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10
Dysrhythmias
Fast & Easy ECGs, 2nd E – A SelfPaced Learning Program
Fast & Easy ECGs, 2E
1
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Origination and Conduction of
Heartbeat
•
•
•
•
Each heartbeat arises as an electrical
impulse from the SA node
It then spreads across the atria
depolarizing the tissue and causing
both atria to contract
The impulse then activates the AV
node but it is slightly delayed there
allowing the atria to finish contracting
and pushing any remaining blood from
their chambers into the ventricles
The impulse then spreads through
both ventricles via the Bundle of His,
right and left bundle branches, and
the Purkinje fibers, causing a
synchronized contraction of the
ventricles and thus, the pulse
Fast & Easy ECGs, 2E
2
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SA Node Depolarization
• Through the property
of automaticity, the
heart’s pacemaker
cells spontaneously
depolarize
• They have what can
be described as an
unstable resting
membrane potential
Fast & Easy ECGs, 2E
3
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SA Node Depolarization
• Because the SA
node reaches it’s
action potential
more quickly than
the other
pacemaker cells, it
is the heart’s
primary
pacemaker
Fast & Easy ECGs, 2E
4
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Nonpacemaker Myocyte
Depolarization
• Phase 4
– In the polarized state, nonpacemaker myocytes
have a resting membrane potential of -80 to
-90 mV which remains stable until the cell is
stimulated
Fast & Easy ECGs, 2E
5
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Nonpacemaker Myocyte
Depolarization
• Phase 0
– Depolarization begins once the myocyte receives an impulse from a
neighboring cell
– Na+ quickly enters the cells through fast Na+ channels, some Ca++ enters the
cells through slow Ca++ channels and the K+ channels close
– With all this Na+ and Ca++ entering the cell, it becomes more positively
charged
– The charge overshoots neutral, rising to about 130 mV
– When a certain level is reached, depolarization of the entire cell occurs
Fast & Easy ECGs, 2E
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Nonpacemaker Myocyte
Depolarization
• Phase 1
– Voltage-gated Na+ channels close, and a small number of the
K+ channels open stopping the fast inflow of Na+ and allowing
some K+ to move out of the cell
– Chloride (Cl-) ions enter the cell
– These ion movements lower the positive charge inside the cell
somewhat
Fast & Easy ECGs, 2E
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Nonpacemaker Myocyte
Depolarization
• Phase 2
– Ca++ enters the cell through voltage-gated L-type Ca++
channels, prolonging the depolarization
– This movement of Ca++ into the cell counteracts the potential
change caused by the movement of K+ out of the cell
– Ca++ then reacts with myosin and actin causing the cell to
contract
I
Fast & Easy ECGs, 2E
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Nonpacemaker Myocyte
Depolarization
• Phase 3
– Ca++ channels close and many K+ channels open allowing a
rapid outflow of K+, causing the cell interior to become more
negatively charged
– Ca++ and Na+ are pulled out of the cell interior by Na+ and Ca++
pumps helping to achieve and maintain the very negative
resting membrane potential of the myocyte
I
Fast & Easy ECGs, 2E
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Absolute Refractory Period
• During this period, no stimulus, no matter how
strong, will depolarize the cell
– Helps assure the rhythmicity of the heartbeat
– Assures that after contraction, relaxation is nearly
complete before another action potential can be
initiated
– Prevents spasm-producing (tetanic) contractions in
the cardiac muscle
• This period includes Phases 0, 1, 2, and part of
phase 3
Fast & Easy ECGs, 2E
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Relative Refractory Period
• During the later phase of repolarization a
sufficiently strong stimulus will depolarize the
myocardium
Fast & Easy ECGs, 2E
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Dysrhythmias
• Refers to any ECG rhythm that differs from
normal sinus rhythm
• Heartbeat may be slower or faster than
normal, irregular, or conduction through the
heart may be delayed or blocked
Fast & Easy ECGs, 2E
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Effects of Dysrhythmias
• Some are of little consequence and simply
annoying while others are life-threatening
medical emergencies that can lead to cardiac
arrest and sudden death
Fast & Easy ECGs, 2E
13
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Effects of Dysrhythmias
• Most common symptom is palpitations, an
abnormal sensation felt with the heartbeat
Fast & Easy ECGs, 2E
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Effects of Dysrhythmias
• Symptoms such as lightheadedness, dizziness,
fainting, chest pain, shortness of breath,
sweatiness, and/or pallor may be seen in
dysrhythmias that cause decreased cardiac
output
• We refer to this as being symptomatic
Fast & Easy ECGs, 2E
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Effects of Dysrhythmias
• Some dysrhythmias slow
the heart rate decreasing
cardiac output
• Others decrease the
stroke volume by making
the heart beat too fast
(which decreases cardiac
output by not allowing
the heart to fill properly)
