EKG REVIEW

Lead Placement

aVF

Marian Williams RN

Correlation of ECG Wave Forms

EKG Distributions
Anteroseptal: V1, V2, V3,
V4
Anterior: V1V4
Anterolateral: V4V6, I,
aVL
Lateral: I and aVL
Inferior: II, III, and aVF
Inferolateral: II, III, aVF,
and V5 and V6

Sistematika Membaca EKG

Rate
Ritme
Aksis
Interval
Infark
Hipertrof

Sinus Rhythms
Originate in the SA node

Normal sinus rhythm (NSR)

Sinus bradycardia (SB)
Sinus tachycardia (ST)
Sinus arrhythmia

Inherent rate of 60 100

Base all other rhythms on deviations from sinus rhythm

Sinus Rhythm

Marian Williams RN

Sinus Bradycardia

Marian Williams RN

Sinus Tachycardia

Marian Williams RN

Sinus Arrhythmia

Marian Williams RN

Atrial Rhythms
Originate in the atria

Atrial fbrillation (A Fib)

Atrial flutter
Wandering pacemaker
Multifocal atrial tachycardia (MAT)
Supraventricular tachycardia (SVT)
PACs
WolffParkinsonWhite syndrome (WPW)

A - Fib

A - Flutter

Wandering Pacemaker

Multifocal Atrial Tachycardia

(MAT)

Pacemaker)
(Rapid
SimilarWandering
to wandering
pacemaker (< 100)
MAT rate is >100
Usually due to pulmonary issue
COPD
Hypoxia, acidotic, intoxicated, etc.
Often referred to as SVT by EMS
Recognize it is a tachycardia and QRS is narrow

SVT

PACs

WolffParkinsonWhite
(AKA - Preexcitation Syndrome)

AV/Junctional Rhythms
Originate in the AV node

Junctional rhythm rate 40-60

Accelerated junctional rhythm rate 60-100
Junctional tachycardia rate over 100
PJCs

Inherent rate of 40 - 60

Junctional Rhythm

Accelerated Junctional

Junctional Tachycardia

Often difficult to pick out so often identifed as

SVT

Ventricular Rhythms
Originate in the ventricles / purkinje fbers

Ventricular escape rhythm (idioventricular) rate

20-40
Accelerated idioventricular rate 42 - 100
Ventricular tachycardia (VT) rate over 102
Monomorphic regular, similar shaped wide QRS
complexes
Polymorphic (i.e. Torsades de Pointes) life
threatening if sustained for more than a few seconds
due to poor cardiac output from the tahchycardia)

Ventricular fbrillation (VF)

Fine & coarse

PVCs

Idioventricular

Accelerated Idioventricular

VT (Monomorphic)

VT (Polymorphic)
Note the twisting of the points

This rhythm pattern looks like

Ribbon in its fluctuations

VF

PVCs

R on T PVCs

A/V Heart Blocks

1st degree
A condition of a rhythm, not a true rhythm
Need to always state underlying rhythm

2nd degree
Type I - Wenckebach
Type II Classic dangerous to the patient

Can be variable (periodic) or have a set

conduction ratio (ex. 2:1)
3rd degree (Complete) dangerous to the
patient

1st Degree Block

2nd Degree Type I

2nd Degree Type II (constant)

P Wave

PR Interval

Uniform

.12 - .20

QRS
Narrow & Uniform

Characteristics
Missing QRS after
every other P wave
(2:1 conduction)

Note: Ratio can be 3:1, 4:1, etc. The higher the ratio, the sicker the heart.
(Ratio is P:QRS)

2nd Degree Type II (periodic)

P Wave

PR Interval

Uniform

.12 - .20

QRS
Narrow & Uniform

Characteristics
Missing QRS after
some P waves

3rd Degree (Complete)

Sinus w/ 1st degree Block

No symptoms are due to the first degree heart
block; symptoms would be related to the
underlying rhythm

2nd Degree Type 1 Wenckebach

PR getting longer and finally 1 QRS drops;
patient generally asymptomatic; can be
normal rhythm for some patients

2nd Degree Type II (2:1 conduction)

Should be preparing the TCP for this patient

3rd degree heart block (complete)

with narrow QRS
Symptoms usually based on overall heart rate
the slower the heart rate the more
symptomatic the patient. Prepare the TCP.

