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OVERVIEW OF EKG AND

TELEMETRY
1. Review of the conduction system
2. EKG waveforms and intervals
3. EKG leads
4. Determining heart rate
5. Determining QRS axis
The electrocardiogram (EKG) is a representation of the
electrical events of the cardiac cycle.

Each event has a distinctive waveform, the study of


which can lead to greater insight into a patients cardiac
pathophysiology.
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
Drug toxicity (i.e. digoxin and drugs which prolong the
QT interval)
Leads are electrodes which measure the difference in
electrical potential between either:

1. Two different points on the body (bipolar leads)

2. One point on the body and a virtual reference point


with zero electrical potential, located in the center of
the heart (unipolar leads)
The standard EKG has 12 leads: 3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads

The axis of a particular lead represents the viewpoint from


which it looks at the heart.
Adapted from: www.numed.co.uk/electrodepl.html
Limb Leads Precordial Leads

Bipolar I, II, III -


(standard limb leads)

Unipolar aVR, aVL, aVF V1-V6


(augmented limb leads)
Rule of 300

10 Second Rule
Take the number of big boxes between neighboring
QRS complexes, and divide this into 300. The result will
be approximately equal to the rate

Although fast, this method only works for regular


rhythms.
www.uptodate.com

(300 / 6) = 50 bpm
www.uptodate.com

(300 / ~ 4) = ~ 75 bpm
(300 / 1.5) = 200 bpm
It may be easiest to memorize the following table:

# of big Rate
boxes
1 300
2 150
3 100
4 75
5 60
6 50
As most EKGs record 10 seconds of rhythm per page,
one can simply count the number of beats present
on the EKG and multiply by 6 to get the number of
beats per 60 seconds.

This method works well for irregular rhythms.


The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

33 x 6 = 198 bpm
The QRS axis represents the net overall direction of the
hearts electrical activity.

Abnormalities of axis can hint at:


Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
By near-consensus, the
normal QRS axis is defined
as ranging from -30 to +90.

-30 to -90 is referred to as a


left axis deviation (LAD)

+90 to +180 is referred to as


a right axis deviation (RAD)
The Quadrant Approach

The Equiphasic Approach


Predominantly Predominantly Equiphasic
Positive Negative
1. Examine the QRS complex in leads I and aVF to determine if
they are predominantly positive or predominantly negative.
The combination should place the axis into one of the 4
quadrants below.
2. In the event that LAD is present, examine lead II to determine
if this deviation is pathologic. If the QRS in II is
predominantly positive, the LAD is non-pathologic (in other
words, the axis is normal). If it is predominantly negative, it is
pathologic.
The Alan E. Lindsay
ECG Learning Center
http://medstat.med.utah.
edu/kw/ecg/

Negative in I, positive in aVF RAD


The Alan E. Lindsay
ECG Learning Center
http://medstat.med.utah.
edu/kw/ecg/

Positive in I, negative in aVF Predominantly positive in II


Normal Axis (non-pathologic LAD)
1. Determine which lead contains the most equiphasic QRS
complex. The fact that the QRS complex in this lead is
equally positive and negative indicates that the net
electrical vector (i.e. overall QRS axis) is perpendicular to
the axis of this particular lead.

2. Examine the QRS complex in whichever lead lies 90 away


from the lead identified in step 1. If the QRS complex in
this second lead is predominantly positive, than the axis of
this lead is approximately the same as the net QRS axis. If
the QRS complex is predominantly negative, than the net
QRS axis lies 180 from the axis of this lead.
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

Equiphasic in aVF Predominantly positive in I QRS axis 0


The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

Equiphasic in II Predominantly negative in aVL QRS axis +150


1. View the slide show
2. Interpret the EKGs
3. Advance slides to review findings
4. Good luck!
1. Take a deep breath
2. Analyze rate
3. Analyze rhythm
4. Look at axis
5. Look for injury/strain/ischemic patterns
6. Look for conduction defecits (RBBB, LBBB)
7. Hypertrophy, meds, toxic effects
8. Make your measurments (PR, QT/QTc, QRS)
Sample EKG #1. Determine rate, rhythm, diagnosis, axis
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.
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).
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.
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.)
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 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 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.
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:

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 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. 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.
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.
The QT/QTc Interval: Calculation and Significance
Measurement: From the beginning of the Q wave to the
end of the T wave
Parameter: 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.
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!)
Rate Cheat Sheet

Besides 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.
Potassium summary:
Digitalis effect summary:

In 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.
Precise axis calculation, anyone?

Remember that it is simply a method of addition. I+III=II. 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?
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.
A. Normal Sinus Rhythm

B. Atrial Fibrillation

C. Normal Sinus Rhythm with Heart Block

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