Fast & Easy ECGs, 2E
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Effects of Dysrhythmias
• Cardiac output can also
be decreased when the
atria don’t contract
properly or contract at
all (eliminating the
atrial kick which
normally pushes blood
into the ventricles
Fast & Easy ECGs, 2E
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Dysrhythmias
• Sometimes the first clinical manifestation of a
cardiac dysrhythmia is sudden death
Fast & Easy ECGs, 2E
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Types of Dysrhythmias
• Include:
– bradycardia
– tachycardia
– early (premature) beats
– dropped beats, or QRS complexes
– irregular rhythms
Fast & Easy ECGs, 2E
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Bradycardia
• Heart rate less than 60 beats per minute
• Can occur for many reasons and may or may
not have an adverse affect on cardiac output
• In the extreme, it can lead to severe
reductions in cardiac output and eventually
deteriorate into asystole
Fast & Easy ECGs, 2E
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Bradycardia
• Can arise from the SA node
– Sometimes this is normal
– Can also be caused by increased parasympathetic
(vagal) tone or a variety of medical conditions
• Can be brought about by failure of the SA node
– Escape pacemaker should arise from the AV node
or ventricles but is likely to result in bradycardia
• Can also be caused by AV heart block
Fast & Easy ECGs, 2E
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Bradycardia
• Can also be seen when the atria repeatedly or
chaotically depolarize and bombard the AV
node so rapidly that not all the impulses are
conducted through to the ventricles
– If the number of atrial impulses reaching the
ventricles falls to less than normal, it results in a
slower than normal ventricular rate
Fast & Easy ECGs, 2E
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Tachycardia
• Heart rate greater than 100 beats per minute
• Has many causes
• Leads to increased myocardial oxygen
consumption
• Extremely fast rates can have an adverse affect
on cardiac output
• When it arises from the ventricles it may lead to
a chaotic quivering of the ventricles called
ventricular fibrillation
Fast & Easy ECGs, 2E
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Tachycardia
• Is referred to as one of
five types:
– narrow QRS complex
regular rhythms,
– wide QRS complex regular
rhythms,
– narrow QRS complex
irregular rhythms,
– wide QRS complex
irregular rhythms,
– wide QRS complexes of
unknown origin.
• Being able to differentiate
between the five types of
tachycardia will help
determine what type of
treatment should be
employed
Fast & Easy ECGs, 2E
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Early Beats
• Fire early, before the SA node has a chance to initiate the impulse
• Can arise from anywhere in the heart, including the atria, AV junction,
or ventricles
• The R-R interval between the normal complex and premature complex
is shorter than the interval between two normal complexes
• Frequent premature beats may progress to atrial, junctional, or
ventricular tachycardia or deteriorate into ventricular fibrillation
I
Fast & Easy ECGs, 2E
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Dropped Beats
• Dropped beats occur when the SA node fails to initiate an
impulse resulting in a pause in the ECG rhythm
• Usually, the SA node recovers and fires another impulse
• If the SA node fails to fire, then an escape pacemaker from
the atria, AV junction, or ventricles initiates an impulse
I
Fast & Easy ECGs, 2E
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Dropped Beats
• Dropped QRS complexes can occur from a partial
or intermittent block at the AV junction
• Some impulses originating from the SA node fail
to conduct to the ventricles, resulting in one or
more dropped ventricular beats
• This is seen as more P waves than QRS complexes
and R-R intervals that are longer wherever there
is a dropped ventricular beat
• Dropped QRS complexes can also occur when a
premature beat arises from the atria but fails to
conduct to the ventricles
Fast & Easy ECGs, 2E
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Irregularity
• Is caused by some type of dysrhythmia
including:
– early beats and dropped beats
– dysrhythmias that speed up and slow down in a
cyclical manner
– those that originate from more than one site
(sometimes from many sites)
– some types of AV heart block
Fast & Easy ECGs, 2E
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Causes and Mechanisms of
Dysrhythmias
• Include
– increased parasympathetic tone
– myocardial hypoxia, injury and infarction
– increased automaticity
– reentry
– triggered beats
– proarrhythmia
Fast & Easy ECGs, 2E
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Increased Parasympathetic Tone
• Stimulation of the parasympathetic nervous
system causes the heart rate to slow and
impulse conduction through the AV node to
be prolonged
• Can lead to bradycardia, sinus arrest and/or
AV heart block
Fast & Easy ECGs, 2E
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Myocardial Hypoxia, Injury, and
Infarction
• An oxygen deprived myocardium is extremely
susceptible to dysrhythmias
• Pulmonary disorders that interfere with adequate
intake of oxygen are major causes of
dysrhythmias
• Damage to portions of the heart’s conduction
