Sample EKG #1.

Determine rate, rhythm,

diagnosis, axis

Interpretation EKG#1
Rate: approx 75/min
Rhythm: Baseline sinus rhythm, P:QRS is 1:1
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.

Sample EKG#2

Interpretation EKG#2
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 3:1. (3 flutter waves to one QRS).

Sample EKG#3

Interpretation EKG#3
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 >1mm 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.

EKG #4

Interpretation of EKG #4:

This 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.)

EKG #5

Interpretation of EKG#5:
Baseline sinus rhythm.
Rate appears normal (60-100)
Axis is physiologic
No evidence of block or conduction abnormality
There is widespread ST segment elevation in all
leads
GLOBAL ST elevation is consistent with
pericarditis

EKG #6

EKG #6 Interpretation:
EKG #6 reveals a baseline sinus rhythm.
Rate approximately 80 bpm
Axis is physiologic
Complexes in V5 greater than 35 mm suggest
LVH
ST segment depression in leads V4-V6 in the
setting of LVH is suggestive of a, strain
pattern.
No evidence of bundle brnach block
ST segment depression in inferior chest
leads

EKG #7

EKG #7 Interpretation:
Baseline sinus rhythm.
Rate of approx 80/min
Axis is physiologic
No evidence of ventricular hypertrophy, but
RAH is possible due to P wave in lead II >0.5
mm.
Possible RBBB because of RSR in V1 and QRS
>0.10
Note pathologic Q waves in II, III, aVF
Pathologic Q waves are >0.04s or >1/3 the
height of the R wave.
Changes consistent with inferior wall
myocardial infarction (old, possibly
transmural).
R wave progression preserved.

EKG #8

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 wave
Possible RVH due to R>S in V1
Note pervasive strain pattern due to RVH
evidenced in precordial leads.
The presence of RAD plus the R>S in V1 is
suggestive of RVH.

Any drug toxicity? EKG#8

EKG Interpretation #8:

Though 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.

EKG #9

EKG #9:
This 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.

EKG #10

EKG #10 Interpretation:

This 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.

Final Rhythm Review

Rhythm interpretation:
-The first strip reveals a prolonged PR
interval, with 1:1 conduction. This rhythm
is a first degree A/V block.
-The second strip is a 4:1 (or 3:1) atrial
flutter.
-The third rhythm strip reveals the typical
atrial fibrillation. Note the fibrillatory
baseline with irregular R to R intervals.

Chamber
enlargement
review:
Name that
hypertrophy?
a) RVH
b) LVH
c) RAH
d) LAH

The EKG findings are consistent with: RVH

Criteria for right ventricular hypertrophy
include:
-Tall R wave in lead V1 (R>S)
-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.