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5.8 Contact Hours

Rhythm Recognition:
Getting to the Heart of the Matter
By Susan Manifold, RN, MS, NP-BC

2014 Gannett Education

All Rights Reserved.



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The purpose of this course is to provide nurses with a step-by-step approach to rhythm analysis
and interpretation to enhance their ability to recognize and interpret cardiac dysrhythmias. After
studying the information presented here, you will be able to:
Describe the components of the cardiac conduction system, incorporating cardiac anatomy
and physiology
Interpret and analyze ECG strips and determine rate, regularity and rhythm
Identify rhythms originating in the sinus node and atria, atrioventricular (AV) node and
ventricles and discuss their significance and treatment
Recognize Type I, II and III AV blocks and discuss their significance and treatment
Identify potentially life-threatening rhythms and discuss initial interventions/approach to
Understand the relationship between coronary blood flow, myocardial infarction and
associated ECG findings

Gannett Education guarantees this educational activity is free from bias.

The planners and authors have declared no real or perceived conflicts of interest that relate to this
educational activity.


Susan Manifold, RN, MS, NP-BC, a nurse practitioner working at the Heart Center for Excellence
in Kalamazoo, Mich., updated this course in 2013. Manifold has more than 25 years of
experience in critical care and emergency nursing, having served in an educator role in those areas.
She has taught at the associate, diploma, undergraduate and graduate nursing levels. Manifold is
also a lecturer for national nurse practitioner meetings, ACLS AHA-certified, a member of the
Michigan Coalition for Nurse Practitioners and an associate member of the American College of


How to Take This Course ........................................................................................ 2

Goal and Objectives ................................................................................................ 3
About the Author .................................................................................................... 3
Introduction ............................................................................................................. 5
Chapter 1: Basic Physiology: The Cardiac Conduction Systems ............................. 7
Chapter 2: The Electrocardiogram .......................................................................... 15
Chapter 3: Sinus Rhythms ........................................................................................ 25
Chapter 4: Atrial Rhythms........................................................................................ 31
Chapter 5: Junctional (Nodal) Rhythms ................................................................... 41
Chapter 6: Ventricular Rhythms ............................................................................... 47
Chapter 7: Atrioventricular (AV) Blocks ................................................................... 55
Chapter 8: Myocardial Infarction and Coronary Vessels ......................................... 61
References ............................................................................................................... 67

...................................................................................................................... 69

Mrs. Smith has been admitted to the observation unit for evaluation of chest pain unrelieved by
nitroglycerin. Her risk factors include a premature family history of coronary artery disease,
diabetes, hypertension and tobacco abuse. After connecting her to an ECG monitor and running a
strip recording you notice unusual-looking beats. What are they? Are they dangerous or not?
Should you notify the physician, initiate emergency protocols or simply continue to monitor
closely? The answer lies within the information ahead.
ECG rhythm recognition and analysis continues to be a major nursing responsibility in the acute
care setting. Since the advent of bedside monitoring and coronary care units in the 1960s, the
ability to understand and interpret a bedside monitor is no longer an expectation of only critical
care and emergency nurses. Medical/surgical nurses need to be competent in ECG rhythm analysis
supported by the notable increased acuity of hospitalized patients requiring ECG monitoring.
ECG tracings can look unintelligible to the untrained eye. However, with an understanding of
basic cardiac physiology and practice, successful ECG interpretation is possible. Gaining
competence in ECG interpretation and rhythm recognition can assist the bedside nurse to
intervene efficiently and effectively in a potentially difficult clinical situation and, ultimately,
improve patient outcomes.

Chapter 1:

Basic Physiology:
The Cardiac Conduction System
Electrocardiographic (ECG) monitoring measures the hearts electrical activity and records it as
waveforms on paper. It is a visual representation of the electrical events in the heart that occur
with each contraction or heartbeat.
The hearts conduction system causes it to contract, resulting in blood flow throughout the body.
This process incorporates an electrical and mechanical event involving cardiac cells with unique
properties. Cardiac cells are of two types: conduction and contractile.1 The conduction cells result
in an electrical event; the contractile cells result in a mechanical event. The electrical event
precedes the mechanical event.
The conduction cells create and conduct electrical signals that stimulate the cardiac muscle to
contract. These cells comprise the sinoatrial (SA) node, also known as the sinus node, and the
atrioventricular (AV) node. These cells result in electrical activation of the myocardium (heart
muscle), which prompts myocardial contraction. Electrical activation is necessary before any heart
tissue can contract.
The contractile cells cause the heart muscle to contract and eject blood to the pulmonary and
systematic circulation. Collectively this process of electrical activation and myocardial contraction
is called a cardiac cycle.1

The Electrical Event

The SA node is a collection of cells within the right atrium of the heart that serves as the primary
pacemaker of the heart. (See Diagram 1.) The SA node remains predominantly under the influence
of the parasympathetic division of the autonomic nervous system, specifically the vagus nerve.
Stimulation of the vagus nerve slows the heart rate via its influence on the SA node. Conversely,
inhibition of the vagus nerve results in an increase or acceleration of heart rate. The sympathetic
division of the autonomic nervous system may also influence heart rate via the SA node due to a
release of stimulatory chemicals known as adrenergic agents or catecholamines, resulting in an
increase in heart rate.2
The conduction cells within the SA node are capable of spontaneously generating an electrical
impulse and thereby start the cardiac cycle by initiating contraction of the heart. This spontaneous
generation of an impulse is termed automaticity.2,3 The SA node cells control the rhythm of the
heart by retaining an automatic or inherent rate of 60 beats to 100 beats per minute (bpm).

Once the electrical impulse in initiated at the SA node, it is propagated through the right and left
atrium to the AV node. The AV node, another collection of conduction cells, is located near the
interatrial septum, or junction, as it is located between the right atrium and ventricle.
The AV node serves as a gatekeeper of impulses it receives, thereby providing a conduction delay
of the impulses it receives. This delay allows the atria to fill the ventricles prior to ventricular
systole. This contribution of blood to the ventricles, provided by the atria, is called atrial kick and
augments total cardiac output up to 30%.1-3 The AV nodes rate of automaticity, or inherent rate, is
40 bpm to 60 bpm and can function as a backup pacemaker if the SA node should fail.4
Diagram 1: Cardiac Conduction System/Pathway

From the AV node, the electrical impulse travels down both ventricles via the bundle of His, also
known as the atrioventricular (AV) bundle, located in the interventricular septum. The His bundle
divides into a right and left bundle branch extending to the Purkinje fibers. (See Diagram 2.) The
left bundle further divides into the left anterior and posterior fascicles. By this process, the
ventricles are activated and ventricular contraction (systole) follows. Ventricular tissues rate of
automaticity or inherent rate is 20 bpm to 40 bpm.3
This completes the electrical portion of the cardiac cycle.

Diagram 2: Complete Pathway of Cardiac Conduction

The Mechanical Event

The electrical events previously described precede and ultimately trigger mechanical events that
occur during each cardiac cycle. There are two phases of the cardiac cycle: systole and diastole.
Systole is the contraction of the ventricles resulting in expulsion of blood into the pulmonary
artery and aorta. Diastole is the filling of the ventricles with blood returning to the atria via the
inferior and superior vena cava and coronary sinus and pulmonary veins.3,4
The electrocardiogram is a visual representation of the electrical activity of the heart, which occurs
due to an exchange of electrically charged ions across the cardiac cell membrane. This exchange of
ions represents a process of depolarization and repolarization.
The resting cardiac conduction cells are polarized; that is, they are electrically negative on the
inside as compared with the outside. (See Diagram 3.) When the cells are stimulated by an
electrical impulse, sodium ions rush into the cells and potassium ions leak out, causing the cells to
become positively charged, or depolarized. (See Diagram 4.) Depolarization of the myocardium
results in myocardial contraction. Once myocardial contraction or systole is complete, ions shift
back to their original places and return the cell to its resting state. This is referred to as
repolarization and represents myocardial relaxation. Electrolytes (sodium, potassium, calcium and
magnesium) influence the process of depolarization and repolarization. Therefore, it is important
to monitor and maintain normal values of these ions.1-4

Diagrams 3 and 4: Polarization and Depolarization

ECG Waveforms and Complexes

The placement of electrodes on the skin transforms the electrical activity of the heart
(depolarization and repolarization) into waveforms and complexes representing the cardiac cycle.
These waveforms and complexes have normal characteristics and timings as follows:1-5
P wave: A small, upright, rounded wave representing atrial depolarization. Atrial contraction
PR interval: Measured from the beginning of the P wave to the beginning of the R wave of the
QRS complex. This interval represents the time it takes for the electrical impulse to pass from the
SA node through the complete cardiac conduction system. Normal PR interval time is between
0.12 and 0.20 seconds.
QRS complex: A tall, spiked waveform arising from the baseline that may be either upright or
inverted representing ventricular depolarization. The normal QRS complex, or ventricular
depolarization, is less than 0.12 seconds. A widened QRS complex may be due to a ventricular
dysrhythmia (Discussed in Chapter 6).
ST segment: The horizontal line between the end of the QRS complex and the beginning of the
T wave. It represents early ventricular repolarization. There are no parameters for timing but there
should be no elevation or depression from baseline. (If noted, it may be indicative of myocardial
ischemia or injury.)
T wave: An upright wave occurring after the QRS complex, representing ventricular
repolarization. Electrolytes and certain clinical conditions can alter its shape.
QT interval: Measured from the beginning of the Q wave to the end of the T wave. Represents
total ventricular depolarization and repolarization time, which should be less than half the time of
the preceding R-R interval (distance between two consecutive R waves of the QRS complex).

U wave: Not normally visualized. If present, it follows the T wave and represents late
repolarization of the ventricle or may indicate electrolyte imbalances.
Collectively, each P-QRS-T complex represents one heartbeat, or cardiac cycle. (Diagram 5) The
horizontal line between the T wave of one beat and the P wave of the next is a time of electrical
inactivity and is called the baseline or isoelectric line.
The atrial contraction on the ECG is manifested by the P-wave. Atrial muscle mass is small so the
electrical charge is small. All atrial dysrhythmias relate to the P wave.
The ventricular mass is larger and creates a bigger deflection on ECG. This is manifested by the
QRS complex. The QRS is altered in ventricular dysrhythmias. It may become wide or narrow.
Diagram 5: The Cardiac Cycle and ECG Complexes.


Diagram 6 ECG Waveforms/Complexes

Chapter Review
The electrical event initiated by the cardiac conduction cells precedes the mechanical event of
myocardial contraction, initiated by contractile cells.
The electrical event is initiated in the SA node, propagated through the atria to the AV node,
bundle of His and Purkinje fibers to the ventricles.
The two phases of the cardiac cycle are systole and diastole.
Electrical stimulation of the heart results in an exchange of ions across the cardiac cell membrane
and the initiation of cardiac depolarization and repolarization.
The waveforms and complexes reflective of depolarization and repolarization are the P wave, QRS
complex, T wave and U wave.
The P wave represents atrial depolarization.
The QRS complex represents ventricular depolarization.
The T wave represents ventricular repolarization.
Each P-QRS-T represents one cardiac cycle, or heartbeat.
Normal segments and intervals for P-QRS-T are:
P-R interval: 0.12 to 0.20 second
QRS complex: 0.06 to 0.12 second
QT interval: less than or equal to one-half the distance between successive R-R intervals


In the diagram below, note the PR interval, QRS complex and QT interval.



