Transcript Left bundle branch block

2.
Evaluate the rhythm.
A Sequential Approach to
Gain familiarity with the "normal" EKG.
EKG’s:
1.
Reading
A Sequential Approach to Reading EKG’s:
It is best to evaluate rhythm on a rhythm strip. If this is not available, look at "pieces" of
the rhythm in each lead (II and V1 generally have prominent P waves).
Determine if the rhythm is regular or irregular.
For irregular rhythms determine if the rhythm is completely irregular ("irregularly
irregular") or if the irregularity is caused by additional or dropped complexes
superimposed on an underlying regular rhythm.
For all rhythms, look for and evaluate P waves in the underlying rhythm first, and then in
relation to any additional or dropped beats
Look at QRS complex morphology, first in the underlying rhythm and then in any
additional beats.
At each step consider the two main questions of rhythm interpretation: where has impulse
formation occurred and how has conduction proceeded.
A Sequential Approach to Reading EKG’s:
3. Calculate rate and axis. Measure intervals. Consider the diagnostic possibilities
suggested by abnormalities found, but do not make final diagnoses yet (except for left
bundle branch block, which makes further interpretation impossible).
4. Evaluate each P wave, QRS, ST segment, T wave and U wave in the following lead
order:
I and aVL
then II, III, and aVF
then V1, V2, V3, V4, V5 and V6 (beginning with R wave
progression), localizing and grouping all abnormalities.
5. Arrive at final diagnoses by critically evaluating each abnormality in relationship to all
others and any available clinical data.
Lead placement
Lead placement
Orientation of the 12 Lead ECG:
It is important to remember that the 12-lead ECG provides spatial information
about the heart's electrical activity in 3 approximately orthogonal directions:
Right
Superior
Anterior
Left
Inferior
Posterior
Each of the 12 leads represents a particular orientation in space, as indicated below (RA
= right arm; LA = left arm, LF = left foot)
Bipolar limb leads (frontal plane):
Lead I: RA (-) to LA (+) (Right Left, or lateral)
Lead II: RA (-) to LF (+) (Superior Inferior)
Lead III: LA (-) to LF (+) (Superior Inferior)
Augmented unipolar limb leads (frontal plane):
Lead aVR: RA (+) to [LA & LF] (-) (Rightward)
Lead aVL: LA (+) to [RA & LF] (-) (Leftward)
Lead aVF: LF (+) to [RA & LA] (-) (Inferior)
Unipolar (+) chest leads (horizontal plane):
Leads V1, V2, V3: (Posterior Anterior)
Leads V4, V5, V6:(Right Left, or lateral)
Standard Limb Leads
Right Sided Leads
normal ECG
ST segment
The normal ECG has the following features:
• P wave - due to atrial depolarization
• PR interval (due to delayed conduction through the AV node) 0.12 - 0.20 seconds
• QRS complex - due to ventricular depolarization
• T wave due to ventricular repolarization
normal ECG
a) The P wave represents atrial activation
b) the PR interval is the time from onset of atrial activation to onset of ventricular
activation. (from the sinus node to the His Bundle purkinje fibers)
c) The QRS complex represents electrical ventricular activation; the QRS duration is
the duration of ventricular activation.
d) The ST-T wave represents ventricular repolarization.
e) The QT interval is the duration of ventricular activation and recovery.
f) The U wave probably represents "after-depolarization" in the ventricles.
Normal Sinus Rhythm
A normal sinus rhythm one would expect the following:
• an ECG with P waves
• a PR interval of 0.12 - 0.20 seconds
• a regular interval between each QRS complex (R-R interval) of 0.60 - 1.0 secs
• a distinct a wave in the CVP trace due to atrial contraction
• there may be minor regular variation in heart rate and pulse pressure associated with
respiration (sinus arrhythmia)
Ps in I, II and aVF are always
upright and always inverted in
aVR
Normal EKG
Ps in V1 and V2 are Diphasic, but
never negative in V2
T wave:
Q
Wave:Always
Amplitude
upright
of Qinwaves
I & IIusually
and inverted
< 4mm
in in
aVR.
all leads
Usually
except
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it may
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or
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and
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isRalways
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PR
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inMeasures
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interval.
