Transcript EKG Basics - Phlebotomy Career Training

EKG Basics
OVERVIEW OF EKG AND
TELEMETRY
Outline
1. Review of the conduction system
2. EKG waveforms and intervals
3. EKG leads
4. Determining heart rate
5. Determining QRS axis
The Normal Conduction System
What is an EKG?
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 patient’s cardiac pathophysiology.
What types of pathology can we
identify and study from EKGs?
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)
Waveforms and Intervals
EKG Leads
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)
EKG 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.
Standard Limb Leads
Standard Limb Leads
Augmented Limb Leads
All Limb Leads
Precordial Leads
Adapted from: www.numed.co.uk/electrodepl.html
Precordial Leads
Summary of Leads
Bipolar
Limb Leads
Precordial Leads
I, II, III
-
(standard limb leads)
Unipolar
aVR, aVL, aVF
(augmented limb leads)
V1-V6
Arrangement of Leads on the EKG
Anatomic Groups
(Septum)
Anatomic Groups
(Anterior Wall)
Anatomic Groups
(Lateral Wall)
Anatomic Groups
(Inferior Wall)
Anatomic Groups
(Summary)
Determining the Heart Rate
Rule of 300
10 Second Rule
Rule of 300
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.
What is the heart rate?
www.uptodate.com
(300 / 6) = 50 bpm
What is the heart rate?
www.uptodate.com
(300 / ~ 4) = ~ 75 bpm
What is the heart rate?
(300 / 1.5) = 200 bpm
The Rule of 300
It may be easiest to memorize the following table:
# of big
boxes
Rate
1
300
2
150
3
100
4
75
5
60
6
50
10 Second Rule
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.
What is the heart rate?
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
33 x 6 = 198 bpm
The QRS Axis
The QRS axis represents the net overall
direction of the heart’s electrical activity.
Abnormalities of axis can hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
The QRS Axis
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)
Determining the Axis
The Quadrant Approach
The Equiphasic Approach
Determining the Axis
Predominantly
Positive
Predominantly
Negative
Equiphasic
The Quadrant Approach
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.
The Quadrant Approach
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.
Quadrant Approach: Example 1
The Alan E. Lindsay
ECG Learning Center
http://medstat.med.utah.
edu/kw/ecg/
Negative in I, positive in aVF  RAD
Quadrant Approach: Example 2
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)

The Equiphasic Approach
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.
Equiphasic Approach: Example 1
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
Equiphasic in aVF  Predominantly positive in I  QRS axis ≈ 0°
Equiphasic Approach: Example 2
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
Equiphasic in II  Predominantly negative in aVL  QRS axis ≈ +150°
EKG Review
1.
View the slide show
2.
Interpret the EKGs
3.
Advance slides to review findings
4.
Good luck!
Recall the approach
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
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 V1V4. 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 (p’s 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 MI’s 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.
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.
The QT/QTc Interval: Calculation and Significance
Measurement:
Parameter:
Abnormalities:
QTc:
Lengthening:
From the beginning of the Q wave to the
end of the T wave
Normal QT intervals range from 0.360.41.
Hypercalcemia will shorten the QT interval
and yield measurements from 0.26-0.36s.
The QT interval varies with heart rate. The
corrected QT interval is calculated by
adjusting your measurement for the
patient’s heart rate. The QT divided by the
square root of the R to R interval typically
gives a QTc around 0.44 seconds.
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, “strain”and is consistent with
repolarization problems in hypertrophied muscle.
For the following strips identify the QRS, QT, Heart Rate, PR, ST, intervals, and
whether or not the rhythm is normal or abnormal. Try your best to identify the
rhythm.
A. Normal Sinus Rhythm
B. Atrial Fibrillation
C. Normal Sinus Rhythm with Heart Block