output and cardiovascular Atrioventricular block
collapse ● Problem in conduction of the heartbeat signal
○ Occurs when erratic signals cause ventricles to from the sinus node to the ventricles
quiver ineffectively, producing no real heartbeat ● occur in any area of the AV conduction system:
○ Most commonly in patients with CAD or LV the AV node, His bundle or the bundle branches
dysfunction ● AV block is usually categorized into three
○ Heart cannot effectively pump blood different types based on ECG findings
causing cardiac arrest
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First- ● 1:1 AV conduction with a prolonged 6. Proarrhythmia
degree PR interval o Asymptomatic to
block ● Signal gets through, but may take o Worsening of symptoms
longer than normal to travel from the 7. Ventricular tachycardia
sinus node to the ventricles o Asymptomatic to
o Hemodynamic collapse
Second- ● Sinoatrial conduction disease 8. Ventricular Fibrillation
degree ● Right coronary infarction o Hemodynamic collapse
block ● Heartbeat signals are lost o Syncope
between the atria and o Cardiac arrest
ventricles
○ Mobitz 1 AV block (Wenckebach C LINIC AL PRESENTATION: C auses
periodicity) o Coronary Artery Diseases and other heart problems
○ Mobitz II AV block o High Blood Pressure
o Congenital Heart Disease
Third- ● Complete heart block: no o Thyroid problems
degree communication between atria and o Diabetes
block ventricles (AV dissociation) so the o Electrolyte imbalance
ventricles beat slowly on their own o Drugs
o Alcohol
o Nicotine

C LINIC AL PRESENTATION: Risk Factors

IV. C LINIC AL PRESENTATION
C LINIC AL PRESENTATION: Signs And Symptoms
Classic Symptoms
1. Lightheadedness
2. Fainting
3. Palpitations
4. Cardiac arrest C LINIC AL PRESENTATION: C omplications

Specific symptoms o Stroke. When your heart quivers, it's unable to

1. AF & Atrial Flutter pump blood effectively, which can cause blood to
○ Palpitations pool. This can cause blood clots to form. If a clot
○ Dyspnea breaks loose, it can travel from your heart to your
○ Fatigue brain. There it might block blood flow, causing a
2. Paroxysmal SVT stroke.
○ Palpitations without provocation o Heart failure. Heart failure can result if your heart
○ Severe: syncope is pumping ineffectively for a prolonged period due
3. Supraventricular Tachycardia to a bradycardia or tachycardia, such as atrial
o Fainting, fibrillation.
o Anginal chest pain
o Palpitations,
o Dizziness V. DIAGNOSIS
o Choking/pressure sensation Electrocardiogram
4. Premature Ventricular C omplexes ● Cornerstone of diagnosis for cardiac rhythm
o Asymptomatic or disturbances
o Mild palpitations ● Records electrical activity of the heart, including
5. Bradyarrhythmias when and for how long a heartbeat occurs
o Dizziness ○ TdP - long QT intervals or prominent U
o Syncope waves
o Fatigue
o Confusion
 C ARDIAC ARRHYTHMIA 5

ALGORITHM

Holter monitoring
● Ambulatory electrocardiography
● Portable ECG device that continuously records
heart rhythm for 24- to 48-hour period of time.
Echocardiography
● Painless ultrasound used to evaluate the size, shape
and motion of valves, septum and walls as well as
changes in chamber size during cardiac cycle
Patch Monitor
● If symptoms occur less frequently - Zio patch - is an
option.
● Adhesive long-term recording device that can store
up to two weeks of continuous recordings of heart
rhythm and automatically detects and records any
cardiac arrhythmias.
Stress test
● monitoring your heart while you work out on a
stationary bike or a treadmill comparing your Algorithm for the treatment of acute (top portion) PSVT
circulation at rest with the same measurements taken and chronic prevention of recurrences (bottom portion)
at maximum exertion
Tilt table test
● While you lie flat on a table, your heart activity and
blood pressure are monitored.

VI. THERAPY OR TREATMENT

A. GENERAL APPROAC H

• Use of antiarrhythmic drugs has declined because

major trials showed increased mortality with use in
several situations, the realization of proarrhythmia
as a significant side effect, and the advancing
technology of nondrug therapies, such as ablation
and the implantable cardioverter-defibrillator (ICD).
 6 CARDIAC ARRHYTHMIA