QT
interval:
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ofinthe
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systole.inNormal
QTc is about
P
are always
upright
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I and
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always
aVR,
inI,III,
S waves
wave: Most
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in aVR
about
16mm,
9mm inverted
in III & aVL,
anddiphasic
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III
0.39
secs
in
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and
0.41
secs
in
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>
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secs
is
ABNORMAL.
aVL,
Ventricular
and Vactivation
middle
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third of of
Leftmore
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than than one
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and aVF.
considered
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apex after
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andonce]
the
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U
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the of
axis
directed
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AXIS
AXIS
Normal axis
Left axis deviation
Right axis deviation
-300 to 1200
-300 to -900
1200 to 1800
Indeterminate (extreme) axis deviation -900 to 1800
AXIS
Normal axis (-30 to +90degrees)
Lead I
Lead
aVF
Positive
Positive
Left axis deviation (-30 to -90) check lead II. To be true left axis
deviation, it should also be down in lead II. If the QRS is upright in Positive
II, the axis is still normal (0 to -30).
Neg
.Right axis deviation
Neg
Positive
Indeterminate axis (-90 to -180)
Neg
Neg
Differential Diagnosis
Left axis deviation
LVH, left anterior fasicular block, inferior wall MI
Right axis deviation
RVH, left posterior fascicular block, lateral wall MI
NORMAL AXIS
LEFT AXIS DEVIATION
If the axis is - 300  Biphasic in lead II, and negative in aVF
If the axis is <300  predominantly negative in lead II and aVF
RIGHT AXIS DEVIATION
Normal QRS width with an axis of >1000
Predominantly positive in leads II and III, and negative in aVL
Early Repolarization
Note diffuse J-point elevation, early R wave transition, with notched downstroke of R
wave in lateral precordial leads. These changes are characteristic of early repolarization
as seen in this EKG of a 28 year old African-American male.
Normal variants or artifacts
Normal
variants
or
artifacts
ischemia
ST Segment Abnormalities
General Introduction to ST, T, and U wave abnormalities
The specificity of ST-T and U wave abnormalities is provided
more by the clinical circumstances in which the ECG changes are
found than by the particular changes themselves.
Thus the term, nonspecific ST-T wave abnormalities, is frequently
used when the clinical data are not available to correlate with the
ECG findings. This does not mean that the ECG changes are
unimportant!
It is the responsibility of the clinician providing care for the patient
to ascertain the importance of the ECG findings.
Factors affecting the ST-T and U wave configuration include:
Intrinsic myocardial disease (e.g., myocarditis, ischemia, infarction,
infiltrative or myopathic processes)
Drugs (e.g., digoxin, quinidine, tricyclics, and many others)
Electrolyte abnormalities of potassium, magnesium, calcium
Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.)
Metabolic factors (e.g., hypoglycemia, hyperventilation)
Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down
the beginning of the ST segment)
Ventricular conduction abnormalities and rhythms originating in the
ventricles
“Secondary” ST-T Wave changes
“Secondary" ST-T Wave changes (these are ST-T wave changes solely due
to alterations in the sequence of ventricular activation)
ST-T changes seen in bundle branch blocks (generally the ST-T polarity is
opposite to the major or terminal deflection of the QRS)
ST-T changes seen in fascicular block
ST-T changes seen in nonspecific IVCD
ST-T changes seen in WPW pre-excitation
ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced
beats
"Primary" ST-T Wave Abnormalities
"Primary" ST-T Wave Abnormalities (ST-T wave changes that are
independent of changes in ventricular activation and that may be the
result of global or segmental pathologic processes that affect ventricular
repolarization)
Drug effects (e.g., digoxin, quinidine, etc)
Electrolyte abnormalities (e.g., hypokalemia)
Ischemia, infarction, inflammation, etc
Neurogenic effects (e.g., subarachnoid hemorrhage causing
long QT)
Causes of ST Elevation
"ELEVATION"
E - Electrolytes
L - LBBB
E - Early Repolarization
V - Ventricular hypertrophy
A - Aneurysm
T - Treatment - Pericardiocentesis
I - Injury (AMI, contusion)
O - Osborne waves (hypothermia)
N - Non-occlusive vasospasm
Differential Diagnosis of ST Segment Elevation
Normal Variant “Early Repolarization”
Ischemic Heart Disease
Acute Pericarditis
Other Causes
Normal Variant "Early Repolarization" (usually concave upwards, ending with
large symmetrical,, upright T waves)
"Early Repolarization":
"Early Repolarization": note high take off of the ST segment in leads V4-6.