Chapter 2:

The Electrocardiogram
The wave of electrical impulses traveling via the SA node to the AV node to the bundle of His to
the bundle branches moves in a right-shoulder-to-left-foot direction (downward and to the left).
Electrodes, placed at various locations on the body, are sensors that pick up the hearts electrical
impulses and transform them into a recording on paper, called the electrocardiogram (ECG/EKG).
The electrodes are placed at specific locations across the chest, known as leads. These leads
provide 12 different views of the hearts electrical activity. The greater the number of leads, the
better the interpretation of the hearts electrical activity. The 12 leads include six standard leads
(the limb leads) that depict cardiac electrical events from six angles in the frontal or vertical
plane. Six additional leads (the chest leads) depict electrical events in the horizontal plane. The
limb leads are leads I, II, III, aVR, aVL and aVF. Leads I, II and III are also called bipolar because
they measure current traveling between a positive and negative pole.
Diagram 7: Limb Leads I, II and III

Lead I: Measures the current traveling between the right and left arms. The right arm is negative;
the left arm is positive.
Lead II: Measures the current traveling between the right arm and left leg. The right arm is
negative; the left leg is positive.
Lead III: Measures the current traveling between the left arm and the left leg. The left arm is
negative; the left leg is positive.
aVR, aVL and aVF are augmented leads, so named because they generate such small waveforms on
the ECG paper that the ECG machine must increase, or augment, the size of the waveforms so
they will be evident on the ECG paper. These leads are positive and unipolar, requiring only one
electrode to make the waveform.


aVR: Measures the current traveling toward the right arm. The electrode is on the right arm.
aVL: Measures the current traveling toward the left arm. The electrode is on the left arm.
aVF: Measures the current traveling toward the left leg. The electrode is on the left leg.
The chest leads (also called precordial) see the heart from the horizontal plane and are named V1,
V2, V3, V4, V5 and V6. (See Diagram 8)
They are located across the chest from the fourth intercostal space, right sternal border to the fifth
intercostal space, midaxillary line. These, like the augmented leads, are unipolar, each one being a
positive electrode.1
Diagram 8 Precordial Chest Lead Placement

Twelve-lead ECGs are used for the diagnosis and recognition of acute coronary syndrome in the
patient who presents to the hospital or clinic with the complaint of chest pain. Twelve-lead ECGs
are often done as well during physical exams and prior to surgery as part of routine health
screening and preoperative evaluation.2,3
Hospitalized patients may require continuous ECG monitoring, or telemetry, if they have a known
history of coronary artery disease or dysrhythmia (abnormal rhythm). These patients are attached
to either a three-lead or five-lead cable, which is then attached to a transmitter to allow continuous
observation of the hearts electrical activity, or ECG rhythm.
The two most common three-lead systems place electrodes on the chest to monitor the cardiac
cycle in Lead II and via a modified chest lead system (MCL-1). (See Diagram 8.) These systems are
used because they typically produce ECG waveforms and complexes that are upright, or positive
(rising above the baseline), thereby allowing for easier interpretation.


Diagram 9: MCL-1

Depicted in Diagram 9 is lead placement for MCL-1 (modified chest lead) with the positive
electrode in the V1 position and the negative electrode just below the left clavicle and adjacent to
the shoulder. The electrodes are connected to color-coded wires, which then are attached to the
monitoring system.
A five-lead system places electrodes on the chest in such a way to allow monitoring in both lead II
and MCL 1. (See Diagram 10.) Additionally, the chest leads (V1 through V6) may be monitored
by moving the chest lead into any of the V1 to V6 lead placement positions.
Diagram 10: 5-lead Monitoring System

ECG Paper
Recordings of ECG rhythms are recorded on small rolls of special paper measuring about 3 inches
wide and several hundred feet in length. A 12-lead ECG is done on 8-by-11- inch paper, using a
recorder that prints a simultaneous view of all 12 leads.


Diagram 11

The ECG paper is ruled into small boxes that are 1 millimeter (mm) in height and width. (See
Tracing 1.) Darker lines are present at every fifth block, horizontally and vertically. These occur
every 5 mm. There are five small boxes horizontally and vertically contained within the darker
lines, or large box. ECG waves and complexes are measured by counting these blocks horizontally
and vertically. Time intervals are determined by counting these boxes along the horizontal axis.
Horizontal counting measures time in seconds. Each small (1 mm) box represents 0.04 seconds.
Each large box, composed on the horizontal axis of five smaller boxes, represents 0.20 seconds
(0.04 seconds x 5 = 0.20 seconds.) Vertical counting measures amplitude, or height, of the
complexes and waves. Amplitude is measured in millimeters.2,3
Each small box measures 1 mm.
Each small box on the ECG paper measures 0.04 seconds.
One large box contains five small boxes.
One large box equals 0.20 seconds. (5 boxes X 0.04 seconds)
With ECG paper it is possible to determine heart rate and time intervals for electrical impulses to
travel from the atria to the ventricles (depolarization and repolarization) by counting and
measuring the boxes.


PR interval: Count the number of small boxes between the beginning of the P and the beginning
of the QRS. Multiply by 0.04 second.
QRS interval: Count the number of small boxes between the beginning and end of the QRS
complex. Multiply by 0.04 second.
QT interval: Count the number of small boxes between the beginning of the QRS and the end
of the T wave. Multiply by 0.04 second.

Approach to the ECG

There are many ways to read an ECG but each person has his or her own method. The aim is to
develop a systematic approach so that nothing is missed.
Developing a systematic approach to the interpretation of the ECG is a critical skill for all
clinicians. The following outlines one such approach.
1. Assess the rhythm of the heart: is it regular or irregular? When the rhythm is regular, the RR
interval or QRS complex is constant. This can be assessed by using calipers or markings on a piece
of paper and comparing successive waves.
2. Always check to see if there is a P wave before the QRS. This reveals if the rhythm is sinus.
Sometimes, the rate may be very fast and the P waves may not be visualized. The P wave shape is
generally smooth, not notched or peaked. P waves are usually upright.
3. Look for Q waves. Assessing for Q waves should be done to look for an acute myocardial
infarction and a patient history may help. It is important to know that small Q waves are normal in
leads III and aVF and in anterolateral leads aVL, l, V5 and V6. Q waves that are more than 1 mm
duration and greater than one-third of the R wave amplitude are considered pathological.
4. Look at the ST segment. Determine if the ST segment is elevated or depressed. ST segment
elevation may be an indication of acute myocardial infarction, angina, pericarditis, myocardial
ischemia or ventricular aneurysm. They may be slightly elevated in some leads over the heart
(precordial leads). The ST segment is almost never normally depressed greater than 0.5 mm in any
5. T wave is generally upright and in the same direction as the QRS complex. In some
asymptomatic adults, isolated T wave inversions may be normal.
6. Learn to measure the QT interval. This interval may be prolonged due to certain medications or
metabolic disorders. It must be corrected for heart rate because it is rate dependent. The QT
interval is usually less than or equal to 0.40 seconds for males and 0.44 seconds for females.


7. If there are dysrhythmias, are they ventricular or supraventricular (another term to describe
atrial dysrhythmias that arise above the AV node).

Determining Heart Rate

ECG is printed on a paper at a speed of 25 mm/second. This is standardized and 5 mm = 0.2
seconds or one large square. Therefore, five large squares represent one second. There are a
number of ways to determine the heart rate.
In method one, shown below, the ECG shows regular R waves. The successive R waves occur after
five large squares (which represents one second). Hence, there is one beat (R wave per second)
and this equals 60 beats per minute (BPM). The squares highlighted in red show the distance
from R-R wave.

In method 2, one can use the ECG grid to calculate heart rate. First, locate a QRS complex at the
beginning of a large square. Then locate the next QRS complex (see below).

If theres another QRS complex separated by one large box, the heart rate is 300 bpm (300/1).
If the QRS complex is separated by two large boxes, the heart rate is 150 bpm (300/2).
If the QRS is separated by three large boxes, the heart rate is 100 bpm (300/3).
If the QRS is separated by four boxes, the heart rate is 75 bpm (300/4) and so on. In the above
ECG, the next QRS complex occurs at the 5th box and hence the rate is 300/5=60 bpm.


Remember this is a rough estimate and depends on regular waves. Most digitally derived ECGs
obtain a reliable heart rate within 1% to 5% of the true heart rate (obtained by pulse
Yet another method to calculate heart rate is to count the number of QRS complexes in a sixsecond interval and multiply by 10.
Tracing 1

Practice: Intervals, Rhythm Patterns

Look at tracing 1 and determine the PR, QRS and QT intervals.
0.20 sec (5 boxes)
QRS: 0.06 sec (1.5 boxes)
QT: 0.32 sec (8 boxes)
In the tracing, the PR interval is normal in that it is between 0.12 and 0.20 seconds. PR intervals
are always calculated every time a rhythm strip is run.
The QRS duration is normal, as it is less than 0.12 seconds. A QRS interval longer than 0.12
seconds represents a delay in conduction time through the ventricle. Beats that originate in the
ventricles or at some point below the AV node always have a conduction time greater than 0.12
Finally, the QT interval is evaluated. This interval is less than or equal to one-half the distance
between successive QRS complexes for a heart rate between 60 and 100. This interval reflects the
depolarization-repolarization process. A prolongation of the interval may be noted during certain
types of drug therapy and increases the susceptibility for a more dangerous ventricular rhythm.3


Another important factor in analyzing ECG tracings is to determine the regularity of the rate. This
refers to the pattern of the recording.
Find an R wave that lies on a darker vertical line and counting to the next consecutive R wave, use
the following sequence of numbers to determine heart rate: 300, 150, 100, 75, 60, 50, 40, 30.
The number sequence changes each time a darker vertical line is encountered. Using Tracing 2,
look at the sixth QRS complex. This complex lies on a darkened vertical line. Counting from this
line to the next darkened vertical line and then to the next nearest QRS complex, you would count:
300, then 150 when you run into the next consecutive R wave. The heart rate is 150 bpm. This is
an approximation only, and in most instances, turns out to be quite accurate.
Tracing 2
Six Second Interval

Calculate the heart rate by counting the number of QRS complexes in the six-second interval
indicated above.
Answer: 80 bpm, as there are eight complexes in the six-second interval; multiply by 10 = 80

A systematic approach to ECG analysis is important. In summary, you should be evaluating:
The waveforms and complexes: P, QRS, T and U (if present)
Intervals and segments: PR interval, QRS complex, ST segment, QT interval.
Heart rate

Chapter Review
The electrocardiogram is a recording of the hearts electrical activity and impulses. The 12-lead
ECG provides 12 different views of the hearts electrical activity and consists of limb and chest
Hospitalized patients requiring ECG monitoring are usually attached to a three- or five-lead cable,
which allows for ECG waveforms and complexes that are easier to interpret.


