RUNNING: EKG INTERPRETATION
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Simulation Lab: Lesson
Module 2 Activity
Presented to
Dr. Eva Stephens
THE UNIVERSITY OF TEXAS
MEDICAL BRANCH at GALVESTON
In Partial Fulfillment
Of the Requirements for the Course
GNRS 5320: Teaching Practicum
By
Caroline Wesonga RN BSN
November 13th 2014
EKG INTERPRETATION
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Basic ECG/Telemetry
The Electrocardiogram
 The tracing recorded from the electrical activity of the heart forms a series of waves and
complexes that have beet arbitrarily labeled PQRST and U waves
 To identify ECG Rhythms, you must know what each wave means, and how it should
appear normally.
 P Wave- generated by the SA node; represent electrical depolarization of
atrium
 PRI interval-should be 0.12-0.20
 QRS complex- The QRS makes the complex and should be 0.8-0.12
 T Wave - Looks a lot like a P Wave, but comes after the QRS and
represent depolarization of the ventricles
 U Waves - does not always occur; likely represent depolarization of the
Purkinje fibers.
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ECG paper is a grid where time is measured along the horizontal axis
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each small square is 1 mm in length and represent 0.4 seconds
each larger square is 5 mm in length and represent 0.2 seconds
so 5 large squares represent 1 second
Basic EKG Interpretation
There are essentially 5 steps for EKG Interpretation
1. Rate (Calculate the Heart Rate)
 The quickest and easiest method to calculate heart rate from an ECG is to
count the number of R-R wave and multiply by 10. If the heart rate is
fast>100bpm it is called tachycardia
 if the rate is slow <60bpm it is called bradycardia
2. Rhythm (measure the regularity or rhythm of the R-wave  Basically do the R wave occur in a regular even pattern? or they are
irregular
3. P Wave (Examine the P wave)
 Does it look normal? is there a P wave before each QRS complex? Are
there extra P waves with no partner QRS? or do you even see any P wave
at all?
4. PRI interval- Measure the P-R interval. Is it within 0.12-0.20 seconds long?
5. QRS-Measure the duration of the QRS complex. Is it 0.08-0.12 seconds long?
EKG INTERPRETATION
Two Methods of Counting Heart Rate
Six Second Method
Ventricular Rate
 Count the number of complete QRS within a period of 6 seconds
 Multiply that number by 10 to determine the number of QRS complexes in a
minute
 Best Used for Irregular Rhythms
Small Box Method
 Count the number of small boxes between two consecutive waveforms (R-R
Interval or
P-P interval) and divide by 1500
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Basic Rhythms to know
Normal Sinus Rhythm
1. Rate
2. Rhythm
3. P Wave: Normal in appearance, regular, One P Wave for every QRS complex
4. PRI interval-0.12-0.20 seconds
5. QRS-0.8-0.12 seconds
You must know what is normal to know what is abnormal!
Sinus Bradycardia
1. Rate-Below 60bpm
2. Rhythm- Regular
3. P Wave - Normal in appearance, regular, P Wave for every QRS Complex
4. PRI Interval-0.12-0.20 seconds
5. QRS- 0.08-0.12
EKG INTERPRETATION
Clinical Significance:
 This rhythm is often seen as a normal variation in athletes, during sleep or in response to
a vagal maneuver or many medications especially beta blockers
Treatment
 Treat the underlying cause, atropine, isuprel or artficial pacing if patient is
hemodynamically compromised
Sinus Tachycardia
1. Rate-100-150bpm
2. Rhythm-Regular
3. P Wave- normal in appearance, regular, one P wave for every QRS Complex
4. PRI-0.12-0.20
5. QRS-0.08-0.12 seconds
Underlying causes
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CHF
hypoxia
PE
Increased temperature
stress
response to pain
Treatment
 Identification of the underlying cause and correction
 if the heart rate is >150bpm it is considered SVT (Supraventricular Tachycardia)
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ATRIAL RHYTHMS
Atrial Tachycardia
1. Rate - 100-150
2. Rhythm-Regular
3. P Wave- May encourch on T Wave
4. PRI interval -Diffciult to measure due to the speed of the rhythm
5. QRS-up to 0.12
Causes
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Anxiety
excitement
exertion
pain
drugs that increase sympathetic tone (epinephrine, dopamine, cocaine)
drugs that block the vagal tone (atropine)
fever
PE
Hyperthyroidism
intravascular volume loss
Clinical significance
 When the ventricular filling time is limited, cardiac output is decreased, decreased
perfusion to other vital organs occur resulting in confusion, dizziness, lightheadedness,
SOB, syncope, heart failure and MI.
Treatment
 consult attending is symptomatic.
 Treatment is based on recognition of the underlying cause.
 Adenosine is often used
EKG INTERPRETATION
Supraventricular Tachycardia
1. Rate- 150-250
2. Rhythm-Regular
3. P Wave- May merge with T. Difficult to see due to the rate
4. PRI - Difficult to measure
5. QRS- upto 0.12
Causes
 Caffeine, tobacco, alcohol, emotional stress, heart failure.