The ST elevation in V2-3 is generally seen in most normal ECG's.
The ST elevation in V2-6 is concave upwards, another characteristic of this
normal variant.
Ischemic Heart Disease (usually convex upwards, or straightened)
Acute transmural injury - as in this acute anterior MI
Persistent ST elevation after acute MI suggests ventricular aneurysm
ST elevation may also be seen as a manifestation of Prinzmetal's
(variant) angina (coronary artery spasm)
ST elevation during exercise testing suggests extremely tight coronary
artery stenosis or spasm (transmural ischemia)
Acute Pericarditis
Concave upwards ST elevation in most leads except aVR
No reciprocal ST segment depression (except in aVR)
Unlike "early repolarization", T waves are usually low amplitude, and
heart rate is usually increased.
May see PR segment depression, a manifestation of atrial injury
Other Causes:
Left ventricular hypertrophy (in right precordial leads with large S-waves)
Left bundle branch block (in right precordial leads with large S-waves)
Advanced hyperkalemia
Hypothermia (prominent J-waves or Osborne waves)
J-point is the point where S wave becomes isoelectric and joins the T wave.
ST segment elevation or depression is measured 2 small boxes away from
the J-point and then, up or down the isoelectric line.
Differential Diagnosis of ST Segment Depression
Normal variants or artifacts:
Pseudo-ST depression (wandering baseline due to poor skinelectrode contact)
Physiologic J-junctional depression with sinus tachycardia (most
likely due to atrial repolarization)
Hyperventilation-induced ST segment depression
Ischemic heart disease
Nonischemic causes of ST depression
Non-ischemic causes of ST depression
RVH (right precordial leads) or LVH (left precordial leads, I, aVL)
Digoxin effect on ECG
Hypokalemia
Mitral valve prolapse (some cases)
CNS disease
Secondary ST segment changes with IV conduction
abnormalities (e.g., RBBB, LBBB, WPW, etc)
Ischemic heart disease
Subendocardial ischemia (exercise induced or during angina attack
Non Q-wave MI
“horizontal"
ST
depression
in lead V6
Reciprocal changes in acute Q-wave MI (e.g., ST depression in leads I & aVL
with acute inferior MI)
Stages of Acute Q-Wave MI
Ist Few Hours
First 24 Hours
First 72 Hours
Evolution of acute anterolateral myocardial infarction at 3 hours
Tomb stoning is less prominent with the onset of T wave inversions in the anterior
precordium. Reciprocal changes are resolving.
Evolution of acute anterolateral myocardial infarction at 24 hours
Prominent Q waves have developed across the anterior precordium and leads I, aVL.
However, ST segment elevation persists.
Evolution of acute anterolateral myocardial infarction at 72 Hours
Q wave pattern in the anterolateral leads is well established.
Persistent ST segment elevation suggests complication by aneurysm or pericarditis
Acute anteroseptal myocardial infarction
a) ST elevation and tall T waves
b) QS deflections in V1, V2 and V3 and V4
Right sided EKG lead placement
Right ventricular infarction (Rt.sided leads)
ST segment elevation in leads V4R and V5R reveals right ventricular involvement
complicating the inferior infarct.
Complicated Acute inferior myocardial infarction
AV
dissociation
Note inferior ST segment elevation as well as atrioventricular dissociation secondary to
complete heart block.
Acute inferior myocardial infarction complicated by Wenkebach
wenckebach
Note inferior ST segment elevation and Q waves as well as progressive prolongation of
the PR interval followed by a dropped beat with grouped beating.
Inferoposterior MI
a)
Tall R in V2,R/S
>1
Q waves in leads II, III & aVF
b) Tall R wave in lead V2 with a duration of > 0.04 secs and R/S ratio equal to or >1
(in patients over 30 years of age without RVH)
Postero-lateral MI
The "true" posterior MI is recognized by pathologic R waves in leads V1-2. These are
the posterior equivalent of pathologic Q waves (seen from the perspective of the
anterior leads). Tall T waves in these same leads are the posterior equivalent of inverted
T waves in this fully evolved MI. The loss of forces in V6, I, aVL suggest a lateral wall
extension of this MI.
Lateral myocardial infarction
ST segment elevation in leads I and aVL associated with inferior reciprocal changes
along with poor R wave progression. Note preexisting anteroseptal MI.