Leads II and MCL-1 are the two monitoring systems primarily used among hospitalized patients
connected to telemetry.
ECG paper is standardized so that one small box on the horizontal plane is 0.04 second and a
large box of five small boxes is 0.20 second.
There are various ways to calculate the heart rate from an ECG tracing:
Dividing 1,500 by the number of small boxes (from R wave to R wave).
Finding an R wave that lies on a darkened vertical line and counting a succession of
numbers: 300, 150, 100, 75, 60, 50, 40 each time a darkened vertical line is encountered;
with the rate being the number associated with the next R wave reached.
Counting the number of QRS complexes in a six-second interval and multiplying by 10.
Using the ECG strip recording below, calculate the heart rate using any of the methods above.
6-second interval

Heart rate: 40: The sinus beat circled lies beyond the six-second interval hash mark at the top of
the ECG strip recording.
6-second interval

Heart rate: 130




Sinus Rhythms
Normal Sinus Rhythm
Normal sinus rhythm is a rhythm that originates from the SA (sinoatrial) node, follows the normal
conduction pathway, is regular and has a rate between 60 to 100 beats per minute. (See Tracing
Under normal circumstances, the electrical stimulus that initiates the cardiac cycle begins in the SA
node and proceeds to the AV node and then down both ventricles via the bundle of His and
Purkinje fibers system. Because the stimulus originates above the ventricles in the SA node, it is
called supraventricular, or above the ventricles. This is the normal response depicted on the ECG
as the P wave and reflects atrial depolarization followed by atrial contraction.
The first step in analyzing an ECG strip should include an analysis of waveforms and complexes.
A P wave should precede each QRS complex and be followed by a T wave. This represents normal
conduction through the heart. Ultimately, with a normal-appearing QRS (with a duration of less
than 0.12 second) and a normal-appearing P wave and PR interval (0.12-0.20 second), it can be
assumed that the conduction from the SA to the AV node and bundle of His is normal; that is,
without any delays or abnormal electrical impulses arising from another electrical focus, or
location within the heart.
Tracing 3: Normal Sinus Rhythm

After looking at the waveforms and intervals, determine the regularity of the rhythm and rate. In
normal sinus rhythm, the rhythm is regular and the atrial and ventricular rates are the same. The
rhythm is described as normal sinus rhythm (NSR) under the following circumstances: (a) The
impulse arises from the SA node and passes through the normal conduction pathway, indicated by
normal appearing waves; (b) There is a normal PR interval; (c) There are normal QRS
configurations; and (d) The heart rate is between 60 bpm to 100 bpm.1
Each rhythm should be evaluated incorporating the following points:
Is the rhythm regular?
What is the atrial and ventricular rate?


Are P waves present?

Are the P waves of normal shape (rounded and upright)?
Is there a P wave preceding each QRS?
What is the duration of the PR interval?
What is the duration of the QRS interval?
Are T waves present of normal shape (rounded and upright)?

Sinus Dysrhythmia
An ECG rhythm not fitting the criteria for NSR is referred to as a dysrhythmia; it is also sometimes
called an arrhythmia, although technically this term is inaccurate, as arrhythmia literally
translates to without rhythm (at all).
The rhythms listed below refer to those originating from an impulse arising from the SA node, the
normal pacemaker of the heart. They do not qualify as NSR, however, because the rhythm, or rate,
is not within defined normal limits as described above.1-3

Sinus dysrhythmia

Sinus bradycardia

Sinus tachycardia

Sinus arrest
A description of each with additional details follows.
Sinus dysrhythmia: A rhythm initiated by the SA node at an irregular rate. Each beat follows the
normal conduction system. (See Tracing 4.) Sometimes the dysrhythmia is cyclical in nature,
corresponding with inspiration and expiration. This may be a normal finding in some people. The
rate may vary (slow, normal, fast).
There are usually no symptoms noted unless the rhythm is associated with a sinus bradycardia or
tachycardia (discussed below) with the treatments corresponding with each.1,3
Tracing 4: Sinus Arrhythmia

Sinus bradycardia: A rhythm that originates in the SA node (P wave preceding each QRS with
normal P-R interval) with a rate less than 60 bpm. (See Tracing 5.) Well-conditioned athletes


frequently have sinus bradycardia. Some medications (e.g., beta-blockers, digoxin, calcium channel
blockers, antiarrhythmics) will decrease the heart rate. It is important to evaluate whether the
patient with sinus bradycardia tolerates the rhythm. This is determined by noting the patients
state of hemodynamics (blood pressure) and level of consciousness. If the rate is too slow to
maintain an effective cardiac output, the blood pressure will fall below normal and the patient may
feel faint or light-headed. This is an example of the patient not tolerating the rhythm.
Tracing 5: Sinus Bradycardia

Quick Check: Sinus Bradycardia

Ventricular Rate
Atrial Rate
P wave
PR interval
QRS complex

Same as ventricular
Normal 0.12 to 2 sec
Normal <0.12 sec


Based on ACLS guidelines, when a patient demonstrates signs and symptoms of poor perfusion
caused by sinus bradycardia, such as altered mental status, light headedness, chest pain or
hypotension, atropine should be given.6 If atropine is ineffective, then IV infusion of betaadrenergic agonists with rate-accelerating effects (dopamine, epinephrine) or TCP can be effective.
Physician consultation should occur for further direction, which may include preparation for
temporary or permanent transvenous pacemaker insertion.
Because the heart rate is influenced by the vagus nerve, which causes slowing of the heart rate,
anything that stimulates this nerve may result in sinus bradycardia. Examples of conditions that
stimulate the vagus nerve include vomiting and pain. When the heart rate drops with these
conditions, it is called a vagal response. When this response or state of bradycardia is sustained
and results in a change in hemodynamics and level of consciousness, it should be treated with the
administration of atropine 0.5 mg IV push.6 The expected result is an increase in heart rate back to
normal (60 bpm to 100 bpm) and normalization of blood pressure and level of consciousness.
Sinus tachycardia: A rhythm that originates within the SA node (P wave preceding each QRS with
normal P-R interval), with a rate greater than 100 bpm, rarely exceeding 180 bpm.1 (See Tracing
6.) As with sinus bradycardia, it is important to determine how the patient tolerates this rhythm.
Elevated heart rates can result in hemodynamic compromise (decreased blood pressure), lightheadedness or chest pain, because of inadequate time for cardiac filling during diastole.
Inadequate filling results in decreased cardiac output and subsequent decreased tissue and organ

perfusion. Patients with a history of heart disease may become symptomatic at lower rates than
those with no pre-existing cardiac history.
Many conditions of noncardiac origin can cause sinus tachycardia: exercise (normal physiological
response), pain, anxiety, fever, hypoxemia, hyperthyroidism and hypovolemia. Therefore,
correction of the possible cause should be considered and may be all that is indicated for
treatment and stabilization.
Tracing 6: Sinus Tachycardia

Quick Check: Sinus Tachycardia

Atrial rate
P wave
PR interval
QRS complex

>100 to 180
Same as ventricular
Normal 0.12 to 0.20sec
Normal <0.12 sec


Sinus arrest/block: This dysrhythmia occurs when the SA node fires its impulse on time, but the
impulse exiting from the SA node to the atrial tissue is blocked. (See Tracing 7.) The beat that the
sinus node initiated is not conducted. The result is that one or more cardiac cycles (P-QRS-T) are
missing as if dropped. It is not a dominant or sustained rhythm, as sinus dysrhythmia, bradycardia,
or tachycardia can be. The underlying rhythm is usually very regular.
This rhythm may occur in response to vagal stimulation (e.g., nausea, pain, fear, hypoxia) coronary
artery disease (CAD), cardiomyopathy or as a side effect of medication (calcium channel blockers,
beta-blockers, digitalis are common culprits).1-3
Tracing 7: Sinus Arrest/Block


Quick Check: Sinus Arrest/Block

Ventricular Rate
Atrial Rate
P wave
PR interval

Same as ventricular
Normal except for
period of sinus arrest
Normal (when P wave is

Regular except for pause
Regular except for pause

Regular except for pause

Note on Tracing 7 that the dominant rhythm is NSR, but a pause is evident. If you mark out the
RR intervals, you will note that exactly one QRS is missing during this time of sinus arrest/block.
In fact, exactly two RR cycles will fit into the pause. In this dysrhythmia, the pause always results
in a multiple of the previous RR intervals.
As with sinus bradycardia and tachycardia, the patient should be evaluated for symptoms of
decreased perfusion such as blood pressure drop, lightheadedness or chest pain. Recurrent and
prolonged pauses will require action. Either alleviate or remove the possible cause or administer
atropine to increase the heart rate.6 As with sinus bradycardia, a temporary or permanent
pacemaker may be considered should the patient remain symptomatic or with unstable vital signs.

Chapter Review
Normal sinus rhythm is a rhythm that originates from the SA node, follows the normal conduction
pathway, is regular and has a rate between 60 and 100 bpm.
Sinus dysrhythmias are rhythms that originate from the sinus node and include sinus dysrhythmia,
bradycardia, tachycardia and sinus arrest/block.
Sinus dysrhythmia is an irregular rhythm arising from the SA node that often corresponds with
inspiration and expiration and is a normal finding in some people.
Sinus bradycardia is a regular rhythm arising from the SA node with a rate less than 60 that may
be induced by vagal stimulation.
Sinus tachycardia is a regular rhythm arising from the SA node with a rate above 100.
Sinus arrest/block is a pause that occurs when the initiation of a SA node impulse is blocked,
resulting in a missed cardiac cycle (P-QRS-T).


Label the following rhythm strips as:

Normal sinus rhythm
Sinus dysrhythmia
Sinus bradycardia
Sinus tachycardia
Sinus arrest

Answer: Sinus dysrhythmia

Answer: normal sinus rhythm

Answer: Sinus bradycardia



Atrial Rhythms
Atrial Dysrhythmias
Atrial dysrhythmias are initiated in the atrial tissue of the heart at a site outside of the normal
pacemaker, the SA node. An abnormal or ectopic focus generates the impulse that is propagated
down the conduction system. The ectopic atrial focus may fire rapidly, usurping or overriding the
sinus node. As a result, atrial rhythms often result in elevated heart rates and patients are usually
symptomatic.1-4 Atrial dysrhythmias to be discussed include:
Atrial fibrillation
Atrial flutter
Premature atrial contractions, multifocal atrial contractions
Atrial tachycardia
Wandering atrial pacemaker
Atrial fibrillation (AF): As the name implies, the atria are fibrillating, or quivering, firing hundreds
of impulses from different locations at the same time. In this rhythm, atrial rates can be as high as
350 bpm to 700 bpm. The quivering atria contract inefficiently, resulting in a reduced filling of
blood into the ventricle. The AV node, usually a gatekeeper or filter of electrical impulses it
receives from the SA node, is bombarded with impulses and cannot depolarize fast enough to let
all of the impulses through. When one of the impulses does get conducted through, it is
propagated normally, generally producing normal-appearing QRS complexes. This rhythm may be
sustained or intermittent.
One of the distinguishing features of atrial fibrillation is the marked irregularity of the ventricular
response.3 The ventricular rate will depend on the degree of blockade (of impulses) at the AV node.
Nomenclature often reflects rate-related severity. For example, AF with a controlled ventricular
response implies that the ventricular rate is normal: between 60 bpm and 100 bpm. A ventricular
rate greater than 100 bpm is called rapid atrial fibrillation. AF with a ventricular rate greater than
150 bpm is said to be uncontrolled. AF with ventricular rates less than 60 bpm is called slow
atrial fibrillation. The QRS could potentially be wider than normal if there is delayed conduction
of the impulse though the ventricle as is seen with a bundle branch block (BBB) or intraventricular
conduction defect.2 This rhythm may be either sustained or intermittent.
Two criteria aid in the diagnosis of AF: the ventricular rate is irregularly irregular, and a P wave is
not discernable. Because there are no P waves, there is no PR interval.
Two serious hemodynamic problems may arise with AF. First, it causes a drop in cardiac output
because of the loss of effective and synchronous atrial contraction (atrial kick). Atrial contraction
contributes up to 30% to overall cardiac output.1-3 Loss of atrial kick may result in dizziness,
lightheadedness, fatigue, shortness of breath or syncope because of a subsequent drop in cardiac
output and blood pressure.


