Dysrhythmia Interpretation Modules 1-6 June 2012

Dysrhythmia Interpretation &
Therapeutic Modalities
Modules I-VI
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Revised: 9/20/10
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Revised: 9/10
Dysrhythmia Interpretation & Therapeutic Modalities

Modules I-VI
Table of Contents
Objectives
4-7
Modules I-VI
Module I
8 - 49
Cardiovascular Structure and Function, Electrocardiography Monitoring,

Introduction to Dysrhythmias, & Sinus Rhythms
Module II
50 65
Atrial Dysrhythmias
Module III
66 74
Junctional Rhythms
Module IV
75 91
Ventricular Rhythms
Module V
92 100
Atrioventricular Blocks
Module VI
101 110
Pacemakers
References
111
Post Test
112 125
Revised: 9/10
Dysrhythmia Interpretation & Therapeutic Modalities

Objectives:
Module I: Cardiovascular Structure and Function, Electrocardiography Monitoring, Introduction to
Dysrhythmias, & Sinus Rhythms
1. Describe the anatomy of the heart.
2. Discuss preload, afterload, and components of cardiac output.
3. Discuss how atrial kick contributes to cardiac output.
4. Differentiate the effects of the sympathetic and parasympathetic nervous systems on the heart.
5. Be able to identify horizontal and vertical measurements on the ECG paper.
6. Name at least two methods for calculating heart rate.
7. Identify correct measurement for PR interval, QRS duration, and QT duration.
8. Be able to identify artifact on the ECG.
9. Describe the ECG characteristics of a sinus rhythm.
10. Describe the ECG characteristics, possible causes, signs and symptoms, and emergency
management of each of the following dysrhythmias that originate in the sinoatrial node :
a. Sinus bradycardia
b. Sinus tachycardia
c. Sinus arrhythmia
d. Sinus block
e. Sinus arrest
Module II: Atrial Dysrhythmias
1. Describe how atrial kick affects cardiac output.
2. Determine the etiology, identifying characteristics, significance and treatment for the following
groups of dysrhythmias:
a. Premature Atrial Contraction (PAC) and blocked PACs
b. Atrial fibrillation
c. Atrial Flutter
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d. Atrial Tachycardia
- Paroxysmal Atrial Tachycardia (PAT)
- Paroxysmal Supraventricular Tachycardia (PSVT)
e. Wandering Atrial Pacemaker
3. Describe the actions, uses, and adverse effects of the most commonly used drugs for the following
types of dysrhythmias:
a. Premature Atrial Contraction (PAC) and blocked PACs
b. Atrial fibrillation
c. Atrial Flutter
d. Atrial Tachycardia
- Paroxysmal Atrial Tachycardia
- Paroxysmal Supraventricular Tachycardia (PSVT)
e. Wandering Atrial Pacemaker
Module III: Junctional Rhythms
junctional rhythms:
a. Premature junctional contraction (PJC)
b. Junctional escape beat
c. Junctional Rhythm
d. Accelerated Junctional Rhythm
e. Junctional tachycardia
2. Describe the most commonly used drugs for the following types of dysrhythmias:
a. Premature junctional contraction (PJC)
b. Junctional escape beat
c. Junctional Rhythm
d. Accelerated Junctional Rhythm
e. Junctional tachycardia
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Module IV: Ventricular Rhythms

ventricular rhythms:
f.
Premature Ventricular Complex/ Contraction (PVC)
g. Ventricular Escape beats

h. Idioventricular Rhythm (Ventricular Escape Rhythm, IVR)
i.
Accelerated Idioventricular Rhythm (AIVR)
j.
Ventricular Tachycardia (VT)

-
Monomorphic VT vs. Polymorphic VT
Torsades de Pointes
k. Ventricular Fibrillation
l.
Pulseless Electrical Activity (PEA)
m. Ventricular Standstill/ Agonal

n. Asystole
2. Describe the most commonly used drugs for the following types of dysrhythmias:
a. Premature Ventricular Complex/ Contraction (PVC)
b. Ventricular Escape beats
c. Idioventricular Rhythm (Ventricular Escape Rhythm, IVR)
d. Accelerated Idioventricular Rhythm (AIVR)
e. Ventricular Tachycardia (VT)
f.
Monomorphic VT vs. Polymorphic VT
Torsades de Pointes
Ventricular Fibrillation
g. Pulseless Electrical Activity (PEA)

h. Ventricular Standstill/ Agonal
i.
Asystole
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Module V: Atrioventricular Blocks

atrioventricular blocks:
a. First-degree AV Block
b. Second-degree AV Block- Type I (Wenckebach or Mobitz I)
c. Second-degree AV Block- Type II (Mobitz II)
d. Third-degree AV block (Complete Heart Block)
2. Describe the most commonly used drugs for the following types of atrioventricular blocks:
a. First-degree AV Block
b. Second-degree AV Block- Type I (Wenckebach or Mobitz I)
c. Second-degree AV Block- Type II (Mobitz II)
d. Third-degree AV block (Complete Heart Block)
Module VI: Pacemakers
1. Identify the primary indications and possible complications of pacemaker therapy.
2. Describe the various methods for pacing (transcutaneous, transvenous, epicardial).
3. Explain the difference between fixed-rate and demand pacemakers.
4. Identify the appearance of pacemakers spikes and the waveform on the ECG produced as a result
of:
a. Atrial pacing
b. Ventricular pacing
Revised: 9/10
Module I: Cardiovascular Structure and Function,

Electrocardiography Monitoring, Introduction to
Dysrhythmias, & Sinus Rhythms
Important Terms- Cardiovascular Structure and Function

Afterload
Affected by pressure and preload. What heart has to pump

against with each contraction.
Aortic Valve
The valve between the left ventricle and the aorta.
Apex
The bottom portion of the heart.
Arteriole
Smaller arteries located between arteries and capillaries.
Artery
A vessel carrying blood away from the heart. With the

exception of the pulmonary artery, carries oxygenated blood.
Atrial Kick
The amount of blood contributed by atrial contraction into the

ventricles. Accounts for 20 - 25 percent of cardiac output.
Capillary
The area in the circulatory system where the exchange of

nutrients takes place.
Cardiac Output
Hemodynamic calculation of heart rate X stroke volume.
Coronary Sinus
Located at the base of the right atrium. It is the area where the
coronary veins return venous blood from the coronary arteries.
Coronary Arteries
Supply the heart muscle with oxygenated blood.
Deoxygenated
Venous blood is deoxygenated.

The venous blood carries 70-75% oxygen, while the arteries
have 95% or greater oxygen.
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Diastole
The relaxation phase of the cardiac cycle.
Mitral Valve
The valve located between the left atrium and left ventricle.
Oxygenated
With oxygen. Arteries carry 95% or greater oxygen.
Parasympathetic
Nervous System
Part of the autonomic nervous system. Stimulation slows

heart rate. Associated with the vagus nerve.
PMI
Point of maximal impulse where the apical pulse can be

palpated. The PMI is normally at the 5th intercostal space,
midclavicular line.
Preload
Amount of fluid coming into the ventricular chambers during

diastole.
Pulmonary Artery
Carries deoxygenated blood from right ventricle to the

pulmonary capillary membrane in the lungs.
Pulmonary Vein
Carries oxygenated blood from the lungs to the left atrium.
Pulmonic Valve
Valve located between the right ventricle and the pulmonary

artery.
Sinus of Valsalva
Located at the base of the aorta on top of the aortic valve.

Is the location where the left and right coronary arteries arise.
Sympathetic
Nervous System
Part of the autonomic nervous system. Stimulation increases

heart rate and strength of contraction.
Systole
The contractile phase of the cardiac cycle.
Tricuspid Valve
The valve located between the right atrium and right ventricle.
Vein
Vessel carrying blood to the heart. Carries deoxygenated blood,

in exception to the pulmonary veins.
Venule
A smaller vein. Part of the circulatory system located

between the capillary and the vein
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CARDIOVASCULAR STRUCTURE AND FUNCTION
The purpose of the heart is to pump oxygenated blood to body tissues. Oxygen is
carried on the hemoglobin of the red blood cell. The blood carries oxygen via the arteries to
capillaries where all body tissues are perfused with oxygen. When tissues are not perfused,
they simply die. The heart has the job of pumping blood to all body tissue.
Anatomy
The heart is a four chambered muscular pump. These chambers are the right atrium,
right ventricle, left atrium, and left ventricle. The right side of the heart pumps deoxygenated
blood to the lungs, and the left side of the heart pumps oxygenated blood to the peripheral
tissues via the vasculature. Since the left side of the heart has to pump blood to entire body,
the muscles of the left side are much thicker than the right. To put it simply, the heart is one
huge plumbing system. The heart, or pump, has to be strong enough to get blood through the
blood vessels (pipes). The pump and the pipes have to be in good working order for the tissues
to receive blood. This blood carries oxygen that provides nutrition to the tissues of the body.
There are four valves located within the heart: the tricuspid valve, pulmonic valve, mitral valve,
and aortic valve. The tricuspid valve is located on the right side of the heart between the right
atrium and right ventricle- Think Tri (try) to be Right! The pulmonic valve lies between the
right ventricle and pulmonary artery. The mitral valve is on the left side of the heart between the
left atrium and left ventricle, and the aortic valve lies between the left ventricle and the aorta.
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10
Systemic Circulation
The circulation of the body is a closed system which carries blood to and from body
tissues. There are approximately 5 liters of blood circulating through the body at one time. The
pulmonary circulation takes blood to the lungs, while the central and peripheral circulation takes
blood to the rest of the body. The functional units of the circulatory system are arteries,
arterioles, capillaries, venules, and veins. An artery is a vessel that goes away from the heart
while a vein returns blood to the heart.
arteries:
large, highly elastic vessels that transport oxygenated blood, with the exception
of the pulmonary artery.
arterioles:
small and controlled for release of blood into the capillaries.
capillaries:
are the exchange point for nutrients, fluids, and other substances to the tissues.
venules:
collect deoxygenated blood from the capillaries.
veins:
transport deoxygenated blood back to the vena cava, with the exception of the
pulmonary veins.
It is best to think of the circulatory system as a closed circuit. The lungs deliver oxygen
to the blood where the oxygen attaches to the hemoglobin of the red blood cell. As the
oxygenated blood travels to the left ventricle, it is then pumped by the heart to the systemic
circulation via arteries, then arterioles. It is at the capillary level of the tissues that perfusion or
oxygenation of body tissues occurs. The tissues then release carbon dioxide and return the
deoxygenated blood via venules and veins to the right side of the heart. The right ventricle then
pumps blood to the alveoli of the lungs to pick up more oxygen. Thus this cycle, via the
circulatory system maintains oxygenation of tissues. If the tissues do not get oxygen, they will
die.
An analogy to the circulatory system is that the oxygen delivered to the alveoli of the
lungs are like passengers at a bus stop. The oxygen waits for the hemoglobin to give it a ride.
There are four receptor sites for oxygen to attach the hemoglobin. The hemoglobin is like a
Honda Accord (a four-seater). The passengers (oxygen) jump onto the Accords (hemoglobin).
The oxygenated blood is then transported via the arteries (freeways), arterioles (side streets) to
the capillary systems throughout the body (your driveway you eat at home). When the
oxygen is used, the deoxygenated blood (empty Accords with waste products) returns via the
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11
venules (side streets) and veins (freeways) to the lungs to expel the waste product as carbon
dioxide. The lungs then pick up more oxygen which is inhaled to continue the cycle.
There are a number of situations that can be applied to this analogy. For example, an
embolus is a road block, while hypertension could be a narrowed road. Hemorrhage could be a
bunch of vehicles driving off a bridge. Im sure you can come up with more of your own!
In order for the cycle to continue, circulation must continue intact, promoting flow from
the lungs, to the left side of the heart, then the systemic circulation and back to the right side of
the heart. The circulatory system diagram on the next page depicts the flow of blood throughout
the body to the various tissues.
Flow of Blood Through the Cardiovascular System

It is best to think of the right and left sides of the heart as separate. Although both sides
of the heart pump together, each ventricle pumps blood to different destinations. The right
ventricle pumps blood to the lungs, while the left ventricle pumps to the systemic circulation.
Deoxygenated blood comes from the systemic circulation after oxygen has been
delivered to the tissues. This blood returns via the venous system to the right atrium via the
inferior and superior vena cava and the coronary sinus. As the blood enters the right atrium, it
travels through the tricuspid valve to the right ventricle. The valves of the heart are one-way
valves that allow blood to pass through them. As the right ventricle fills, the pressure of blood in
the right ventricle closes the tricuspid valve. When the right ventricle contracts,
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12
blood then passes through the pulmonic valve into the pulmonary artery. An artery is any
vessel carrying blood away from the heart. The pulmonary artery is the only artery in the body
that carries deoxygenated blood. The pulmonary artery branches to pulmonary arterioles, then
branches to capillaries. They branch to millions of capillaries, where each capillary hugs an
alveolus (air sac). It is at the alveolar-capillary membrane that the exchange of gases takes
place. We have been told many times that we inhale oxygen and exhale carbon dioxide. The
oxygen we inhale at room air is 21% oxygen. Although we do exhale carbon dioxide, included
in this exhaled gas is approximately 16 to 17% oxygen. If you think about it, if we did not exhale
oxygen, CPR would not work.
Once the carbon dioxide and oxygen is exhaled, oxygen is inhaled and an exchange of
gases or diffusion occurs at the millions of alveolar capillary membranes in the lungs. It is at
this location that oxygen attaches to the hemoglobin receptor sites on the red blood cell. The
oxygenated blood is carried by the pulmonary vein to the left atrium. From the left atrium, blood
passes through the mitral valve into the left ventricle. When the left ventricle fills with blood, the
mitral valve closes. As the left ventricle contracts, blood flows through the aortic valve, to the
aorta.
At the base of the aorta, positioned on top of the aortic valve, is an area called the Sinus
of Valsalva. The Sinus of Valsalva provides the opening to the coronary arteries which supplies
the heart muscle itself with blood. The aorta carries blood via the vasculature to the capillaries
which provide nutrients to the body tissues. At the capillary level, oxygen is delivered to the
tissues and carbon dioxide is picked up. The blood then travels through the venous system
back to the right side of the heart.
Coronary Arteries
The coronary arteries supply the heart muscle with blood. This is not the circulation that
flows through the heart, but is the blood supply that feeds the heart muscle. The coronary
arteries arise at the base of the aorta directly above the aortic valve. At the Sinus of Valsalva
the right and left coronary arteries arise. As a result of the structural location of the coronary
arteries on top of the aortic valve, filling occurs during diastole, or the backflow of the coronary
arteries. Systolic contraction of the ventricles is too strong for filling to occur during systole.
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13
The right coronary artery feeds the right side of the heart while the left coronary artery
divides into the left anterior descending and the circumflex branches. The circumflex branch
wraps around the back of the heart. The heart muscle receives oxygen and nutrients via
capillaries. Venous blood from the coronary arteries returns via the coronary veins to the
coronary sinus, located at the base of the right atrium. It is blockage of these coronary arteries
from emboli, atherosclerosis or spasm that causes a heart attack or myocardial infarction.
Coronary arteries
The right and left coronary arteries each feed or perfuse different areas of the heart.
Blockage of a specific area may predispose the patient to different types of dysrhythmias. The
following table outlines the possible effects of blockage of each of the coronary arteries:
Right Coronary Artery
Left Anterior Descending
Left Circumflex
Right Atrium
Anterior 2/3 of the Septum
Left Atrium
Right Ventricle
Anterior Left Ventricle
Posterior Left Ventricle
Sinoatrial Node
Lateral Left Ventricle
Inferior Wall of the left ventricle
Atrioventricular Bundle
Apex
in one out of ten people
Posterior Portion of the Left

Ventricle
Inferior Wall of the left ventricle
in 9 out of 10 people
An important concept to understand is that people differ anatomically.
everyones coronary arteries predictably feed the same portion of the heart.
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As a result, not
14
Position of the Heart

The heart is located in the center of the chest, and is tilted toward the left side. The
base (top) of the heart is directed upward, back and to the right, while the apex (bottom) is
directed down, forward, and to the left. The PMI is the point of maximal impulse. During
ventricular contraction, the apex moves forward striking the left chest wall which can be
palpated as a light tap. The PMI is normally palpated at the left 5th intercostal space, midclavicular line. The significance of the PMI is that the normal position of the PMI may change
with certain conditions such as obesity, enlargement of the heart, or myocardial infarction.
PMI is normally palpated at the 5th ICS,