Subendocardial Ischemia
Anterolateral ST segment depression is consistent with diffuse subendocardial ischemia
vs. non-Q wave MI.
Unstable angina vs. non-Q wave myocardial infarction
ST segment depression in leads V2 through V5 supports acute ischemic syndrome with
no “Q” waves.
Non-Q Wave MI
Non Q MI
Recognized by evolving ST-T changes over time without the formation of
pathologic Q waves (in a patient with typical chest pain symptoms and/or
elevation in myocardial-specific enzymes)
Although it is tempting to localize the non-Q MI by the particular leads
showing ST-T changes, this is probably only valid for the ST segment
elevation pattern
Evolving ST-T changes may include any of the following patterns:
a) Convex downward ST segment depression only (common)
b) Convex upwards or straight ST segment elevation only (uncommon)
c) Symmetrical T wave inversion only (common)
d) Combinations of above changes
Non-Q Wave MI
a)
Convex downward ST segment depression only (common)
b)
Convex upwards or straight ST segment elevation only
(uncommon)
c)
Symmetrical T wave inversion only (common)
The Pseudoinfarcts
pseudoinfarcts
These are ECG conditions that mimic myocardial infarction either by simulating
pathologic Q or QS waves or mimicking the typical ST-T changes of acute MI.
IHSS (may make normal septal Q waves "fatter" mimicking pathologic Q waves)
LVH (may have QS pattern or poor R wave progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimic true posterior MI)
Complete or incomplete LBBB (QS waves or poor R wave progression in V1-V3)
Pneumothorax (loss of right precordial R waves)
Left anterior fascicular block (may see small q-waves in anterior chest leads)
Acute pericarditis (the ST segment elevation may mimic acute transmural injury)
CNS disease (may mimic non-Q wave MI by causing diffuse ST-T wave changes)
COPD and cor pulmonale (loss of R waves V1-3 and/or inferior Q waves with RAD)
Arrhythmias
How to think about arrhythmias and conduction disturbances
Arrhthmia algo
p
a
u
s
e
s
A fully compensatory pause
usually follows a premature
complex, where the R - R
interval produced by two
sinus initiated QRS
complexes on either side of
the premature complex
equals twice the normally
conducted R - R interval
Atrial Premature Beat (APB)
A
P
C
•
•
•
•
an abnormal P wave
as P waves are small and rather shapeless the difference in an APB is
usually subtle. The one shown here is a clear example.
occurs earlier than expected
followed by a pause - but not a full compensatory pause
Premature Ventricular Complex
P
V
C
QRS complex appears bizarre usually greater than 120msec
T wave is large and opposite in direction to the QRS complex
A fully compensatory pause usually follows a PVC
PVC
Interpolated PVC
•
•
•
Sinus rhythm with a PVC that has no
effect on the sinus rate. Although not
easily seen, there is often PR prolongation
due to retrograde concealed penetration
into the AV node.
Ventricular Bigeminy
Bi
ge
mi
ny
a ventricular premature beat follows each normal beat
QT prolongation
Marked QT Prolongation
• ECG rhythm strip of a 12 year old
male with recurrent unexplained
syncope and Long QT syndrome. ECG
strip shows marked QT prolongation.
• Low amplitude notched T waves are
often associated with LQT type 2,
associated with HERG gene mutations
that cause defects in IKr.
F
i
b
Atrial Fibrillation
A
Atrial fibrillation (AF) is thought
to be due to multiple wavelets of
conduction produced by reentry.
Perpetuation of AF depends on
the relative dimensions of the
atria and the size of the reentrant
circuit.
Compared
with
atrial
flutter, in which there is one
reentrant circuit and organized
atrial activity, atrial fibrillation
demonstrates no organized atrial
contraction. This leads to blood
stasis, the formation of clots, and
the possibility of embolic events.
Thus, most patients with chronic
atrial
fibrillation
are
given
anticoagulants to reduce the risk
of embolic events such as strokes.
Atrial Fibrillation
A
F
i
b
No P waves. Narrow complex QRS with irregular RR intervals. Ventricular rate
is controlled in this EKG.
Atrial Fib complicating inferior MI
A
F
i
b
Preexcited QRS complex with Atrial Fibrillation
W
P
W
in
Af
ib
•
The shortest RR interval is 190 msec, suggesting a high risk pathway that may be
associated with rapid rates and degeneration to ventricular fibrillation. Catheter
ablation should be strongly considered in patients such as this.