A second problem is an increased threat of blood clots, as the blood in the atria is allowed to pool
when the atria are fibrillating rather than contracting completely. Pooled blood may form clots and
precipitate MI, stroke or pulmonary embolism. As a result, many patients with AF are
anticoagulated with warfarin unless the potential risks of anticoagulation would outweigh the risks
of untoward bleeding.7 (Level ML) The decision for anticoagulation is individually determined for each
person with AF.
The 2011 guideline update for AF advises the clinician on use of the addition of clopidogrel to
aspirin therapy for those patients unable to tolerate warfarin or comply with the required testing
associated with this medication.7
Dabigatran (Pradaxa), a direct thrombin inhibitor, is a therapeutic option to anticoagulate an
individual in nonvalvular atrial fibrillation to prevent strokes that could result from systemic
emboli formation (in lieu of warfarin).8 (Level ML)
Rivaroxaban (Xarelto) is a Factor XA inhibitor found to be noninferior to warfarin for the
prevention of stroke in patients with nonvalvular atrial fibrillation and is yet another therapeutic
option to be used in place of warfarin among patients with atrial fibrillation.8 (Level ML)
For all anticoagulants, the most worrisome complication is bleeding. Close monitoring and patient
education are therefore crucial in addition to appropriate patient selection for these drugs. Most
certainly the estimated benefit of anticoagulation must outweigh any and all risks associated with
their use.
Detailed prescribing information is available at the National Library of Medicine, which maintains
a drug information portal with additional information from the U.S. Food and Drug
Tracing 8: Atrial Fibrillation

Tracing 9a
Atrial Fibrillation With Controlled Ventricular Response


Tracing 9b
Rapid Atrial Fibrillation

Quick Check: Atrial Fibrillation

Ventricular Rate
Atrial rate
P wave
PR interval
QRS complex

60 to 100 if controlled
Normal or widened if BBB

Irregularly irregular
Irregular, fibrillatory

Some of the clinical conditions associated with atrial fibrillation include COPD, pneumonia,
valvular heart disease, pericarditis, acute illness, hypoxia, digitalis toxicity, hyperthyroidism,
coronary artery disease and pulmonary embolism. Atrial fibrillation occurs more frequently in
older patients (> age 65) and in association with increased sympathetic nervous system activity.
The treatment objectives for atrial fibrillation consist of ventricular rate and rhythm control.2
Medications such as digitalis, beta-blockers, calcium channel blockers and antiarrhythmics may be
used. Antiarrhythmic agents, such as propafenone (Rhythmol), flecainide (Tambocor), ibutilide
(Corvert), dofetilide (Tikosyn), sotalol (Betapace), amiodarone (Pacerone) and dronederone
(Multaq) may be used to convert the rhythm back to NSR (or used selectively to maintain NSR).
Electrical cardioversion, AV node ablation or pacing can be done if the medications do not control
the rhythm and the patient is hemodynamically unstable or symptomatic (e.g., dizzy or short of
Droneradone (Multaq) is the newest antiarrhythmic agent, which is used in treatment of
paroxysmal atrial fibrillation or after conversion of persistent atrial fibrillation to normal sinus
rhythm. The 2011 guidelines on atrial fibrillation caution against using droneradone for patients
with Class IV (severe) heart failure or a recent episode of decompensated heart failure in the past
Atrial flutter: This dysrhythmia results when one single ectopic focus in the atrium fires regularly at
a rapid rate, producing fluttery or sawtooth P waves. The ectopic focus supersedes the SA node
and predominates. Atrial flutter results from a re-entrant circuit with circular activation most often
in the right atrium near the tricuspid valve.2


Tracing 10: Atrial Flutter

The flutter or sawtooth-shaped waves signaling atrial depolarization may occur at a rate in excess
of 250 bpm. This rate is too fast for the AV node to depolarize, so many of the impulses never get
through to the ventricle. The ventricular rate may range from 60 bpm to 180 bpm, depending on
the degree of AV node blockage. The ventricular rhythm may be regular or irregular, depending on
the degree of AV blockage.
There may be two, three, four or more flutter waves before the QRS. If ventricular depolarization
follows regularly at set intervals, the rhythm will be regular. (See Tracing 10.) Depending on the
number of P waves preceding the QRS, the rhythm may be denoted as a ratio; e.g., 3:1 response if
there are three P waves for each QRS complex. The P waves march out regularly, with one often
being buried in (hidden within) the QRS. As with atrial fibrillation, the QRS could potentially be
wider than normal if there is delayed conduction of the impulse through the ventricle, as is seen
with a bundle branch block or intraventricular conduction defect.2
Less commonly, there may be an irregular response from the ventricle. The number of flutter waves
before each QRS will vary. This would be called atrial flutter with variable ventricular response.
(See Tracing 11.)
Tracing 11: Atrial Flutter with Variable Ventricular Response

Quick Check: Atrial Flutter


Ventricular Rate
Depends on AV block
QRS complex
Normal or widened
Atrial Rate
Very rapid, up to >300 Regular
P wave
Sawtooth, flutter-like
PRI (PR interval)
*A variable atrial flutter will cause the rhythm to become irregular


Clinical conditions that may cause atrial flutter include any condition that results in an
enlargement of the atrial chamber and an increase in atrial pressure.2 Clinical conditions
associated with AF may also result in the development of atrial flutter; e.g., COPD, pneumonia,
hypoxia, valvular heart disease, hyperthyroidism, CAD, pericarditis, digitalis toxicity and cardiac
This dysrhythmia is more rare and potentially more unstable and serious than atrial fibrillation. If
the AV node does not block out a controlled number of impulses, ventricular rates in excess of
250/min are possible, resulting in symptoms associated with decreased cardiac output.
As with atrial fibrillation, the treatment of this dysrhythmia consists of administering rate- or
rhythm-controlling drugs. If the patient is hemodynamically unstable, synchronized cardioversion
should be administered immediately.2-4
Premature atrial contraction (PAC): A premature atrial contraction is a single beat that is
prematurely conducted by an irritable focus within the atrium. (See Tracing 12.) It arises before
the regular beat arising from the SA node is due. This premature beat produces a P wave that
varies in shape from that obtained with normal atrial depolarization arising from the SA node. It
is followed by a normal-appearing QRS as the impulse follows down the same conduction
pathway once it reaches the AV node. Theres often a pause that follows the QRS of a premature
atrial contraction that occurs as the sinus nodes resets itself, or repolarizes, in preparation for the
next electrical impulse.
Tracing 12

PACs often occur in response to stimulation or irritability of the atrial tissue caused by caffeine,
amphetamines, ephedrine or tobacco. Increased sympathetic nervous system activity stimulation
(e.g., fear, excitement, anxiety) or an electrolyte abnormality may also result in a PAC. They may
signal impending heart failure, ischemia, hyperthyroidism or hypoxia. The treatment is to avoid
stimulants and treat or avoid the underlying cause. Often, PACs are benign, representing no
pathology and presenting no hemodynamic compromise; therefore, requiring no treatment.
Medications such as beta-blockers or calcium channel blockers may be used if a person is
symptomatic with the PACs.1-3


Quick Check: Premature Atrial Contraction

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)

Same as ventricular
Varies from sinus P wave
Varies from sinus PRI


Atrial tachycardia (AT): This dysrhythmia often starts and stops suddenly and is designated as
paroxysmal (paroxysmal atrial tachycardia or PAT; or supraventricular tachycardia or SVT). (See
Tracing 13.) This rhythm is distinctive in that it occurs suddenly and is self-limiting. It occurs from
a burst of three or more PACs in a row that resets the pacemaker of the heart to a rhythm that is
much faster than normal. Once the impulse is conducted through the AV node, it follows a normal
conduction through the ventricle. The QRS is of normal appearance and duration unless there is
abnormal conduction through the ventricle. Heart rates may range from 150 to 250 bpm. The P
wave associated with the PAC varies from that associated with the normal sinus rhythm.
The ratio of P waves to QRS complexes is 1:1. The P wave may be difficult to detect due to the
rapid rate and as it may be hidden within the previous ST segment or T wave. The PRI may be
indiscernible as a result.
Tracing 13: Atrial Tachycardia

This dysrhythmia may result in hemodynamic instability, because the ventricles are not allowed to
fill and empty adequately due to the rapid rate. Cardiac output, therefore, drops, resulting in a
corresponding fall in blood pressure and symptoms of syncope/lightheadedness. The longer the
rhythm is sustained, the greater the possibility for hemodynamic compromise and symptoms.
Increased irritability or stimulation of the atria caused by caffeine or increased CNS stimulation
(fear, excitement, anxiety) may precipitate this dysrhythmia. Other causes may signal more serious
disorders such as digitalis toxicity (most common), hyperthyroidism, CAD, heart failure, electrolyte
imbalances, hypoxia or COPD.2
Young, healthy people can tolerate this rhythm without symptoms, but those with heart disease
may develop symptoms rapidly.


Quick Check: Atrial Tachycardia

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)


150 to 250
Normal or widened
Same as ventricular
Variable if seen
Variable if seen


To treat this rhythm, vagal maneuvers intended to stimulate the parasympathetic system may be
initially tried, such as having the patient cough or bear down (Valsalva maneuver). If these do not
work, medications may be used to interrupt the rhythm. Adenosine (Adenocard) is the primary
drug of choice for treatment of this dysrhythmia. Adenosine, a naturally occurring nucleoside, acts
on the AV node to slow conduction and inhibit re-entry pathways. It is given as a 6 mg IV bolus
rapidly (over one to three seconds) followed by a saline bolus of 10 mL to 20 mL. Another 12 mg
may be administered if the dysrhythmia is not eliminated in one to two minutes.6 Adverse
reactions include asystole (complete lack of electrical activity) and hypotension, but these are
usually very transient and self-limiting due to the short half-life of adenosine, less than 10 seconds.
Other medications that may be used include digoxin, intravenous calcium channel blockers or
beta-blockers. If medication-induced conversion of this rhythm does not work, electrical
cardioversion may be done if the rhythm persists with hemodynamic compromise and symptoms.
Wandering atrial pacemaker (WAP): This dysrhythmia occurs when multiple foci within the atria
depolarize, resulting in cardiac conduction. (See Tracing 14) The foci wander from different sites
in the atria, creating variable P wave configurations, usually three or more different P wave
morphologies, and PR intervals. This rhythm is often intermittent, alternating with normal sinus
Due to variations in the location of initiation of the beat, the shape of the P wave and PR interval
may vary from beat to beat.
Tracing 14: Wandering Atrial Pacemaker

Used with permission of Frank G. Yanowitz, MD, the ECG Learning Center and Intermountain Healthcare.

