Introduction to

Electrocardiography III

John C. Evans, MD
Fellow
Division of Cardiovascular Medicine
Oregon Health and Science University
9/25/07

Disclaimer
Some of these slides were made using images found on the web. In
particular ABC of Electrocardiography by Morris and Brady from the
British Medical Journal. Please use the web to track down the images
and use the respective pages. Dont rat Dr. Luft out to the publishers. If
you are a publisher, dont sue me; its Dr. Luft.

Lecture Topics:
Lecture 1
Introductory Approach to ECG Interpretation

Lecture 2
Introduction to Rhythm Analysis

Lecture 3
Introduction to clinical ECG changes/Ischemia

ECGinterpretation
identification
standardization
rate
rhythm
axis
intervals
voltage/chambers/hypertrophy
geography/ischemia/infarction

Bradycardia
Sinus bradycardia
Sinus arrest with subsidiary pacemaker
Ectopic atrial
Junctional
Ventricular

Block
Second degree Type I (Wenckebach)
Second degree Type II
Complete Heart Block

Bradycardia Algorithm
Regular?
AV dissociation?

How irregular?

If AV dissociated

Irregularly Irregular

And A>V: heart block

Atrial Fibrillation

And V>A: ventricular pacemaker

Wandering Pacemaker

If notLook for the P waves

Sinus
Ectopic Atrial focus
Junctional
Ventricular

Grouped
Second Degree Block

Tachycardia
Wide Complex
Ventricular Tach

SVT w/ aberrancy
-preexisting
-rate-related
-AVRT

Narrow Complex
Regular
Sinus Tach
Atrial Flutter
AV Reentry Tach
AVN Reentry Tach
Atrial Tach
Junctional Tach

Irregular
Atrial Fib
Multifocal AT
Variable Conduction

Anatomy

Anatomy

Lead location of ST changes can allow wall

segment localization of Infarct/ischemia

Lead Localization

R wave progression
Normally
No q anteriorly
R:S should
increase until V5
R:S should be 1:2
by V3 and 1:1 by
V4
Septal q laterally

Lead localization can correlate with

coronary anatomy
Left Anterior
Descending Artery:
Anterior and lateral leads
V1-V4
Right Coronary Artery:
Inferior leads: II, III, aVf
Left Circumflex: Lateral
leads V4-V6, I, aVL
(notorious for being ECG
silent)

Plaque Rupture

STEMI Evolution

Hyper acute T waves - minutes

ST elevation (Injury/Acute MI) - hours

Deep Q waves with ST elevation (Recent MI) - days

Q waves with T wave inversion (Age indeterminant) weeks

Q wave with normalization of T wave (Old) - months

ST Elevation

The ST segment
elevation may
fuse with the
QRS and T wave
- yielding a
Tombstone
complex.

Reciprocal ST Depression

ST depression often
develops at in leads
opposite the sight of
infarction.
Known as reciprocal
depression.
Can be helpful to confirm
STEMI.
May represent mirror
image phenomenon.

Acute Anterior
LAD artery distribution

ST elevations

Reciprocal depressions

Acute Inferior Infarct

Right Coronary Artery Distribution

Reciprocal depression

ST elevation

Old Inferior Infarct (Q waves)

Q waves are considered significant or pathological if they are >

30msec wide and/or > 1/4 of the R wave amplitude.
Q waves in III and aVR can be normal (even if significant).
Look for an anatomic pattern!

Acute Lateral MI
Left Circumflex or Diagonal artery

ST elevations

Reciprocal depressions

Old Lateral Infarct

Lateral Infarct

Inferior/Posterior Infarct

Posterior Infarct vs. LAD Ischemia

Represent ST Elevations
behind V1-V3

ST Depressions V1-V3

Flip or
Use a
Mirror!

Difficult to Diagnose STEMI

RV Infarction (with IMI)

Right sided leads with

ST elevation
Inferior STEMI

Complications of STEMI
Complications can include: pericarditis, CHF, VSD,
papillary muscle rupture (acute MR), aneurysm
formation, thrombus, and LV rupture.

LV rupture

LV aneurysm

ST Segment Elevation
CausesofSTsegmentelevation

Acutemyocardialinfarction
Benignearlyrepolarization
Leftbundlebranchblock
Leftventricularhypertrophy
Ventricularaneurysm
Coronaryvasospasm/Printzmetal'sangina
Pericarditis
Brugadasyndrome
Subarachnoidhaemorrhage

Pericarditis

Pericarditis
ST Segment Elevation

PR Depression

Early Repolarization

Early Repolarization

Vasospasm

Baseline

Spasm

Spasm Resolving

Reversible ST segment Elevation Associated

With Vasospasm

ST Elevation in LBBB
Up to 5mm of
discordant ST
elevation may
be normal.

Infarction in LBBB
Note >5mm discordant
elevation in V2-V4.
Note > 1mm
concordant ST elevation
in V5 and V6.
This may represent
acute infarction.

T waves
Different T wave morphologies can
represent ischemia.
T wave abnormalities can also reflect
normal variation, youth, electrolyte
abnormalities, drugs, CNS abnormalities,
lead misplacement, etc.
T waves should generally be <10mm tall
and be approximately >1/8 the height of
the R wave.
T wave inversion in III, aVR and V1 may
be normal. T wave inversion
V1-V3
seen in juvenile pattern.

T Waves (biphasic)
Biphasic T waves are frequently
associated with ischemia and
acute coronary syndrome.
Usually seen in V1-V3.
Correlate with LAD disease.
Sometimes referred to as
Wellens waves.

T waves
Tall T waves (> 10mm) may
represent ischemia.
Also seen with hyperkalemia
and young patients.

T waves

T waves (non-specific)

T waves

T waves (Deep, Symmetrical)

ST Depression
ST segment
depression may
also represent
ischemia.
Like T wave
inversions and ST
elevations, it is not
specific to
ischemia.

ST Depression
Note deep,
downsloping ST
depressions.
High probability
of ischemia
(espically if new
or associated
with chest pain).

ST Depression (Digoxin
Toxicity)

ST Depression (LVH)

Hyperkalemia

Elevated K+ can result in deadly

rhythms.

The typical progression of EKG change

with rising potassium is roughly:

1.
2.
3.

Peak T waves (tall) K+>6

QRS widening and P flattening K+>7
Sinusodial tachycardia K+>8

Hyperkalemia (Peaked T Waves)

Hyperkalemia (Sinusodal VT)

Hyperkalemia (Sinusodial)

Hyperkalemia needs immediate treatment.

Cardiac membrane stabilization with calcium.
Insulin, glucose, beta2 agonists, K-exalate, or hemodialysis to bring down
potassium.

Other electrolyte abnormalities

Hypokalemia
U waves
ST depression
QTU

Hypo/hypercalcemia
Hypo/hypermagnesemia

Back to axis
Left axis deviation

LAFB
LVH
IMI
AMI

Right axis deviation

RVH
LMI
WPW
Lead misplacement
LPFB

So much more
Blocks
Block above and below the AV node
Complete heart block with a-fib

Syndromes

Lown-Ganong-Levine
Brugada
ARVD
Short QT

Findings of systemic disease

Infiltrative
Hypothermia

So remember.

ECGinterpretation
identification
standardization
rate
rhythm
axis
intervals
voltage/chambers/hypertrophy
geography/ischemia/infarction

Thank you

Dr. Luft for his slides

Ryan Palmer for all his help
The facilitators of the small groups
You (questions AND feedback are greatly
appreciated)