EKG Self Study Guide

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EKG Self Study Guide

1. View the slide show
2. Interpret the EKGs
3. Advance slides to review findings
4. Good luck!

Companion to 12-lead EKG InterpretationBen
Lawner, NREMT-PNSUCOM Division of EMS Training
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Recall the approach
1. Take a deep breath2. Analyze rate3. Analyze
rhythm4. Look at axis5. Look for
injury/strain/ischemic patterns6. Look for
conduction defecits (RBBB, LBBB)7. Hypertrophy,
meds, toxic effects8. Make your measurments (PR,
QT/QTc, QRS)
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(No Transcript)
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Sample EKG 1. Determine rate, rhythm, diagnosis,
axis
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Interpretation EKG1
Rate approx 75/min Rhythm Baseline sinus
rhythm, PQRS is 11 Axis Physiologic Injury ST
elevation is present in the anterior, septal, and
literal leads. Massive ST segment elevation is
present in V2-V6, with moderate ST elevation that
obscures visualization of the QRS complex in lead
one. Changes are consistent with LCA occlusion.
Other R wave progression is difficult to
determine secondary to the pathological ST-T
changes. No evidence of chamber enlargement or
hypertrophy.
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Sample EKG2
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Interpretation EKG2
The EKG reveals an atrial flutter at a rate of
approx 100 per minute. The QRS complexes are
narrow and reveal a physiological axis. There is
evidence of a premature ventricular complex,
readily identifiable in the lateral chest leads.
No evidence of ischemia or infarction. No
evidence of R or L bundle branch block. Atrial
flutter is conducted at approx 31. (3 flutter
waves to one QRS).
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Sample EKG3
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Interpretation EKG3
The EKG reveals an irregularly irregular rhythm
suggestive of atrial fibrillation. The rate is
variable, with a controlled or slow ventricular
response. The axis is physiologic. ST-T changes
suggestive of ischemia/injury are present in
leads II, III, and aVF. ST elevation of gt1mm in
limb leads is indicative of a possible inferior
wall myocardial infarction. Reciprocal changes
are seen in leads one and aVL. Early R wave
progression.
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EKG 4
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Interpretation of EKG 4This EKG reveals a
baseline sinus rhythm. Rate cannot be determined
definitively. The QRS is wide V1 reveals an RSR
pattern consistent with a right bundle branch
block. The axis is physiologic but is not easy to
determine because of ST elevation present in
leads III and aVF (inferior wall). Other abnormal
T changes are seen (T wave inversion) in leads
V1-V4. ST segment depression is present in the
lateral chest leads as well. No evidence of
chamber enlargement. ST elevation in III and aVF
with reciprocal depression in I and aVL may be
consistent with an inferior wall MI (RCA lesion.)
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EKG 5
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Interpretation of EKG5Baseline sinus
rhythm.Rate appears normal (60-100)Axis is
physiologicNo evidence of block or conduction
abnormalityThere is widespread ST segment
elevation in all leadsGLOBAL ST elevation is
consistent with pericarditis
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EKG 6
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EKG 6 InterpretationEKG 6 reveals a baseline
sinus rhythm. Rate approximately 80 bpmAxis is
physiologicComplexes in V5 greater than 35 mm
suggest LVHST segment depression in leads V4-V6
in the setting of LVH is suggestive of a, strain
pattern.No evidence of bundle brnach blockST
segment depression in inferior chest leads
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EKG 7
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EKG 7 Interpretation Baseline sinus
rhythm.Rate of approx 80/minAxis is
physiologicNo evidence of ventricular
hypertrophy, but RAH is possible due to P wave in
lead II gt0.5 mm. Possible RBBB because of RSR
in V1 and QRS gt0.10Note pathologic Q waves in
II, III, aVFPathologic Q waves are gt0.04s or
gt1/3 the height of the R wave.Changes consistent
with inferior wall myocardial infarction (old,
possibly transmural). R wave progression
preserved.
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EKG 8
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Interpretation of EKG 8 Baseline sinus rhythm,
rate approx 80. Right axis deviation, as
evidenced by a primarily negative complex in lead
I.Possible RAH due to large lead II P
wavePossible RVH due to RgtS in V1Note pervasive
strain pattern due to RVH evidenced in precordial
leads. The presence of RAD plus the RgtS in V1 is
suggestive of RVH.
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Any drug toxicity? EKG8
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EKG Interpretation 8Though the picture has
poor resolution, it is clear that the lateral
leads reveal a pattern of digoxin toxicity. Even
though rate is impossible to determine, the
cored-out and depressed ST segments in the
lateral precordial leads suggest digoxin
toxicity. Furthermore, the irregular R to R
intervals hint at a baseline rhythm of atrial
fibrillation. Many patients take digoxin for
chronic atrial fibrillation. Moderate left axis
deviation.
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EKG 9
