09 26 2011

MS3 ECG Workshop

Diagnostic Pearls

J.B. Esterson, MD

Ischemic ECG Changes

Both of these can progress to MI

ST Depression (subendocardial injury):

same as seen in Non-STEMI, but markers neg.
Symmetric T Inversion (transmural ischemia):
same as seen in
i Non-STEMI,
N STEMI bbut markers
k neg.

ECG Presentations of
A t Coronary
Acute
C
E
Events
t

09 26 2011

Acute Ischemia

ST depressions (1 mm) or T inversions (2 mm)

Biomarkers negative
g
Prolonged = Unstable Angina

Acute Infarction

ST Elevation MI (Q, Transmural)

Biomarkers may be positive

Biomarkers may be negative if early (Injury)

Non-ST Elevation MI (Non-Q, Non-transmural)

ST depressions
p
((1 mm)) or T inversions ((2 mm))
Biomarkers positive

Stress-induced Ischemia
Thaler 1999)
(adapted from Thaler,

09 26 2011

Early Repolarization
J point and ST
Concave upwards
Most commonly V 22--4
No reciprocal ST

Associated
J point slurring or notching
Tall T waves
No serial change; with exercise, age

Usuallyy Healthy,
Healthy
y, no Sx , male > female, y
young,
g athlete
Some evidence: sudden death Inferior and ? Lateral leads

DDx - subepicardial
p
injury
j y (STEMI),
(
), p
pericarditis

ST : Pericarditis vs. MI
ST elevations all
leads (except aVR
and isoelectric
leads)

ST elevations
regional

09 26 2011

Right Bundle Branch Block

(from Huszar, Basic Dysrhythmias, 1994)

Right Bundle Branch Block: Criteria

QRS prolongation

.12 sec

Incomplete if < .12 sec.

Secondary R wave (R') in right precordial leads

(especially V1)
R' wave is wider and taller than the R wave

Wide S wave in lateral leads (I, aVL, V5-6)

Secondary ST-T changes (opposite direction)
4

09 26 2011

Left Bundle Branch Block

(from Huszar, Basic Dysrhythmias, 1994)

Left Bundle Branch Block: Criteria

QRS pprolongation
g

.12 sec

Absent Q wave lateral leads (I, V5-6)

V5 6)
Broad R wave I,
I V5-6
Usually slurred and notched

Secondary ST-T changes (opposite direction)

LAD common
5

09 26 2011

Injury
j y - ECG Changes
g
ST Elevation (transmural injury)
Not always truly transmural
Usually progresses to ST Elevation MI
With elevated markers and pathologic Q

Rarely can present as rest Variant Angina

(Prinzmetals Angina) without MI

Evolution of STEMI
T
Tall T

Path. Q

ST

Path. Q

T upright

L ST
Less

ST normall

Path. Q

Hyperacute

Injury / Acute

Evolving

Old
6

09 26 2011

Left Ventricular Hypertrophy

(adapted from Lilly, Pathophysiology of Heart Disease, 1998)

Left Ventricular Hypertrophy (LVH)

Increased QRS voltage (chest & limb leads
best)
ST-T
T changes ((Strain)
Strain ) common
Secondary ST
in left sided leads
Abnormal
b
l left
l f axis
i deviation
d i i (LAD)
(
)
Left atrial enlargement (LAE)
QRS slight prolongation (up to .12)
7

09 26 2011

Right Ventricular Hypertrophy

(adapted from Lilly, Pathophysiology of Heart Disease, 1998

Typical RVH Pattern

(RV mass approaches LV mass)

Right axis deviation (usually > 110 )

RS ratio V1 > 1 (usually tall R) often qR
Deep S waves left precordial leads
Slight prolongation QRS duration (up to .12)
12)
Secondary ST-T changes (Strain) common
in right sided leads
Occasional RAE (right atrial enlargement)
8

09 26 2011

Hyperkalemia
yp
ECG Effect

K+ Level

T wave peaked,
k d tall,
ll andd narrow

> 5.5
55

QRS prolongation (T will widen)

> 6.5

P wave

> 7.0

amplitude,

duration

P-R interval

> 7.0

P wave disappears

> 8.8

QRS sine wave (can occur earlier)

> 8.8

Hyperkalemia (Lead II) Progression

09 26 2011

Atrial Fibrillation

Atrial Fibrillation
No definite P shape can be determined
Atrial impulses very rapid and irregular, 400-700 bpm
Fibrillatory waves coarse or fine

Ventricular response
Always
y irregularly
g
y irregular
g
((unless complete
p
AV block))
Rate: untreated usually 100-180
QRS shape normal

10

09 26 2011

Atrial Flutter
Block

Atrial Flutter
F ((flutter)) waves
Shape: Saw tooth (undulating baseline)
Rate: 250 350 bpm

QRS
Shape: normal
Rate: < F rate, may have variable block
New onset usually 2:1 block (HR 150)

If 1:1 conduction, suspect WPW!

11

09 26 2011

Premature Ventricular Complexes

Wide and different from sinus QRS
Not preceded
d d bby premature P
Morphology
Uniform
Multiform

ST-T different from sinus

Significance clinical setting

Ventricular Tachycardia

3 or more consecutive PVCs

Abrupt onset and termination
Rate 140-200
QRS > .14,
14 different from sinus
Not preceded by P wave
AV dissociation common
Differentiate from supraventricular

12

09 26 2011

2nd Degree AV Block Type I

(from Scheidt, 1983)

Second Degree AV Block, Type I

AV nodal site of block

Progressive PR followed by non-conducted P
G
Grouped
d beating
b i
QRS usually narrow
Transient. reversible
Excessive vagal
g tone
AV node ischemia / blocking drugs

Usually benign prognosis

Rarely progresses to 3rd degree AV block

13

09 26 2011

2nd Degree AV Block Type II

Second Degree
g AV Block Type
yp II

PR constant followed by non-conducted

non conducted P
Grouped beating
QRS usually
ll wide:
id Hi
His-Purkinje
P ki j system
Extensive disease
Bi / Trifascicular block
Progression to complete AV block
Slow escape ventricular rhythm
Syncope / sudden death - pacemaker

14

09 26 2011

Thi d D
l t )H
k
Third
Degree (C
(Complete)
Heartt Bl
Block

3rd Degree or Complete AV Block

Sinus impulses do not activate the ventricle

Regular P-P intervals, regular R-R intervals
Variable PR intervals
inter als
Atrial rate > ventricular rate
QRS originates
i i
in
i AV Node,
d His,
i Bundles,
dl
Purkinje fibers, Ventricles
Drugs, MI, conduction
d i disease,
di
congenital,
i l
hypertension, valvular, myocardial dis.
Rx: Pacer usually
ll Px: related
l d to etiology
i l

15