system can result in blockage of impulse
formation and/or conduction
• Sometimes myocarditis can precipitate
dysrhythmias
Fast & Easy ECGs, 2E
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Increased Automaticity
• Results from
stimulation of
the
sympathetic
nervous
system
• Causes the
cells to
spontaneously
depolarize
more quickly
• The resulting
heart rhythm
depends on
where the
impulse
originates
I
Fast & Easy ECGs, 2E
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Increased Automaticity
• If it is the SA node, the rhythm remains normal but
faster than 100 beats per minute
• If it is an ectopic focus, any number of dysrhythmias
may ensue
– May cause a single, occasional early beat or it can
produce a sustained abnormal rhythm
• Sustained rhythms produced by an ectopic focus in the
atria or atrioventricular junction are less dangerous
than those that arise from the ventricles
Fast & Easy ECGs, 2E
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Causes of Increased Automaticity
• Emotional stress or physical exercise, caffeine,
amphetamines, ischemia, hypoxia, atrial
stretching or dilation hyperthyroidism, or a
myriad of other medical conditions, such as
hypovolemia, congestive heart failure, etc
Fast & Easy ECGs, 2E
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Reentry
• Occurs when
an electrical
impulse
reenters a
conduction
pathway
rather than
moving from
one end of the
heart to the
other and
then
terminating
Fast & Easy ECGs, 2E
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© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Reentry
• Some hearts have an accessory pathway located
between either the right atrium and the right ventricle or
the left atrium and the left ventricle
– These accessory pathways allow electrical impulses to
bypass the AV node and depolarize the ventricles
• Some hearts have a dual conduction pathway through
the AV node
• Under the right circumstances, reentry can occur in both
accessory pathways and dual conduction pathways
through the AV node
Fast & Easy ECGs, 2E
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Reentry
• Depending on the timing, reentry can
generate a sustained abnormal circuit rhythm
• Reentry circuits are responsible for a number
of dysrhythmias, including atrial flutter, most
paroxysmal supraventricular tachycardia, and
ventricular tachycardia
Fast & Easy ECGs, 2E
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Reentry
• A unique form of reentry is referred to as
fibrillation
– Results when there are multiple micro-reentry
circuits in the heart chambers and they are
quivering due to chaotic electrical impulses
• Atrial fibrillation occurs in the atria
• Ventricular fibrillation occurs in the ventricles
Fast & Easy ECGs, 2E
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Triggered Beats
• Occur when problems at the level of the ion
channels in individual heart cells lead to partial
repolarization
– Partial repolarization causes repetitive ectopic firing
called triggered activity
• Depolarization produced by triggered activity is
known as afterdepolarization and can bring about
atrial or ventricular tachycardia
• Are relatively rare but can result from the action
of antidysrhythmic drugs, cell injury, and other
conditions
Fast & Easy ECGs, 2E
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Proarrhythmia
• Refers to the development of new or a more
frequent occurrence of pre-existing
dysrhythmias that are caused by
antidysrhythmic therapy or drugs used to
treat other conditions
Fast & Easy ECGs, 2E
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Dysrhythmias
• Can originate from the SA node, atria, AV
junction, or ventricles and can occur due to AV
heart block
Fast & Easy ECGs, 2E
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Identifying Dysrhythmias
• Examination of the ECG rhythm on the ECG
monitor must be done in a systematic,
organized way
Fast & Easy ECGs, 2E
42
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Lead II
• Is the most
commonly used
lead for
identifying
dysrhythmias
• Has an
excellent view
of normal
conduction of
the impulse
through the
heart
Fast & Easy ECGs, 2E
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Modified Chest Lead 1 (MCL1)
• Is another lead
used for continuous
cardiac monitoring
• Place positive
electrode in the
fourth intercostal
space in the right
sternal border
(same position as
precordial lead V1)
I
Fast & Easy ECGs, 2E
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Modified Chest Lead 1 (MCL1)
• Is effective for monitoring the QRS complexes
of dysrhythmias, P wave changes, AV bundlebranch defects, and premature ventricular
beats
• Is helpful in differentiating between the
different types of tachycardia
(supraventricular versus ventricular)
Fast & Easy ECGs, 2E
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Treatment of Dysrhythmias
• Many dysrhythmias require no treatment as
they are either benign or resolve on their own
• The method used to manage dysrhythmias
depends on whether or not the patient is
stable or unstable
• Patients who are symptomatic are considered
unstable because symptoms indicate
decreased cardiac output
Fast & Easy ECGs, 2E
46
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Treatment of Dysrhythmias
• Several treatment options are available to