 Hemodynamic effects- may decrease cardiac output
Treatment
Treat rate by doing vagal stimulation, adenosine, cardio version, sedation, oxygen
Atrial Flutter
1. Rate-250-300bpm
2. Rhythm-regular but can be irregular
3. P Wave- No definable P Waves present. Usually saw tooth pattern is present
4. PRI interval- unable to determine
5. QRS- 0.8-0.12 seconds
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Clinical significance
 With rapid ventricular response are the same as Atrial Tachycardia.
 The Atria do no contract and empty as they normally do causing as loss of the atrial kick
and a reduction of as much as 25% of the cardiac output
Causes
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It occurs in diseased hearts eg valvular (esp. Mitral) disease.
CHF
cardiomyopathy
Acute MI
COPD
PE
After cardiac surgery
Treatment
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Depend on the clinical condition
Beta blockers, Calcium Channel blocker, digitalis
DC cardio version
Control rate with Calcium Channel Blockers
Convert Rhythm with Cardioversion, amiodarone
Atrial Fibrillation
1. Rate-Atrial rate is usually slow, normal or fast aka (Afib with RVR)
2. Rhythm: Irregularly Irregular "Hallmark for this Dysrhythmia"
3. P Wave- No present, usually saw tooth
EKG INTERPRETATION
4. PRI- Unable to determine
5. QRS- 0.08-0.12
Causes
 Associated with COPD, CHF
 chronic ischemic disease, valvular disease, hyperthyroidims, sleep apnea, hypertensive
disease
 Clinical significance
 The Atria do not contract and empty as normal causing loss of the Atrial kick and a
reduction of as much as 25% of the cardiac output.
Treatment
Atrial Fibrillation <48Hours
 Oxygen
 ABCD-(Amiodarone, Beta Blockers, Calcium Channel Blockers), Direct Current
Cardioversion
Atrial Fibrillation >48 hours
 Oxygen
 ABC- (Amiodarone, Beta Blocker, Calcium Channel Blockers)
 Delay cardioversion until the patient is antiocoagulated and atial thrombi excluded
Premature Atrial Contractions
1. Rate- Dependents on the underlying rhthym - slow, normal or fast
2. Rhythm- Irregular because of the premature beats
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3. P Wave- P wave of PAC usually has different shape than the sinus P wave because they
originate from a different atrial pacemaker
4. PRI-PAC interval may be different from underlying rhythm
5. QRS- up to 0.12 seconds
Clinical Significance
 Isolated PACs may occur in persons with apparently healthy hearts and are not
significant
 in persons with heart disease, however, frequent PACs may indicate enhanced
automaticity of the atria, or a reentry mechanism resulting from a variety of cause such as
CHF or Acute MI
 in addition, PACs may warn of or initiate more serious supraventricular arrhythmias such
as atrial tachycardia, atria flutter or atrial fibrillation
Causes
May be associated with
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emotional stress or excessive caffeine intake
sympathomimetic agents (epinephrine, isuprel)
hypothyroidism
various types of structural heart disease and increase in frequency with age
Treatment
 Digitalis
 Beta Blocker
 Calcium Channel Blockers
VENTRICUALAR RHYTHMS
Ventricular Tachycardia
1. Rate- Greater than 100bpm
EKG INTERPRETATION
2. Rhythm- Usually Regular
3. P Wave- None or buried in the QRS Complex
4. PRI - Unable to measure
5. QRS- Wide, a bizzare morphology > 0.12
Ventricular Tachycardia is three or more consecutive PVCs
Clinical significance
 Signs and symptoms vary depending of the nature and severity of cardiac disease
 cardiac output decreased as much as 25% or more
 Considered a life threatening arrhythmia
Causes
physiologic
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ishchmia
hypotension
hypoxia
hypokalemia
heart failure
Treatment
If pulse is present
 Amiodarone or lidocaine
 synchronized cardioversion
 treat underlying cause (Stable -treat with medication, if unstable cardiovert)
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If Pulse is absent
 Treat at V-Fib- immediate defrillation and ACLS protocols, identification of the
underlying cause is also needed
Ventricular Fibrillation
1. Rate- Unable to measure
2. Rhythm- Erratic, irregular, cannot measure
3. P Wave- Unable to measure
4. PRI - Unable to measure
5. QRS- Unable to measure
Causes
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Acute myocardial Infarction
Digitalis toxicity
Drug overdose
Electrocusion
Treatment
Follow ACLS Protocol
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CPR
Epinephrine
Amiodarone
Magnesium
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EKG INTERPRETATION
Premature Ventricular Contractions
1. Rate- Slow, normal or fast
2. Rhythm- Underlying rhythm consistent with occasional premature ventricular beats
3. P Wave- Related to underlying rhythm, PVCs has no P-wave
4. PRI- Related to underlying rhythm
5. QRS- Related to underlying rhythm. PVC is >0.12 seconds
Clinical significance of PVCs
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not uncommon in normal adult of all ages
occurs more frequently with advancing age
young adults may have PVCs because of anxiety or excessive caffeine intake
common with mitral valve prolapse
may be seen with virtually any type of heart diseases
most common arrhythmia seen with acute MI
Causes