A
F
l
u
t
t
Atrial Flutter circuit
Atrial flutter is a macro reentrant circuit
in the right atrium. The circuit involves
conduction in a counterclockwise (or
clockwise) direction from the low
posterior right atrium near the tricuspid
valve annulus (TA), the posteroseptal
region near the coronary sinus os, the
interatrial septum, the high lateral right
atrium, and down the crista terminalis to
the isthmus between the inferior vena
cava and the TA. The region of the
posterior right atrium is thought to be
the slow zone of conduction in the
circuit. Evidence that supports this
theory are data showing that atrial
flutter can be entrained with atrial
pacing. Electrophysiologists have
developed techniques allowing to ablate
the critical regions of the circuit causing
atrial flutter, thus, rendering the circuit
inoperable.
Atrial Flutter
A
F
l
u
t
t
e
r
“F”
wave
s
Atrial rate of 300 bpm with upright “FLUTTER” waves inferiorly. This is consistent
with typical atrial flutter.
A
Flutt
er
Atrial
Flutter
With 2:1
AV
Conduction
Atrial flutter with 2:1 AV block is one of the most frequently missed ECG rhythm
diagnoses because the flutter waves are often hard to find. In this example two flutter
waves for each QRS are best seen in lead III and V1. The ventricular rate at 150 bpm
should always prompt us to consider atrial flutter with 2:1 conduction as a diagnostic
consideration.
SVT
Supraventircular Rhythms
SVT
1. Do you see any P waves?? How do they look? Are they
upright, preceding, following or buried in relation to the QRS?
2. What is the ventricular rhythm? Look at the QRS and its
duration?
3. Now wonder about the AV conduction with the above
information!! Are the P and QRS related with normal intervals??
4. Are there any unusual complexes?
SVT
P always related to QRS
SVT
P precedes QRS with a fixed PR interval
Normal Sinus rhythm nstee
P precedes QRS with a fixed prolonged PR interval
First Degree AV block
P precedes QRS with a variable PR interval
and a variable p morphology
Wandering pacemaker
Multifocal atrial tachycardia
P precedes/follows/buried in relation to the QRS
Non Sinus (inverted Ps)
Junctional (P follows QRS)
P sometimes related to QRS
progressive lengthening of PR interval
with intermittent dropped beats
Second degree Type I (wenckebach)
sudden dropped beats without prior PR lengthening
but with fixed prolonged PR interval
Second degree Type II Mobitz
P never related to QRS
QRS complexes < P waves
Third degree AV block
Narrow QRS with adequate HR - Junctional
Wide QRS with a low HR - Escape Rhythm
QRS complexes > Pwaves
AV Dissociation
a)
P waves follow the QRS
b) QRS regular with a normal duration
S
V
T
Supraventricular Tachycardia
S
V
T
Supraventricular Tachycardia
Electrocardiographic patterns of narrow complex tachycardia
Narro
w
compl
ex
Tachy
cardia
The most important clue to the mechanism of a
narrow complex tachycardia is the relationship
of the P wave to the QRS complex.
No visible P wave often means that the P
wave is buried in the QRS complex. This is
usually due to typical atrio-ventricular (AV)
nodal reentry.
With typical AV nodal reentry, the P wave
may also be located just at the start or end of
the QRS complex, giving a qRs or Rsr′ pattern.
When the P wave is located close to the
previous QRS complex, it is identified as a
short-RP tachycardia. This is often seen with
accessory pathway–mediated tachycardia and
is due to retrograde atrial activation over the
accessory pathway.
AVNRT—atrioventricular nodal reentry tachycardia
Electrocardiographic patterns of narrow complex tachycardia
The most important clue to the mechanism of a
narrow complex tachycardia is the relationship
of the P wave to the QRS complex.
The P wave may also be far from the
previous QRS complex and are classified as a
long-RP tachycardia.
If the P wave is inverted, it may be the result
of atypical AV node reentry, or it may be using
a slowly conducting accessory pathway in the
retrograde direction.
AVNRT—atrioventricular nodal reentry tachycardia
N
ar
ro
w
co
m
pl
ex
ta
ch
yc
ar
di
a
Narrow complex tachycardia
Diagram of atrioventricular (AV) nodal reentry
AV
N
reen
try
Schema for
typical atrioventricular
node reentrant
tachycardia (AVNRT).