Once the stimulus passes through the AV node, it is conducted normally through the ventricle,
producing normal and uniform-appearing QRS waves. Wandering atrial pacemaker may be

mistakenly diagnosed as AF due to the irregular nature of the rhythm. Heart rates may range from
60 bpm to 100 bpm and in some cases may be bradycardic.2,3
When the ventricular rate is above 100 bpm, this dysrhythmia is referred to as multifocal atrial
tachycardia or MAT and is often seen among people with severe COPD.

Quick Check: Wandering Atrial Pacemaker

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)
*Rates >100 for MAT


60 to 100, may be
Same as ventricular


This rhythm may be seen in healthy people during sleep or in athletes.1

Wandering atrial pacemaker may be caused by side effects from medications that may affect serum
electrolytes, such as diuretics; it can also be caused by hypoxia, vagal stimulation or MI. It is often
associated with no symptoms. If the heart rate slows too much, a person could experience
symptoms of decreased cardiac output such as weakness or fatigue.2
Treatment is based on determining and treating the underlying cause. In people with no preexisting cardiac disease and without symptoms, nothing other than surveillance for symptoms may
be necessary.
Tracing 15: Multifocal Atrial Tachycardia


Chapter Review
Atrial dysrhythmias include atrial fibrillation, atrial flutter, premature atrial contractions, atrial
tachycardia and wandering atrial pacemaker.
Atrial fibrillation is typically irregularly irregular and may result in a drop in cardiac output because
of loss of atrial kick.
Atrial flutter may result in a variable ventricular response and is associated with characteristic
flutter, or sawtooth-shaped P waves.
Premature atrial contractions refer to a premature beat arising from an irritable focus within the
atrium. They are often benign and may result from CNS stimulation or stimulating medications or
Paroxysmal atrial tachycardia starts and stops suddenly, precipitated by a PAC and resulting in
hemodynamic compromise if it is sustained or the patient's pre-existing clinical condition is
compromised. Heart rates may range from 150 bpm to 250 bpm.
WAP and MAT differ with respect to rate. Treatment depends on symptom presentation.
List the following rhythm strips as
Atrial fibrillation
Atrial flutter
Premature atrial contractions
Paroxysmal atrial tachycardia
Wandering atrial pacemaker

Answer: Atrial Flutter


Answer: Atrial fibrillation

Answer: Sinus rhythm with PAC



Junctional (Nodal) Rhythms

Junctional rhythms come from an impulse that arises in the area surrounding the AV node at the
AV junction and include the bundle of His. They are also referred to as nodal rhythms and may
arise when the SA node fails or is suppressed. Depending on where in the AV junction the impulse
originates (high, mid or low region), the P wave will be inverted, buried or follow the QRS.1-3
For example, an electrical impulse may spread backward (retrograde) into the atria, resulting in an
inverted P wave, or forward (antegrade), resulting in a P wave of an alternate shape or morphology
when compared with an impulse arising from the SA node. The P wave may be completely
undetected or be buried within the QRS; it may even occur after the QRS if the junctional
impulse reaches the ventricles before the atria or if the atria and ventricles are depolarized at the
same time.
The junctional impulse follows an alternate conduction pathway, which results in a variable PR
interval, usually shortened, because the impulse originates at a location that is closer to the
ventricle (nodal region), requiring less time for conduction to the ventricles.1 Rhythms arising from
the junctional region are categorized as:

Junctional rhythm
Premature junctional contraction or complex
Accelerated junctional rhythm
Junctional tachycardia

Junctional rhythm: This is a very regular rhythm, as the impulse originates from a single site in the
nodal or junctional region. Junctional rhythms occur when there is failure of SA node firing,
initiation of impulses in the SA node less than 40 bpm, or when there is blockage of a beat
originating in the SA node.2 (See Tracing 16.) A normal-appearing QRS is usually produced as the
impulse is propagated into the ventricles following the normal conduction pathway. The inherent
rate of the AV nodal region is 40 bpm to 60 bpm.2 Therefore, heart rates in true junctional (nodal)
rhythms are also between 40 bpm to 60 bpm.
Junctional rhythms with heart rates from 60 bpm to 100 bpm are referred to as accelerated
junctional rhythms, reserving the term junctional tachycardia for those junctional origin rates
greater than 100 bpm.
Impulses firing at the AV junction located in the middle of the heart results in abnormal
depolarization, which may spread backward (retrograde) into the atria or forward (antegrade) into
the ventricles.1 As a result, P waves may be absent, inverted, or follow the QRS. Sometimes the P
wave is buried within the QRS and not seen at all if the atria and ventricles are depolarized at the
same time. The PR interval is short (< 0.12 second) because the impulse originates at a location
that is closer to the ventricle (nodal region), thus requiring less time for conduction.


Tracing 16: Junctional Rhythm

P waves are absent in this junctional rhythm. The heart rate is approximating 60 bpm.
Potential causes of junctional rhythms include an electrolyte abnormality, myocardial ischemia,
valvular heart disease, stimulant drugs, caffeine or digoxin toxicity.2,4 Treatment may not be
necessary if the heart rate is within normal limits and there are no adverse physiological effects
noted (stable blood pressure and mental status). Removal of the underlying cause may be the only
remedy indicated.

Quick Check: Junctional Rhythm

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)

40 to 60
Same as ventricular
Inverted, absent, or following the QRS
None or <0.12 sec if P wave present


Premature junctional (nodal) contraction (PJC/PNC): A premature beat arising from the AV nodal
or junctional area that comes before a normal beat and is followed by a pause before the
underlying rhythm resumes. (See Tracing 17.) A premature junctional (nodal) contraction
(PJC/PNC) is distinct in that the P wave is of a different shape (often inverted) from that of the
underlying rhythm. The P wave may be absent, inverted or following the QRS. If the P wave occurs
before the QRS, the P-R interval is shortened (<0.12 second).1,2 Because the ventricles usually
depolarize normally, the QRS complex has a normal duration of less than 0.12 sec.2,3
The characteristics of the waveforms: P wave, PR interval and QRS complex are identical to that
described in the section on junctional rhythms.
The distinguishing feature is that the PJC/PNC occurs prematurely in the cardiac cycle. Causes and
treatment modalities are the same as that described for junctional rhythms.


Tracing 17: Premature Junctional Contraction

Accelerated junctional rhythm: This rhythm is a junctional rhythm with a ventricular rate >60 and
<100 bpm.2 (See Tracing 18.) Remember that the inherent junctional rate is normally 40 to 60
bpm, so a junctional rhythm with a HR greater than >60 and <100 bpm qualifies as an accelerated
junctional rhythm. The characteristics of the waveforms: P wave, PR interval and QRS complex are
identical to that described in the section on junctional rhythm. The distinguishing feature is based
on the heart rate only. Causes and treatment modalities are the same as that described for
junctional rhythms.
Tracing 18: Accelerated Junctional Rhythm

Junctional tachycardia: This is a rhythm originating from the AV junctional region with a rate
>100 bpm.1 It is usually a result of the firing of an irritable focus in the AV junction that takes over
as the pacemaker of the heart. Morphology of the P and QRS are the same as those in the already
described junctional rhythms. It may be paroxysmal, as is the case in Tracing 19.
The characteristics of the waveforms: P wave, PR interval and QRS complex are identical to that
described in the section on junctional rhythms. The distinguishing feature is based on the heart
rate only. Causes and treatment modalities are the same as that described for junctional rhythms.
This rhythm may be caused by digitalis toxicity, heart disease, an increase in myocardial oxygen
demand, stimulants or anything else that may provoke the sympathetic nervous system. Adverse effects
include a decrease in cardiac output and corresponding drop in blood pressure as the increased heart
rate results in incomplete ventricular filling. Treatment may consist of medications to decrease the rate:
beta-blockers, calcium antagonists or adenosine.3,4 Attempts should be made to treat the underlying


Tracing 19: Junctional Tachycardia

Chapter Review
The inherent rate of the AV nodal/junctional region is 40 to 60 bpm.
P waves in junctional rhythms may be inverted, absent (buried within) or follow the QRS.
PR intervals are <0.12 second in junctional rhythms.
QRS intervals and morphology are normal.
A premature junctional contraction (PJC) comes early in the R-to-R interval and is followed by a
Accelerated junctional rhythm is characterized as a junctional rhythm with a rate of 60 to 100
Junctional tachycardia is characterized as a junctional rhythm with a rate >100 bpm.
Label each of the following strips as
Junctional rhythm
Premature junctional contraction
Accelerated junctional rhythm
Junctional tachycardia

Answer: Premature junctional contraction (2)


Answer: Junctional rhythm

Answer: Junctional tachycardia




Ventricular Rhythms
Ventricular rhythms originate from an irritable focus in the ventricle. Most of these rhythms are
problematic in that they result in a drop in cardiac output.1-5 Some are potentially life-threatening.
The inherent rate of the ventricle is 20 bpm to 40 bpm. Impulses originating in the ventricle are
very slow, because they do not follow the normal, well-traveled conduction system. Cardiac output
is decreased because of the slower rate and the loss of atrial kick, which may contribute up to
30% to cardiac output.1-3
In some cases, ventricular dysrhythmias may achieve rates up to 250 bpm or higher. This
accelerated ventricular rate causes cardiac output to drop and results in acute hemodynamic
instability and eventual cardiovascular collapse in a short time; thus, the serious nature of these
dysrhythmias and the importance of recognizing them and intervening quickly.
Ventricular beats have wide, bizarre, larger than normal QRS complexes >0.12 second. Theres no
preceding P wave, because the impulse is initiated in the ventricle. T waves associated with the
ventricular beat occur in the opposite direction of the QRS as the impulse follows an alternate
pathway with depolarization. A change in repolarization follows.
The ventricular rhythms discussed in this section are:
Premature ventricular complexes (PVCs)
Ventricular tachycardia
Torsades de pointes
Ventricular fibrillation
Idioventricular rhythm
Premature ventricular contractions (PVCs): These beats are similar to all other premature beats in
that they interrupt the normal cardiac cycle by coming before the next sinus beat is due.
As with all ventricular beats, there is no preceding P wave. P waves generated from the sinus node
may be noted on the ECG recording, but they are not related to the PVC. The P waves represent
atrial depolarization without conduction or initiation of a cardiac cycle. The P waves are usually
upright and normally appearing, if they are seen. There is no measurable PR interval. The QRS is
wide (>0.12 second) and bizarre. The T wave slopes off in the opposite direction to the QRS.1-3
They can occur at any rate. There may be a compensatory pause that follows the PVC. This pause
exceeds the usual RR interval associated with the underlying sinus rhythm.
PVCs usually signal electrical irritability within the heart. Anything that disrupts normal electrolyte
shifts during depolarization and repolarization may case ventricular irritability and PVCs.


