Beruflich Dokumente
Kultur Dokumente
Therapeutic Modalities
Modules I-VI
Revised: 9/20/10
Students may not retake the same home study topic within 2 years of completion for
CEU credit.
California CNAs are ineligible to complete home studies for CEU credit.
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Table of Contents
Objectives
4-7
Modules I-VI
Module I
8 - 49
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
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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
1. Determine the etiology, identifying characteristics, significance and treatment for the following
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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j.
Torsades de Pointes
k. Ventricular Fibrillation
l.
f.
Torsades de Pointes
Ventricular Fibrillation
Asystole
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Aortic Valve
Apex
Arteriole
Artery
Atrial Kick
Capillary
Cardiac Output
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
Deoxygenated
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Diastole
Mitral Valve
The valve located between the left atrium and left ventricle.
Oxygenated
Parasympathetic
Nervous System
PMI
Preload
Pulmonary Artery
Pulmonary Vein
Pulmonic Valve
Sinus of Valsalva
Sympathetic
Nervous System
Systole
Tricuspid Valve
The valve located between the right atrium and right ventricle.
Vein
Venule
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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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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:
capillaries:
are the exchange point for nutrients, fluids, and other substances to the tissues.
venules:
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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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.
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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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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:
Left Circumflex
Right Atrium
Left Atrium
Right Ventricle
Sinoatrial Node
Atrioventricular Bundle
Apex
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As a result, not
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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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WHAT IS MEASURED
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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Excitability:
Conductivity:
Contractility:
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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
40 to 60 times/minute
20 to 40 times/minute
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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
**Enhances Automaticity
**Suppresses Automaticity
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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 ++
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.
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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.
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SA Node
60-100 bpm
Purkinje system
20-40 bpm
AV Junction
40-60 bpm
Important Terms
Antegrade conduction
Automaticity
Block
Re-entry
Retrograde conduction
Usurpation
Vagal stimulation
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.
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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.
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Acute MI
Artifact
Depolarization
Isoelectric line
J point
The location at the end of the QRS complex which indicates the
change from the QRS complex to the ST segment.
P wave
PR interval
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
S-T segment
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
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Somatic tremor
T wave
Time
U wave
Voltage
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.
J-point
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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 -
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 -
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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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:
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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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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.
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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.
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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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rr rr
r rrr
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
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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.
B.
4.
C.
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
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
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3 boxes = 100
4 boxes = 75
5 boxes = 60
6 boxes = 50
7 boxes = 43
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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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.
3.
4.
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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.
3.
4.
5.
6.
7.
8.
a.
b.
c.
d.
e.
9.
Search for any ectopic beats. Are the premature or escape beats?
10.
a.
b.
c.
d.
e.
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Sinus Rhythms
Aberrant Conduction
Asymptomatic
Bradycardia
Dysrhythmia
Etiology
Symptomatic
Tachycardia
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.
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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
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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
B. Identifying Characteristics
1. Rhythm - Regular
2. Rate - < 60 (40 59 is the most common)
3. P Waves - Normal in size and shape
4. P-R Interval - Normal (0.12 to 0.20 seconds)
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
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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.
B. Identifying Characteristics
1. Rhythm - Regular
2. Rate - 100 - 150 / min
3. P Waves - normal in size and shape
4. P-R Interval - Normal (0.12 to 0.20 seconds)
5. QRS Duration - Normal (< 0.12 seconds)
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.
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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)
B. Identifying Characteristics
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.
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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
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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.
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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
Flutter
Nonconducted
A area in heart fired, but did not progress through the conduction
system.
Paroxysmal
Premature
Occurring early.
Supraventricular
Occurring above the ventricle. Can include rhythms that are sinus, atrial,
and junctional.
Vagal maneuvers
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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
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.
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(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
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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.
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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
B. Identifying Characteristics
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.
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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.
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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
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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.
B. Identifying Characteristics
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.
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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
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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:
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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.
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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).
B. Identifying Characteristics
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.
5. QRS Duration - Normal (< 0.12 seconds)
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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).
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Escape Beat
Idiojunctional
Inverted
Retrograde Conduction
Compensatory Pause
Noncompensatory Pause
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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
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.