Midclavicular line.
Phases of the Cardiac Cycle

The heart also has phases of contraction and relaxation or filling that occur in the atria
and ventricles. The contractile or pumping phase is called systole, while the relaxation or filling
phase is called diastole. During diastole, blood enters the atria and flows passively into the
relaxed ventricles. Remember, the valves of the heart are one-way valves allowing the blood to
flow passively. When atrial systole occurs and the atria contract, blood is pumped into the
ventricles allowing for better filling of the ventricles. As the ventricles fill they begin to contract.
This pressure causes the tricuspid and mitral valves to close. As the ventricles contract, blood
is pushed out of the pulmonic and aortic valves. Therefore, blood flows into the ventricles in two
phases; the passive ventricular filling phase (75 - 80% of blood) and the contraction of the atria
(20 - 25% of blood). The contribution of the atrial contraction to ventricular filling is called atrial
kick.
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15
Hemodynamic Parameters
Knowledge of hemodynamic parameters in the heart is important to understanding
disease processes, interventions, and drug treatments. Hemodynamics is the movement of the
blood and the forces involved. To understand this concept, you need to know about preload,
afterload, and cardiac output. These concepts are probably very new to you, yet understanding
them will help you in your care of patients.
Preload is what comes to the heart before contraction. Preload is the fluid or filling of the
chamber before contraction. The heart muscle is much like a rubber band. The more you
stretch it, the better it will contract. This stretch is accomplished in the heart through filling of the
chambers with blood. Therefore, preload is related to the amount of blood in the ventricle
before contraction. If a person is overhydrated, preload will increase. If a person is dehydrated,
preload will decrease.
Afterload is what comes after ventricular contraction or the resistance against which the
heart must pump blood. Afterload is determined by two conditions; the blood volume ejected
from the ventricle and the compliance of the vascular space into which the blood is ejected.
Think of afterload as a hose nozzle. If the hose nozzle is wide open, afterload is decreased due
to increased compliance and decreased resistance. If the hose nozzle is almost closed,
afterload will increase because the water has so much resistance to push against. Now, if you
increase or decrease the amount of water that comes from the nozzle, there will be a further
effect on the afterload. Think of afterload of the left ventricle as blood pressure. Increased
blood pressure is increased afterload, while decreased blood pressure is decreased afterload.
Each side of the heart has its own preload and afterload. Preload is the filling of each
chamber while afterload is the pressure and volume of blood the chamber has to pump against.
Most of the time these measurements are obtained via the use of a pulmonary artery (SwanGanz) catheter which is placed in the right side of the heart. The preload of the right side of the
heart is reflected as the central venous pressure (CVP) and the afterload of the right side is
reflected as the pulmonary vascular resistance (PVR). The preload of the left ventricle is the
pulmonary capillary wedge pressure (PCWP) and the afterload is the systemic vascular
resistance (SVR).
The body is constantly trying to maintain cardiac output. Cardiac output is affected by
the heart rate and stroke volume.
Heart rate is the pulse, or the number of ventricular
contractions per minute. Stroke volume is the amount of blood ejected by the heart with each
beat. The formula for cardiac output is:
Cardiac Output = Heart Rate X Stroke Volume
The body is always trying to keep in balance with this formula. For example, if someone
had a Myocardial Infarction (heart attack), the stroke volume would decrease because of the
weakened heart muscles inability to pump out enough blood. To keep in balance, the heart
rate would have to increase. On the other hand, the person who is athletic has built up the
heart muscle so well that the stroke volume increases. As a result, he/she can manage well,
with a slow heart rate, to meet the cardiac output.
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Review of Hemodynamic Parameters

PARAMETER
WHAT IS MEASURED
C.O. cardiac output
How much blood is ejected by the heart each

minute
CVP central venous pressure
The amount of volume returning to the right

side of the heart (Right Ventricular preload)
PCWP pulmonary capillary wedge pressure
The amount of volume returning to the left side

of the heart (Left Ventricular preload)
PVR pulmonary vascular resistance
The resistance the right ventricle has to pump

against to eject blood into the pulmonary
artery (Right Ventricular afterload)
SVR systemic vascular resistance
The resistance the left ventricle has to pump

against to eject blood into the aorta (Left
Ventricular afterload)
Cardiac Muscle
Most of the heart has heart muscle tissue. This muscle tissue is involuntary, meaning
we cannot control its contractions. The heart muscle cells have the ability to lengthen and
shorten, much like a rubber band. The heart muscle has interconnecting, overlapping bands
that can shorten and lengthen The more the heart muscle is stretched, to a certain point, the
better contraction will occur. In other words, like a rubber band, the further you stretch it the
better is will shoot. With the heart muscle, this stretching is achieved with the filling of the
ventricle with blood. As a result, the more blood that enters the chamber, the better stretch, and
thus better contraction. This concept, called Starlings Law of the Heart helps explain the
importance of adequate blood volume to create better stretch then contraction.
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Cardiac Muscle Properties

The heart muscle has properties which allow for conduction of electrical impulses.
These properties of the heart muscle are:
Automaticity:
the ability to generate an impulse
Excitability:
the ability to respond to stimulation
Conductivity:
the ability to transmit impulse
Contractility:
the ability to respond with pump action (pulse)
As a result of these properties the heart spontaneously and rhythmically initiates

impulses that are transmitted through the conduction system to excite the heart muscle and
stimulate muscular contraction. Electrical activity precedes contraction. Once the heart has
been stimulated, contraction occurs which is validated by a pulse. It is possible to have
electrical activity occurring without pump action. At times, especially during a cardiac arrest
situation, many drugs are given to the patient to enhance the electrical activity of the heart.
These drugs make the heart muscle especially excitable. The electrical activity that occurs
shows on the ECG. When the heart muscle cannot respond with pump action, the patient
essentially has no pulse and CPR must be initiated. This situation is called PEA or pulseless
electrical activity. Remember to always validate what you see on an ECG by assessing your
patient and checking the pulse.
Conduction System of the Heart
The heart has its own conduction system which is able to function as a result of the
cardiac muscle properties listed above. The electrical impulses of the heart usually begin in the
sinoatrial node (SA), an area located in the upper part of the right atrium. From the SA node,
the impulse travels via interatrial tracts to the left atrium and through internodal tracts to the
atrioventricular node (AV). At this point, the impulse pauses to allow time for the ventricles to fill
with blood. The impulse then travels to the Bundle of His, then to the right and left bundle
branches. From the bundle branches, the impulse goes to the Purkinje fibers which line the
inside of the ventricular musculature. After the Purkinje fibers are innervated, contraction
should occur. As a result, electrical conduction of the heart precedes contraction.
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Interatrial
Tracts
Internodal Tracts
To review, the conduction system of the heart proceeds in the following order:
Sinoatrial (SA) node
Internodal and Interatrial tracts
Atrioventricular (AV) node
Bundle of His
Right & Left bundle branches
Purkinje fibers
Ventricular muscle
Under normal circumstances, the SA node is the pacemaker. The reason the SA node
is usually the pacemaker is because it has a leakier cell membrane that allows cells to
depolarize spontaneously without waiting for an outside source. Sinus node cell membranes
are more leaky to sodium ions, therefore activate more rapidly to pace the heart. The rule of
thumb is that the part of the heart that beats the fastest will be the pacemaker of the
heart. For example, if the ventricles beat faster than the SA node, the ventricles will become
the pacemaker of the heart, as happens in ventricular tachycardia. Other areas of the heart,
besides the SA node have the property of automaticity and can be the pacemaker of the heart.
The SA node is usually the pacemaker of the heart because it beats the fastest. The part of the
heart that beats the fastest will be the pacemaker for the time being. Each area of the heart has
inherent rates for initiating impulses:
Inherent Rates
Sinus Node (pacemaker):
AV Junctional Tissue (1 backup pacemaker):
His Purkinje System in Ventricles (2 backup pacemaker):
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60 to 100 times/minute
19
The pacemaker sites other than the SA node are backup systems for the heart. If the
SA node were to fail for some reason, the AV nodal area could take over as the pacemaker. If
the AV nodal area were to fail, the ventricles could pace the heart at 20 to 40 times per minute.
These areas can be enhanced or suppressed by the Autonomic Nervous System which
innervates the heart.
Autonomic Nervous System
The rate of impulse formation is determined by the autonomic nervous system, which
branches into the sympathetic and parasympathetic nervous systems. The sympathetic branch
speeds the rate of impulses, while the parasympathetic branch slows the rate of impulse
formation. The heart actually functions best as a balance of these two systems. When
sympathetic innervation to the heart is excessive, the heart rate increases. When
parasympathetic innervation to the heart is excessive, the heart rate decreases. There are
examples of this occurring in our own body. When we are frightened, we release epinephrine, a
sympathetic substance which results in an increased heart rate. The parasympathetic nervous
system is associated with the vagus nerve. The vagus nerve can be stimulated by the Valsalva
Maneuver, which may be caused by excessive straining as in a bowel movement. This results
in the release of acetylcholine, which slows the heart.
SYMPATHETIC NERVES
Supply both atria and ventricles
PARASYMPATHETIC NERVES (Vagus)

Supplies mainly the SA and AV nodes with
little effect on the atrial muscle and no effect
on ventricular muscle
Stimulation causes release of the hormone

Norepinephrine which causes:
Increased rate of SA node discharge
Increased excitability
Stimulation causes release of the hormone

acetylcholine which causes:
Slowing of SA node
Slows rate of conduction through the
AV node
**Enhances Automaticity
**Suppresses Automaticity
TOTAL EFFECT increased overall activity of

the heart
TOTAL EFFECT decreased overall activity

of the heart
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REVIEW OF AUTONOMIC NERVOUS SYSTEM

Excitability and Conductivity
All areas of the heart have the ability to respond to and transmit electrical impulses.
They respond to and transmit electrical impulses by the process of DEPOLARIZATION. At rest
cardiac cells are negatively charged on the inside and are POLARIZED. Once depolarized the
cell returns to its normal electrical state through a process called REPOLARIZATION.
a.
The cell is POLARIZED when it is in a resting state. Potassium is in the inside and
sodium is on the outside.
Na +
Ca ++
Electroloytes are positively charged but cell wall is negatively charged.

b.
A stimulus to the cell, such as the electrical current from the SA node changes the
permeability of the cell membrane. The cell membrane becomes leaky and
DEPOLARIZATION occurs. The leaky cell membrane allows sodium, potassium and
calcium to cross the cell membrane. Depolarization is the stimulation of the cell.
c.
The cells have to get back to their initial resting state to prepare for another electrical
impulse. The cells get back to their original states passively through a process
called REPOLARIZATION; a relaxation of the cells.
This process of going from a polarized state to a depolarized state and then
repolarization happens from cell to cell in rapid succession. This is called CONDUCTION.
Revised: 9/10
21
Action Potential
The action potential is the process of depolarization and repolarization of a single
myocardial cell. The action potential has various phases that indicate the stages of
depolarization and repolarization. These phases correlated to the electrocardiogram (ECG)
waveform and cycle.
ACTION POTENTIAL OF A SINGLE MYOCARDIAL CELL
If you were to look at the horizontal portion of the action potential as a time line, you
would see that depolarization (0) occurs very rapidly, while repolarization (1, 2,&3) takes a very
long time.
Phases of the Action Potential
0 = rapid depolarization of the cell
1 = initial stage of repolarization
2 = slowing down of repolarization to allow the cardiac muscle a more sustained contraction
3 = sudden acceleration of rate of repolarization. Inside of the cell becomes negative again
4 = resting membrane potential, or polarized state
Refractory Periods
During repolarization, the individual cardiac cells regain normal excitability, and during
this process go through varying periods of excitability known as refractory periods. The
refractory periods represent times when the cells are partially or completely resistant to any
stimuli, or when another beat could occur. Later in the book, this concept will be presented in
more depth.
Revised: 9/10
22
Review of Structure and Function

Basically, the heart is a muscular pump. The left side of the heart is thicker than the
right side since it has to pump to a large area of peripheral tissues via the vasculature. The
right side of the heart pumps blood only to the lungs, where carbon dioxide and oxygen is
exhaled. Through the lungs oxygen is inhaled and attaches to the hemoglobin of the red blood
cell. The left side of the heart then pumps oxygenated blood to the capillaries of the body. The
coronary arteries arise from the Sinus of Valsalva off of the aorta and supply the heart muscle
with oxygenated blood. Blockage of these arteries is the cause of a myocardial infarction. The
cardiac muscle has specific properties of automaticity, excitability, conductivity, and contractility
that allows for the integration of electrical activity then contraction of the heart muscle. The
heart, with this electrical activity has its own conduction system. The impulse begins at the SA
node, through interatrial and internodal tracts to the AV node, Bundle of His, bundle branches,
then to the Purkinjes fibers in the ventricles. Once the Purkinje fibers are innervated,
ventricular contraction occurs. The autonomic nervous system divides into the sympathetic and
parasympathetic branches. The sympathetic speeds the heart rate while the parasympathetic
branch slows the heart rate. The cardiac cycle is divided into systole, the contraction phase,
and diastole, the filling phase.
Hemodynamic parameters of preload, afterload, and cardiac output are important to
understand. Preload is what comes before ventricular contraction and is directly related to fluid
volume. Afterload is what comes after ventricular contraction and is related to the vascular
resistance and the volume of blood to be ejected from the ventricle. Afterload of the right
ventricle is reflected as pulmonary vascular resistance, or pulmonary artery pressure, while
afterload of the left ventricle is reflected as systemic vascular resistance or as blood pressure.
Lastly, the formula for cardiac output is heart rate x stroke volume. Our body strives to keep the
cardiac output in balance either by changing the heart rate or adjusting the stroke volume.
The systemic circulation includes the blood vessels of the body. The arteries and
arterioles transport oxygenated blood to the capillaries. The venules and veins then transport
the deoxygenated blood back to the right side of the heart. It is at the capillary level that the
exchange of oxygen and nutrients occur.
Revised: 9/10
23
SA Node
60-100 bpm
Purkinje system
20-40 bpm
AV Junction
40-60 bpm
Important Terms
Antegrade conduction
Conduction that occurs in a downward manner

from atria to ventricles.
Automaticity
Quality of the conduction system that

automatically initiates a stimulus.
Block
Impulse is prevented from continuing on

the conduction pathway.
Re-entry
When an impulse re-enters the conduction

system in a retrograde manner rather
than terminating.
Retrograde conduction
Conduction that returns backwards through

the conduction system.
Usurpation
When a lower pacemaker takes over.
Vagal stimulation
Stimulation of the parasympathetic nervous

system resulting in a decrease in heart rate.
Normally, the heart is paced by the spontaneous activity of the sinus node at a regular
rate consistent with the physiological demands of the body. The automatic impulses generated
in the sinus node normally dominate all the fibers of the heart. When this rhythm is disturbed or
its conduction is interfered with, the term arrhythmia or dysrhythmia is used. The term
arrhythmia actually means without rhythm while the term dysrhythmia means difficult or
disturbed rhythm. These terms are generally used interchangeably, although dysrhythmia is
the more accurate term.
Revised: 9/10
24
Normal Mechanism of Rhythm Formation

The area of the heart that beats the fastest will pace the heart.
1. The sinus node is the pacemaker of the heart because its cell membrane leaks Na+ ions
more readily and therefore, the sinus node is the first to reach an action potential and
depolarize the rest of the heart.
2. Other areas of the conduction system such as the AV node or the ventricles are merely
potential pacemakers that become active solely in the case of emergency.
3. The sinus node may DEFAULT as pacemaker due to DECREASED AUTOMATICITY.
This sinus slowing allows the escape of lower pacemaker centers which are now firing
faster than the SA node.
a. Junctional rhythms - escape rhythms from the junction or AV nodal area
b. Idioventricular - escape rhythms from the ventricles
Even though these rhythms are abnormal, the escape mechanism that takes over is
normal, thus placed under normal mechanisms of rhythm formation.
4. Causes of decreased automaticity and depression of cardiac cells leading to bradycardia
and possible escape rhythms are:
a. Vagal stimulation
b. Hypothermia
c. Electrolyte imbalance as hyperkalemia & hypercalcemia

d. Drugs such as digoxin and Inderal
Abnormal Rhythm Formation

1. The sinus node may lose its job as the pacemaker due to INCREASED AUTOMATICITY
of other myocardial cells that now beat faster than the sinus node. Both escape beats and
premature beats are considered ECTOPIC BEATS.
2. The sinus node pacemaker loses its function because the other area of the heart beat
faster, shutting off the sinus node mechanism. This is called USURPATION of the
pacemaker function. This is not because the SA node failed; another pacemaker fired
faster.
3. May be seen as PREMATURE BEATS or tachycardia from the atria, junction, or ventricles.
4. Causes of increased automaticity leading to premature beats or tachycardia rhythms:
a. sympathetic stimulation
b. hyperthermia
c. electrolyte imbalance such as hypokalemia and hypocalcemia
d. hypoxia and hypercapnia
e. cardiac dilatation
f. ischemia and injury
g. drugs - toxins
h. stimulants as caffeine, alcohol, or tobacco
i. metabolic diseases (hyperthyroidism)
j. mechanical stimulation (Swan-Ganz & pacemaker placement)
k. acquired damage (trauma)
l. diseases of the heart itself such as valve disease, hypertrophy, and aneurysms
Revised: 9/10
25
m. congenital abnormalities
Normal Impulse Conduction
The conduction system is one continuous electrical system. Impulses will travel in either
direction depending upon where the stimulation occurs. If the impulse starts at the SA node,
impulses will travel downward or antegrade. However, if the impulse starts at the AV node the
impulse will travel down to the ventricle and back or retrograde up to the atria.
1. Antegrade Conduction - normal impulses proceed downward from the sinus node to the
Purkinje system.
2. Retrograde Conduction - reverse conduction is possible from the Purkinje system to the
atria. Premature ventricular contractions (PVCs) may conduct through the system in a
retrograde manner and activate the atria. In this situation, the P wave may appear
inverted or may be seen following the QRS.
Abnormal Impulse Conduction
1. Conduction disturbances and dysrhythmias occur if there is a delay or block somewhere
in the conduction system.
a. A block in the sinus node would not allow the impulse to progress to the atria
(no P wave, no QRS, no T wave).
b. With a block in the AV node, the impulse may have trouble getting from the atria to
the ventricles (1st, 2nd, 3rd degree block).
c. A block in the bundle branches causes abnormal ventricular conduction (a wide,
bizarre QRS).
2. Conduction disturbance in a small area can develop into a unidirectional block and may
cause re-entry dysrhythmias. Re-entry occurs when an impulse is able to re-enter an
area that was just recently depolarized and repolarized. Conduction occurs in a circuit.
Re-entry phenomena usually allow for faster depolarization and is the cause of many
tachycardias.
CONDUCTION AND DEFECTS
A - impulse travels down the Purkinje fiber and terminates at the ventricular muscle.
B- impulse travels down the Purkinje fiber but is blocked before reaching the ventricular
muscle
C - impulse travels down the Purkinje fiber, reaches the ventricular muscle, but does not
terminate there. The impulse re-enters the conduction system, permitting re-excitation
of the ventricular muscle.
Revised: 9/10
26
Important Terms- Electrocardiography, Monitoring, and ECG

12-lead ECG
Views the heart from 12 angles to help in determining infarction,

hypertrophy, axis deviation, and bundle branch blocks.
Acute MI
Blockage of the coronary artery from atherosclerosis, spasm,

or embolus results in death of heart muscle.
Artifact
Extra events recorded on the ECG that do not relate to actual

electrical activity of the heart.
Depolarization
The electrical stimulation of cells.
Isoelectric line
The flat horizontal line on the ECG that represents no

electrical activity (the base line).
J point
The location at the end of the QRS complex which indicates the
change from the QRS complex to the ST segment.
Large box method
A method for determining heart rate on regular rhythms. The

number of large boxes between two QRS complexes is divided
into 300 to obtain the minute heart rate.
P wave
PR interval
Wave representing atrial depolariztion.

