Download Understanding the 12-lead ECG, part II

BundleBundle-branch blocks
Understanding the
12-lead ECG, part II
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Right bundlebundle-branch block (RBBB)
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Appears as a wider than normal QRS
complex
Occurs when one of the two bundle
branches can’t conduct the impulse
Most common cause: ischemic heart
disease
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Left bundle branch block (LBBB)
Impulse conduction to right ventricle is
blocked
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Examine lead V1 to
identify RBBB
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ECG show delayed or positive R wave
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Key identifier is QRS complex wider than
0.12 second, with positive R wave in V1
Most common electrocardiogram (ECG)
abnormality
Electrical impulses don’t reach left
side of the heart
QRS wider than 0.12 second
Key to recognizing LBBB
is a wide downward
S wave or rS wave in
leads V1 and V2
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What do you think?
What do you think?
•Sinoatrial block, type II
•Sinoatrial block, type II
•Second-degree atrioventricular (AV) block,
type I
•Second-degree atrioventricular (AV) block,
type I
•Second-degree AV block, type II
•Second-degree AV block, type II
•Nonconducted atrial premature impulse
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•Nonconducted atrial premature impulse
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What do you think?
•Second-degree AV block, type II
P waves occur regularly in this tracing;
Some of them are conducted to the ventricles while others
are blocked; therefore, it is second-degree AV block.
In this tracing, when the P waves are conducted, the PR
intervals do not lengthen; therefore, this is second-degree AV
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block, type II.
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Recognizing
myocardial infarction (MI)
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Series of predictable ECG changes occur in
MI
- pauses in the middle of a regular rhythm.
- there are no extra P waves during the pauses -- an
indication that this is not AV block.
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- the pause is exactly twice the length of the shorter cycle,
indicating regularly firing sinus impulses that fail to conduct
to the atrium at times;
STST-segmentsegment-elevation MI
(STEMI)-serious type
(STEMI)--serious
of MI, associated with
more complications,
higher risk of death
This is SA block. Because the pause is
twice the shorter cycle, it is type II.
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Characteristic changes in AMI
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ST elevation
ST segment elevation over area of
damage
ST depression in leads opposite
infarction
Pathological Q waves
Reduced R waves
Inverted T waves
• Occurs in the early
stages
R
ST
• Occurs in the leads
facing the infarction
P
Q
• Slight ST elevation may
be normal in V1 or V2
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Deep Q wave
• Only diagnostic change of
myocardial infarction
R
• At least 0.04 seconds in
duration
ST
P
T
Q
T wave changes
• Depth of more than 25%
of ensuing R wave
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• Late change
R
ST
P
• Occurs as ST elevation
is returning to normal
T
• Apparent in many leads
Q
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Sequence of changes in evolving
AMI
Bundle branch block
Anterior wall MI
Left bundle branch block
R
I II III
aVR aVL aVF
V1 V2 V3
V4 V5 V6
I II III
aVR aVL aVF
V1 V2 V3
R
R
ST
T
V4 V5 V6
ST
P
P
Q S
P
T
Q
Q
1 minute after onset
1 hour or so after onset
A few hours after onset
R
ST
P
ST
P
T
T
P
T
Q
Q
Q
A day or so after onset
Later changes
A few months after AMI
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Inferior wall STEMI
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Inferior infarction
Inferior infarction
Elevated ST segments in
leads II, III, and aVF,
aVF,
which monitor the heart’s
inferior or bottom wall
I II III
Right
coronary
artery
Septal MI
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V1 V2 V3
V4 V5 V6
Area of the heart perfused
by the right coronary artery
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aVR aVL aVF
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AnteriorAnterior-wall STEMI
Perfused by the left anterior
descending (LAD) coronary artery
STST-segment elevation seen in leads
V1 and V2, the precordial or chest
leads located on the anterior chest
wall over the septum
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Directly to the left of the septal area
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Also perfused by the LAD
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Most muscular, powerful
pumping wall of the heart,
responsible for large
proportion of cardiac output
ST elevation seen in V3 and V4
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Anterior infarction
LateralLateral-wall STEMI
Anterior infarction
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I II III
aVR aVL aVF
V1 V2 V3
V4 V5 V6
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Left
coronary
artery
Perfused by the circumflex artery
Muscular, contributes significantly to the
heart’s pumping ability
Monitored by precordial (chest) and
frontal (limb) leads
STST-segment elevation will appear in
leads I, aVL, V5, V6
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Lateral infarction
Lateral infarction
I II III
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Common dysrhythmias
Left
circumflex
coronary
artery
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Sinus bradycardia
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Sinus bradycardia
Sinus rhythm slower than 60 beats per
minute
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Commonly caused by ischemic heart
disease causing sinoatrial (SA) node to
malfunction
Signs and symptoms: hypotension,
lethargy, fatigue, chest pain,
difficulty breathing
Also seen in MI, some medications (such
as betabeta-blockers), and wellwell-conditioned
athletes
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Sinus tachycardia
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Sinus rhythm faster than 100 beats per
minute
Related to physiologic cause: fever,
infection, pain, physical exertion, anxiety,
shock, hypoxia
May need betabeta-blocker if cause unknown
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Atrial fibrillation (AF)
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Common dysrhythmia
Irregular heart rhythm with no meaningful
P waves
Atrial kick lost, atrias quiver due to depolarization
of atrial cells
Causes irregular ventricular rate, 40 to 180 beats
per minute
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Premature ventricular
contractions (PVCs)
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Wide abnormal premature QRS
complex
Due to conduction through the
ventricle instead of HisHis-Purkinje
system
QRS greater than
0.12 second
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Ventricular tachycardia (VT)
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Rapid rate, 100 to 250 beats per minute
Wide, bizarre, QRS complex followed by
large T wave
Patient may be unconscious, pulseless,
pulseless,
apneic-initiate CPR
apneic--initiate
If patient awake, treat as medical
emergency
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Hypercalcemia
Shortened QT interval (short/absent ST segment)
Digitalis
Scooping of ST segment
Shortening of QT interval
Low amplitude of T wave
Elongation of PR interval
High amplitude of U wave
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Digitalis poisoning
Digitalis poisoning
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Atrial tachycardia with AV block
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1st degree AV Block
ƒ Mobitz I
ƒ AF with accelerated junctional rhythm
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Digitalis poisoning
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Bidirectional VT
ƒ Ventricular bigeminy
Tricyclic antidepressants (TAD)
HYPOTHERMIA
Sinus tachycardia with a prolonged QRS interval
Sinus bradycardia with first-degree AV block is evident.
Rightward axis
Tall R wave in lead aVR
Markedly abnormal repolarization changes suggests TAD poisoning
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The downstroke of each QRS complex is slurred and is
typical of a J (Osborne) wave (↓).
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