RSPT 2325 Cardiopulmonary Diagnostics Unit 1 Basic EKG
interpretation
by Elizabeth Kelley Buzbee AAS, RRT-NPS, RCP
Reading assignment:
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Ellis EKG Plan and simple pp. 83 to 166 for rules.
Wilkin’s Assessment Chapter 10
Egan’s Fundamentals pp. 1100-11007
Objective for this unit include:
1. The student will review A & P notes regarding conduction, paper speed, counting rates
and intervals used in basic EKG interpretation steps and inherent rates of various parts
of the heart.
2. The student will be able to identify and troubleshoot the 4 types of artifacts. pp. 51
3. Discuss the importance of standardization of the EKG tracing prior to diagnostic EKG.
pp50-51
4. The student will know the rules for the following sinus rhythms, the clinical significance
of each and be able to recognize the arrhythmia from a 6 second strip :
 Normal sinus rhythm [NSR] pp 83
 Sinus tachycardia pp 85,
 Sinus bradycardia pp. 83
 Sinus arrest pp. 87
 Sinus arrhythmia pp. 86
5. The student will know the rules for the following atrial rhythms, the clinical significance
of each and be able to recognize the arrhythmia from a 6 second strip :
 Wandering pacemaker pp. 103
 Premature atrial contraction PAC pp. 105
 Paroxysmal atrial tachycardia PAT pp. 106
 Atrial flutter pp. 107
 Atrial fibrillation pp. 108
 Supraventricular tachycardia SVT pp. 110
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6. The student will know the rules for the following junctional rhythms, the clinical
significance of each and be able to recognize the arrhythmia from a 6 second strip :
 premature junctional contraction PJC pp. 125
 junctional escape pp. 126
 junctional bradycardia pp. 125
 accelerated junctional pp. 127
 Junctional tachycardia pp. 128
7. The student will know the rules for the following ventricular rhythms, the clinical
significance of each and be able to recognize the arrhythmia from a 6 second strip :
 PVC pp. 137
 Idioventricular pp. 141
 Accerated idioventricular pp. 142
 Agonal rhythem pp. 140
 V tachycardia pp 143
 V fibrillation pp 144
8.
9.
10.
11.
12.
13.
 Torsades de pointes pp. 143
 Asystole flat line pp. 145
The student will know the rules for the following A-V blocks rhythms, the clinical
significance of each and be able to recognize the arrhythmia from a 6 second strip :
 First degree block pp. 161
 Second degree block type I [Wenckebach] pp. 162
 Second degree block type II pp. 163
 Third degree AV block pp 165
The student will recognize the EKG tracing associated with digitalis overdose and various
electrolyte imbalences. pp338-340
The student will recognize the appearance of an abnormal ST segment and be able to
determine the clinical significance of the ST seg deviation. pp345-348
The student will understand the significance of an axis deviation and how these
deviations can be caused by hypertrophy or infaction. pp.433-441
The student will understand the significance of the cardiac stress test and the angiogram
in diagnosis of heart disease. pp. 453-455
The student will understand the indications and contraindications for the use of the
halter monitoring of the EKG over 24 hours
Lecture EKG
1. The student will review A & P notes regarding conduction, paper speed,
counting rates and intervals used in basic EKG interpretation steps and
inherent rates of various parts of the heart.
 First march out the P waves to see if the atrial beat is regular; if not regular is it
because the rate changed, or there is a single abnormal beat or is the whole thing
irregular.
 Do the same for the R or S waves to see if the ventricular beat is regular. You should
be able to use the same notches for both atrial and ventricular rhythms
 The next thing we do is calculate the HR of the atria and of the ventricles; never
assume they are the same unless both P and QRS marched out with the same notches
on the paper.
 We measure the PRI; start at the beginning of the P to the point where the isoelectric
line goes down to the Q or up to the R
 We measure the QRS;
 Note if the ST segment is elevated or depressed
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Note if the P of the next impulse starts on down slope of the preceding T wave.
QT intervals pp. 30: beginning of the QRS to the end of the T wave is the QT
interval. This should be half the distance between the RR intervals at normal rates. If
the QT is prolonged, there is increased chance of lethal arrhythmias
2. The student will be able to identify and troubleshoot the 4 types of artifacts.
pp. 51
 Tremors can cause artifact. Make sure the leads are on tight and cover the
patient if she is cold. With tremors we can usually make out the QRS complexes
and even the P and T waves.
 Baseline sway. The entire baseline moves up and down, frequently associated
with the breathing. Check the leads and clean the skin with alcohol to get rid of
lotion or sweat
 60 cycle interference: caused by other electrical equipment. Ask the nurse
what you can disconnect for the 2 minutes of the study
 Broken recording: sudden loss of impulse, check connections and get another
machine
3. Discuss the importance of standardization of the EKG tracing prior to
diagnostic EKG. pp 50-51
 Standardization: check the calibration of the equipment. Failure to
standardize will make the reading inaccurate A 1 mlvolt impulse should cause the
stylus to jump 2 big blocks tall. [10 mm.]
4. The student will know the rules for the following sinus rhythms, the clinical
significance of each and be able to recognize the arrhythmia from a 6 second
strip :
Sinus arrhythmia arise from the SA node; tend to be the most benign because the
conduction is pretty much normal with normal Stoke volumes and Cardiac Outputs