Time interval from the beginning of the P wave to the
beginning of the QRS complex. Represents atrial firing to the
beginning of ventricular depolarization. Normal range is 0.12 0.20 seconds.
Q-T interval
Interval from the beginning of the QRS to the end of the T wave.
QRS duration
Interval from the beginning of the QRS to the end of the QRS
wave. Normal range is below 0.12 seconds.
Refractory Periods Various periods in the ECG complex where the heart can or
cannot accept a new impulse.
Repolarization
The passive recovery phase of the ECG which occurs after

depolarization.
S-T segment
Interval from end of the QRS complex to the beginning of the T

wave.
Six-second method A method for determining heart rate with regular or irregular
rhythms. The number of QRS complexes in 6 seconds is
multiplied by 10 to calculate minute heart rate.
Small box method
Revised: 9/10
A method for calculating heart rate for regular rhythms. The

number of small boxes between two QRS complexes is divided
into 1500 to obtain minute heart rate.
27
Somatic tremor
Electrical artifact that results from muscle shaking; seizures.
T wave
Repolarization of the ventricle.
Time
Measured on the horizontal plane of the ECG.
U wave
At times is seen after the T wave. May be indicative of

Ischemia, hypokalemia, or incomplete repolarization.
Voltage
Measured on the vertical plane of the ECG.
Vulnerable period
The area from the peak of the T wave back to the baseline. Early
beats hitting on this area may result in Ventricular Tachycardia or
Ventricular Fibrillation.
ELECTROCARDIOGRAPHY, MONITORING AND ECG

The electrocardiogram or ECG (EKG) represents electrical activity of the heart. This
book provides methods to learn to read the ECG. ECG or EKG may be used interchangeably,
since they both represent the electrocardiogram.
The electrocardiogram only measures electrical activity of the heart. The ECG does not
verify contraction of the heart. This can be determined only by pulse or blood pressure.
The wave of depolarization and repolarization spreading through the heart can be
recorded on paper through the use of the ECG. The ECG waveform has specific names that
correlate with various activities occurring in the heart.
J-point
Definition of components of the ECG configuration

Isoelectric line - baseline that indicates no electrical activity is occurring
P wave - represents depolarization of the atria or the spread of electrical activity
through the atria. The P wave is normally upright in Lead II. If the P wave is of normal
size and shape, it may be assumed that the stimulus began in the SA node.
PR Interval - the period from the start of the P wave to the beginning of the QRS
complex. It is the time taken for the original impulse to reach the ventricles,
including the delay at the AV node.
Revised: 9/10
28
Normal = 0.12 - 0.20 seconds. A prolonged PR interval indicates a longer than normal delay in
the impulse getting through the AV node.
QRS Complex - represents depolarization of the ventricles.
Q wave - first negative wave (in front of a positive wave) Q waves that are at
least 1/4 the depth of the R wave are abnormal and may be indicative
of a myocardial infarction.
R wave - positive wave (above the isoelectric line)
S wave - negative wave after a positive wave
**Note:
Not all ECG complexes will have all of the components of the QRS.
Some may only have an R, or an R and an S.
Others may only have a QS wave.
QRS Duration - measured from the beginning of the QRS to the end of the QRS.
Normal Range = < 0.12 seconds. A prolonged QRS duration may indicate a block
in the bundle branches.
Q-T Interval - includes the QRS complex and T wave. Normal ranges will vary with
age and heart rate.
Normal = 0.36 - 0.44 seconds
T wave -
represents repolarization or recovery of the ventricles. The T wave is normally

upright in lead II. Inversion of the T wave may indicate ischemia occurring in
the heart. Flat T waves may be an indication of potassium deficiency, while
tall, peaked T waves may indicate hyperkalemia or early ischemia.
S-T segment - the interval between the completion of depolarization & repolarization
of the ventricular muscle. The S-T segment seen from the end of the QRS to
the beginning of the T wave. Elevation of the S-T segment may indicate an
injury pattern occurring in the heart.
U wave -
comes after the T wave. May be seen as normal, or may be indicative of

potassium deficiency or ischemia or incomplete repolarization of the ventricles.
J point -
the point on the QRS complex where a distinct change is seen in direction, from
the QRS to the ST segment. It is important to identify the J point to determine
accurate measurement of the QRS duration and as a reference to calculate ST
elevation or depression .
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29
Configurations of the QRS Complex

Not all components of the QRS complex are present on each persons ECG. In fact, a
large Q wave is abnormal and may indicate that an MI has occurred in the past. Below are
some examples of variations of the QRS complex. Even though parts of the QRS may not be
present, it is still referred to as the QRS complex.
The prime () indicates a second wave of the same. The second R wave is termed
prime. The capital letter or lower case letter of the Rr indicates which peak is the tallest. If the
first R is taller, it gets the capital. If the second R is taller, it gets the capital letter.
As you can see, the QRS complex can have many different shapes. It is important to
understand this so that you can correctly measure intervals such as the PRI and the QRS
duration.
Revised: 9/10
30
The ECG paper that comes out of the cardiac monitor is a graph paper that comes out at a
speed of 25 mm/Sec. Some machines can have a paper speed of 50 mm/Sec. or other
variations, but the standard is 25 mm/Sec.
Rule #1: Horizontal measurement on the paper = TIME
1 small box = 0.04 seconds
1500 small boxes = 60
seconds or 1 minute
1 large box = 0.20 seconds
5 large boxes = 1
second
300 large boxes = 60
seconds or 1 minute
1 inch on the ECG paper = 1
6 inches on the ECG paper = 6
second of time
seconds
The ECG paper will usually have some sort of marking on the paper to indicate a 1
second, 3 second or 6 second period of time. This paper has markings in 1 second intervals on
the top of the page.
Rule #2: Vertical measurement on the paper = VOLTAGE
1 small box
1 large box
10 small boxes
=
=
=
1 mm (millimeter) or .1 mV (millivolt)
5 mm
.5 mV
10 mm
1 mV
LEAD SYSTEMS
Leads are a method of recording electrical activity within the heart. It takes two wires,
one positive (+) and one negative (-) to make a lead. The leads view the heart from different
angles. There are 12 established leads, each viewing the heart from a different angle. The
electrical field extends to the body surface where it is measured by electrodes and then
waveforms on paper. Electrodes are patches that the wires attach to and measure the voltage
difference between two electrodes. There are 4 principles of electrocardiography that you
must know to understand lead systems:
Revised: 9/10
31
1. No electrical current flowing yields no voltage

difference shown as an ISOELECTRIC LINE
2. Current flowing towards a (+) electrode will

record a positive or upright wave.
3. Current flowing away from a (+) electrode, or to

a (-) electrode records a negative or downward
wave.
4. Current flowing perpendicular to the leads axis
will record a biphasic wave.
Remember, the leads only view the heart from different angles. The electrical forces of
the heart progress from the SA node down to the ventricles. That is saying that the electrical
forces go down and to the left of the heart. This is called the mean cardiac vector. Any lead
with its positive electrode down at the left or at the foot area should record an upright P wave
and QRS complex. This is because the electrical current (of the heart) is flowing toward a
positive electrode.
WHEN PLACING THE LEADS, THINK WHITE ON THE RIGHT, SMOKE OVER FIRE!
LEAD II
The most common monitoring lead is lead II since it produces an upright P wave and
QRS that are easy to see.
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SUMMARY OF ECG CHANGES THAT OCCUR WITH ACUTE MI

THE THREE IS
The road to an MI (myocardial infarction) includes 3 predictable changes on the
ECG. These changes will show only on the leads that view the part of the heart
where the injury occurs.
I.
II.
III.
Ischemia = ST depression and/or T wave inversion

Injury = ST elevation
Infarct = Q waves
NORMAL EKG COMPLEX
ISCHEMIA (inverted T waves) - The first change to occur.
INJURY (elevated ST segments) - The second change to occur.
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33
INFARCTION (development of Q waves) - The last and permanent change.
Q-Wave
As mentioned before, Q waves are abnormal if they are (25%) the depth of the R
waves height and at least 0.04 seconds wide. During the acute phase of a myocardial
infarction, T waves will initially invert, then ST segments will elevate. Q waves may not show up
for over a day. Eventually, the ST segments will return to normal, T waves will return to an
upright position, but the Q waves will remain forever as the wave of depolariztion passes
through dead or infarcted tissue. The location of an MI is determined by analyzing the 12 lead
EKG. Changes will be seen in the leads that correlate with the infarction in that area, and must
be visualized in 2 or more leads of the same group to be considered significant.
ARTIFACT
Artifact is extraneous electrical activity that shows up on the EKG that is not occurring
with the patients heart. Artifact can sometimes be confused with a number of
dysrhythmias and must be differentiated by physical assessment of the patient. Good
electrode contact is essential to obtaining a picture without artifact.
Suggestions for good electrode placement:
1.
Place on a stable part of the body. For example, do not place electrode on
the clavicle where there may be a lot of movement with respirations. Or do
not place under pendulous breasts, where each time the person breathes it
taps against the electrode
2.
Place on a smooth part of the skin. You may need to shave the area where
the electrode is attached.
Assure that the electrode has adequate amounts of conductive gel on the
inside. If the gel is dried out, a poor reading may occur.
3.
4.
Make sure the wires are in good working order for continuous monitoring.
5.
Electrodes need to be affixed firmly to the skin. If the patient is perspiring,

you may need to change the electrodes often. Tincture of Benzoine on the
skin may help the leads stay on.
Revised: 9/10
34
Types of artifact that can occur are:

60 cycle interference - interference from electrical equipment and may be caused from
improper grounding of equipment. A magnifying glass will show exactly sixty even, regular,
spikes in a 1 - second interval on the ECG tracing. Check all the equipment to see what may be
causing the interference and have the equipment replaced or repaired. Prehospital causes may
be electric blankets or heating pads,
60 cycle interference shows as thick lines of up and down spikes.
Wandering Baseline - the baseline of the EKG will wander with the persons respirations.
Changing the electrode to a different position may help. This artifact is sometimes unavoidable.
Revised: 9/10
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Somatic or Muscle Tremor - can occur with chilling, seizures or tension. This will show as a
grossly uneven, tremulous baseline. Artifact will continue until the condition stops.
CPR Artifact - when CPR is done, compressions show up on the ECG tracing.
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36
Calculating Heart Rates

Each time an ECG strip is analyzed, the heart rate must be calculated. Since we dont
always have a full minute strip, we need to determine ways to calculate the heart rate with a
smaller strip. Before determining the method for calculating heart rate, it is important to know if
the heart rhythm is regular or irregular. A regular heart rhythm is one that has an equal
distance from one QRS complex to the next QRS complex. An irregular rhythm would not have
the same distance from one QRS complex to the next.
R R R R R R
These Rs are regular
rr rr
r rrr
These rs are irregular
One method that can aid in determining regularity is to take a blank piece of paper and
mark a line for 3 QRS complexes in a row on the blank sheet of paper. Then take the 3 lines of
the paper and move them to the next set of QRS complexes. Another method is to use a
caliper to march out the regularity of a strip. If the lines match up or march out with the new
QRSs, the rhythm is regular. If they do not match, the rhythm is irregular. If less than three
small boxes difference between the narrowest and widest R-R interval on 6 second strip, than
the strip is regular. Look at the rhythm strips below and determine if they are regular or irregular:
Strip A
Strip B
Revised: 9/10
37
You should have said that Strip A was regular and Strip B was irregular, since the QRS complexes in A
were equal distance apart and the QRS complexes in B were not equal.
Methods for Calculating Heart Rate

A.
Six Second Method - approximate

1.
2.
3.
4.
B.
Large Box Method

1.
2.
3.
4.
C.
Take six seconds on the ECG paper

Count the number of QRS complexes in the six seconds
Multiply this number by 10 to give the minute heart rate
Accuracy
a. Safe to use with irregular rhythms
b. May also be used with regular rhythms
One large box on the ECG paper equals 0.20 seconds, so there are 300
large boxes in a minute or 60 seconds
Count the number of large boxes between 2 QRS complexes.
Divide this number into 300
For Example:
a. if there are 3 large boxes between two QRS complexes,
divide 3 into 300 = rate of 100 per minute
b. if there are 5 large boxes between two QRS complexes,
divide 5 into 300 = rate of 60 per minute
Accurate for regular rhythms only
Small Box Method

1.
One tiny box on the ECG paper equals 0.04 seconds, so there are 1500
small boxes in 60 seconds
2.
Count the number of small boxes between two QRS complexes
3.
Divide this number into 1500
For Example:
a. if there are 15 small boxes between two QRS complexes
then divide 15 into 1500 for a rate of 100
b. if there are 25 small boxes between two QRS complexes
then divide 25 into 1500 for a rate of 60
4.
Accurate for regular rhythms only
he most accurate method for regular rhythms other than taking a full minute strip
Revised: 9/10
38
Table for Large Box Method

To calculate the heart rate, count the number of 0.20 squares (or large boxes)
between two QRS complexes (300 divided by X = HR)
1 box = 300
2 boxes = 150
3 boxes = 100
4 boxes = 75
5 boxes = 60
6 boxes = 50
7 boxes = 43
Table for Small Box Method

To calculate the heart rate, count the number of 0.04 squares (or small boxes)
between two QRS complexes (1500 divided by X = HR)
Number of Squares = Heart Rate of X

4----------------375
5----------------300
6----------------250
7----------------214
8----------------188
9----------------168
10---------------150
11---------------136
12---------------125
13---------------115
14---------------107
15---------------100
16----------------94
17----------------88
18----------------83
19----------------79
20---------------75
21---------------72
22---------------68
23---------------65
24---------------63
25---------------60
26---------------58
27---------------56
28---------------54
29---------------52
30---------------50
31---------------48
32---------------47
33---------------45
34---------------44
35---------------43
36---------------42
37---------------41
38---------------40
39---------------38
40---------------37
41---------------37
43---------------35
44---------------34
45---------------33
46---------------33
47---------------32
48---------------31
49---------------31
50---------------30
You really only need to know 1 or 2 methods for calculating heart rate. The important
factor is to know that in the absence of a full minute strip to count heart rate, you may use any
of these methods for regular rhythms. For irregular rhythms, the six-second method is the only
method that can be used.
MEASURING THE PRI (PR Interval)
The P wave represents atrial depolarization. The PR interval is measured from the beginning
of the P wave to the beginning of the QRS. Normal PRI is 0.12- 0.20 seconds. A prolonged
PRI indicates that the impulse is delayed as it passes through the atria or AV Node.
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MEASURING THE QRS DURATION

The QRS represents ventricular depolarization and is measured from the beginning of the QRS
to the end of the QRS. Normal QRS duration is < 0.12 seconds. A wide QRS that follows a P
wave indicates that the impulse was delayed as it traveled down the bundle braches.
MEASURING THE QTI (QT Interval)
The QT interval represents total ventricular activity (the time from ventricular depolarization to
ventricular repolarization) and is measured from the beginning of the QRS to the end of the T
wave. The duration of the QT interval varies according to age, gender, and heart rate. To
quickly determine if the QTI is normal or prolonged, measure the interval between two
consecutive R waves and divide by two. Measure the QT interval. If the QT interval is less
than half of the R-R interval, it is probably normal. If the QT interval is more than half of the
R-R interval, it is considered prolonged. A prolonged QT interval puts the patient at risk for
developing life threatening dysrhythmias because this prolongs the vulnerable period during the
ventricular refractory period.
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40
Refractory Periods
During repolarization, the individual cardiac cells regain normal excitability, and during
this process go through varying periods of excitability known as refractory periods. There are
times in these periods when the cells are partially or completely resistant to any stimuli, when
another beat could not occur.
1.
Absolute Refractory Period - Cardiac cells are unable to respond to any stimulus
regardless of strength.
This area extends from the Beginning of the QRS to the initial part of the T wave.
2.
Relative Refractory Period - A strong stimulus can cause an impulse.

This area is on the T wave.
3.
Vulnerable Period - A stimulus hitting at this time is sensitive and vulnerable to

electrical chaos such as ventricular tachycardia or ventricular fibrillation.
This area is located at the peak of the T wave and back to the baseline.
4.
Supernormal Period - A weak stimulus can initiate the heart.

This occurs after the T wave.
ARP (absolute refractory period)

RRP (relative refractory period)
V (vulnerable period)
SN (supernormal period)
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SYSTEMATIC APPROACH FOR ANALYZING CARDIAC RHYTHMS

When analyzing an individual ECG, it is essential that the analysis be done in a standard, sequential
manner. Failure to analyze the strip systematically can result in missing important details and drawing
incorrect conclusions.
Each and every time you analyze a strip, follow this step-by-step approach.
1.
Determine the regularity of the QRS complexes (rhythm). This allows you to determine the
method for obtaining rate.
REGULAR?
- use any method
IRREGULAR? - use the six second method or obtain a full minute strip
2.
Calculate the heart rate.

a. Determine the atrial rate (P)
b. Determine the ventricular rate (QRS)
3.
Examine the P waves.

a. First, determine if P waves are present.
b. Examine the contour.
1. P waves should be upright in leads II.
2. Each P wave should be similar shape.
c. Observe the position of the P waves in respect to the QRSs. Normally each P wave
should be followed by a QRS, and each QRS should be preceded by a P wave.
4.
Measure the QT Interval.
5.
Measure the PR Interval.
6.
Measure the QRS Duration.
7.
Measure the ST Segment.
8.
a.
b.
c.
d.
e.
9.
Identify the T-Wave.