PHARMACOLOGIC NON- PHARMACOLOGIC
Vaugnhan – Williams C lassification
All anti-arrhythmic drugs act by altering the movement of
electrolytes within the electrical conduction pathways of
the myocardium. The Vaughan Williams classification
system groups drugs according to their ability to block
the movement of one or more of these ions across the
myocardial cell membrane.
o C lass I drugs act by blocking the fast sodium
channels and therefore delay the rise in phase 0 of the
action potential. This group can be further subdivided
into: class IA drugs which increase the duration of the
action potential; class IB, which shorten the action
potential; and class IC, which have no effect on action
potential duration.
o C lass II drugs act by modifying the sympathetic
stimulation of heart rate by blocking the beta-
adrenoceptors. Although, these drugs do not affect the
action potential in most myocardial cells, they increase
the time taken to reach the threshold potential during
phase 4 in the specialised pacemaker cells, hence
slowing sinoatrial (SA) nodal and atrioventricular (AV)
nodal firing.
o C lass III agents act by blocking the potassium
channels and therefore prolonging the plateau of phase
2, delaying repolarisation, and increasing the refractory
period and preventing further excitation.
o C lass IV agents block the movement of calcium ions
during phase 2 (plateau phase) of the action potential.
In addition, calcium movement is the primary
determinant of depolarisation in SA and AV nodal
pacemaker cells and the nodes are therefore
particularly sensitive to the effects of calcium channel
blockers

*drugs are in the next page

 C ARDIAC ARRHYTHMIA 7

CLASS 1A – Na CHANNEL BLOCKERS

CLASS 1B – Na CHANNEL BLOCKERS

CLASS 1C – Na CHANNEL BLOCKERS

 8 CARDIAC ARRHYTHMIA

C LASS II – BETA BLOC KERS

C LASS III – K+ C HANNEL BLOC KERS

C LASS IV – C a C HANNEL BLOC KERS

 C ARDIAC ARRHYTHMIA 9

OTHER ANTIARRHYTHMIC DRUGS
 10 CARDIAC ARRHYTHMIA
VII. CLINICAL PRACTICE GUIDELINES
2017 AHA/AC C /HRS Guidelines for Management
of Patients with Ventricular Arrhythmias
Non Arrhythmic Medications
ELEC TROLYTES
● Administration of potassium and magnesium
has been proposed as helpful adjuncts in the
prevention of VA.
DEFIBRILLATION
● This therapy can be delivered by a transvenous
IC D ( Implantable C ardioverter
Defibrillator). These device can monitor the
heart rhythm continuously and deliver therapy in
response to a tachycardia that meets
preprogrammed detection rates and arrhythmia
duration.
VIII. JOURNALS
Burden of Arrhythmia in Recreational Marijuana
users
● Marijuana or C annabis is widely used as a
recreational substance worldwide. Case reports
have reported cardiac arrhythmias immediately
following recreational marijuana use
● The study identified 2,459,856 weighted
hospitalized marijuana users between 2010 and
2014, out of these, 66,179 (2.7%) patients
experienced arrhythmias
● Among hospitalizations with known marijuana
use, the 45–64 years age group showed highest
arrhythmia incidence whereas 65–84 years age
group showed a maximum rise in arrhythmia
incidence over time.
● The prevalence of arrhythmias in hospitalized
male and female marijuana users nearly
increased two-fold between 2010 and 2014;
7464 to 14,195 in males and 1876 to 3800 in
females, p b 0.001. Males with recreational
marijuana use more often experienced
arrhythmias.
● There were consistently increasing trends of all-
cause arrhythmia (2145 in 2010 to 3183 in 2014,
trend p = 0.03) and Afib (1405 in 2010 to 2252
in 2014, p = 0.03) in hospitalized marijuana
users. The frequency of AF, SVT, VFib, and VT
per 100,000 hospitalized marijuana users also
increased 1.3 to 1.4 fold between 2010 and
2014 (p b 0.001).
Secondhand smoke and cardiac arrhythmia
● The authors conducted the study using mice.
Mice were exposed to secondhand tobacco
smoke in a chamber specifically designed to test
health effects associated with inhaled toxins.
The smoke levels were set to be similar to those
found in public areas where smokers are
present.
● Following four, eight and 12 weeks of exposure
for six hours a day, five days a week, the
animals' hearts were tested using high-speed
imaging and electrocardiograms for changes in
electrical activity. To test susceptibility to
arrhythmias, hearts were paced at fast heart
rates. They also were tested for levels of
calcium, which regulates heart contraction and
contributes to abnormal rhythms. The results
were compared to hearts of mice exposed only
to filtered air.
● The researchers found that hearts from mice
exposed to filtered air responded normally, but
the hearts from mice exposed to secondhand
smoke could not tolerate fast rates, especially at
12 weeks of exposure. They also found that
calcium levels in these hearts did not respond
quickly enough, causing beat-to-beat instability,
or cardiac alternans.
● "The high incidence of cardiac alternans is
particularly concerning because we know that
patients with this condition are at significantly
higher risk for arrhythmias and sudden cardiac
death,"