Three usual etiologies for PVCs are hypokalemia, heart disease (coronary artery disease or heart
failure) and hypoxia. Other causes include digoxin toxicity, stimulants, stress, caffeine, pain or
anxiety. Each of these etiological factors may cause the heart to become irritable and the
ventricle to fire off an early beat.
Infrequent PVCs may occur in healthy people without an identifiable cause or symptoms. Persons
with weakened hearts or underlying coronary heart disease with PVCs are at risk for symptoms of
lightheadedness or hemodynamic instability.
Occasional or rare PVCs are usually benign, posing no risk to the patient. Frequent PVCs (six or
more per minute) and PVCs that are very close to the preceding T wave warrant concern.4 In these
situations, the PVC may lead to lethal dysrhythmias such as ventricular tachycardia, ventricular
fibrillation, or Torsades de pointes.
When the PVCs all look similar (unifocal, see Tracing 20), it can be assumed they are arising from
the same single focus. When there are multiple-appearing PVCs (multifocal, see Tracing 21) it
indicates there are multiple irritable foci conducting these impulses from the ventricle. This
indicates a much more unstable rhythm that has an increased likelihood of degenerating into a
lethal dysrhythmia.
Tracing 20: Unifocal PVCs

Tracing 21: Multifocal PVCs

When a PVC occurs close to or at the same time as the T wave, it is called R-on-T phenomenon.1
(See Tracing 24.) The R wave of the PVC occurs at the same time as the T wave of the preceding
beat. At this time of ventricular repolarization, the ions are lining up on either side of the cell
membrane waiting for the next signal to stimulate ion movement and cardiac contraction. If the
PVC occurs at this vulnerable time, the conduction cells will assume the ventricular rhythm as the
dominant one, which can lead to significant hemodynamic instability.


Tracing 22: R-on-T phenomenon

Quick Check: Premature Ventricular Contraction

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)

Variable, depends on underlying rhythm

Bizarre >0.12 sec
Depends on underlying rhythm
Normal or inverted
No relationship to the PVC


PVCs may occur singly, in clusters of two or more or in repeating patterns. PVCs that occur in
pairs are called couplets. PVCs that occur every other beat are known as bigeminy; those that occur
every third beat are known as trigeminy.
Infrequent PVCs should be approached based on symptoms and cardiac history with an attempt
to first find out the cause and correct it. If the potassium is low, for example, it needs to be
repleted. Oxygen should be administered, and any electrolyte imbalances should be corrected. Pain
should be treated.
If the patient is without symptoms or history of heart disease, the dysrhythmia likely wont require
treatment. If the patient does have symptoms and a history of heart disease, the physician may
choose to treat the PVCs with IV medications such as beta-blockers or antiarrhythmic agents,
depending on whether there is any structural heart disease.4
Ventricular tachycardia (VT): In this rhythm, commonly called V tach, three or more PVCs occur
in a row and the ventricular rate exceeds 100 bpm. This in an extremely unstable rhythm and may
precede sudden cardiac death (SCD).1-5 (See Tracing 23.) It may be paroxysmal or sustained. If it
is short lasting (< 30 seconds), it is may be tolerated and does not necessitate immediate
treatment. If sustained > 30 seconds, this rhythm is poorly tolerated and often life threatening. V
tach requires immediate recognition and treatment.
Theres usually no P wave due to the lack of atrial activity, which is superseded by the ventricle. If
P waves are seen, they are not related to the QRS complex. Theres no measurable PR interval. The
QRS is wide (>0.12), bizarre and uniform, indicating that the impulse originates from the same
location in the ventricle. In this case, the rhythm may be described as monomorphic (similar
shape) ventricular tachycardia. The rhythm is regular. The QRS complexes appear as large


sawtooth waves. The amplitude, or size, of the complex is increased. The T wave slopes off in the
opposite direction as the QRS and is often obscured by the preceding QRS when the rate exceeds
100 bpm. Ventricular rates may reach up to 200 bpm.1
Tracing 23: Ventricular Tachycardia

Quick Check: Ventricular Tachycardia

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)


> 100 bpm

Bizarre >0.12 sec
Unable to determine
Usually not seen

Ventricular tachycardia is caused by many of the same factors causing PVCs: heart disease,
electrolyte abnormalities, hypoxia, digoxin toxicity and stimulants. The R-on-T phenomenon can
precipitate ventricular tachycardia.
When this dysrhythmia is seen, the first step in patient evaluation is to determine how it is
affecting the patients clinical signs and symptoms. In the presence of a pulse, initial treatment
consists of administering supplemental oxygen. If the patient is without signs of cardiac instability
(hypotension, change in mental status, syncope, shortness of breath), antiarrhythmic agents or
rate-controlling medications may be ordered. Continuous, close monitoring is essential. If the
patient becomes unstable with signs of cardiac instability, immediate synchronized cardioversion
is indicated.4,6
Per the 2011 American Heart Association ACLS Guidelines, the initial approach for stable wide
complex tachycardias calls for obtaining prompt IV access and a 12 lead ECG if the patients
condition will allow for this added diagnostic step. Adenosine may be considered initially if the
stable, wide complex tachycardia is regular and monomorphic as both a form of treatment and as a
diagnostic aid. Protocols follow for antiarrhythmic boluses and infusions for either procainamide,
amiodarone or sotalol, all with guidance from expert consultation.6
If the patient deteriorates and a pulse is undetected, initiation of ACLS protocol for pulseless
arrest is required: unsynchronized defibrillation accompanied by CPR, a vasopressor medication,
such as epinephrine and/or vasopressin, and antiarrhythmic therapy (amiodarone).6


Some ventricular tachycardias can be treated with radiofrequency ablation (RFA) to abolish the
ectopic focus within the ventricle. This may be performed by a cardiologist specializing in the
treatment of cardiac dysrhythmias or electrophysiology (EP). An automatic implantable cardiodefibrillator (AICD) is used for patients with recurrent VT or those at risk for VT due to reduced
cardiac output or heart failure.3
Torsade de pointes: A special form of VT, Torsade de pointes, is a ventricular dysrhythmia that
arises from multiple ectopic foci within the ventricle and may also be called polymorphic VT.
Torsade de pointes means twisting about the points, which describes the QRS complexes that
appear to rotate or twist about the isoelectric baseline.1-3
This rhythm is characterized by a prolonged QT interval that precedes its onset. QRS complexes
are wide and bizarre (>0.12 second) with increased amplitude. Ventricular rates may range from
150 to 250 bpm.2 There are no discernable P waves. T waves slope off in the opposite direction of
the QRS but are often indiscernible due to the increased rate. This may be paroxysmal, starting
and stopping suddenly, and has the potential to deteriorate into ventricular fibrillation at any time.
Tracing 24: Torsade de Pointes

The cause of this form of ventricular tachycardia is often reversible. A metabolic derangement
(hypokalemia, hypomagnesemia or hypocalcemia) or drug toxicity (particularly drugs that prolong
the QT interval) may precipitate Torsades. Other causes include all of those that may precipitate
PVCs or ventricular tachycardia.
Treatment of Torsades de pointes is aimed at correcting the underlying cause, especially if the
cause is due to a specific drug therapy. Magnesium sulfate or overdrive pacing may also be ordered
by the physician in an attempt to break the triggered mechanism for the rhythm.2
Continuous, close monitoring of the patient with this rhythm is necessary. If the patient
deteriorates, and a pulse is undetected, initiation of ACLS protocol for pulseless arrest is required,
which includes unsynchronized defibrillation accompanied by CPR, epinephrine and/or
Prevention of Torsade de Pointes in the hospital setting was released as a Scientific Statement
from the AHA in 2010. Particular emphasis is placed on medical conditions and medications
known to be risk factors. Healthcare providers are also guided on the discernment of this
potentially lethal rhythm and ECG/telemetry monitoring methods.11 (Level ML)


Ventricular fibrillation: Also referred to as V-fib, this rhythm is a chaotic pattern of electrical
activity arising from multiple ectopic foci in the ventricles. (See Tracing 25.) It is a lethal
dysrhythmia often responsible for sudden cardiac death.1-4 V-fib is always an emergency, patients
are never stable, and it must be treated quickly to avoid death. In this rhythm, the ventricles are
quivering or fibrillating (as in atrial fibrillation) and as a result, cardiac out and blood pressure fall
quickly. The patient rapidly loses consciousness.
Tracing 25: Ventricular Fibrillation

Ventricular fibrillation represents completely disorganized and chaotic electrical activity. There are
no discernable P waves, QRS complexes or T waves. Markedly reduced cardiac output results in a
lack of tissue and organ perfusion and an undetectable pulse.
Possible causes of this dysrhythmia include all of those discussed for VT and Torsades de pointes.
Treatment consist of immediate defibrillation and CPR following the ACLS protocol for pulseless
Idioventricular rhythm: This rhythm has been referred to as a rhythm of last resort.1 It is a
ventricular escape rhythm with rates ranging from 20 bpm to 40 bpm. (See Tracing 26.) An
idioventricular rhythm (idio in this context means all on its own or spontaneously) results
when the electrical impulse initiating a cardiac cycle, whether at the SA node, atrial tissue or AV
node, fails or is blocked. The automaticity or inherent rate of the ventricle takes over as the main
pacemaker of the heart. The ventricles beat to provide a heartbeat and save the patients life.
Hemodynamic instability is certain due to the slow heart rate and subsequent decreased cardiac
output. Symptoms of decreased perfusion to tissues and organs are obvious and noted by
decreased levels of consciousness and severe hypotension.
P waves are either absent or totally unrelated to the QRS complex. Therefore, the PR interval is
indiscernible. The QRS complex is wide (> 0.12 sec). T waves slope off in the opposite direction
from the QRS. The ventricular rhythm is usually regular. (See tracing 27.)
If the rate ranges from 40 bpm to 60 bpm, then it is referred to as an accelerated idioventricular
rhythm (AIVR).


Tracing 26: Idioventricular Rhythm

Tracing 27: Accelerated Idioventricular Rhythm

Quick Check: Idioventricular Rhythm

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)

20 to 40
>0.12 sec
None or if present unrelated to QRS


The cause of IVR is usually serious cardiac disease: myocardial infarction, acute myocardial
ischemia, digoxin toxicity, hypoxia or metabolic imbalances. Accelerated IVR is seen frequently
following a myocardial infarction or when blood flow to the coronary arteries is re-established
with thrombolytics or percutaneous intervention. In this setting, AIVR may be referred to as a
reperfusion dysrhythmia.
Treatment includes initiation of ACLS protocol for severe bradycardia or pulseless arrest should a
pulse become undetectable. Placement of a temporary pacemaker may be considered based on
expert consultation.

Chapter Review
The inherent rate of the ventricle is 20 bpm to 40 bpm.
Ventricular dysrhythmias often result in hemodynamic instability and are considered life
threatening of they occur frequently or are allowed to persist.
Usual etiologies for ventricular dysrhythmias are similar and include electrolyte abnormalities,
heart disease, digoxin toxicity, hypoxia, stimulants or pain.
PVCs may occur in healthy people without an identifiable cause or symptoms.