Upright?
Inverted?
Flat?
Peaked?
Biphasic?
Search for any ectopic beats. Are the premature or escape beats?
10.
a.
b.
c.
d.
e.
Determine the origin of the rhythm:

Sinus?
Atrial?
Junctional?
Ventricular?
Pacemaker (artificial)?
**Follow this procedure for analyzing all rhythms.
Revised: 9/10
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Sinus Rhythms
IMPORTANT TERMS- SINUS RHYTHMS

Arrhythmia
Without rhythm; A rhythm that is disturbed.
Aberrant Conduction
Conduction that takes a different pathway through the Atria or

ventricles. Usually results in a wider QRS complex.
Asymptomatic
Patient is free of symptoms even though an abnormal rhythm is

present.
Bradycardia
In general, a heart rate below 60.
Dysrhythmia
A rhythm that is disturbed.
Etiology
The cause of a problem.
Symptomatic
When the patient has symptoms such as hypotension,

dizziness, or chest pain.
Tachycardia
In general, a heart rate above 100 in the adult patient.
Sinus rhythms originate in the sinoatrial (SA) node. Normal Sinus rhythm is the most
desired rhythm and will comprise most of the rhythm strips that you will see in the clinical
setting. There are other rhythms that originate in the sinus node and differ in rate or rhythm.
They will be discussed in this section.
Revised: 9/10
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NORMAL SINUS RHYTHM

A. Etiology
Since sinus rhythm is normal, there is no etiology.
B. Identifying Characteristics
1. Rhythm - Regular
2. Rate - 60 to 100/min
3. P Waves - Normal in size and shape. Upright and before each QRS
4. P-R Interval - Normal (0.12 to 0.20 seconds)
5. QRS Duration - Normal (< 0.12 seconds) unless there is a right or left
bundle branch block or aberrant conduction
C. Significance 1.
There are no signs and symptoms since it is a normal rhythm.
2.
In children the rate may vary from 90 in a 3-year old to 150 in an infant.
D. Treatment - None
Revised: 9/10
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SINUS BRADYCARDIA
A. Etiology
1. Damage to the SA node
2. Normal in athletes and sleep
3. Physiologic response to increased vagal tone from the Valsalva maneuver,
coughing, suctioning or carotid massage.
4. Pathologic response to increased intracranial pressure, glaucoma, hypothermia,
hypothyroidism, or M.I.
5. Drug response to Digoxin, Inderal or Morphine Sulfate
1. Rhythm - Regular
2. Rate - < 60 (40 59 is the most common)
3. P Waves - Normal in size and shape
5. QRS Duration - Normal (< 0.12 seconds)
C. Significance
1. Potential dangers are that slow rate may lead to blocks or escape rhythms
2. May allow for an irritable focus to take over
3. May cause a decrease in cardiac output and decreased level of consciousness
4. May develop congestive heart failure post-M.I.
D. Treatment
1. If asymptomatic - none
2. If symptomatic- Bradycardia Algorithm (AHA)
IV/ O2/ 12-lead ECG/ Differential Diagnosis (treat cause)
a. Atropine 0.5 mg IV q 3-5 min, max 3 mg
b. Pacing (Transcutaneous, Transvenous)
c. Dopamine 2 - 20 mcg/kg per min
d. Epinephrine Drip at 2 - 10 mcg/min
Revised: 9/10
45
SINUS TACHYCARDIA
A. Etiology
1. Physiologic response to exercise, excitement, and anxiety.
2. Stimulants such as coffee, tea, alcohol, and nicotine.
3. Response to sympathomimetic medications such as Epinephrine (Adrenalin)
4. Pathologic response to fever, shock, CHF, MI, chronic lung disease, hypotension,
thyrotoxicosis, anemia, pain or hypoxemia.
1. Rhythm - Regular
2. Rate - 100 - 150 / min
3. P Waves - normal in size and shape
C. Significance
1. In the presence of an MI (myocardial infarction) may lead to ischemia and or CHF.
2. May cause a decreased filling time in the ventricles. If the diastolic filling time is
short (i.e. tachycardia), the ventricles dont have time to fill with blood.
Decreased filling = decreased stretch = decreased C.O.
3. Impaired filling of the coronary arteries with oxygenated blood. The coronary
arteries arise from the Sinus of Valsalva on top of the aortic valve. They fill
during diastole. Tachycardias may prevent complete filling of the coronary arteries
which may lead to myocardial ischemia.
D. Treatment
Treat the underlying cause of the tachycardia, not the rhythm itself. For example,
if the person has a fever, decrease the fever. If the person is hypoxemic, treat the
Hypoxemia.
Revised: 9/10
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SINUS ARRHYTHMIA
A. Etiology
1. Common in children
2. Considered benign
3. Can be from drugs which influence vagal tone such as digoxin and morphine
4. Rate varies with respirations from vagal influences:
a. Rate increases with inspiration (decreased vagal tone)
b. Rate decreases with exhalation (increased vagal tone)
1. Rhythm - Irregular. This rhythm is cyclically irregular, speeding and slowing with each
Respiratory cycle.
2. Rate - usually normal at 60 - 100/min
3.
P Wave - normal in size and shape
4.
P-R Interval - Normal (0.12 to 0.20 seconds)
5.
QRS - Normal (< 0.12 seconds)
C. Significance
1. Usually not symptomatic
2. Pulse will be irregular so the rhythm is sometimes confused with other dysrhythmias
D. Treatment None, unless the overall rate is too slow or too fast then treat as bradycardia or
tachycardia.
Revised: 9/10
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SINUS ARREST and SINUS BLOCK

A. Etiology
1. Failure of the SA node to fire resulting in the absence of an entire PQRST
sequence for one or more cardiac cycles. The SA node takes a rest.
2. Pathologic causes are MI, hypersensitive carotid sinus, overdose of digoxin or
quinidine, and hyperkalemia.
3. Physiologic response to increased vagal tone.
1. Rhythm - Irregular
2. Rate - Usually Slow
3. The entire PQRST sequence is absent for one or more cardiac cycles.
4. To calculate the length of the pause that occurs, measure the number of small
boxes from the R wave before the pause to the next R wave. Multiply the number
of small boxes by 0.04 seconds to calculate how many seconds long the pause is.
Sinus Arrest
Since the SA node fails to initiate an impulse for a time, the node has to reset itself.
a. the rhythm before and after the pause is sinus rhythm.
b. the next beat that comes in has a P wave
c. P- P interval is disturbed. The next P wave after the pause returns off cycle.
SA node fails to
fire
Revised: 9/10
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Sinus Block
The impulse originates in the SA node but is blocked within the sinus node.
The SA node continues to fire regularly, even though some are blocked.
a. the rhythm before and after the pause is sinus rhythm.
b. the next beat that comes in has a P wave
c. P- P interval is undisturbed. The next P wave after the pause returns
on cycle.
C. Significance of Sinus Arrest and Sinus Block

1. These rhythms are not significant if backup pacemakers take over to keep the heart
rate adequate to prevent complete asystole.
2. They are dangerous if ectopic rhythms such as ventricular tachycardia or
ventricular fibrillation take over as a result of irritability that may occur from the
slow rate..
D. Treatment
1. If asymptomatic and infrequent - none
2. If symptomatic- Bradycardia Algorithm
IV/ O2/ 12-lead ECG/ Differential Diagnosis (treat cause)
a. Atropine 0.5 mg IV q 3-5 min, max 3mg
b. Pacing (Transcutaneous, Transvenous)
c. Dopamine 2 - 20 mcg/kg per min
d. Epinephrine Drip at 2 - 10 mcg/min
Review of Sinus Rhythms

This completes the section on sinus rhythms. Remember that sinus rhythms originate in
the SA node. Normal Sinus Rhythm, sinus bradycardia, and sinus tachycardia are differentiated
by rate alone. Sinus arrhythmia has a varying rhythm that speeds and slows with respirations.
Sinus arrest and sinus block are similar in that there is a pause with each, followed by a
PQRST. The only difference is that sinus arrest has a disturbed P-P while sinus block has an
undisturbed P-P.
Revised: 9/10
49
Module II: Atrial Dysrhythmias
IMPORTANT TERMS- ATRIAL DYSRHYTHMIAS

Atrial Kick
Atrial filling of the ventricle which can account for 20 to 25% of cardiac
output.
Ectopic/ectopy
A beat occurring in the wrong place, not from the sinus node.
Fibrillation
A quivering chamber resulting from multiple firings.
Flutter
Rhythmic, rapid firing within a chamber.
Nonconducted
A area in heart fired, but did not progress through the conduction
system.
Paroxysmal
Referring to sudden start or stop.
Premature
Occurring early.
Supraventricular
Occurring above the ventricle. Can include rhythms that are sinus, atrial,
and junctional.
Vagal maneuvers
Intentional interventions to stimulate the vagus nerve.

Examples are the Valsalva Maneuver, coughing, or carotid massage.
Revised: 9/10
50
ATRIAL DYSRHYTHMIAS
Normally rhythms originate in the SA node, the normal pacemaker of the heart.
Sometimes, the SA node loses its pacemaking role. As a result, the pacemaking function is
taken over by another site along the conduction system. The site with the fastest inherent rate
usually controls the pacemaking function.
Rhythms that originate in the atria are called ATRIAL DYSRHYTHMIAS.
Atrial
dysrhythmias are caused when the atrial rate becomes faster than the sinus rate, either by
irritability (usurpation).
As with the sinus rhythms, impulses originating in the atria will travel through to the AV
junction, through the ventricles, to the Purkinje fibers. This mechanism will give atrial rhythms a
normal shaped, narrow QRS complex.
Since atrial rhythms originate in the atria, and not the SA node, the atrial conduction will be
faster and rougher than the sinus rhythms.
Atrial dysrhythmias always produce
tachyarrhythmias, and will not produce bradyarrhythmias (unless induced by medication) or
escape beats/rhythms. The P waves in atrial rhythms will be atypical and can be:
flattened
notched
peaked
saw tooth
diphasic or biphasic
Common features of atrial dysrhythmias are:
narrow QRS - impulse originates above the ventricles
atypical P wave (usually not rounded)
Remember that in the cardiac cycle, about 75-80% of blood passively fills the ventricles
from the atria. Then, the atria contract causing the other 20-25% of blood to enter the
ventricles. This is called the atrial kick. When atrial dysrhythmias interrupt the normal
contraction of the atria, they can negatively impact cardiac output by affecting that additional 2025% of blood that would normally enter the ventricles.
Revised: 9/10
51
PREMATURE ATRIAL CONTRACTION
(PAC)
A. Etiology
A PAC arises from the premature discharge of an atrial ectopic focus. PACs occur in
the presence of a sinus rhythm as the underlying rhythm.
A PAC is not a rhythm itself, but considered an ectopic beat.
Ectopic Focus - is a site of origin of a cardiac complex other than the normal SA node.
Ectopy - a conducted premature or escape complex from a site other than normal.
Can be caused from:
1. Stimulants such as caffeine, tobacco, or alcohol
2. Hypoxia
3. Digitalis toxicity
4. Ischemia/ Injury
B. Identifying Characteristics: When identifying a PAC, there are actually 2 jobs for you:
Identify the underlying rhythm
Locate the ectopic beats
For example, a person could be in: Sinus tachycardia (underlying rhythm) with
2 PACs (ectopy)
1.
Rhythm irregular
a. The basic underlying rhythm is regular, but is interrupted by a sudden, premature
beat. It is the premature beat that causes the rhythm to look irregular.
b. There may be a regularity to the irregularity
1. bigeminal PACs - every other beat a PAC
2. trigeminal PACs - every third beat a PAC
2. Rate - usually normal or tachycardic

3. P waves
a. Premature
b. Differently shaped from the sinus P wave. May be flattened, notched, peaked,
diphasic.
c. May be hidden in the preceding T wave if the P wave comes really early. The
preceding T wave will look different if there is a P wave hidden in it.
4. PR Interval - will generally be within normal range of 0.12 to 0.20 seconds, but
could be shorter or longer than the PR intervals seen in the underlying rhythm.
5. QRS - usually normal but can be prolonged if the impulse passes through an
aberrant pathway
Revised: 9/10
52
6. Usually non-compensatory or incomplete compensatory pause.

Note the second beat below that comes earlier than expected, followed by an incomplete
compensatory pause.
NONCONDUCTED OR BLOCKED PAC

Sometimes, a premature atrial contraction (PAC) may be completely blocked at the AV node.
When this happens, you will see a premature P wave that is not followed by a QRS because it
was not conducted down to the ventricles.
DIFFERENTIATING PACS FROM SINUS ARRHYTHMIA

It is important to differentiate PACs from sinus arrhythmia. In sinus arrhythmia, the irregularity
of the R-R will be cyclic with each cycle gradually prolonging then speeding up and is
asscociated with the respiratory cycle. In PACs, the underlying rhythm will be regular with a
sudden, premature beat.
Revised: 9/10
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Revised: 9/10
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Sinus Arrhythmia
PAC
C. Significance of PACs
1. May indicate an underlying problem such as CHF
2. May be precursor to other atrial dysrhythmias
3. A PAC falling on the vulnerable period of atria may produce atrial fibrillation or atrial flutter
D. Treatment
1. Treat the underlying cause
2. Treat occasionally with amiodarone, beta blockers, or calcium channel blockers.
Revised: 9/10
55
ATRIAL TACHYCARDIAS
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)
PAROXYSMAL ATRIAL TACHYCARDIA (PAT)
Atrial tachycardia occurs when there is a repetitive recycling of an ectopic atrial focus. In
PSVT the pacemaker is a single, irritable site that lasts seconds to hours. PSVT is usually
initiated by a PAC. This is thought to be a re-entry rhythm.
A. Etiology
1. Emotional stress, fatigue (mental or physical)
2. Caffeine, alcohol, tobacco
3. PSVT has a paroxysmal (sudden or abrupt) start or stop
4. Atrial Tachycardia is present and may have gradually reached the tachycardia range
1. Rhythm - regular
2. Rate - Atrial - 150 to 250 /min
Ventricular - 150 to 250
3. P wave - different from the sinus P wave, but is often buried in the preceding T wave.
4. PR Interval - may vary but is sometimes difficult to measure since the P waves are
obscured.
5. QRS - Usually normal (< 0.12 seconds) but may be wider than normal if
aberrant conduction is present.
6. Variations
a.Atrial Tachycardia - rhythm with rate 150 to 250 present on the paper
b.PSVT (paroxysmal supraventricular tachycardia) - paroxysmal means sudden
onset or sudden termination. The tachycardia begins abruptly with a PAC and may
end as suddenly as it started. The criteria is the same as atrial tachycardia but you
see it start or stop abruptly.
7. 3 or more PACs in a row is a run of Atrial Tach or SVT.

8. The difference between supraventricular tachycardia (SVT) and paroxysmal
supraventricular tachycardia (PSVT) is that PSVT had a sudden onset or abrupt stop.
Rhythms that are supraventricular were initiated above the ventricles.
This incudes sinus, atrial, or junctional tachycardias.
Revised: 9/10
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Atrial Tachycardia
PSVT
C. Significance
1. Usually tolerated in young.
2. In the elderly may lead to myocardial ischemia, myocardial infarction (M.I.) or
pulmonary edema.
3. Person may feel short of breath and feel weak and dizzy depending upon how fast
the heart rate is.
4. PAT frequently occurs in people with normal hearts and is caused by stress or
anxiety, usually not causing any real problems in these individuals.
D. Treatment
1. Vagal Maneuvers
a. Valsalvas maneuver (bearing down as if you were having a bowel movement
while holding your breath or blow through an occluded straw). The increased
intrathoracic pressure stimulates the vagus nerve.
Revised: 9/10
57
b. Carotid sinus massage (use with caution)

Contraindications
Patient >50
History o f CVA or heart disease
Carotid bruit or thrills.
Unequal carotids
Procedure
Begin with right carotid
Massage 15 to 20 seconds
Wait 2 to 3 minutes, go to left carotid. Only one carotid at a time
2. Asymptomatic or Hemodynamically Stable (BP in normal range):
a. Adenosine
6 mg RAPID IV push, may repeat in 1-2 minutes at 12 mg RAPID
IV push, then 12 mg RAPID IV push
follow each dose immediately with a 10-20 cc flush
Blocks conduction through AV node
May produce transient asystole
Short half-life (4-10 seconds)
Drug Interactions
b. Beta blocker ONLY if NO history of heart disease or CHF
Metoprolol, 5 mg slow IV over 2-5 mins, may repeat in 5 min
c. Calcium channel blocker
Diltiazem, 0.25 mg/kg slow IV over 2 min, may repeat in 15 mins
at 0.35 mg/kg slow IV
d. Amiodarone
150 mg IV infusion over 10 mins
3. Symptomatic (dropping blood pressure or showing signs of left ventricular failure):
Synchronized Cardioversion (MD Order required)
Unlike defibrillation, which is a random shock to the heart to disrupt the
rhythm, the synchronization allows the machine to pick up on the R waves of
the patients rhythm so that the shock is not delivered on the vulnerable
period of the T wave which may precipitate ventricular tachycardia or
ventricular fibrillation.
Disrupts the ectopic (re-entry) focus to allow the SA node to regain control of
the rhythm.
Treat according to PSVT algorithm
Revised: 9/10
58
The Monitor Marking the QRSs for Synchronized Cardioversion