Normal sinus rhythm [NSR] pp 83
o
o
o
o
o
Rhythmic of atria and ventricle: both A and V march out and they march
out together
P waves: identical, precedes QRS, one for every QRS
Rate of atria and ventricle: both are exact and are between 60- 100
PRI wave: is between .12- .20 second
QRS wave: is less than .12 seconds
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Sinus tachycardia pp 85
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Sinus bradycardia pp. 83
Clinical significance: the most likely cause of sinus tachycardia would be [1]
hypoxemia, [2] increased WOB, [3] fever[4] medications that cause tachycardia such
as atropine [5] thyroid storms[6] MI
o Rhythmic of atria and ventricle: both A and V march out and they
march out together
o P waves: identical, precedes QRS, one for every QRS
o Rate of atria and ventricle: both are exact and is 101-160 BPM
o PRI wave: is between .12- .20 second
o QRS wave: is less than .12 seconds

Clinical significance: causes include: [1] stimulation of the vagus nerve by tactile
stimulation of the back of the throat such as during suctioning, [2] MI [3] sometimes
hypoxia [4] lower blood sugar [5] digitalis OD [6] sinus brady is common in trained
athletes
o Rhythmic of atria and ventricle: both A and V march out and they march
out together
o P waves: identical, precedes QRS, one for every QRS
o Rate of atria and ventricle: both are exact and is less than 60 BPM
o PRI wave: is between .12- .20 second
o QRS wave: is less than .12 seconds
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Sinus arrest pp. 87
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Sinus arrhythmia pp. 86
Clinical significant: occasionally, the SA node fails to fire and a lower escape beat
from the AV node or the ventricle will step in to keep the beat, then it returns to
sinus. This can happen when
o Rhythmic of atria and ventricle: normal till there is a pause
o P waves: normal except for pause; identical, precedes QRS, one for every
QRS
o Rate of atria and ventricle: both are exact and are between 60- 100
o PRI wave: is between .12- .20 second before the pause; may be shorter after
pause
o QRS wave: is less than .12 seconds; may be different after the pause
Clinical significant: is a benign finding with children and small adults in which
the HR speeds up and slows down with breathing; rarely associated with heart
disease
o Rhythmic of atria and ventricle: the A and V are both irregular;
frequently associated with the patient’s breathing pattern
o P waves: identical, precedes QRS, one for every QRS
o Rate of atria and ventricle: both are exact and are between 60- 100
o PRI wave: is between .12- .20 second
o QRS wave: is less than .12 seconds
Practice strips on page 89-96; quiz questions will come from these
5. The student will know the rules for the following atrial rhythms, the clinical significance
of each and be able to recognize the arrhythmia from a 6 second strip :
Atrial arrhythmias arise from myocardial cells in the atria, but not the SA node. As a rule
the conduction in the AV node and ventricle is normal so the cardiac output and stroke
volumes are normal.
1. Wandering pacemaker pp. 103
In this rhythm, different atrial cells are acting as pacemakers rather than the SA
node. This happens when patient has hypoxemia, or MI or as a side effect of some