Ventricular tachycardia may be monomorphic or polymorphic and degenerate into ventricular

fibrillation, resulting in sudden cardiac death.
Torsade de pointes is a potentially life-threatening dysrhythmia that is usually reversible and most
often caused by an agent that causes QT prolongation preceding its onset, such as drug toxicity or
metabolic derangement (hypokalemia, hypomagnesemia or hypocalcemia).
Ventricular fibrillation is unmistakable and always results in severe cardiovascular collapse, thereby
requiring early defibrillation and initiation of ACLS.
Accelerated idioventricular rhythms are serious and unstable, and may be seen after administration
of thrombolytics or coronary revascularization and may be referred to as reperfusion dysrhythmias.
Label each of the following strips as:
Premature ventricular complexes (PVCs)
Ventricular tachycardia
Torsades de pointes
Ventricular fibrillation
Idioventricular rhythm

Answer: Ventricular tachycardia

Answer: Premature ventricular complexes (unifocal)

Answer: Torsade de Pointes



Atrioventricular (AV) Blocks

Atrioventricular (AV) blocks are dysrhythmias that represent a disruption or delay in the normal
pathway of conduction. The rhythm originates at the SA node and follows the normal conduction
pathway to the AV node. All P waves conduct to the AV node. These rhythms may also be referred
to as a SA exit block, which identifies a conduction delay distal to the pacemaker (SA node) site.12
Once the impulse reaches the AV node, it is either delayed or completely blocked, resulting in
either a delay or interruption of conduction to the ventricles. The site of block may occur at the
AV node, bundle of His (AV bundle) or bundle branches. The underlying rhythm is sinus. Heart
rates can be normal or slowed. The clinical effect, or symptoms, depend on how many impulses are
blocked and how slow the ventricular rate is. Treatment, if indicated, is aimed at increasing the
heart rate and improving conduction of the impulse.
The types of AV blocks to be discussed are:
Second-degree (Type I and II)
First-degree AV block: This type of AV block occurs when impulses from the SA node are
consistently delayed through the AV node.1-4 (See Tracing 28.) All impulses arriving at the AV
node get through; they just take longer. The delay in transmission is seen on the ECG as a
prolonged PR interval of >0.20 sec.
Tracing 28: First-Degree AV Block

Quick Check: First-Degree AV Block

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)


Usually 60 to 100
< 0.12 sec
Same as ventricular
Prolonged, > 0.20 sec

The heart rate associated with this rhythm may vary from bradycardic to tachycardic but is usually
normal. P waves are normal appearing. The P-R interval is prolonged (>0.20 second) and is

constant. QRS complexes are normal appearing unless associated with a bundle branch block.
With normal heart rates, the patient with first-degree AV block is usually asymptomatic.
This rhythm may be seen in healthy people. It may also occur in association with inferior wall
myocardial infarction, hyperkalemia, vagal stimulation or administration of medications that slow
the conduction time through the AV node.2 The treatment, if needed, is to determine and remove
the underlying cause. Progression of this rhythm into a higher degree of atrioventricular block is
possible and therefore requires periodic evaluation for symptoms and monitoring.
Second-degree AV block type I (Mobitz I or Wenckebach): This dysrhythmia, or block, is usually
transient. (See Tracing 29.) It occurs when the AV node becomes progressively sicker, slowing the
conduction of impulses it receives until complete conduction fails. The PR intervals grow
progressively longer until there is a P wave with no QRS to follow.
The atrial rate is regular, ranging between 60 bpm to 100 bpm, and exceeds the ventricular rate.
The ventricular rate is irregular due to successive PR prolongation. The P waves are normal in
configuration. The PR interval gradually prolongs until a QRS is dropped. The QRS is usually of
normal configuration and duration but may be prolonged (>0.12 second) because the conduction
disturbance occurs lower in the conduction system, therefore prolonging the amount of time
required to conduct through the ventricles.12 Collectively, the QRS complexes seem to appear as
though they are grouped.
Tracing 29: Second-Degree AV Block Type I

Quick Check: Second-Degree AV Block Type I

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)

Irregular or a grouped pattern

Usually < 0.12 sec
Usually 60 to 100
Upright, uniform
Progressively lengthens


Patients with this rhythm are usually asymptomatic. It may occur normally among athletes and
children.3 This block retains the potential to progress to a more advanced AV block. Possible
causes include heart disease, digitalis toxicity and heart rate-lowering medications. Treatment
consists of determining and treating or removing the underlying cause. Atropine can be given if
the heart rate is slow and the patient becomes symptomatic. If symptoms are progressive, a
transcutaneous pacemaker can be used if atropine does not increase the heart rate. Most patients
with second-degree AV block type I require nothing more than careful observation.1-3

Second-degree AV block type II (Mobitz II): In this type of block an electrical impulse generated
from the SA node is blocked at the bundle of His. The impulse is intermittently blocked, creating a
rhythm where two or more P waves are conducted for each QRS complex or ventricular beat. (See
Tracing 30.) Second-degree AV block type II is more rarely seen than type I and much more
dangerous due to its potential to deteriorate into a more advanced AV block such as third-degree
or complete heart block (CHB).
Tracing 30: Second-Degree AV Block Type II

Quick Check: Second-Degree AV Block Type II

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)


Variable and slow

Normal or >0.12sec
Usually 60 to 100
Upright, uniform
Normal and consistent


The atrial rhythm is regular, ranging from 60 to 100 bpm. The ventricular rate is irregular and less
than the atrial rate due to dropped beats. The P waves are normal appearing. The PR intervals are
constant and of normal duration. The QRS may be narrow if the block is around the AV juncture
and widened if the block is at the bundle branch/Purkinje region. The ventricular response (QRS
complex) may have a variable conduction rate in comparison with atrial contraction (P waves).
When two or more successive atrial impulses are blocked, the conduction disturbance is called
high-grade AV block.1-3 The number of P waves to QRS complexes is referred to as a ratio; e.g.,
2:1, 3:1. As the number of P waves compared with QRS complexes increases, the amount of
blockage increases and becomes more ominous.
If the ventricular rate (heart rate) is slow, the patient may have signs of decreased cardiac output
such as light-headedness, syncope or hypotension. Causes of type II second-degree block include
heart disease and degenerative changes in the conduction system.1-5
Treatment for this rhythm includes supplemental oxygen and prompt initiation of either a positive
chronotropic (heart rate-increasing) medication: atropine, dopamine or epinephrine as per ACLS
protocol, transcutaneous or transvenous pacing.6


Tracing 31: 2:1 and 3:1 (Variable) Second-Degree AV Block

Third-degree AV block: This type of block (also called complete heart block) occurs when the sinus
node sends out an electrical impulse as usual, but the transmission to the AV node is completely
blocked. (See Tracing 31.) The junctional tissue at the AV node or the ventricles starts initiating
beats at their inherent rates to initiate a cardiac cycle. If the AV node takes over as pacemaker, the
inherent rate will be between 40 to 60 bpm. If conduction occurs lower in the system into the
ventricle, the rate may be as low as 20 to 40 bpm. These beats from junctional or ventricular origin
are referred to as escape beats. In this rhythm, the sinus and AV node are not working in
coordination with each other. It is generally a life-threatening rhythm requiring prompt recognition
and treatment.
Analysis of the ECG reveals no relationship whatsoever between the P wave and QRS complex.
Atrial rates are usually normal, ranging from 60 to 100 bpm; the ventricular rate is typically slow,
ranging from 20 to 60 bpm. In some cases, the ventricular rate may be higher than 60 bpm, which
would be referred to as third-degree AV block with an accelerated junctional or ventricular
response.3 P waves will be present with a consistent P-P interval. The P waves are not associated
with any of the QRS complexes, so the P-R interval varies. Some P waves may be hidden inside the
QRS complex or T waves. The QRS complex may be of normal duration (<0.12 second) if the
resultant heartbeat is from a junctional focus near the AV node, or wide (>0.12 second) if from a
ventricular focus. The QRS complexes march out in a regular pattern.
Tracing 32: Third-Degree AV Block

Quick Check: Third-Degree AV Block

Ventricular Rate
QRS complex
Atrial Rate
P wave
PRI (PR interval)

20 to 60
Normal or >0.12sec
Usually 60 to 100
Upright, uniform
Varies (No consistent relationship
between P waves and QRS complexes)



This is the most serious form of heart block and may result in signs of significantly compromised
cardiac output (hypotension, syncope). In some rare cases, if this rhythm occurs gradually and the
heart has time to compensate for the slow ventricular rate, it can occur without significant
Causes of this rhythm include significant heart disease, medication side effects (digoxin toxicity,
beta-blockers, calcium antagonists), hypoxia and congenital heart defects.2-5
When symptomatic, treatment for third-degree AV block includes urgent external pacing, or an
ACLS directed administration of positive chronotropic (or heart rate-increasing) medications
(atropine, dopamine or epinephrine) until transvenous pacing can be initiated.6
Chapter Review
The underlying rhythm is sinus. All P waves are conducted with the site of blockage distal to the
SA node.
The site of conduction blockage may be at the AV node, bundle of His (AV bundle) or bundle
With AV blocks, the clinical effect depends on how many impulses are blocked, how slow the
ventricular rate is and how the block affects the heart.
First-degree, second-degree (types I and II) and third-degree are all types of AV block rhythms.
First-degree AV block is the least dangerous, but it can degenerate into a more severe block.
Second-degree AV block Type II is more serious than Type I AV block and may require placement
of a pacemaker.
Third-degree AV block, also called complete heart block, is the most serious of AV blocks, often
requiring immediate treatment, including the initiation of ACLS treatment protocols.
Label each of the following strips as:
Second-degree type I
Second-degree type II


Answer: Second-degree AV block type I

Answer: Third-degree AV block

Answer: First-degree AV block



Myocardial Infarction
and Coronary Vessels
In general, the three coronary vessels that cause myocardial infarction/ischemia include the left
anterior descending, circumflex and right coronary artery. When the right coronary artery is
occluded, patients develop an inferior wall MI. When the left anterior descending coronary artery
is occluded, an anterolateral MI develops. When the circumflex coronary artery is occluded, a
lateral wall MI develops.
Diagram 12 below shows the right coronary artery and its course to the inferior aspect of the
heart. The left main coronary artery gives rise to the left anterior descending coronary artery,
which when occluded causes an anterolateral MI. The circumflex coronary artery (not shown) also
comes off the left main coronary artery and at the back of the heart. When occluded, it gives rise
to a lateral wall MI.
Diagram 12

ECG and Myocardial Infarction

The diagnosis of an MI is noted with accompanying characteristic 12-lead ECG changes.
Abnormal (elevated) serum cardiac enzymes often are measured in the setting of myocardial
infarction as well. Within hours of an MI, the ECG will show changes that are often quite

prominent. The first changes after an MI may be noted on the ECG as abnormal appearing T
waves. The T wave is often prominent or accentuated. You may instead note T wave flattening or
inversion, signaling a lack of adequate coronary blood flow leading to an MI if left untreated. This
is followed by Q waves and return of the ST segment to baseline (Diagrams 13 and 14).
Diagram 13


Diagram 14

Another simplified view of the progressive ECG changes that occur following an MI

Localization of an MI on the ECG

The ECG can also help localize the myocardial infarct by assessing changes in particular leads. In
general, one should look at the following leads for specific infarct locations:

V3 to V6
I, aVL, V5,V6

Blood vessel
Circumflex/obtuse marginal

To confirm the MI and occlusion of the coronary artery requires an angiogram.