Sedate patient, if possible:
-
Valium 5 to 10 mg IV, or
Versed 2.5 - 5 mg IV
Administer slowly
May cause hypotension and/or respiratory depression
Administer to produce amnestic effect
Set up for Synchronized cardioversion
Energy Settings
50 J (PSVT/Atrial Flutter)
100J
200J
300J
360J
Revised: 9/10
59
ATRIAL FLUTTER
With atrial flutter, the atria become so irritable that they fire faster than 250 times per minute.
They are said to be fluttering. This creates a repetitive cyclic pattern in the atria resulting in
sawtooth waves. Atrial flutter is thought to be a re-entry rhythm at the atrial level.
Atrial flutter looks similar if held upright or upside down.
A. Etiology
1. Presence of atrial flutter is usually indicative of some pathologic process in the heart.
2. Emotional stress.
3. Transient rhythm in response to pulmonary embolism or thyroid storm.
1. Rhythm - Regular or Irregular
2. Rate - Atrial rate is 250 to 350 /min (Occasionally up to 450). Ventricular rate varies and
may be: 1/2 to 1/3 to of atrial rate depending upon the block.
For Example:
2:1 Block - If Atrial rate
300, Ventricular rate
150
3:1 Block 300
100
4:1 Block 300
75
3. P Wave - are not called P waves but F or flutter wave
a. Saw tooth or Picket Fence with an undulating baseline
b. F waves are continuous throughout the cycle (even under the QRSs)
4. PR Interval - since there are no P waves, there is not a PR interval
5. QRS Duration - normal (< 0.12 seconds) but may be wider if aberrant
conduction is present.
6. If conduction ratios vary, it is called atrial flutter with variable AV block.
Atrial Flutter with 3:1 Block
Revised: 9/10
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Atrial Flutter with 4:1 Block
Atrial Flutter with Variable Conduction
C.
Significance
1. Ventricular filling time is decreased if ventricular response is rapid - The ventricles
dont have enough time to fill with blood between each beat.
2. Loss of atrial kick - the AV node protects each atrial impulse (300 per minute) from
reaching the ventricles. Since there is fluttering of the atria, there is loss of atrial kick
which can result in a decreased filling of the ventricles and decreased contractility.
D.
Treatment
Rate control : Calcium channel blockers, beta blockers
Convert Rhythm : Amiodarone or synchronized countershock
Anticoagulation therapy may be needed
Revised: 9/10
61
ATRIAL FIBRILLATION
In atrial fibrillation the atria become so irritable that they are no longer beating but quivering
ineffectively. The atria fire at a rate of 400 to 600 times per minute. The AV node takes these
impulses through to the ventricles randomly, resulting in an irregular, chaotic rhythm. Atrial
Fibrillation is thought to be a rhythm of multiple areas of re-entry into the atria.
A. Etiology
1. Pathologic conditions of the heart - valvular disease, or congestive heart failure.
2. Pressure from congestive heart failure can have back-up pressures that stretch the
atrial myocardium which produces irritability.
B. Identifying Characteristics - irregular rhythm, no P waves
1. Rhythm: very irregular
2. Rate:
Atrial rate 400 to 600 but immeasurable

Ventricular rate varies with the number of impulses conducted to the
ventricles
Controlled - ventricular response (rate) below 120

Uncontrolled - ventricular response (rate) above 120
3. P waves: absent. Fibrillatory waves f are seen and vary in size and shape.
Fine - fibrillatory line almost straight
Coarse - fibrillatory line more bumpy
4. PR Interval - not measurable
5. QRS Duration - normal (< 0.12 seconds) unless aberrant conduction is present
Revised: 9/10
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Uncontrolled Atrial Fibrillation (Rate above 120)
Controlled Atrial Fibrillation (Rate below 120)
C. Significance
1. Loss of Atrial Kick - since atria are fibrillating, there is no distinct atrial contraction to
provide extra filling to the ventricles.
2. Thrombus formation - can occur with fibrillating atrium. When rhythm is converted to
sinus rhythm the resulting atrial contraction can result in pulmonary emboli
(right atrium) or a stroke (left atrium).
D. Treatment
Digitalis to increase AV block to control ventricular rate (long term)
Rate control: Calcium channel blockers, beta blockers (acute)
Convert Rhythm : Amiodarone (caution) or synchronized countershock (for
symptomatic atrial fibrillation- must be anticoagulated first if long standing atrial
fibrillation)
Anticoagulation therapy may be needed.
Revised: 9/10
63
WANDERING ATRIAL PACEMAKER
In Wandering Atrial Pacemaker (WAP) the pacemaker of the heart shifts between the SA
node, atria, and AV node.
A. Etiology - The sinus node defaults for some reason and slows allowing other pacing foci
to take over (escape mechanism). The foci can also become irritable and usurp the
pacing function of the SA node. If the irritability increases more, the WAP may be seen
at a tachycardic rate known as multifocal atrial tachycardia (MAT).
1. Rhythm - Usually irregular
2. Rate - varies depending if it is from escape mechanism which would give a slow rate,
or from an irritable focus which would give it a fast rate.
3. P waves - vary in size and shape depending on the site of the pacemaker. Some
sources say there should be P waves of at least 3 different shapes.
4. PR Interval - varies depending upon the pacemaker site.
Wandering Atrial Pacemaker (rate below 100)
Revised: 9/10
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Multifocal Atrial Tachycardia (rate above 100)
C. Significance - only significant depending upon the rate. If the rate is too fast or too
slow, patient may have symptoms.
D. Treatment - usually none. No suppressive drugs should be given as this may be a
backup pacemaker situation. If symptomatic MAT, use beta-blockers, calcium channel
blockers, Amiodarone (no cardioversion).
Review of Atrial Rhythms

This completes the section on atrial rhythms. Remember, atrial rhythms originate in the
atria, not the sinus node. Since the impulse originates in the atria, the P wave will be of a
different shape than that of the sinus node. PACs are early beats coming from the atrium.
They are called ectopics. You will have two jobs: identifying the underlying rhythm and
identifying the ectopic.
Atrial tachycardia and PSVT are rhythms originating in the atria at a rate of 150 to 250 per
minute. The difference between the two is that PSVT is paroxysmal, and has a sudden start or
sudden stop. Atrial flutter has the atria fluttering at 250 to 350 times a minute with a saw tooth
baseline. The AV node usually takes impulses through in a rhythmic pattern, resulting in block
of 2:1, 3:1, 4:1, or other variations. Atrial fibrillation has the hallmarks of an irregular rhythm and
no P waves. Wandering Atrial Pacemaker (WAP) has the pacemaker of the heart wandering
between the SA node, atria, and AV node. Characteristics are different shaped P waves and,
usually, an irregular rhythm. Multifocal Atrial Tachycardia (MAT) is the same thing as WAP but
with a rate over 100.
Revised: 9/10
65
Module III: Junctional Rhythms
IMPORTANT TERMS- JUNCTIONAL RHYTHMS

Antegrade Conduction
Conduction occurring in a downward manner toward

the ventricles.
Escape Beat
Occurs when a higher pacemaker doesn't fire. The beat

'escapes' from a lower pacemaker as a backup. (Rescue
Beat)
Idiojunctional
The same as junctional escape rhythm.
Inverted
Upside down (as in the P waves in junctional rhythm).
Retrograde Conduction
Conduction that returns to the atria in a backwards

manner.
Compensatory Pause
Normal beat following the premature complex occurs when

expected (the period between the complex before and
after the premature beat is the same as two normal R-R
intervals)
Noncompensatory Pause
Normal beat following the premature complex occurs

earlier than expected (less than two normal R-R intervals)
Also referred to as incomplete compensatory pause.
Revised: 9/10
66
JUNCTIONAL RHYTHMS
Remember that the AV node is responsible for conducting impulses from the SA node
and the atria down the conduction pathways into the ventricles. It is considered the gatekeeper
of the conduction system. The AV node has the ability to hold impulses or even block them
from getting through to the ventricles. The one property the node does not have is the ability to
initiate impulses. Localized tissues around the AV Node and the Bundle of HIS to the
bifurcation. This area is called the AV junction. Dysrhythmias that originate in the AV junction
are called junctional rhythms. It is not the primary pacemaker, but will assume responsibility for
the heart if:
The SA node fails to fire
The impulse from the SA node is blocked as it leaves the SA node
The rate of the SA node is very slow
The SA node impulse transmits through the atria but is blocked at the AV node
With junctional rhythms, the pacemaker is located in the middle of the heart. The electrical
system of the heart is one continuous electrical system. As a result, when an impulse starts in
the junctional area, the spread of the impulse occurs in two directions:
a. antegrade (downward) to the ventricles
b. retrograde (backward) to the atria
With junctional rhythms, the impulses traveling to the atria and the ventricles may show up
on the ECG paper at varying intervals. Since the impulse is traveling retrograde to the atria
(and traveling towards a negative electrode), the P wave will be inverted with a short P-R
interval. The impulse traveling to the ventricles does so in an antegrade fashion (towards a
positive electrode), and shows as an upright QRS.
Revised: 9/10
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ALL JUNCTIONAL RHYTHMS SHARE A JUNCTIONAL LOOKING BEAT.

This beat has the following criteria:
1.
An inverted P wave before the QRS, buried in the QRS or after the QRS. It is as
though the impulse is racing to get to the paper. If the impulse gets to the atria
first, you will see the P wave inverted before the QRS. If the impulse reached
the ventricles first, you will see a QRS without a P wave. In this case the P is
either buried in the QRS or comes after the QRS.
2.
PR is interval below 0.12 seconds when the P precedes QRS.
INVERTED P
a. Before QRS
b. Hidden in QRS
c. After the QRS
Revised: 9/10
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PREMATURE JUNCTIONAL CONTRACTIONS (PJC)

A PJC, like a PAC, is not an entire rhythm, but an ectopic beat. You will need to identify the
underlying rhythm and identify the ectopic beat.
A. Etiology
An irritable focus within the AV junction fires early and produces a single ectopic beat.
1.
2.
3.
4.
Ischemia or insult to the AV junction

Hypoxemia
Digitalis toxicity
Overstimulation
1. Rhythm Appears irregular because of the premature beats, but underlying rhythm may
be regular
2. Rate - Normal, bradycardia, or tachycardia
3. P wave -Junctional type - inverted before QRS, buried in the QRS, or inverted
behind. Will generally see no P wave before QRS or inverted P wave
4. PR Interval - Short, below 0.12 seconds when seen before the QRS. There will be
no PR interval if the P wave occurs in the QRS or behind the QRS.
5. QRS duration -usually normal (< 0.12 seconds) resembles the QRS of the underlying
rhythm
6. Compensatory Pause - usually incomplete
PJC
C. Significance - PJCs are considered benign unless they trigger junctional tachycardia.
Pulse will be irregular.
D. Treatment - usually none, but can treat the underlying cause. May respond to drugs
used to treat PACs. Amiodarone, Bata blockers, or Calcium Channel Blockers (ABC).
Revised: 9/10
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JUNCTIONAL ESCAPE BEAT

A junctional escape beat occurs when the SA node fails to fire. The protective mechanism of
the AV node and junctional areas lets a beat escape to keep the heart rate adequate. A
junctional escape beat is a protective mechanism. It occurs when the SA node fails or pauses
for more than 1 second.
A. Etiology - failure of a higher center in the conduction system to fire.
1. Rhythm appears irregular due to the pause. The underlying rhythm may be regular.
The underlying rhythm is the rhythm that is present before the pause.
2. Rate - overall rate may be slow due to the pause. Underlying rate can be normal,
bradycardia or tachycardia.
3. P waves - the beat coming in after the pause will have a Junctional type P wave which
is inverted before, buried in, or after the QRS.
4. PR Interval - on the beat after the pause (the escape beat) it will be short (less than 0.12
seconds) if there is a P wave preceding the QRS. If no P wave precedes the QRS, there
will not be a PR interval.
5. QRS duration - normal (below 0.12 seconds)
JUNCTIONAL ESCAPE BEAT
Much like sinus arrest, except beat after the pause is junctional.
C. Significance - none if the overall rate is adequate to maintain cardiac output. This is a
protective mechanism.
D. Treatment - ESCAPE BEATS ARE NOT TREATED. They prevent slow rates or
asystole. If patient is symptomatic, you would treat as you would a sinus bradycardia
(atropine and/or transcutaneous pacing).
Revised: 9/10
70
JUNCTIONAL ESCAPE RHYTHM
(sometimes called junctional rhythm or idiojunctional)
A. Etiology
With depression of the SA node, the junction takes over as a backup pacemaker.
The SA node defaults allowing the junction to take over.
1.
2.
3.
4.
Insult to the SA node

Increased vagal tone in the SA node
Hypoxemia
Digitalis Toxicity
1. Rhythm - regular
2. Rate - 40 to 60/min (inherent rate of the junction)
3. P waves - Junctional type P waves - inverted before, during, or after the QRS
4. PR interval - less than 0.12 seconds if the P is before the QRS. If the P is not before
the QRS, there will not be a PR interval
5. QRS duration - normal (< 0.12 seconds)
JUNCTIONAL RHYTHM
C. Significance - Rhythm may not cause any serious problems unless the heart rate is too
slow to maintain cardiac output. There may be loss of atrial kick leading to further decrease in
cardiac output. Because of the slow rate, ventricular escape or irritability may occur.
D. Treatment - DO NOT SUPPRESS THE RHYTHM. If the patient is symptomatic, treat
according to the ACLS Bradycardia Algorithm.
Revised: 9/10
71
ACCELERATED JUNCTIONAL RHYTHM

Accelerated junctional rhythm results from increased automaticity in the junctional area
which usurps the function of the SA node.
A. Etiology
2. Insult to the AV junction
3. Acute MI
1. Rhythm - regular
2. Rate - 60 to 100/min (between inherent rate of the junction and tachycardia rate)
3. P waves - Junctional P waves. Inverted before, during, or after the QRS.
4. PR Interval - below 0.12 seconds or no PR if the P wave does not come before the
QRS complex.
5. QRS duration - normal (below 0.12 seconds)
ACCELERATED JUNCTIONAL RHYTHM
C. Significance - likely to cause no problems since the heart rate is at a normal range.
May cause difficulty with the loss of atrial kick in compromised hearts leading to left
ventricular failure. Usually benign.
D. Treatment - Usually requires no treatment. If therapy is required, drugs such as
Amiodarone or Procainamide might be used to slow the rate of the junctional
focus so the SA node can regain control. If caused by digitalis toxicity, the medication
should be held. If symptomatic (due to bradycardia), atropine and/or transcutaneous
pacing should be considered.
Revised: 9/10
72
JUNCTIONAL TACHYCARDIA
An irritable site within the AV junction speeds up to override the SA node for control of the
heart. This irritable focus is thought to be an automatic tachycardia in the AV junction. May
start with a single PJC reentering. 3 or more PJCs in a row is considered to be a short run of
junctional tachycardia.
A. Etiology
1. Insult to the AV junction
3. Acute MI
4. Theophylline administration
1. Rhythm - regular
2. Rate 101-150
3. P waves - junctional type P waves. P wave is inverted before, buried in, or after the
QRS.
4. PR Interval - short (below 0.12 seconds) if the P wave is before the QRS. Otherwise
there will be no PR interval.
5. QRS duration - normal (< 0.12 seconds)
*May be difficult to distinguish from atrial tachycardia when the P waves cannot be seen.
JUNCTIONAL TACHYCARDIA
C. Significance - Has the same problems of any of the tachycardias resulting in decreased
filling time for the ventricles. May increase myocardial ischemia, due to incomplete filling of the
coronary arteries, frequency and severity of chest pain, extend myocardial infarction, and
predispose patient to ventricular dysrhythmias if associated with an acute coronary syndrome.
Loss of atrial kick may put patient into left ventricular failure.
Revised: 9/10
73
D. Treatment depends on severity of symptoms. If no symptoms, only observation needed.

1. Same as atrial tachycardias
a. Vagal maneuvers
b. Oxygen and IV access
c. IV adenosine to determine origin of rhythm (pharmacological differential
diagnosis)
d. Drugs beta-blocker or calcium channel blocker (if no
contraindications exist), or amiodarone
2. If rhythm is result of digitalis toxicity, hold drug. If result of Theophylline
administration, the infusion should be slowed or stopped.
Review of Junctional Rhythms

The most important thing to remember is that ALL JUNCTIONAL RHYTHMS SHARE A
JUNCTIONAL TYPE BEAT. This junctional beat has the criteria of:
1) Inverted P wave before the QRS, buried in the QRS, or after the QRS.
2) PR interval of the P wave before the QRS, when short is < 0.12 seconds.
3) QRS is normal (< 0.12 seconds)
A premature junctional contraction is an ectopic beat that comes early. This ectopic beat has
the junctional P wave. A junctional escape beat is an ectopic beat that comes late. It is much
like sinus arrest. In sinus arrest there is a pause, and the next beat that comes in has a sinus P
wave in front of it. In a junctional escape beat, the beat after the pause has a junctional type P
wave. Junctional rhythm, accelerated junctional, and junctional tachycardia are all the same
except they differ in rate criteria. All three of these rhythms share a junctional type P-wave, but
the rate varies:
Junctional - 40 to 60
Revised: 9/10
Accelerated - 60 to 100
Tachycardia - over 100
74
Module IV : Ventricular Rhythms
IMPORTANT TERMS - VENTRICULAR RHYTHMS

Pairs (Couplets)
Two sequential premature ventricular complexes (PVCs)
Runs or Bursts
Three or more PVCs in a row
Bigeminy
Every other beat is a PVC.
Trigeminy
Every third beat is a PVC
Unifocal
Coming from the same sight and having the same shape.
Multifocal
Coming from different sites and have different shapes.
Monomorphic
Coming from the same sight and have the same morphology.
Polymorphic
Coming from different sites and have different morphology.
Compensatory Pause
The timing and spacing to the next beat after an ectopic.

PVC's usually have a full or complete compensatory pause.
Opposite Polarity
A description of ventricular beats where the QRS is in an upward

direction while the T wave is downward, or the T wave is
upward while the QRS is downward.
R-on-T Phenomenon
A PVC that hits in the vulnerable portion of the T wave. May

precipitate ventricular fibrillation or ventricular tachycardia.
Revised: 9/10
75
VENTRICULAR RHYTHMS
With Ventricular dysrhythmias, the impulse originates in the ventricles. The inherent
pacemaker rate of the ventricles is between 20-40 beats per minute (BPM). Since these
rhythms do not originate above the bifurcation of the Bundle of HIS, depolarization of the
ventricles is usually slower resulting in a wide and bizarre QRS complex and there is no
depolarization of the atria that occur, therefore no P-wave is seen. Since it is the ventricles that
produce the cardiac output, disturbances in this area are very serious and can precede cardiac
arrest.
PREMATURE VENTRICULAR COMPLEX/ CONTRACTION (PVC)
When an irritable ectopic focus from the ventricle fires an impulse, a PVC occurs. It is a
premature beat (occurring earlier than expected) that has characteristics of originating from the
ventricles (wide, bizarre QRS with no preceding P-wave).
A. Etiology
1. Hypoxia, anoxia, hypotension, anemia
2. Ischemic heart disease
3. Electrolyte imbalance (low potassium or magnesium)
4. Myocardial Infarction
5. Myocarditis, pericarditis
6. CHF
7. Stress, tiredness, smoking, overeating, caffeine
8. Hypoglycemia
9. Sepsis
1. Rhythm appears irregular due to the premature beat, but underlying rhythm may be
regular
2. Rate - varies depending on underlying rhythm
Revised: 9/10
76
Identifying characteristics (cont.)