mediations, vagal stimulation. This is generally benign
 Rhythmic of atria and ventricle: slightly irregular due to the
changing PRI;
 P waves: are not uniform—at least three different types of P waves,
precedes QRS, one for every QRS
 Rate of atria and ventricle: WNL
 PRI wave: is between .12- .20 second, but varies within normal
 QRS wave: is less than .12 seconds
2. Premature atrial contraction PAC pp. 105
When atrial myocardium is irritated and fires early, we have premature atrial
contraction. Frequent PAC can be a sign of early heart failure, patient may advance to
atrial tachycardia or atrial fibrillation. Can be caused by tobacco and coffee,
hypoxemia
 Rhythmic of atria and ventricle: can be WNL. But interrupted by
premature beats
 P wave: the PAC will look different from the NSR P waves; may come so
early that it is buried in the T wave of the last complex
 Rate of atria and ventricle: this can occur at any rate
 PRI wave: WNL, but
 QRS wave: WNL, unless the PAC did not conduct
3.
Paroxysmal atrial tachycardia PAT pp. 106 three or more
PAC in a row.
PAT are associated with irritation such as tobacco and coffee, hypoxemia. Could
be an early sign of heart failure and can progress to atrial fibrillation. Watch the T
waves because the P could be buried in them
 Rhythmic of atria and ventricle: underlying rhythm is interrupted by
these PAT
 P wave: will differ from the underlying NSR, but look the same within
the PAT
 Rate of atria and ventricle 160-250 BPM
 PRI wave: WNL
 QRS wave: WNL
4.
Atrial flutter pp. 107 in this rhythm, we have a single irritable myocardial
cell in the atria is firing. There are more P than QRS because not all the impulses
get through the AV node. This implies heart disease, but could show up with PE
and valve problems, thyroid storm or lung disease.
 Rhythmic of atria and ventricle: the atrial will march out, but may
not march out with ventricles
 P wave: saw-toothed flutter waves interrupted by normal QRS complexes
 Rate of atria and ventricle: rate of atria 250-350 & is higher than
ventricle rate; look for ratio of A:R may be 2:1 or 3:1 ratio
 PRI wave: cannot count
 QRS wave: WML
5.
Atrial fibrillation pp. 108 in this rhythm, we have hundreds of atrial
impulses. This can result in a PE because of poor blood flow into and out of the
atria. Can decrease CO by 15-30%. This is one of the most common arrhythmias
in the hospital and many of these patient are placed on blood thinners to prevent
PE or strokes. If recent onset, less than 48 hours, we can treat with cardioversion.
 Rhythmic of atria and ventricle: completely irregular with both A
and V
 P wave: cannot find individual P
 Rate of atria and ventricle: atrial R is 350-700 with the Ventricular
rate varied: ventricular rate above 100, is uncontrolled A-fib, ventricular
rate at 100 is rapid A-fib and ventricular rate less than 60 is slow A-Fib.
 PRI wave: cannot find
 QRS wave: WNL
6.
Supraventricular tachycardia SVT pp. 110 . This is a catch-all name
for tachycardias that originate are above the ventral. Could be atrial tachy, sinus
tachy, or junctional tachy but the rate is so fast that we cannot differentiate. This
will result in decreased CO due to rate being so fast, the SV is down
 Rhythmic of atria and ventricle: is regular
 Rate of atria and ventricle: atrial rate is above 130 BPM
 PRI wave: cannot measure because cannot find P