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EKG 9This rhythm strip reveals a profound
bradycardia. There is no relationship between the
atria (P waves) and QRS complexes. This is
consistent with complete A-V dissociation, or
third degree heart block. This rhythm frequently
requires emergent pacing.
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EKG 10
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EKG 10 InterpretationThis EKG reveals a
baseline sinus rhythm (ps are difficult to
discern.) The rhythm is a sinus tachycardia at
approximately 100 per minute. Massive ST segment
elevation is present in leads II, III, and aVF.
Reciprocal changes (depression) in leads I and
aVL. Note that the precordial chest leads (v4R to
V6R) are placed on the right side of the chest.
ST segment in a right-sided EKG likely
indicates an inferior wall MI that involves the
RIGHT ventricle. Be careful when giving these
patients NTG. Administration of nitrates, due to
the alteration of venous preload, can precipitate
hypotension. Treat these MIs with fluid first.
The axis is physiologic, no evidence of chamber
enlargement. R wave progression is not of value
in this EKG because of the right sided chest
leads.
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Final Rhythm Review
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Rhythm interpretation -The first strip reveals
a prolonged PR interval, with 11 conduction.
This rhythm is a first degree A/V block. -The
second strip is a 41 (or 31) atrial
flutter. -The third rhythm strip reveals the
typical atrial fibrillation. Note the
fibrillatory baseline with irregular R to R
intervals.
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The QT/QTc Interval Calculation and
Significance Measurement From the beginning of
the Q wave to the end of the T
waveParameter Normal QT intervals range from
0.36- 0.41.Abnormalities Hypercalcemia will
shorten the QT interval and yield measurements
from 0.26-0.36s.QTc The QT interval varies
with heart rate. The corrected QT interval is
calculated by adjusting your measurement for
the patients heart rate. The QT divided by
the square root of the R to R interval
typically gives a QTc around 0.44 seconds.
Lengthening Diseases, drugs, and toxins can
prolong the QT interval and precipitate
attacks of lethal ventricular arrhythmias.
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Long QT syndrome, Romano-Ward Syndrome EKG
The QTc, adjusted for rate, would almost
certainly be greater than 0.44 seconds. You can
see in this example that the QTc is approximately
0.5-0.6 seconds (almost 3 large boxes!)
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Rate Cheat SheetBesides calculating the number
of R waves in a 3 or 6 second strip and
multiplying by 20 or 10 seconds, simply divide
the number of small (0.04s) units between
consecutive R waves into 1500. -The heart rate
can also be calculated from the R to R interval.
Simply divide the number of large boxes (0.2s)
between consecutive R waves into 300. -15 large
boxes is a three second strip! -30 large boxes
represents a six second strip! -For irregularly
irregular rhythms, try to calculate rate with a
decent time interval, preferably greater than a 3
second strip.
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Potassium summary
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Digitalis effect summaryIn addition to a wide
variety of atrial conduction defects, ventricular
ectopy, and heart blocks, early digitalis
toxicity manifests itself as a shortening of the
QT interval in addition to scooped-out appearing
ST segments.
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Precise axis calculation, anyone? Remember that
it is simply a method of addition. IIIIII. The
mean QRS vector will also point 90 degrees away
from the most isoelectric lead. Leads with large
amplitude R waves will shift the mean QRS vector
in their general direction. Remember about
dropping those stubborn perpendiculars?
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Chamber enlargement review Name that
hypertrophy? a) RVHb) LVHc) RAHd) LAH
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The EKG findings are consistent with
RVH Criteria for right ventricular hypertrophy
include-Tall R wave in lead V1 (RgtS)-qR
pattern in V1-Right axis deviation-T wave
inversion in right to mid precordial leads
possible-Commonly due to ASD! -The pattern of T
wave inversion is called, strainand is
consistent with repolarization problems in
hypertrophied muscle.
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Biphasic P waves, P waves with a terminal
negative component or notched P waves are
consistent with..?
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Left Atrial Hypertrophy! What about the following
EKG tracing?
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Right atrial enlargementFactors suggesting
right atrial enlargement include-Tall, humped P
waves-May be higher than 2.5 mm-Patient history
may be significant for asthma, COPD, or pulmonary
hypertension
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A zebra says, Good-bye What syndrome is
typical of the following EKG features?-Short PR
interval-Bouts of tachycardia-Upsloping R wave,
deltawave-Often abberant conduction through
ventricles (widegt0.10s QRS)-The name of this
zebra is. -Next slide for answer and EKG.
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Lead two reveals the short PR, delta wave, and
the wider-appearing QRS typical of
Wolff-Parkinson-White syndrome.