3. P-wave - since impulse originates in the ventricles no P-wave is present
4. PR interval none
5. QRS Complex, ST segment, and T wave
a. QRS is premature - must occur before next expected beat
b. QRS is wide and bizarre 0.12 seconds or greater
c. ST segment and T wave are in opposite polarity to the QRS of the PVC
Unifocal PVCs
d. The above strip shows an example of Unifocal PVCs. They have the same morphology
(shape) indicating that they have come from the same irritable ectopic focus within the ventricle.
The following strip is an example of Multicocal PVCs. They have different shapes indicating
that the premature impulses have come from different sites within the ventricles.
Multifocal PVCs
Revised: 9/10
77
Bigeminy - Every other beat is a PVC
Pairs - Two sequential PVCs occurring in a row
Run or Burst Three or more PVCs occurring in a row.

together, this is sometimes referred to as a Salvo.
Revised: 9/10
When there are 3 PVCs
78
R-on-T phenomenon When a PVC hits on the vulnerable portion of the T-wave, it may (but
not always) precipitate a more serious ventricular dysrhythmia such as V-tach or V-fib.
R-on-T precipitating V-fib
C. Significance
1. One of the most common dysrhythmias and can occur in both healthy and unhealthy
individuals at any time.
2. In the normal heart, they are not considered dangerous or significant. Frequency tends to
increase with age.
3. In ischemic heart disease or electrolyte imbalance, they are considered dangerous
beats that warn of ventricular irritability that can lead to serious and lethal rhythms
such as ventricular tachycardia or ventricular fibrillation.
4. Individually, PVCs have no real hemodynamic significance.
They are usually
asymptomatic but if PVCs are frequent, they may cause a decrease in cardiac
output and symptoms.

5.
Patients experiencing PVCs may complain of palpitations, a racing heart,

skipped beats, or chest/neck discomfort.
Revised: 9/10
79
Treatment (cont.)
D. Treatment
1. Depends on the underlying cause, the patients signs and symptoms, and the clinical
situation.
2. Treat the underlying cause (i.e. if low potassium or magnesium, give electrolyte
replacement). Routine use of medications to treat PVCs is no longer recommended,
although when high or increasing in frequency, Amiodarone 150 mg over 10 minutes,
followed by continuous infusion may be used.
3. In the setting of acute coronary syndrome:
-
Ensure adequate oxygenation

Relieve pain
Identify and treat any precipitating causes (hypoxia, heart failure, electrolyte
abnormalities, or acid-base abnormalities)
4. Dangerous PVCs that should be treated (all indicate increased irritability within the
ventricles and a higher risk of developing a more serious ventricular dysrhythmia):
a. more than 6 per minute
b. increasing in frequency
c. occurring in pairs or triplets
d. multifocal - indicates more than one irritable site
e. R-on-T phenomenon
VENTRICULAR ESCAPE BEAT

A ventricular escape beat is an ectopic beat that occurs after a pause when the
supraventricular pacemakers (SA Node and junctional area) fail to fire as the back-up
pacemakers. The impulse fires from the ventricle to try and maintain cardiac output. This is a
compensatory mechanism. It is different from a PVC because it occurs later than expected
(versus earlier).
A. Etiology
A ventricular escape beat occurs when the SA node fails to fire and the junctional area
fails to back up the SA node.
1. Rhythm appears irregular due to the escape beat, but underlying rhythm may be
regular
Revised: 9/10
80
2. Rate - underlying rate is usually normal or slow, but overall rate may be slow due to
the pause
3. P wave - absent on escape beat following the pause.
4. PR Interval - not applicable
5. QRS - the QRS complex following the pause will be wide and bizarre, like any other
ventricular originated beat
Ventricular escape beat vs. PVC
PVC
Notice the PVC above comes earlier than expected.
ESCAPE BEAT
The ventricular escape beat above comes after a pause.
C. Significance - rate may be slow, but this is an escape mechanism that is working to
keep the overall rate of the heart adequate to maintain cardiac output.
D. Treatment
1. DO NOT SUPPRESS - treat the overall slow rate if causing symptoms
2. If symptomatic, treat as a symptomatic bradycardia
- Atropine 0.5 mg IVP (may repeat to max of 3mg)
- Transcutaneous pacing (TCP)
- Consider Epinephrine (2-10 mcg/min) or Dopamine (2-10 mcg/kg/min)
Revised: 9/10
81
IDIOVENTRICULAR RHYTHM ( IVR OR VENTRICULAR ESCAPE RHYTHM )

The ventricles act as a backup pacemaker. Ventricular escape rhythm occurs when the
entire rhythm arises from the ventricles because the higher pacemakers have ceased function.
The rate of this rhythm is at the inherent rate of the ventricles (20 to 40 per minute).
A. Etiology
Idioventricular rhythm is the most dangerous of the escape rhythms and occurs only
when higher pacemakers have failed.
1. Rhythm usually regular
2. Rate - slow at 20 to 40 beats/minute
3. P waves - absent
4. PR Interval - not applicable
5. QRS, ST, T - QRS wide above 0.12 seconds, bizarre, with ST and T in opposite
direction to the QRS
C. Significance
1. Rate is very slow and undependable. The pacemaker may stop firing at any time,
leaving the patient in ventricular standstill.
2. Rate may be too slow to maintain cardiac output.
3. Since there are no P-waves, there is a loss of atrial kick.
D. Treatment
1. DO NOT SUPPRESS - its all that is left to pace the heart.
Revised: 9/10
82
- Atropine 0.5 mg IVP (may repeat to max of 3mg)

ACCELERATED IDIOVENTRICULAR RHYTHM (AIVR OR ACCELERATED VENTRICULAR
ESCAPE RHYTHM)
A. Etiology
AIVR occurs when an automatic focus in the ventricles fires between 40 and 100 times per
minute. This is a benign escape rhythm that is often transient. It is common within the first 12
hours of myocardial infarction as well as after successful reperfusion therapy.
1. Rhythm - regular
2. Rate - 40 to 100 per minute
3. P waves - none
4. PR Interval - none
5. QRS, ST, T - entire rhythm comes from the ventricle with wide, bizarre, QRSs. ST
and T wave are opposite direction to the QRS complex
C. Significance - this is a backup pacemaker mechanism

D. Treatment
1. DO NOT SUPPRESS
- Atropine 0.5 mg IV (may repeat to max of 3mg)
Revised: 9/10
83
VENTRICULAR TACHYCARDIA (VT)

Ventricular tachycardia is due to a rapid discharge from an ectopic ventricular focus. The
rhythm is sometimes preceded by PVCs and indicates advanced myocardial irritability. The
rate of ventricular conduction takes over the SA node as the pacemaker.
A. Etiology - same as PVCs
1. Rhythm - usually regular
2. Rate - Ventricular rate of greater than 100. Atrial rate is not measurable.
3. P waves - usually cannot be seen. In slower rates, P-waves may march through
the rhythm but have no relation to the QRS due to AV dissociation.
4. PR Interval - none
5. QRS - wide and bizarre with a duration 0.12 seconds or greater, ST segment and T wave
will be in the opposite direction of the QRS. May be monomorphic (from same ectopic
focus) or polymorphic (indicating impulse originating from different foci)

Monomorphic VT- same morphology (shape) of QRS
Polymorphic VT- varying morphologies
Revised: 9/10
84
C. Significance
1. Indicates extreme myocardial irritability and can cause loss of consciousness.
2. May progress to ventricular fibrillation and death.
3. May be tolerated in some but causes a decrease in cardiac output leading to
dizziness, angina, CHF, pulmonary edema, or shock.
D. Treatment (ACLS Algorithm for Unstable tachycardia and Pulseless VT/VF)
1. Determine if pulse or no pulse.
2. VT with a pulse
- Oxygen and IV access
- STABLE: Amiodarone 150 mg over 10 minutes, Repeat as needed to maximum
dose of 2.2 g in 24 hours.
- UNSTABLE (symptomatic related to heart rate usually >150: altered mental status,
ongoing chest pain, hypotension, or other signs of shock): Immediate synchronized
cardioversion at 100J
3. Pulseless VT
- Immediate defibrillation with 1 shock (200J with Biphasic defibrillator, 360J with
Monophasic defibrillator)
- Five cycles of CPR, followed by another shock, epinephrine 1mg IV/IO (may
repeat every 3-5 minutes) or 1 dose of vasopressin (40 units IV/IO to replace the
first or second dose of epinephrine)
- Consider antiarrhythmics: Amiodarone 300 mg IV/IO once (may repeat using
150 mg IV/IO once) or Lidocaine (1-1.5 mg/kg first dose, then 0.5-0.75 mg/kg
IV/IO, maximum 3mg/kg)
TORSADES DE POINTES
Polymorphic VT that occurs in the presence of a long QT interval is called Torsades de pointes.
This is a French term meaning twisting of the points. The QRS changes shape, amplitude,
and
width
and
often
appears
to
twist
around
the
isoelectric
line.
Revised: 9/10
85
Torsades (cont.)
A. Etiology
1. Medications (antibiotics like erythromycin, antifungals such as fluconazole, antihistamines,
cardiac medications such as quinidine, Procainamide, Amiodarone, sotalol)
2. Hypothyroidism
3. Subarachnoid hemorrhage
4. Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)
5. Myocarditis
B. Significance - May be irritated by traditional treatment for VT. If a polymorphic VT is noted,
it is important to try and determine if the patients QT interval just before the tachycardia was
normal or prolonged. If prolonged, this indicates Torsades and must be treated differently.
Regular VT would be treated with Amiodarone. However, Amiodarone can prolong the QT
interval further worsening Torsades.
C. Treatment Magnesium, loading dose 1-2 gm IV/IO diluted in 10 ml D5W given over 5-20
minutes. If no pulse, same as ACLS algorithm for pulseless VT/VF but consider Magnesium
instead of Amiodarone or Lidocaine.
VENTRICULAR FIBRILLATION
Ventricular fibrillation (VF) is a chaotic ventricular rhythm where the entire ventricular muscle
twitches and quivers erratically. There are no effective contractions of the heart. There is no
cardiac output. In most cases the rhythm is triggered by PVCs or V-tach but can occur
spontaneously without preceding signs of ventricular irritability.
A. Etiology - A lethal dysrhythmia, incompatible with life. Can occur from
ventricular irritability or suddenly without preceding signs or symptoms.
1. Rhythm - totally irregular
2. Rate - not measurable
3. There are no P, QRS, ST, or T waves, only chaotic undulations of the baseline. May
appear as coarse or fine VF.
Revised: 9/10
86
Coarse VF
Fine VF
C. Significance
1. No cardiac output - patient is apneic, pulseless, and clinically dead.
2. Therapy must be instituted within two to three minutes or the chance for survival is
poor. Irreversible brain death occurs within four to six minutes.
3. If fine VF is suspected, always check rhythm in another lead and/or increase gain to
differentiate from asystole.
D. Treatment (ACLS algorithm for Pulseless VT/VF)
-
Revised: 9/10
Immediate defibrillation with 1 shock (200J with Biphasic defibrillator, 360J with
Monophasic defibrillator)
Five cycles of CPR, followed by another shock, epinephrine 1mg IV/IO (may
repeat every 3-5 minutes) or 1 dose of vasopressin (40 units IV/IO to replace the
first or second dose of epinephrine)
87
Consider antiarrhythmics: Amiodarone 300 mg IV/IO once (may repeat using

150 mg IV/IO once) or Lidocaine (1-1.5 mg/kg first dose, then 0.5-0.75 mg/kg
IV/IO, maximum 3mg/kg)
Pulseless Electrical Activity (PEA or Electromechanical Dissociation- EMD)

A. Conduction of electrical impulses is occurring without contraction of the myocardium.
B. No pulse or blood pressure. Lethal Rhythm!
C. Almost any rhythm can be seen on the monitor (usually bradycardic with wide or narrow
QRS)
D. Treatment (ACLS Algorithm for Asystole/PEA)
- CPR for 5 cycles
- Epinephrine 1mg IV/IO every 3-5 minutes or Vasopressin 40 units IV/IO in place
of first or second dose of epinephrine
- Consider Atropine 1mg IV/IO for slow PEA rate less than 60 beats/min, may
repeat every 3-5 minutes (up to 3 doses)
- Search for and treat the underlying cause
Possible Causes of PEA

2ways to remember!
Think PATCH 4 MD
Pulmonary embolism
Acidosis
Tension pneumothorax
Cardiac Tamponade
Hypovolemia (most common cause of PEA)
Hypoxia
Heat/Cold (hypothermia/ hyperthermia)
Hypo/ Hyperkalemia (and other electrolytes)
Myocardial infarction
Drug overdose
The Hs and Ts
Hypovolemia (most common cause)

Hypoxia
Hypothermia
Hypo/ Hyperkalemia
Hypoglacimia
Hydrogen ions (acidosis)
Tauxins (Drugs or poisons)
Trauma
Tampinad (Cardiac)
Tension Pneumothorax
Thrombas Cardiac
Thrombas Pulmanary
Is there a pulse with that?

Revised: 9/10
88
VENTRICULAR STANDSTILL
A. Etiology -Ventricular standstill is a lethal dysrhythmia that occurs when the AV node is completely blocked down and no lower pacemaker takes over. There are two types of
ventricular standstill:
Primary - The impulse from the SA node are blocked and no ventricular impulses occur.
Because they fire from the SA node to activate the atria, you will see P-waves.
1.
2.
3.
4.
5.
Rhythm - atrial rhythm regular, no ventricular rhythm

Rate - atrial rate is the sinoatrial (SA) rate. Ventricular rate is 0.
P waves - sinus P waves
PR interval - none since there are no QRSs present
QRS - absent
Secondary - may follow primary standstill. Atrial rate is missing. Evidence of ventricular
electrical activity is present at a slow rate but pulse is absent. This is sometimes referred to as
an Agonal rhythm which is used to describe a dying heart. Also a form of PEA.
1.
2.
3.
4.
5.
Rhythm - regular or irregular

Rate - atrial rate is absent, ventricular rate is <20 beats/min
P wave - absent
PR interval - not applicable
QRS - wide and bizarre 0.12 seconds or greater
Revised: 9/10
89
Ventricular standstill (cont.)

C. Significance In both primary and secondary standstill, the patient has no pulse and is
clinically dead. Must be treated as asystole.

- CPR for 5 cycles
- Consider Atropine 1mg IV/IO for slow PEA rate, may repeat every 3-5 minutes
(up to 3 doses)
ASYSTOLE
A. Etiology
In asystole there is no electrical activity occurring. Asystole may be a primary event in
cardiac arrest or may follow ventricular tachycardia or ventricular fibrillation. The rhythm shows
up on the strip as a straight line.
B. Important points to consider with asystole:
1. If the rhythm is unclear and possibly fine ventricular fibrillation, treat as V-fib. (Do flat line
protocol)
2. Asystole should always be confirmed in 2 leads.
C. Significance - patient is clinically dead

- CPR for 5 cycles
Revised: 9/10
90
Consider Atropine 1mg IV/IO for slow PEA rate, may repeat every 3-5 minutes
(up to 3 doses)
Review of Ventricular Rhythms
The ventricular rhythms are the most life threatening and require immediate recognition and
treatment. All ventricular rhythms share a QRS which is wide (above 0.12 seconds) and
bizarre. P-waves are generally not present since the impulse originates in the ventricles. If
P-waves are present, they bear no relation to the QRS complexes (AV Dissociation).
PVCs are early beats originating in the ventricle. They can occur in any rhythm, come
early, and have a ventricular looking QRS. Ventricular escape beats are ectopic beats that
occur after a pause in which a higher (Supraventricular) pacemaker fails to fire. This is a
compensatory mechanism of the heart to maintain cardiac output. Rhythms that come entirely
from the ventricle are differentiated by rate alone are:
Idioventricular rhythm (Ventricular Escape rhythm)
Accelerated Idioventricular rhythm (AIVR)
Ventricular tachycardia (VT)
Rate 20-40
Rate 40-100
Rate > 100
Torsade de Pointes is a type of polymorphic ventricular tachycardia where the QRSs flip
from upward to downward. It is treated differently from traditional ventricular tachycardia.
Ventricular standstill is differentiated by primary and secondary. With primary standstill, only P
waves occur with no QRS complexes at all. In secondary standstill, QRS complexes show at a
rate of <20, but there is no pulse to correspond. Asystole occurs when there is no electrical
activity occurring and shows as a flat line.
Revised: 9/10
91
Module V: Atrioventricular Blocks
IMPORTANT TERMS - ATRIOVENTRICULAR BLOCKS

AV junction
Located between the atria and ventricles. Also called the

junctional area.
Dissociated
Not related to each other. For example, the P-waves do not have
any relation to the conduction of the QRS.
Transient
Temporary; comes and goes.
Revised: 9/10
92
An atrioventricular block (AVB) is defined as a delay or interruption in the conduction between

the atria and ventricles. The impulse originates in the SA node, but has trouble getting through
the AV node to the ventricles. AV Blocks are classified two ways- by the degree of the block
and by the site of the block:
Degree of the block (differentiated by the PR Interval):
Partial blocks
o First-degree AV block
o Second-degree AV block (type I and type II), and 2:1
Third-degree or complete AV block
Site of the block (determined by the QRS duration):
AV node
Infranodal
o Bundle of His
o Bundle branches
With first-degree AV blocks, the impulses from the sinoatrial (SA) node are only delayed (not
blocked). In second-degree AV blocks, the impulses are intermittently blocked, and in thirddegree AV block there is a complete block in conduction of impulses between the atria and
ventricles.
FIRST-DEGREE AV BLOCK
In first-degree AV block, the sinus impulse is delayed in traveling through the AV node,
resulting in consistently prolonged PR intervals.
A. Etiology
1. Insult to the AV node
2. Hypoxemia
Revised: 9/10
93
3.
4.
5.
6.
M.I.
Digitalis toxicity
Ischemic diseases of the conduction system
Hyperkalemia
1. Rhythm - Regular
2. Rate - normal, bradycardia, or tachycardia
3. P wave - normal sinus P-wave
4. PR interval - constantly prolonged >0.20 seconds
C. Significance - usually there are no other signs or symptoms.