 QRS wave: WNL
Practice strips on page 110-117; quiz questions will come from
these
6. The student will know the rules for the following junctional rhythms, the clinical
significance of each and be able to recognize the arrhythmia from a 6 second strip :
Junctional beats come from the AV node and can be escape beats trying to compensate
for a SA node that fails or early [premature beats] associated with irritation
 premature junctional complexes PJC pp. 125 PJC can be
caused by the same irritants that trigger atrial tachycardia
 Rhythmic of atria and ventricle: is regular until early beat comes in
before the next P is due
 P Wave: will be absent, or retrograde [upside down /or following the
QRS]
 Rate of atria and ventricle: same as underlying rhythm
 PRI wave: if the p wave precedes the QRS, it will be less than .12
seconds; if not cannot measure
 QRS wave: WNL
 Junctional escape pp. 126 because the AV node is pacing the
heart, the rate will generally be lower [about 40-60] this is due to the
failure of the SA node to fire and can be caused by vagal simulation,
ischemia of the SA node, or heart disease. This can decrease the CO.
 Rhythmic of atria and ventricle: is regular until SA node stops [sinus
arrest] and new beat starts
 Rate of atria and ventricle: between 40-60
 P Wave will be absent, or retrograde [upside down /or following the
QRS]
 PRI wave: if the p wave precedes the QRS, it will be less than .12
seconds; if not, cannot measure
 QRS wave: WNL
 Junctional bradycardia pp. 125 because the higher pacemaker
failed the AV node is attempting to trigger the heart. This can be caused
by anything that causes Sinus arrest and will lead to decreased CO
 Rhythmic of atria and ventricle: regular
 Rate of atria and ventricle: less than 40 BPM
 P Wave will be absent, or retrograde [upside down /or following the
QRS]
 PRI wave: if the p wave precedes the QRS, it will be less than .12
seconds; if not, cannot measure
 QRS wave: WNL
 Accelerated junctional pp. 127 this could be associated with
escape or irritation. In this tracing, the HR is basically normal and the CO
is ok.
 Rhythmic of atria and ventricle: regular
 Rate of atria and ventricle: between 60-100
 P Wave will be absent, or retrograde [upside down /or following the
QRS]
 PRI wave: if the p wave precedes the QRS, it will be less than .12
seconds; if not, cannot measure
 QRS wave: WNL
 Junctional tachycardia pp. 128 this is associated with irritation,
can also be called Supraventricular tachycardia because not known if
junctional or atrial or sinus origin
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Rhythmic of atria and ventricle: regular
Rate of atria and ventricle: more than 100 BPM
P wave will be absent, or retrograde [upside down /or following the QRS]
PRI wave: if the p wave precedes the QRS, it will be less than .12
seconds; if not, cannot measure
 QRS wave: WNL
Practice strips on page 128-132; quiz questions will come from these
7. The student will know the rules for the following ventricular rhythms, the
clinical significance of each and be able to recognize the arrhythmia from a
6 second strip :
Ventricular rhythms tend to be dangerous, because the originating pacemaker cannot
produce a good stroke volume and the CO is down. Some of these rhythms require CPR
because they have no pulse rate.