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b. Hidden in QRS
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B. Identifying Characteristics
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).
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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).
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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.
B. Identifying Characteristics
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.
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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.
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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
2. Digitalis toxicity
3. Acute MI
4. Theophylline administration
B. Identifying Characteristics
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.
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Accelerated - 60 to 100
74
Runs or Bursts
Bigeminy
Trigeminy
Unifocal
Coming from the same sight and having the same shape.
Multifocal
Monomorphic
Coming from the same sight and have the same morphology.
Polymorphic
Compensatory Pause
Opposite Polarity
R-on-T Phenomenon
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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
B. Identifying Characteristics
1. Rhythm appears irregular due to the premature beat, but underlying rhythm may be
regular
2. Rate - varies depending on underlying rhythm
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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
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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.
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
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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:
-
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
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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
ESCAPE BEAT
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)
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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.
2. If symptomatic, treat as a symptomatic bradycardia
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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.
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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.
B. Identifying Characteristics
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.
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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
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
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.
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.
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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.
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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.
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Dissociated
Not related to each other. For example, the P-waves do not have
any relation to the conduction of the QRS.
Transient
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3.
4.
5.
6.
M.I.
Digitalis toxicity
Ischemic diseases of the conduction system
Hyperkalemia
B. Identifying Characteristics
1. Rhythm - Regular
2. Rate - normal, bradycardia, or tachycardia
3. P wave - normal sinus P-wave
4. PR interval - constantly prolonged >0.20 seconds
5. QRS Duration - Normal (< 0.12 seconds)
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3. hypoxemia
4. increased vagal tone to the AV node
B. Identifying Characteristics
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
B. Identifying Characteristics
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.
5. QRS Duration - Normal (< 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. 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.
3. hypoxemia
4. increased vagal tone to the AV node
B. Identifying Characteristics
1. Rhythm - regular
2. Rate varies, but often slow
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D. Treatment
1. If treatment is necessary, use ACLS algorithm for symptomatic bradycardia (pacing).
3. digitalis toxicity
4. insult to the AV node
B. Identifying Characteristics
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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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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100
Fixed rate
Transcutaneous
Epicardial
Transvenous
Sensitivity
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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
Methods of Insertion
A.
B.
C.
D.
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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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103
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.
Revised: 9/10
104
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
Revised: 9/10
105
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
Undersensing
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Oversensing
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.
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109
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.
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.
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110
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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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
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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.
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113
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
Revised: 9/10
114
a.
b.
c.
d.
Atrial fibrillation
Wandering atrial pacemaker
Sinus Rhythm with PAC
Atrial flutter
a.
b.
c.
d.
Revised: 9/10
115
a.
b.
c.
d.
Atrial fibrillation
Multifocal Atrial Tachycardia
Atrial flutter
PSVT
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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a.
b.
c.
d.
Junctional rhythm
Sinus rhythm with a junctional escape beat
Accelerated junctional rhythm
Sinus rhythm with a pause
a.
b.
c.
d.
Junctional rhythm
Accelerated junctional rhythm
Junctional tachycardia
Sinus rhythm
Revised: 9/10
118
a.
b.
c.
d.
a.
b.
c.
d.
Revised: 9/10
119
a.
b.
c.
d.
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.
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.
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.
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121
a.
b.
c.
d.
First-degree AV block
Second-degree AV block, type I
Second-degree AV block, type II
Third-degree AV block
a.
b.
c.
d.
First-degree AV block
Second-degree AV block, type I
Second-degree AV block, type II
Third-degree AV block
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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.
a.
b.
c.
d.
First-degree AV block
Second-degree AV block, 2:1 conduction
Second-degree AV block, type II
Third-degree AV block
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.
First-degree AV block
Second-degree AV block, type I
Second-degree AV block, type II
Second-degree AV block, 2:1 conduction
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123
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.
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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
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CEP#08593
Nevada CNA
LVN/LPN
RN
Behavioral Science
RCP
) ______________________
* CA. CNAs are not eligible to receive credit for Self-Study Modules*
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Signature below verifies that you have completed this module yourself and the information given above is accurate.
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?
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2
2
2
2
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3
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4
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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
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