D. Treatment - usually none, but atropine may reverse.
SECOND-DEGREE AV BLOCK Type I (Mobitz I or Wenckebach)

This type of block is a form of intermittent block, since only some of the sinus impulses
are prevented from reaching the ventricles. The block is thought to occur at the level of the AV
node. Since the AV node primarily receives its blood supply from the right coronary artery, this
type of block is more frequently seen with inferior M.I.s. With Wenckebach, the impulses are
progressively delayed through the AV node, being a little slower with each beat. The PR
interval gets progressively longer until the QRS is dropped.
Revised: 9/10
94
A. Etiology 1. insult to AV node

2. acute M.I.
3. hypoxemia
4. increased vagal tone to the AV node
1. Rhythm:
P to P is regular
R to R is irregular
Irregularity is cyclic
2. Rate: Usually slow but may be normal More P-waves than QRSs
3. P-waves - sinus P-wave. At times there will be more than one P-wave for each QRS.
4. PR Interval - PR gets longer and longer with each QRS until a QRS is missing
(dropped)
5. QRS Duration - normal (<0.12 seconds)
6. Cyclic Pattern
C. Significance
1. Usually transient. If occurring in conjunction with acute MI, the patient should be observed
for increasing AV block.
2. There may be no hemodynamic changes unless the rate is very slow.
3. With an inferior MI, it is viewed as benign. With an anterior MI, it may be a warning sign
that a higher degree of block may occur at any time.
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D. Treatment
1. Usually no treatment unless the rate is slow causing symptoms
2. If treatment is necessary, use ACLS algorithm for symptomatic bradycardia algorithm
(atropine and/or temporary pacing).
SECOND-DEGREE AV BLOCK Type II (Mobitz II)
Second-degree AV block, type II is another form of intermittent block, but is thought to occur
at the bundle branches rather than at the AV node. Because the bundle branches receive their
primary blood supply from the left coronary artery, anterior M.I.s are typically associated with
blocks that occur at the level of the bundle branches (such as second-degree type II). Type II
blocks have a greater chance of progressing to complete heart block.
Remember: two = trouble
A. Etiology 1. degenerative changes to the conduction system
2. anterior M.I.
3. hypoxemia
4. organic heart disease
1. Rhythm - usually irregular
2. Rate - Usually slow because QRSs are dropped or blocked Whenever you have a slow
rate on a rhythm strip, look carefully to be sure a Type II block is not present.
3. P-waves - Sinus P, occasionally more than one P-wave for every QRS.
4. PR Interval - PRI of conducted beats may be normal or constantly prolonged.
C. Significance
1. Slow heart rate can decrease cardiac output and blood pressure resulting in shortness
of breath, restlessness, and chest pain.
2. Usually not transient and may progress to complete heart block or ventricular
standstill.
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D. Treatment
1. If treatment is necessary, use ACLS algorithm for symptomatic bradycardia algorithm
(temporary pacing).
2. Pacemaker often used since this block can progress to third-degree heart block.
SECOND DEGREE TYPE 2 AV BLOCK 2:1 CONDUCTION

2:1 AV Block is a type of second degree heart block where there is a fixed ratio of conduction
through to the ventricles. The PR interval remains constant before the conducted beats. There
will be two P-waves for every QRS, and the rhythm will be regular. Sometimes, the term highgrade or advanced second-degree AV block may be used to describe two or more consecutive
P waves that are not conducted. There may be a 3:1 or 4:1 conduction ratio where only every
3rd (3:1) or 4th (4:1) P-wave is conducted.
A. Etiology 1. insult to AV node
2. acute M.I.
3. hypoxemia
4. increased vagal tone to the AV node
1. Rhythm - regular
2. Rate varies, but often slow
3. P-waves - Sinus P-waves, 2 P-waves for every QRS.

4. PR Interval - PRI of conducted beats may be normal or constantly prolonged.
5. QRS Duration - Normal (<0.12 seconds) or wide (>0.12 seconds)
C. Significance
1. Slow heart rate can decrease cardiac output and blood pressure resulting in shortness
of breath, restlessness, and chest pain.
2. Must monitor closely to make sure it does not progress to a higher degree of block.
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D. Treatment
1. If treatment is necessary, use ACLS algorithm for symptomatic bradycardia (pacing).
THIRD-DEGREE AV BLOCK (complete heart block)

In third-degree block the area below the AV node in the Bundle of HIS or Bundle Braches
shuts down completely. The SA node fires, but no impulses are conducted through to the
ventricles. Backup pacemakers, such as the AV junction or the ventricles, will hopefully
reestablish or allow some heart rate. Complete AV dissociation is noted.
A. Etiology
1. ischemic diseases of the conduction system
2. acute M.I
3. digitalis toxicity
4. insult to the AV node
1. Rhythm - regular
2. Rate Usually slow
3. P-waves - sinus P-waves that have no relationship to the QRSs.
4. PR Interval - varies greatly. No relation to QRSs (pseudo or false PR Interval).
5. QRS Duration - Narrow or wide depending upon backup pacemaker:
Junction narrow (<0.12)
Ventricles wide (>0.12)
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(Third Degree AV Block, cont.)

C. Significance
1. Hemodynamic status is dependent upon the ventricular rate
a. near normal rate mild to no symptoms
b. slow rate - decreased cardiac output causing symptoms (Dyspnea, chest pain,
light-headedness, changes in LOC, hypotension, pallor, diaphoresis)
2. Extremely Dangerous - the lower pacemakers are usually very slow and unreliable,
particularly if the backup pacemaker is coming from the ventricles. The slow rate may
cause irritability or ventricular standstill.
D. Treatment
1. Depends on the ventricular rate and whether or not the patient is symptomatic:
a. Asymptomatic: standby pacemaker needed in case patient becomes symptomatic
b. Symptomatic: prepare for transcutaneous pacing and/or transvenous pacemaker
insertion, and Dopamine or Epinephrine drips.
Review of Atrioventricular Blocks

To review, atrioventricular blocks occur because the area of, or below, the AV node is sick.
The sinus node fires impulses at a normal rate, but the impulse is delayed or blocked when
attempting to get through the AV node. AV blocks are categorized by degrees, with third degree
being the most dangerous. The degree of the block can be differentiated by the PR interval. AV
blocks can also be classified by the site of the block, which is determined by the width or
duration of the QRS.
THE KEY TO IDENTIFYING AV BLOCKS IS THE PR INTERVAL
First-degree AV block is just like sinus rhythm except the PR interval is constantly
prolonged greater than 0.20 seconds. There are 2 types of second-degree AV block. Type I is
often called Wenckebach and is characterized by a PR interval that gets longer and longer until
a QRS is dropped. This is a cyclic rhythm. The P to P will be regular, but the R to R is
irregular in Wenckebach. Type II second degree heart block has intermittent blocking of
impulses through the AV node. The PR interval will be constant (fixed). Type II block is more
dangerous than Type I and is more likely to progress to complete heart block. 2:1 block is a
type of second-degree heart block in which there is a fixed ratio of conduction to the ventricles.
The R to R is regular, and there are 2 P-waves for every QRS. Third-degree AV block is the
most dangerous because there is a total block below the AV node. The sinus node beats on its
own as does a backup pacemaker which may be the junction or the ventricles. There is no
relationship between the P waves and the QRSs (Pseudo/ false PR Interval).
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Symptoms will depend upon the overall ventricular heart rate of the patient, and in general
you will see slower heart rates with the higher degrees of blocks. The slow heart rate will
decrease cardiac output and therefore cause symptoms such as dyspnea, chest pain, lightheadedness, changes in LOC, hypotension, pallor, or diaphoresis. If a patient is symptomatic,
they are treated using the ACLS algorithm for symptomatic bradycardia regardless of the type of
block. In higher degrees of blocks, temporary pacing may be required over the use of atropine.
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Module VI: Pacemakers
IMPORTANT TERMS - PACEMAKERS

Demand Pacing
Pacemaker fires only when needed as determined by

preset intervals.
Fixed rate
Pacemaker fires at a set rate regardless of what is

happening with the patient's own rhythm.
Transcutaneous
Electrodes are placed on the skin to pace.
Epicardial
Pacemaker leads are placed directly onto or through the

Epicardium under direct visualization (surgery).
Transvenous
Pacemaker inserted through a venous route for entry into

the right atria or ventricle.
Sensitivity
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The extent to which the pacemaker recognizes intrinsic electrical

activity.
101
Purpose
Pacemakers are battery-operated, electronic devices with a pulse generator that delivers an
electrical stimulus to the heart through electrodes placed in contact with the endocardium,
attached directly to the epicardium, or placed on the skin. This electrical current will depolarize
or activate the heart at a predetermined rate or cycle.
Indications
A. Slow Heart Rate
1.
2.
3.
4.
5.
6.
Symptomatic bradycardia
Symptomatic second-degree Type II AV block
Third-degree AV block
Prophylactically during surgical procedures
Medication toxicity (digitalis, quinidine)
Sick sinus syndrome
B. Fast Heart Rate

To override a tachycardic dysrhythmia (Supraventricular or ventricular) which is refractory
to pharmacologic therapy or electrical countershock.
Methods of Insertion
A.
B.
C.
D.
Transthoracic (Epicardial wires)

Temporary Transvenous
Permanent Transvenous
Transcutaneous
A. Transthoracic (Epicardial wires)

1. Placed during open heart surgery for prophylactic use post operatively. Pacer wires
attach directly to the epicardium.
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Atrial wire
Ventricular wire
B. Temporary Transvenous
1. Pacing catheter is inserted through the venous system into the right atrium or ventricle.
2. Pacer wires are attached to an external battery-operated pulse generator.
C. Permanent Pacemaker
1. Pacing catheter is inserted transvenously into the right heart against the endocardium.
2. The proximal end of the catheter is directed through a subcutaneous tunnel and joined to
the battery-powered pulse generator that is placed in a pocket beneath the skin in the
anterior chest just below the right or left clavicle.
Pulse Generator
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D. Transcutaneous Pacing
1. A noninvasive emergency pacemaker that provides temporary pacing until a
temporary transvenous pacing electrode can be inserted.
2. Large electrodes (pacing pads) are placed at the V3 position and at the midback position.
Electrocardiographic Considerations
A. Pacemaker Spike: The electrical stimulus delivered by the pacemaker produces a sharp
narrow deflection called a spike or pacemaker artifact. The spike immediately precedes
the chamber paced. If the atrium is paced, the spike precedes the P-wave. If the ventricle
is paced, the spike precedes the QRS. The shape of the pacemaker induced P or QRS
will differ significantly from the spontaneous beat.
ATRIAL PACEMAKER- Notice the pacemaker spikes immediately before the P-wave.
ATRIAL AND VENTRICULAR PACING (DUAL CHAMBER PACEMAKER)- Notice the

pacemaker spikes before both the P-wave and QRS.
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B. Pacemaker Capture: When a spike occurs and is followed by a waveform, then capture
has occurred. The chamber that is being paced has been depolarized. The spike can
appear upright or inverted. When a spike occurs and there is no waveform following it, this
is considered loss of capture. An electrical stimulus has been delivered, but has failed to
cause depolarization.
Pacing Modalities
A. Fixed-rate pacemaker (continuous asynchronous): The pacemaker fires at a set rate
regardless of the patients own intrinsic rate.
Danger: pacemaker stimulus may fall on the vulnerable period of the T wave causing
a serious ventricular dysrhythmia (R-on-T phenomenon).
B. Demand Pacemaker: A demand pacemaker fires only when the patients heart rate falls
below the pacemakers preset rate. It senses the patients heart beat and fires only when
needed. These pacers can work in two ways:
1. rate - pacer rate is set at 70, if patients heart rate falls below 70 then pacer starts
pacing
2. timing intervals the pacemaker has a preset time set in milliseconds until the next Pwave or QRS is expected to come in. If the patients own P-wave or QRS does not
come in by that time, the pacemaker will fire. These are programmable pacers that can
have parameters set individually for the P-wave or QRS depending upon whether there
are pacing wires in the atria, ventricle, or both.
In addition to single chamber pacemakers (pacing wire is either in the atrium or the
ventricle) and dual chamber pacemakers (pacing wires are in both the atrium and the ventricle
and the device is able to pace both chambers), there is also something called a biventricular
pacer. With a biventricular pacer, there are pacing wires in the atrium and both left and right
ventricles. This type of pacemaker is indicated for those patients with moderate to severe heart
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failure and the goal is to synchronize the ventricles to beat together in a more organized
fashion. This is sometimes referred to resynchronization therapy.
Lt. Ventricular
wire
Atrial wire
Complications
Rt. Ventricular
wire
A. Pacemaker Failure
1. Failure to Capture
What will you see? Pacer spike noted not followed by a waveform. Patient
may experience bradycardia, hypotension, and fatigue.
What may be the cause?
Displacement of pacing lead wire
milliamps (mA) set too low
battery failure
fractured pacing lead wire
increased stimulation threshold due to medications ,electrolyte
imbalance, or increased fibrin formation on catheter tip
Nursing Action: - check connections (on temporary pacer)
- replace battery (on temporary pacer)
- increase the output or milliamps (on temporary pacer)
- turn patient on either side
- call doctor
- Atropine or Isoproterenol as needed
- CPR if needed
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Failure to capture
2. Failure to Sense (Undersensing fires when it should not)

What will you see? Pacemaker fails to sense the patients own underlying
rhythm and fires anyway. Pacer spikes will be seen at
inappropriate times (i.e. after the QRS or on T-wave).
Displacement of pacing lead wire
millivolts (mV) set too low
battery failure
increased sensing threshold due to medications, electrolyte
2. Failure to Sense (Undersensing) cont.

Nursing Action: - increase sensitivity (mV) (on temporary pacer)
- replace battery
- call doctor
Undersensing
(Notice the pacer spike found on the T-wave)
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3. Oversensing (Does not fire when it should)

What will you see? Pacemaker senses extraneous electrical signals (artifact, T
or P-waves, etc.) and thinks they are the patients underlying
rhythm, therefore it fails to fire when needed. The spikes
may come at a rate slower than the pacemakers preset rate
or be absent altogether.
millivolts (mV) set too high
battery failure
increased sensing threshold due to medications, electrolyte
Nursing Action: - increase sensitivity (mV) (on temporary pacer)
- replace battery
- call doctor
Oversensing
Wheres the spike?
Notice in the above strip there is a missing spike at the expected interval. The
pacemaker interpreted the blocked P-wave as conducting through to the ventricles so it
failed to fire.
4. Complications of specific methods

A. Transutaneous Pacing
a. Pain- if possible, medicate the patient
b. Tissue damage and burns with prolonged pacing- avoid any topical medications
or patches underneath pads and shave area where pads will be placed.
c. Loss of capture and pacing threshold changes- pads must be replaced
periodically if used continuously (check with manufacturer on frequency).
B. Temporary Transvenous Pacing
a. Bleeding, infection, pneumothorax, hematoma
b. Cellulitis, phlebitis
c. Dysrhythmias, lead displacement
d. Right ventricular perforation, cardiac tamponade
C. Permanent Pacing
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a. During insertion: bleeding, pneumothorax, dysrhythmias, air embolism,

thrombosis.
b. Long-term: infection, electrode displacement, heart failure, pacemaker induced
dysrhythmias, right ventricular perforation and/or cardiac tamponade
Routine Nursing Care

A. Dressing change per facility policy
B. Check insertion site for signs of infection
C. Document:
1. Rate, output setting (mA), sensitivity (mV) for temporary pacers
2. Permanent pacemaker settings (if known, i.e. VVI 60)
2. Rhythm strip documenting both paced rhythm and patients own rhythm if
possible (may need to pause the pacer or lower the rate to capture this).
3. Document the percent of time the patient has been in their own rhythm and paced
rhythm.
i.e. Pacemaker site clean and dry without
redness or swelling. Pacemaker rate
set at 70, mA 3.0, mV 1.5. Underlying sinus bradycardia rate 40,
ventricular paced 50% of time.
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Review of Pacemakers
Pacemakers are battery-operated, electronic devices with a pulse generator that delivers
an electrical stimulus to the heart. They consist of pacer wire electrodes placed in contact with
the endocardium, attached directly to the epicardium, or placed on the skin. These wires are
attached to a pulse generator that will deliver the electrical stimulus directly to the atrium,
ventricle, or both in order to cause a depolarization of the chamber. This electrical current will
depolarize or activate the heart at a predetermined rate or cycle.
Pacemakers are primarily used for bradydysrhythmias and the newer devices also have
antitachycardic functions. Pacemakers can be single chamber (ventricular) or dual chamber
(atrial and ventricular). Dual chamber pacemakers are hemodynamically more compatible with
the heart since the atrial kick is intact. Ventricular pacemakers originate from the ventricle and
generate a ventricular beat that is seen on the ECG as wide and bizarre.
Pacemakers can be temporary or permanent. Temporary pacemakers have a generator

box outside of the body, while permanent pacemakers have a generator placed under the skin.
Temporary pacing can be achieved through transcutaneous, transthoracic, or transvenous
methods. Permanent pacing can be accomplished transvenously through one of the subclavian
veins.
On the ECG, a pacer beat will show as a vertical spike. The spike can be up or down, but
must precede the chamber paced and capture the chamber producing a marked P-wave and/or
QRS complex. Pacemakers are classified according to the chamber paced.
Pacemakers can be demand or asynchronous (fixed rate). Fixed-rate pacers are rarely
used because of the danger of R-on-T phenomenon. Demand pacemakers are set to come in
on demand only. The pacemaker is set to come in either when the heart rate falls below a
preset limit or by timing intervals.
Pacemaker complications can occur because of improper placement, inappropriate voltage

to capture, or generator battery failure. A pacemaker that is not functioning properly can exhibit
failure to capture, undersensing, or oversensing.
Other complications can be infection,
pericarditis, ventricular perforation, or lethal dysrhythmias.
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References
Aehlert, B. (2006). EGCs Made Easy (3rd ed.). St. Louis: Mosby Elsevier.
American Heart Association. (2006). Advanced Cardiovascular Life Support Provider Manual.
SkillMasters (2003). Expert ECG Interpretation. Lippincott Williams & Wilkins.
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DYSRHYTHMIA INTERPRETATION & THERAPEUTIC MODALITIES