ST Elevation and non-ST

Elevation MIs
When myocardial blood supply is abruptly
reduced or cut off to a region of the heart,
a sequence of events occur beginning with
ischemia (inadequate tissue perfusion),
followed by necrosis (infarction), and
eventual fbrosis (scarring) if the blood
supply isn't restored in an appropriate
period of time.
The ECG changes over time with each of
these events

ECG Changes
Ways the ECG can change include:
ST elevation &
depression

T-waves

Appearance
of pathologic
Q-waves

peaked
inverted

flattened

ECG Changes & the Evolving

MI
There are two
distinct patterns
of ECG change
depending if the
infarction is:

Non-ST Elevation

ST Elevation

ST Elevation (Transmural or Q-wave), or

Non-ST Elevation (Subendocardial or non-Q-wave)

ST Elevation Infarction
The ECG changes seen with a ST elevation infarction are:

Before injury Normal ECG

Ischemia

ST depression, peaked T-waves,

then T-wave inversion

Infarction

ST elevation & appearance of

Q-waves

Fibrosis

ST segments and T-waves return to

normal, but Q-waves persist

ST Elevation Infarction
Heres a diagram depicting an evolving infarction:
A. Normal ECG prior to MI
B. Ischemia from coronary artery
occlusion results in ST depression (not
shown) and peaked T-waves
C. Infarction from ongoing ischemia
results in marked ST elevation
D/E. Ongoing infarction with appearance
of pathologic Q-waves and T-wave
inversion
F. Fibrosis (months later) with persistent
Q- waves, but normal ST segment and
T- waves

ST Elevation Infarction
Heres an ECG of an acute inferior wall MI:
Look at the
inferior leads
(II, III, aVF).
Question:
What ECG
changes do
you see?
ST elevation
and Q-waves

Extra credit:
What is the
rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!

Non-ST Elevation Infarction

Heres an ECG of an inferior wall MI later in time:
Now what do
you see in
the inferior
leads?
ST elevation,
Q-waves and
T-wave
inversion

Non-ST Elevation Infarction

The ECG changes seen with a non-ST elevation infarction are:

Before injury Normal ECG

Ischemia

ST depression & T-wave inversion

Infarction

ST depression & T-wave inversion

Fibrosis

ST returns to baseline, but T-wave

inversion persists

Non-ST Elevation Infarction

Heres an ECG of an evolving non-ST elevation MI:
Note the ST
depression
and T-wave
inversion in
leads V2-V6.

Question:
What area of
the heart is
infarcting?

Anterolateral

12 Lead Comparison Chart

(Main ones are highlighted)

ST elevation in V2 V5
(Anterior wall)

ST elevation in II, III & aVF

(Inferior wall with LBBB)

ST Elevation
Inferior Wall II, III, aVF

ST elevation in II, III, aVF

(Inferior wall - note reciprocal changes)
Watch for hypotension

ST elevation in V1 V6, I & aVL

(Anteroseptal with lateral extension)
Extensive anteroseptal
Watch for heart block

ST elevation V2-V5
Watch for heart block

Left Ventricular
Hypertrophy

Left Ventricular Hypertrophy

Compare these two 12-lead ECGs. What
stands out as different with the second one?

Normal

Left Ventricular Hypertrophy

Answer: The QRS complexes are very tall

(increased voltage)

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized
by tall QRS complexes?
As the heart muscle wall thickens there is an increase in
electrical forces moving through the myocardium resulting
in increased QRS voltage.

LVH

Increased QRS voltage

ECHOcardiogram

Left Ventricular Hypertrophy

Specifc criteria exists to diagnose LVH using a
12-lead ECG.
For example:

The R wave in V5 or V6 plus the S wave in V1 or V2

exceeds 35 mm.

However for now, all

you need to know is
that the QRS
voltage increases
with LVH.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

A 16 yo young man ran into a guardrail while riding a motorcycle.

In the ED he is comatose and dyspneic. This is his ECG.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

What is the rate?

Approx. 132 bpm (22 R waves x 6)

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

What is the rhythm?

Sinus tachycardia

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

What is the QRS axis? Right axis deviation (- in I, + in II)

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

What are the PR, QRS PR = 0.12 s, QRS = 0.08 s, QTc = 0.482 s
and QT intervals?

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

Is there evidence of
atrial enlargement?

No (no peaked, notched or negatively

deflected P waves)

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

Is there evidence of
No (no tall R waves in V1/V2 or V5/V6)
ventricular hypertrophy?

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

Infarct: Are there abnormal

Q waves?
30

30

30

30

Yes! In leads V1-V6 and I, avL

Any

R40

20

Any

R50

30

Any

30

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

Infarct: Is the ST elevation

or depression?

Yes! Elevation in V2-V6, I and avL.

Depression in II, III and avF.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

Infarct: Are there T wave

changes?

No

SUMMARY Rate Rhythm Axis Intervals Hypertrophy

Infarct

ECG analysis: Sinus tachycardia at 132 bpm, right axis deviation,

long QT, and evidence of ST elevation infarction in the
anterolateral leads (V1-V6, I, avL) with reciprocal changes (the
ST depression) in the inferior leads (II, III, avF).
This young man suffered an
acute myocardial infarction after
blunt trauma. An
echocardiogram showed
anteroseptal akinesia in the left
ventricle with severely
depressed LV function
(EF=28%). An angiogram
showed total occlusion in the
proximal LAD with collaterals
from the RCA and LCX.

End of Module VII b

Reading 12-Lead ECGs
Proceed to Module VII b Practice Quiz on your iROCKET
Course