PVC premature ventricular complexes pp. 137 these
are signs of irritation associated with drugs. Low potassium or hypoxemia. 6 or
more PVC in a minute are serious, multifocal PVC are worse than uniform PVC
because uniform PVC imply there is only one foci of irritation. A PVC that falls on
the T wave [R on T] can quickly progress to V-tach or V-fib
 Rhythmic of atria and ventricle: underlying is interrupted
 Rate of atria and ventricle: underlying rate can be normal or
tachycardia
 P wave: not present in this; QRS comes before the P is due
 PRI wave: cannot measure in the PVC
 QRS wave: is wide and bizarre goes in the opposite direction from other
QRS. Another carateristic of the PVC is that there is a compensatory
pause in which nothing happens then the normal beat returns. If you
march out the beat you will see that the next P wave after the PVC comes in
right on schedule. Not all PVC have compensatory pauses
Manifestations of PVC
 Uniform PVC: each PCV is basically identical
 Multifocal PVC: more than one type of PVC
 Couplets pairs of PVC then some normal beats
 Bigeminy: normal beat alternating with a PVC
 Trigeminy: two normal beats then a PVC followed by two normal PVC

Idioventricular pp. 141 Because both the SA node and the AV
node have failed, the ventricle is trying to keep the heart going. These
impulses create little CO and if there is no pulse, the patient will require
CPR
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Rhythmic of atria and ventricle: no atrial beat, ventricle is regular
Rate of atria and ventricle: atrial none, ventricular 20-40 BPM
P wave : absent
PRI wave: absent
QRS wave: wide and bizarre with T wave in the opposite direction
Accerated idioventricular pp. 142 Occationally after
successful reperfusion after s/p MI, the irritable ventricle will fire at a near
normal rate. Tends to be self-limiting
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Rhythmic of atria and ventricle: irregular or regular
Rate of atria and ventricle: : atrial none, ventricular 60-100 BPM
P wave : absent
PRI wave: absent
QRS wave: wide and bizarre with T wave in the opposite direction

Agonal rhythem pp. 140: the last firing of the dying heart, as
each myocardial cell tries to restart the heart. Patient is dying. There will
be little or no CO, and no pulse so CPR needs to be done
 Rhythmic of atria and ventricle: no atrial, ventricle irregular
 Rate of atria and ventricle: less than 20 BPM [occasionally one or two
faster]
 P wave : absent
 PRI wave: absent
 QRS wave: wide and bizarre with T wave in the opposite direction

V tachycardia pp 143
basically a run of PVC eventually becomes
V-tachycardia. Pt will have no CO, no pulse so we need to be doing CPR
 Rhythmic of atria and ventricle: usually very regular
 Rate of atria and ventricle: no atrial, ventricular rate is 100BPM or
more
 P wave : absent
 PRI wave: absent
 QRS wave: wide and bizarre with T wave in the opposite direction

V fibrillation pp 144: hundreds of ventricular cells are firing.
No
CO, no pulse, we need to do CPR
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Rhythmic of atria and ventricle: total chaos
Rate of atria and ventricle: cannot count
P wave : absent
PRI wave: absent
QRS wave: just wavy spiky baseline and cannot find T waves
Torsades de pointes pp. 143: a form of V-tachycardia caused
by cardiac drugs such as quinidine or procainamide, usually followed by Vfib
8.
 Looks like V-tachy but the impulses get smaller and larger so that it looks
like thread on a spindle

Asystole flat line pp. 145: no CO, no pulse need to do CPR
Flat line
Practice strips on page 148-154; quiz questions will come from these
9. The student will know the rules for the following A-V blocks rhythms, the clinical
significance of each and be able to recognize the arrhythmia from a 6 second strip :
In AV blocks we see slow conduction through the AV junction. The problems will be found in
the PRI intervals. These problems happen because of infarction at the junction, or digitalis
OD or side effect of beta blockers or Ca Channel blockers

First degree block pp. 161. Needs to be watched for increased block.
Rarely causes decreased CO
 Rhythmic of atria and ventricle: regular
 Rate of atria and ventricle: normal rates for both
 P wave: normal
 PRI wave: prolonged, but a QRS follows every P wave
 QRS wave: normal
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Second degree block type I [Wenckebach] pp. 162 Is
a transitional phase that gets worse. Can be caused by MI and digitalis
 Rhythmic of atria and ventricle: irregular
 Rate of atria and ventricle: atrial rate faster than ventricular rate, but
atrial rates 60-100
 P wave: more P waves than QRS
 PRI wave: prolonged, longer, longer, longer then dropped conduction so
that QRS doesn’t follow the P, then cycle starts over
 QRS wave: normal
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Second degree block type II pp. 163 Can be caused by MI and
digitalis. If decreasing CO. patient needs a pacemaker
 Rhythmic of atria and ventricle: irregular
 Rate of atria and ventricle: rates within normal, but atrial rates faster
than ventricular
 P wave: more P waves than QRS
 PRI wave: normal then occasionally a P is not followed by QRS
 QRS wave: normal