POST TEST
Choose the Single Best Answer for the Following and Place on the Answer Sheet Provided:
1. What is the main function of the heart?
a. To pump oxygenated blood to tissues and deoxygenated blood back to the lungs
b. To carry waste from the body to be excreted
c. To generate nerve impulses for skeletal muscle movement
d. All of the Above
2. Which of the following are components of cardiac output?

a. Contractility
b. Heart Rate
c. Stroke Volume
d. Both b & c
3. What effect does the parasympathetic nervous system have on the heart?
a. Increases heart rate
b. Increases force of contraction
c. No direct effect
d. Decreases heart rate
4. Preload refers to ______________.
a. The excitability of cardiac muscle cells
b. Volume returning to the heart
c. The resistance the heart has to pump against
d. The pressure gradients of the valves
5. Electrical stimulation of cells is ______________ and electrical relaxation of cells is
____________.
a. Preload, afterload
b. Automaticity, excitability
c. Depolarization, repolarization
d. Afterload, preload
6. Duration in seconds of one small box is _____ and voltage in millimeters of one small
box is _____.
a. 0.04 sec, 1 mm
b. 0.12 sec, 3 mm
c. 0.08 sec, 2 mm
d. 0.10 sec, 1 mm
7. Which of the following methods can be used to calculate heart rate on an ECG strip?
a. Count the number of R waves on a six second strip and multiply by 10
b. Count the number of small boxes between R-R intervals and divide by 1500
c. Count the number of large boxes between R-R intervals and divide by 150
d. Both a & b
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112
8. Measured from the beginning of the QRS to the end of the QRS.
a. PR interval
b. QRS duration
c. QT interval
d. ST segment
9. Measured from the beginning of the P wave to the beginning of the QRS.
a. PR interval
b. QRS duration
c. QT interval
d. ST segment
10. Which of the following are causes of artifact on an ECG?
a. 60 cycle interference
b. Muscle tremors
c. CPR
d. All of the above
11. Sinus rhythms originate in which area of the conduction system?
a. Purkinje system
b. SA node
c. AV junction
d. Atrial Tissues
12. What is one of the defining characteristics of sinus arrhythmia?
a. Irregular rhythm related to respirations
b. Heart rate <60
c. Failure of SA node to fire resulting in a disturbed P-P cycle
d. All of the above
13. Measure the PRI and QRS duration in the following strip:
a.
b.
c.
d.
PRI 0.12, QRS 0.08

PRI 0.14, QRS 0.12
PRI 0.20, QRS 0.06
PRI 0.24, QRS 0.18
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14. Analyze the following six second strip:
a.
b.
c.
d.
Sinus rhythm
Sinus bradycardia
Sinus tachycardia
Sinus block
a.
b.
c.
d.
Sinus rhythm
Sinus bradycardia
Sinus tachycardia
Sinus block
a.
b.
c.
d.
Sinus rhythm
Sinus bradycardia
Sinus tachycardia
Sinus block
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114
17. Atrial dysrhythmias will generally have a QRS that is:

a. Widened (>0.12)
b. Narrow (<0.12)
a. Absent
b. Narrow ( <0.24)
18. Atrial kick is:
a. The quivering of the atria that occurs with atrial fibrillation
b. When the atria contract
c. When the remaining 20-25% of blood is ejected into the ventricles
d. Both B & C
19. Identify the following strip:
a.
b.
c.
d.
Atrial fibrillation
Wandering atrial pacemaker
Sinus Rhythm with PAC
Atrial flutter
a.
b.
c.
d.
Multifocal atrial tachycardia

Atrial fibrillation
Sinus Rhythm with PACs
PSVT
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21. When giving Adenosine for stable atrial tachycardias:

a. The dose is 6 mg RAPID IV push, may repeat in 1-2 minutes at 12 mg RAPID IV
push
b. You should see transient asystole
c. You must follow each dose immediately with a 10-20 cc flush
d. All of the above
22. Identify the following rhythm:
a.
b.
c.
d.
Atrial fibrillation
Multifocal Atrial Tachycardia
Atrial flutter
PSVT
23. What classification of medications is given in atrial dysrhythmias to control rate?

a. Calcium channel blockers or beta blockers
b. Diuretics
c. Anticoagulants
d. Alpha adrenergics
a.
b.
c.
d.
Atrial flutter
Controlled atrial fibrillation
Sinus arrhythmia
Uncontrolled atrial fibrillation
25. Thrombus formation can occur with fibrillating atrium, therefore the patient must be on
what type of medication?
a. Calcium channel blockers or beta blockers
b. Diuretics
c. Anticoagulants
d. Alpha adrenergics
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26. What is the difference between Wandering Atrial Pacemaker (WAP) and Multifocal Atrial
Tachycardia (MAT)?
a. WAP has a ventricular rate <100 and MAT has a ventricular rate >100
b. WAP is a regular rhythm and MAT is irregular
c. WAP has a widened QRS (>0.12) and MAT has a narrow QRS
d. Nothing
27. What is the one distinction that junctional rhythms share?
a. inverted P wave before the QRS, buried in the QRS, or after the QRS
b. Wide QRS complex (>0.12)
c. Tachycardic rates
d. Originate in the ventricles
28. What is the difference between junctional rhythm, accelerated junctional rhythm and
junctional tachycardia?
a. The width of the QRS
b. The rate
c. The PR interval
d. Whether the P wave is inverted, buried, or after the QRS
29. Identify the following six second strip:
a.
b.
c.
d.
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Sinus rhythm with PJCs

Junction rhythm
Accelerated junctional rhythm
Junctional tachycardia
117
a.
b.
c.
d.
Junctional rhythm
Sinus rhythm with a junctional escape beat
Sinus rhythm with a pause
31. The treatment for junctional tachycardia:

a. Depends on the severity of symptoms
b. May include vagal maneuvers
c. May include giving beta-blockers or calcium channel blockers if no contraindication
exists
d. All of the above
a.
b.
c.
d.
Junctional rhythm
Junctional tachycardia
Sinus rhythm
33. Which of the following medications may cause a junctional tachycardia?

a. Amiodarone
b. Theophylline
c. Digoxin
d. Both B & C
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118
a.
b.
c.
d.
Sinus rhythm with PACs

Sinus rhythm with PJCs
Sinus rhythm with PVCs
35. What distinction do ventricular rhythms share?

a. Rates of less than 40
b. Wide and bizarre QRS complex (>0.12)
c. They are all fatal
d. Originate in the junctional area
36. Why are PVCs that occur more than 6 per minute, increasing in frequency, multifocal, or
occurring in pairs more dangerous than isolated PVCs?
a. Because they are harder to treat
b. Because they always indicate myocardial ischemia
c. Because they indicate ventricular irritability and an increased risk of developing a
more severe ventricular dysrhythmia
d. They are not any more dangerous
a.
b.
c.
d.

Idioventricular rhythm
Accelerated Idioventricular rhythm
Ventricular tachycardia
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119
a.
b.
c.
d.

Ventricular tachycardia
39. When treating the rhythm in question #38, you assess that the patient has a pulse but
appears to be asymptomatic. What would you expect to do next?
a.
b.
c.
d.
Immediate synchronized cardioversion

Give Amiodarone 150 mg over 10 minutes IV
Give Cardizem 10 mg/hr IV drip
Shock x 1 at 200J followed by 5 cycles of CPR
40. Now the patient with the rhythm in question #38 has lost his pulse. You have shocked
one time and have done 5 cycles of CPR. What drug and dosage would you expect to
give next?
a. Magnesium 1-2 gm IV/IO
b. Amiodarone 150 mg over 10 minutes IV
c. Amiodarone 300 mg IV/IO
d. Atropine 1 mg IV/IO
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120
a.
b.
c.
d.
Monomorphic Ventricular tachycardia

Torsades de Pointes
Ventricular fibrillation
42. Why would you not want to give Amiodarone to a patient with Torsades?
a. It can prolong the QT interval (thereby worsening Torsades)
b. It causes Amiodarone lung
c. It is too expensive
d. Because Amiodarone levels in Torsades are already high
43. Identify the following six second strip of a pulseless patient:
a.
b.
c.
d.
Sinus rhythm with PVC

Secondary ventricular standstill or agonal rhythm
Asystole
44. Which of the following is NOT a cause of PEA?

a. Tamponade
b. Drug overdose
c. Hypovolemia
d. Carotid artery stenosis
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45. What distinction is found with first-degree AV blocks?

a. Progressively lengthening PR interval
b. Wide and bizarre QRS complex (>0.12)
c. Constantly prolonged PR interval
d. Rapid heart rate
a.
b.
c.
d.
First-degree AV block
Second-degree AV block, type I
Second-degree AV block, type II
a.
b.
c.
d.
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48. The patient with the rhythm in question #47 has now started complaining of chest pain
and feeling dizzy. Their blood pressure is now 85/49. What would you expect to do
next?
a.
b.
c.
d.
Immediate synchronized cardioversion

Prepare for transcutaneous pacing
Administer Amiodarone 150mg over 10 minutes
Hope that a cardiologist comes
a.
b.
c.
d.
Second-degree AV block, 2:1 conduction
50. Which of the following blocks may progress to a third-degree AV block without warning
and should be monitored very closely?
a.
b.
c.
d.
Second-degree AV block, 2:1 conduction
51. Which two AV blocks have irregular R to R intervals?

a. First-degree and Second-degree, type I
b. First-degree and Third-degree
c. Second-degree, type I and Second-degree, type II
d. Third Degree and 2:1 block
52. Which medication would be given for symptomatic bradycardia?
a. Atropine
b. Amiodarone
c. Lopressor
d. Aspirin
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53. Which of the following is NOT an indication for pacemaker therapy?

a.
b.
c.
d.
Third-degree heart block

Symptomatic bradycardia
Sinus rhythm with first-degree AVB
Sick sinus syndrome
54. Of the following statements, which is INCORRECT about pacemaker spikes on an

ECG?
a.
b.
c.
d.
They appear vertical

May be positive or negative
Indicates depolarization of the chamber paced
May be seen before the P-wave or QRS
55. Capture is:

a. Indicative that depolarization of the chamber has occurred
b. When the patient has finally agreed to pacemaker insertion
c. Indicated by a pacer spike on the ECG
d. When the pacemaker generator fails to fire
56. When reading the patients chart, you note that they have a VVI pacemaker. This
means:
a. Atrium paced, Atrium sensed, response triggered by a sensed signal
b. Both chambers paced, both chambers sensed, response both inhibited and triggered
c. Ventricle paced, ventricle sensed, response inhibited by a sensed signal
d. Ventricle paced, atrium sensed, response triggered by a sensed signal
57. You are taking care of patient with a temporary pacemaker and you notice the following
on the monitor. What does this indicate?
a.
b.
c.
d.
Both atrium and ventricles are being paced normally

Undersensing
Loss of capture
Oversensing
Revised: 9/10
124
58. Based on the strip in #6, what action(s) would you possibly take?
a. Check all connections and battery
b. Increase the milliamps
c. Increase the millivolts
d. Both a and b
59. Which of the following would not be a possible complication of transcutaneous pacing?
a.
b.
c.
d.
Burns
Loss of capture and pacing threshold changes
Pain
Ventricular perforation
60. Documentation should include pacemaker rate and settings, output and sensitivity
settings (if temporary pacer), patients underlying rhythm and percentage of time in
paced rhythm.
a. True
b. False
Revised: 9/10
125
SELF STUDY MODULE ANSWER SHEET

TOPIC:
Dysrhythmia Interpretations & Therapeutic Modalities
13.0 CONTACT HOURS
CEP#08593
TO RECEIVE CREDIT FOR THIS MODULE:

A. Successfully complete examination (>80%)
B. Fill out evaluation form
C. Turn in this completed form by:
-Placing it in the return slot in the Self Study
Box at your facility (Contract Hospitals only)
-Mail it to: Flex Ed
3340 Riverside Dr., Suite F
Chino, CA 91710
A certificate will be sent to you, or to your

hospital, within four weeks.
We cannot accept faxed copies or photocopies
of this answer sheet.
Nevada CNA
LVN/LPN
RN
Behavioral Science
RCP
***All information below must be included to receive credit. ***

Name: ___________________________________ Telephone (
) ______________________
Address: _______________________________City __________________ Zip _________________

License Type (i.e. RN, RCP) ____________
License Number ______________________
* CA. CNAs are not eligible to receive credit for Self-Study Modules*
Last 4 digits of Social Security Number (for ID purposes only):_______ Employer: ______________________
Signature below verifies that you have completed this module yourself and the information given above is accurate.
Signature ___________________________________ Date Completed: _________

Dysrhythmia Interpretations & Therapeutic Modalities - Circle the Correct Response:
1. A B C D
11. A B C D
21. A B C D
31. A B C D
41. A B C D
51. A B C D
2. A B C D
12. A B C D
22. A B C D
32. A B C D
42. A B C D
52. A B C D
3. A B C D
13. A B C D
23. A B C D
33. A B C D
43. A B C D
53. A B C D
4. A B C D
14. A B C D
24. A B C D
34. A B C D
44. A B C D
54. A B C D
5. A B C D
15. A B C D
25. A B C D
35. A B C D
45. A B C D
55. A B C D
6. A B C D
16. A B C D
26. A B C D
36. A B C D
46. A B C D
56. A B C D
7. A B C D
17. A B C D
27. A B C D
37. A B C D
47. A B C D
57. A B C D
8. A B C D
18. A B C D
28. A B C D
38. A B C D
48. A B C D
58. A B C D
9. A B C D
19. A B C D
29. A B C D
39. A B C D
49. A B C D
59. A B C D
10. A B C D
20. A B C D
30. A B C D
40. A B C D
50. A B C D
60. True
False
EVALUATION OF MODULE
1.
2.
3.
4.
5.
6.
Poor
The content of this module was:
1
The module was easy to understand:
1
The objectives were clear:
1
This module applies to my work:
1
I learned something from this module:
1
Would you recommend this module to others?
2
2
2
2
2
3
3
3
3
3
4
4
4
4
4
5 6
5 6
5 6
5 6
5 6
Yes
Excellent
7 8 9 10
7 8 9 10
7 8 9 10
7 8 9 10
7 8 9 10
No
Comments:
Revised: 9/10
126

Dysrhythmia Interpretation Modules 1-6 June 2012

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Dysrhythmia Interpretation &

3340 Riverside Drive, Suite F

Things to keep in mind when submitting a FLEX ED Home Study

According to Flex Ed policies:

Dysrhythmia Interpretation & Therapeutic Modalities

Cardiovascular Structure and Function, Electrocardiography Monitoring,

Dysrhythmia Interpretation & Therapeutic Modalities

Module IV: Ventricular Rhythms

Premature Ventricular Complex/ Contraction (PVC)

g. Ventricular Escape beats

Accelerated Idioventricular Rhythm (AIVR)

Ventricular Tachycardia (VT)

Monomorphic VT vs. Polymorphic VT

Pulseless Electrical Activity (PEA)

m. Ventricular Standstill/ Agonal

Monomorphic VT vs. Polymorphic VT

g. Pulseless Electrical Activity (PEA)

Module V: Atrioventricular Blocks

Module I: Cardiovascular Structure and Function,

Important Terms- Cardiovascular Structure and Function

Affected by pressure and preload. What heart has to pump

The valve between the left ventricle and the aorta.

The bottom portion of the heart.

Smaller arteries located between arteries and capillaries.

A vessel carrying blood away from the heart. With the

The amount of blood contributed by atrial contraction into the

The area in the circulatory system where the exchange of

Hemodynamic calculation of heart rate X stroke volume.

Supply the heart muscle with oxygenated blood.

Venous blood is deoxygenated.

The relaxation phase of the cardiac cycle.

With oxygen. Arteries carry 95% or greater oxygen.

Part of the autonomic nervous system. Stimulation slows

Point of maximal impulse where the apical pulse can be

Amount of fluid coming into the ventricular chambers during

Carries deoxygenated blood from right ventricle to the

Carries oxygenated blood from the lungs to the left atrium.

Valve located between the right ventricle and the pulmonary

Located at the base of the aorta on top of the aortic valve.

Part of the autonomic nervous system. Stimulation increases

The contractile phase of the cardiac cycle.

Vessel carrying blood to the heart. Carries deoxygenated blood,

A smaller vein. Part of the circulatory system located

CARDIOVASCULAR STRUCTURE AND FUNCTION

small and controlled for release of blood into the capillaries.

collect deoxygenated blood from the capillaries.

Flow of Blood Through the Cardiovascular System

Right Coronary Artery

Left Anterior Descending

Anterior 2/3 of the Septum

Anterior Left Ventricle

Posterior Left Ventricle

Lateral Left Ventricle

Inferior Wall of the left ventricle

in one out of ten people

Posterior Portion of the Left

Position of the Heart

PMI is normally palpated at the 5th ICS,

Phases of the Cardiac Cycle

Review of Hemodynamic Parameters

C.O. cardiac output

How much blood is ejected by the heart each

CVP central venous pressure