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stimulants
Myocardial ischemia or infarction
digitalis toxicity
cardiac surgery
hypoxia
cardiomyopathy
 electrolyte imbalances
Treatment
 search for potentially reversible causes and contributors, particularly hypoxia,
hypokalemia, hypomagnesaemia and certain drug stimulant drugs
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EKG INTERPRETATION
Asystole
1. Rate-None
2. Rhythm- None
3. P-Wave- May be present but no QRS to follow
4. PRI - Unable to measure
5. QRS- Unable to measure
Clinical Significance
Cardiac output and a palpable pulse are absent resulting in
 loss of consciousness
 seizure
 Apnea
 Death
Treatment
ACLS Protocols
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CPR
Epinephrine
Atropine
Determine the cause of asystole
consider end of life decision
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HEART BLOCKS
First Degree Heart Block
1. Rate- Variable
2. Rhythm- Variable
3. P Wave- Normal shape, one P Wave for each QRS
4. PRI- Widened-greater than >0.20
5. QRS- 0.08-0.12
Clinical Significance
 First degree AV Block produces no signs and symptoms
 Because it can progress to a higher-degree AV Block under certain conditions (eg
excessive administration of beta blocker or calcium channel blockers and acute inferior or
right ventricular MI), the patient may require observation and ECG monitoring
Causes
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Inferior MI
ischemic acute MI
digitalis toxicity
hyperkalemia
Increased vagal tone
acute rheumatic fever
myocarditis
Treatment
 Generally does not require specific treatment
 treat the underlying cause
 Atropine
 observe progression to a more advanced AV Block
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Second Degree AV Block Type 1 - Mobitz 1 (Wenchebach)
1. Rate- Variable
2. Rhythm- Regular
3. P Wave- Normal Morphology with regular P to P interval
4. PRI- The PRI is progressively longer until the impulse from the AV node is completely
blocked resulting in an absent QRS complex (longer, longer, longer Drop is a Wenckenback
block)
5. QRS- 0.08-0.12 Seconds
 P wave occurs at regular interval, the PR interval progressively lengthen from beat to
beat until a P wave that is not followed by a QRS complex occur.
 Mobitz I is usually asymptomatic because the ventricular rate remains nearly normal and
cardiac output is not usually affected
Causes
 increased parasympathetic (Vagal) tone
 effects of medications eg (Digitalis, Beta-blockers, Calcium Channel Blockers and
Hyperkalemia
 acute inferior MI
 digitalis Toxicity
Treatment
 if ventricular rate slows and patient is symptomatic, protocol for symptomatic
bradycardia is initiated
 Atropine, external or transvenous pacing, dopamine or epinephrine given to increase
blood pressure
 Temporary and resolves spontaneous
 normal variant in athletes because of physiological increase in vagal tone
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Second Degree AV Block (Mobitz Type II)
1. Rate- Variable
2. Rhythm- Usually Regular
3. P Wave- Normal Morphology with constant P-P interval
4. PRI - The PRI interval may be normal or prolonged, but is constant until one P wave is not
conducted to the ventricles
5. QRS- Normal or widened (Because this is usually associated with a bundle branch block)
Clinical Significance
 It is more serious than type 1. Mobitz II is usually associated with an anterior wall MI. It
is not associated with increased vagal tone or drug toxicity.
 It is less common but more severe than Mobitz I.
 It has the potential to progress suddenly to 3rd degree with little or no warning.
Causes
 it can occur after an acute anterior MI
 not associated with increased vagal tone or drug toxicity
Treatment
 external pacemaker while preparations are made for insertion of a temporary or
transvenous pacemaker
Third Degree AV Block
1. Rate- Atrial rate is usually normal, ventricular rate is usually less than 70bpm. The atrial rate
is always faster than the ventricular rate
2. Rhythm- Irregular
3. P Wave- Normal Morphology with constant P to P interval, but have no identifiable
relationship to the QRS complexes
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4. PRI-The PRI may be normal or prolonged
5. QRS- Normal or widened
Clinical Significance
 If ventricular rate is within normal limits, patient may be symptomatic of minor
symptoms such as weakness, fatigue, dizziness and exercise intolerance
 If ventricular rate is extremely slow, cardiac output is decreased and symptoms such as
hypotension, dyspnea, heart failure and chest pain seen.
 Atrial and ventricular contractions are unrelated due to complete blocking of the atrial
impulses to the ventricles. (The atria and the ventricles are not talking with one another).
 Can progress to asystole.
Causes
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Digitalis toxicity
acute infection
MI
degeneration of the conductive tissue
Treatment
 External pacing and atropine for acute
 permanent pacing for chronic complete heart block
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References
Beasley, B. (2003). Understanding EKGs: A Practical Approach (3rd Ed.). Prentice Hall:
Upper Saddle River, NJ.
Brosche, T., A. (2009). The EKG Handbook. Jones and Bartlett Publishers: Sudbury, MA