Third degree AV block pp 165 Can be caused by MI. can decrease
the CO and the pulse rate. Needs pacemaker
 Rhythmic of atria and ventricle: march out A and march out V, but
the two have different rhythms
 Rate of atria and ventricle: different; atrial 60-100, but ventricular
20-60
 P wave: looks normal; not always has a QRS
 PRI wave: varies
 QRS wave: if the block is lower than the junction, the QRS will be wide.
Practice strips on page 166-173; quiz questions will come from these
10. The student will recognize the EKG tracing associated with digitalis overdose and various
electrolyte imbalances. pp338-340

Digitalis

 can cause the ST segment to ‘sag’ much like the look of an MI
 PRI can be prolonged with digitalis toxicity
Normal potassium is 3.5-5.
 If potassium is lower than normal we can see flattened T waves and wavy
U waves following the T
 If potassium levels are high [above 6], we see tall spiky, pointy T waves,
 if the potassium rises to 8 the QRS gets longer and the patient is close to
cardiac arrest
 Calcium problems:
 High Ca can cause the ST segment to shorten & the QT interval to be
shortened
 Low Ca can cause the prolonged QT
11. The student will recognize the appearance of an abnormal ST segment and be able to
determine the clinical significance of the ST segment deviation. pp345-348
 The normal ST segment should be on the same line as the PRI. If the ST
segment is raised above the PRI there is evidence of myocardial injury.
 Concave elevated ST segments pericarditis, but could also be MI
 Convex elevated ST segment MI in progress
 Depressed ST segment implies ischemia [lose of blood flow before infarction]
12. The student will understand the significance of an axis deviation and how these
deviations can be caused by hypertrophy or infarction. pp. 308-309
Vector with normal conduction
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
The total vector [direction] of all the electrical energy of the myocardial
conduction is from right to left, from top to bottom and from front to back. This
is seen as the normal axis which is between zero and +90 degrees. When there is
a problem with the myocardium, we may see changes in the vectors which will
change the axis.
If you draw a circle over the chest with the heart in the middle, then create
notches 180 degrees around the circle you will have an axis.
-90
Indeterminate axis deviation
Left axis deviation
-/+ 180
0
Right axis deviation
Normal axis
+90
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Normal is axis is from zero to +90
The axis will deviate from infarction
The axis will deviate to hypertrophy
We find cor pulmonale because there is an axis deviation toward the right [right
ventricular hypertrophy]
 To look for axis deviation we have to look at the 12 lead EKG
13. The student will understand the significance of the cardiac stress test and
the angiogram in diagnosis of heart disease. pp. 433-445
 Indications for cardiac stress test is to establish the presence of coronary artery
occlusion in a patient who has a history of exercise induced SOB or angina, or a
person with a strong family history of MI, or to assess the patient post coronary
artery bypass surgery, or as a follow up to a rehab program
 The patient is placed on EKG monitor and worked on a treadmill or ergo-bike
until sufficient work [85% of the target HR] causes the HR to rise to maximal
level and starts causes changes in the EKG or the patient’s symptoms [HR,
systemic BP chest pain, fatigue.]
 Radioisotopes are injected into the vein and the chest is scanned before and
several hours after exercise to study the perfusion of the myocardium.
 Patients who cannot exercise such as persons with arthritis, can be stressed
pharmacologically with a drug such as adenosine which causes tachycardia.
 Persons with problems with coronary blood flow will have problems with the
cardiac stress test because obstruction will not allow blood to flow into the
myocardium as needed.
 Persons with positive cardiac stress tests will be followed by an angiogram of the
coronary circulation to see if the occlusion is present. Cardiac stress testing
14. The student will understand the indications and contraindications for the
use of the holter monitoring of the EKG over 24 hours. pp. 453-456
Holter monitoring of an ambulatory EKG of the patient over several hours [12-24 hours]
is indicated when a person has a history of syncopy or near-syncopy, it is indicated when
patients are suspected of arrhythmias or who have sporatic chest pain or SOB. Once a
patient has been started on a cardiac drug we can monitor the effect of the drug by
performing a 24 hour monitoring of the EKG.
Because the holter monitor is usually done as an outpatient, it is contra-indicated for
severe symptoms that might be better treated and monitored in the hospital.