treat dysrhythmias and are employed on the
basis of the mechanism or etiology of the
dysrhythmia
• Commonly used treatments include physical
maneuvers, electricity therapy, and the
administration of certain medications
Fast & Easy ECGs, 2E
47
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Electrical Therapy
• Synchronized cardioversion
• Defibrillation
• Pacing
Fast & Easy ECGs, 2E
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Physical Maneuvers
• Vagal maneuvers
Fast & Easy ECGs, 2E
49
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Medications
• For slow heart rates, a drug that blocks the effects of the
parasympathetic nervous system, such as atropine, may be
initially used
• The bradycardic patient may also be treated by directly
stimulating the sympathetic nervous system through the
use of drugs that have sympathomimetic properties, such
as epinephrine or dopamine
• Medications referred to as antidysrhythmics can be used to
suppress tachydysrhythmias and ventricular fibrillation
• There are many classes of antidysrhythmic medications
with different mechanisms of action and many different
individual drugs within these classes
Fast & Easy ECGs, 2E
50
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Medications
• Although drug therapy is used to prevent
dysrhythmias, nearly every antidysrhythmic drug
has the potential to act as a proarrhythmic
• Several groups of drugs slow conduction through
the heart, without actually preventing the
dysrhythmia
– These drugs are used to control the rate of a
tachycardia and make it tolerable for the patient
• Anticoagulant medications and antiplatelet drugs
can reduce the risk of clotting that is associated
with certain dysrhythmias
Fast & Easy ECGs, 2E
51
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• Each heartbeat arises as an electrical impulse
from the SA node and spreads across the atria,
depolarizing the tissue, causing both atria to
contract
• The impulse then activates the AV node where it
is delayed slightly
• The impulse then spreads through both ventricles
via the Bundle of His, right and left bundle
branches, and the Purkinje fibers, causing a
synchronized contraction of the primary pumping
chambers of the heart
Fast & Easy ECGs, 2E
52
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• Through the property of automaticity, the
heart’s pacemaker cells spontaneously
depolarize
• Because the SA node reaches it action
potential more quickly than the other
pacemaker cells, it is the heart’s primary
pacemaker
Fast & Easy ECGs, 2E
53
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• In the polarized state, the myocytes have a resting
membrane potential of -80 to -90 mV • In nonpacemaker myocytes, this membrane potential
remains stable until the cell is stimulated
• The temporary change in electrical potential that
occurs between the inside and the outside of a nerve
or muscle fiber when a nerve impulse is transmitted
is called the action potential
• The action potential of the myocytes consists of five
phases labeled 0 to 4
Fast & Easy ECGs, 2E
54
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• One of the things we look for during
examination of the ECG is the presence of
dysrhythmias
• A dysrhythmia is an ECG rhythm that differs
from normal sinus rhythm
• Some dysrhythmias are of little consequence
and simply annoying while others are lifethreatening medical emergencies that can
lead to cardiac arrest and sudden death
Fast & Easy ECGs, 2E
55
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• The most common symptom of dysrhythmias is
palpitations
• Symptoms such as lightheadedness, dizziness,
fainting, chest pain, shortness of breath,
sweatiness, and/or pallor may be seen in
dysrhythmias that cause decreased cardiac
output
– Referred to as being symptomatic
• Sometimes the first clinical manifestation of a
cardiac dysrhythmia is sudden death
Fast & Easy ECGs, 2E
56
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• Types of dysrhythmias include bradycardia,
tachycardia, early (premature) beats, dropped
beats, or QRS complexes and irregular rhythms
• Causes and mechanisms of dysrhythmias include
increased parasympathetic tone, myocardial
hypoxia, injury and infarction, increased
automaticity, reentry, triggered beats, and
proarrhythmia
• Dysrhythmias can originate from the SA node,
atria, AV junction, or ventricles and can occur due
to AV heart block
Fast & Easy ECGs, 2E
57
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• Typically, dysrhythmias can be identified
through the use of one lead, most commonly
lead II
• Another lead commonly used to detect
dysrhythmias is the MCL1
• Examination of the ECG rhythm on the ECG
monitor must be done in a systematic,
organized way
Fast & Easy ECGs, 2E
58
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.
Summary
• Many dysrhythmias require no treatment as they
are either benign or resolve on their own
• Managing dysrhythmias depends on whether or
not the patient is stable or unstable
• Patients who are symptomatic are considered
unstable because symptoms indicate decreased
cardiac output
• Many treatment options are available to treat
dysrhythmias including physical maneuvers,
electricity therapy, and the administration of
certain medications
Fast & Easy ECGs, 2E
59
© 2013 The McGraw-Hill Companies, Inc. All rights reserved.