Anterolateral MI
Sometimes a myocardial infarction will involve more than one coronary artery, such as occurs with
anterolateral MI. This type of MI is recognized by observing ST segment changes in leads I, aVL
and precordial leads overlying the anterior and lateral surface of the heart (V3 to V6).
Anterolateral wall MI occurs because of coronary artery disease in the left anterior descending or
circumflex coronary artery. Dysrhythmias that may be seen with this MI include right or left
bundle branch blocks, or type II second-degree heart block. Image below is from a patient with an
anterolateral MI.


Diagram 15

Lateral Wall MI
A lateral wall MI occurs when there is occlusion of the left circumflex or the obtuse marginal
coronary artery with ECG changes seen in leads I, aVL,V5 and V6 alone. Due to the coronary
anatomy it is much more common to note changes consistent with anterolateral MI because the
circumflex artery is a branch of the left main coronary artery. As a result, the left anterior
descending artery is often involved as well with associated ECG changes noted V3, V4.
Diagram 16


Inferior Wall MI
Inferior wall MI occurs when there is occlusion of the right coronary artery (image 10). On the
ECG, inferior wall MI will present with changes in leads II, III and aVF. The Q waves are often
largest in lead III and smallest in lead II.
Diagram 17

Chapter Review
Occlusion of one of the three coronary vessels will result in myocardial infarction/ischemia. This
results in damage to the area of the heart supplied by the corresponding coronary artery.
Right coronary artery occlusion results in an inferior wall myocardial infarction.
Left anterior descending artery occlusion results in an anterolateral wall myocardial infarction.
Circumflex artery occlusion results in a lateral wall myocardial infarction
Characteristic ECG changes occur with myocardial infarction. Cardiac enzymes will be elevated in
the setting of myocardial infarction.
T wave changes may be one of the first ECG changes noted after a myocardial infarction.
The 12-lead ECG can help to localize the MI by associated changes in specific leads.
An anterolateral MI is associated with ECG changes in leads I, avL, or V3-6.
Lateral wall MI is associated with ECG changes in leads I, avL, V5,6.
Inferior wall MI is associated with ECG changes in II, III, aVF.


Label each of the following strips as:

Anterolateral wall MI
Lateral wall MI
Inferior wall MI

Answer: Inferior wall MI

With progressively increased acuity among hospitalized patients, bedside ECG monitoring is more
common, requiring nurses to hone their skills and gain competency in ECG interpretation. In
support of these needs, in 2004, practice guidelines were issued from the AHA on electrographic
monitoring in hospital settings and this has set the standard for continuous cardiac dysrhythmia
telemetry monitoring.13
In closure, this continuing education course has been developed to allow nurses to update their
clinical skills and competencies in ECG rhythm analysis with the intended ultimate result of
improved patient outcomes.



Cardiovascular Care Made Incredibly Easy. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.


Knechtel MA. EKGs for the Nurse Practitioner and Physician Assistant. New York, NY: Springer Publishing Co.;


Jenkins P. Nurse to Nurse ECG Interpretation. New York, NY: McGraw-Hill Cos.; 2010.


Chulay M, Burns SM. AACN Essentials of Critical Care Nursing. 2nd ed. New York, NY: McGraw-Hill Co. Inc.;


Woodrow P. An introduction to electrocardiogram interpretation: part I. Emerg Nurse. 2010;18(1):28-35.


Sinz E, Navarro K, Soderberg ES, eds. Advanced Cardiac Life Support. Provider Manual. Dallas, TX: American
Heart Association; 2011.


Wann LS, Curtis A, January C, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with
atrial fibrillation (Updating the 2006 guideline). A Report of the American College of Cardiology Foundation /
American Heart Association Task Force on Practice Guidelines. Circulation. 2011;123:104-123. Published December 20, 2010. Accessed February 10, 2014.

8. You JJ, Singer DE, Howard PA, et al. Antithrombotic therapy for atrial fibrillation: Antithrombotic therapy and
prevention of thrombosis, 9th ed; American College of Chest Physicians evidenced-based clinical practice
guidelines. Chest. 2012;141(2 Suppl):e531S-575S. Published February 2012. Accessed
February 10, 2014.
9. National Institute of Health Drug Information Portal. National Library of Medicine Web site. Accessed February 10, 2014.
10. Camm AJ, Lip GYH, DeCatarina R, et al. 2012 focused update of the ESC guidelines for the management of
atrial fibrillation: an update of the 2010 ESC guidelines for the management of atrial fibrillation developed
with the special contribution of the European Heart Rhythm Association. Europace. 2012;14(10):385-1413.
11. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of Torsade de pointes in hospital settings: a scientific
statement from the American Heart Association and the American College of Cardiology Foundation.
Circulation. 2010;121(8):1047-1060. Published February 8,
2010. Accessed February 10, 2014.
12. Yanowitz FG. ECG learning center Web site. Published 2006. Accessed February 10, 2014.
13. Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings: an
American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical
Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized
Electrocardiology and the American Association of Critical-Care Nurses. Circulation. 2004;110(17):2721-2746. Published October 2004. Accessed February 10, 2014.



1. The electrical events associated with each cardiac contraction or
heartbeat include:
a. Exchange of ions across the cell membrane resulting in myocardial
b. Spontaneous generation of an impulse in the pacemaker cells, i.e.,
the SA node
c. Return of the myocardial cell to its resting state (repolarization)
d. Propagation of the electrical impulse from the SA, through the AV
node, and finally through the Purkinje system
e. All of the above
2. The following is characteristic of the sinoatrial (SA) node:
a. Intrinsic rate of 40 bpm to 60 bpm
b. Is capable of spontaneously generating an electrical impulse
c. Located near the interatrial septum, or junction
d. Serves as a gatekeeper, delaying impulses to allow time for the
ventricles to fill
3. The ECG is from a 71-year-old in the CCU. It shows:


Sinus bradycardia
First-degree heart block
Third-degree heart block
Atrial fibrillation



A 67-year-old was admitted to the ICU because of chest pain. The

night nurse printed out the ECG strips from four different leads and
they are shown below. The patient most likely developed:


Ventricular fibrillation
Ventricular tachycardia
Atrial flutter
Torsades de pointes

A 29-year-old female presents to the ED with complaints of

palpitations, vague chest pain and diaphoresis. She claims that she
got scared when a man approached her on the street and demanded
her purse. The resulting panic attack led to these symptoms. However,
she is worried because the palpitations have now been going on for at
least 60 minutes. Her vitals are stable and her ECG strip is shown
below. She most likely has:


Atrial tachycardia
Ventricular tachycardia
Atrial flutter



A 67-year-old female treated with hydrochlorothiazide for her

hypertension presents to the ED with dizziness. Blood work reveals
hypokalemia. The ECG done is shown below. She most likely has


A 57-year-old male in the ICU has the following rhythm. His BP is

65/35, pulse is barely palpable and his pulse oximetry is 86% on 100%
oxygen facemask. The next step in his management is:


Peaked T waves
Torsades de pointes
Atrial tachycardia
Ventricular tachycardia

Start amiodarone
Administer 2 liters NS fluid bolus
Start lidocaine

The following are typical characteristics of the 12-lead ECG recording:

a. Six limb leads and six chest leads
b. Limb leads I, II, III, aVR, aVL, aVF
c. Chest leads: V1 through V6
d. Used for diagnosis and recognition of acute coronary syndrome
e. All of the above



The following characterize the standard ECG paper used for

a. Comprised of small boxes measuring 0.05 second
b. Comprised of large boxes measuring 0.10 second
c. Comprised of small boxes that are 2 millimeters (mm) in height and
d. All of the above
e. None of the above

10. The normal values for the ECG waves and complexes are:
a. PR interval 0.12 to 0.20 second
b. QRS duration greater than 0.12 second
c. QT interval variable and greater than or equal to one-half the
distance between successive QRS complexes
d. T wave denoted as a negative deflection from the isoelectric line
11. A systematic approach to ECG analysis includes:
a. Evaluation of waveforms and complexes: P wave, QRS complex, T
wave and U wave (if present)
b. Intervals and segments: PR interval, QRS duration, ST segment, QT
c. Heart rate
d. Rhythm/regularity
e. All of the above
12. What is the heart rate of this patient?



13. If a rhythm is irregular, yet of sinoatrial node origin (sinus) with similar
looking P waves preceding each QRS, and a rate of 60 bpm to 100
bpm, the rhythm is called:
a. Sinus bradycardia
b. Sinus dysrhythmia
c. Sinus arrest
d. Sinus tachycardia


14. To determine whether a patient is tolerating a rhythm, the following

should be evaluated/assessed:
a. Blood pressure and level of consciousness
b. Exercise capacity
c. Blood sugar
d. Body mass index (BMI)
15. Sinus bradycardia is associated with:
a. Heart rate less than 60 bpm
b. Inverted P waves
c. A prolonged PR interval
d. All of the above
16. Sinus tachycardia is identified as or associated with:
a. Anxiety, fear, pain, fever
b. b. Hyperthyroidism and/or hypovolemia
c. Potential hemodynamic compromise due to inadequate time for
cardiac filling
d. Heart rates in excess of 100 bpm
e. All of the above
17. What is the rhythm of this patient?




18. This rhythm is noted on the ECG as a pause that occurs when the
sinus node fires an impulse on time, but the impulses exit from the
sinus node to the atrial tissue is not conducted. This rhythm is:
a. Sinus bradycardia
b. Sinus dysrhythmia
c. Wandering atrial pacemaker
d. Sinus block


19. The treatment of atrial tachycardia may include:

a. Electrical cardioversion
b. Beta-blockers
c. Digoxin
d. Calcium channel blockers
e. All of above
20. Atrial tachycardias (paroxysmal atrial tachycardia/PAT or
supraventricular tachycardia/SVT) may be treated with the following:
a. Atropine
b. Adenosine
c. Isoproterenol
d. Lidocaine
21. A 62-year-old male admits to the ED with a complaint of chest pain.
Blood tests reveal an elevated cardiac enzyme and a 12-lead ECG is
done with abnormal findings. These ECG changes reflect:


A normal variant
Lateral wall infarction
Anterolateral wall myocardial infarction
Inferior wall myocardial infarction

22. Premature ventricular contractions (PVCs) are most dangerous if they

a. Multifocal
b. Appear wide and bizarre
c. Occur after the T wave
d. Occur every third beat
23. Potential causes of PVCs include:
a. Heart disease
b. Hypoxia
c. Hypokalemia
d. Anxiety, pain, stress
e. All of the above


24. The following dysrhythmias are potentially life threatening and

require initiation of ACLS protocol:
a. Supraventricular tachycardia with a rate of greater than 150 bpm
b. Ventricular fibrillation
c. Ventricular tachycardia
d. Idioventricular rhythm
e. All of the rhythms
25. What type of AV block is associated with progressively longer PR
intervals and an eventual dropped QRS complex?
a. First-degree
b. Second-degree type II
c. Third-degree
d. Second-degree type I (Wenckebach)