Schema
for atypical
atrioventricular node
reentrant tachycardia
(AVNRT).
Slow pathway fibers begin in or around the coronary sinus (CS) or posteriorly and travel superiorly
and anteriorly to converge on the compact AV node, which is in the superior interventricular septum.
Fast pathway fibers travel superior and anterior to the compact AV node.
AV nodal
reentry
Inverted P
150 /min
A
V
N
R
T
a) Onset and termination are abrupt
b) Episode ia initiated almost always by a premature atrial beat with a > PR interval
c) Heart rate is usually between 140 and 220/min
d) P - QRS complex resemble a junctional beat with inverted P in II, III, aVF.
e) P waves may superimpose on, follow or rarely precede QRS
f) QRS may be normal or wide secondary to an preexisting IVCD or secondary to an
aberrant ventricular conduction.
Junctional Tachycardia
Junctional
Tachycardia
a) Heart rate between 120/min and 220/min with minute to minute variations
b) Normal QRS duration unless associated with aberrant conduction
c) Rhythm generally regular, but may be irregular resembling A Fib or MAT
d) Retrogade P wave may be seen following the QRS, but AV dissociation is common
with slower rhythms
W
P
W
Wolf
Parkinson
White
Syndrome
• The short PR interval is due to a bypass track, also known as the Kent pathway.
By bypassing the AV node the PR shortens.
• The delta wave represents early activation of the ventricles from the bypass tract.
• The fusion QRS is the result of two activation sequences, one from the bypass tract
and one from the AV node.
• The ST-T changes are secondary to changes in the ventricular activation sequence.
Wolf Parkinson White Syndrome
W
P
W
Wolf
Parkinson
White
Syndrome
W
P
W
a)
A PR interval of <0.12 sec, with normal P wave
b) Abnormally wide QRS complex with a duration of 0.11 sec or more
c)
The presence of an initial slurring of the QRS complex, The delta Wave
d) Secondary ST segment and T wave changes
e)
The frequency association of paroxysmal tachycardia
Conduction over an accessory pathway
Conduction over an accessory pathway
The morphology of a QRS complex in patients with
an accessory pathway (AP) is an excellent example
of fusion.
Conduction over an AP is influenced by drugs,
sympathetic states, and its location along the
atrioventricular annulus. If there is no antegrade
conduction, the AP may still conduct in the
retrograde direction but is considered concealed,
because it is not apparent on the ECG.
When conduction over the AP is minimal and
atrioventricular (AV) node conduction
predominates, the QRS becomes a fusion of
conduction over the AV node–His-Purkinje system
and the AP.
H-P—His Purkinje; LA—left atrium; LV—left
ventricle; PVC—premature ventricular complex;
RA—right atrium; RV—right ventricle.
Conduction over an accessory pathway
When conduction to the ventricle over the AP
predominates compared with AV nodal conduction,
the QRS represents a fusion of conduction over the
AV node–HPS and the AP, but the larger the
portion of the ventricle activated by the AP, the
wider the QRS complex appears.
If ventricular activation is only over the AP, as
with maximally preexcited tachycardias, it is
difficult to distinguish the complex from
ventricular tachycardia.
H-P—His Purkinje; LA—left atrium; LV—left
ventricle; PVC—premature ventricular complex;
RA—right atrium; RV—right ventricle.
Wide complexd tachycardia
Differential Diagnosis of Wide-Complex Tachycardia
VT
SVT with aberrancy (atrial fibrillation/flutter)
Antidromic AV reentry via WPW accessory pathway
Atrial fibrillation, atrial flutter, atrial tachycardia, or
AV nodal reentry in setting of WPW with rapid
conduction down accessory pathway
Bundle branch reentry
EKG Distinction of VT from SVT with Aberrancy
Favors VT
Favors SVT
with Aberrancy
Duration:
RBBB: QRS > 0.14 sec.
LBBB: QRS > 0.16 sec.
< 0.14 sec.
< 0.16 sec.
Axis:
QRS axis -90° to ±180°
Normal
Morphology:
Precordial concordance
If LBBB:
V1 duration > 30 ms
S wave > 70 ms
S wave notched or slurred
V 6:
qR or QR
If RBBB:
V1: monophasic R wave
qR
If triphasic, R > R1
V 6:
R<S
R wave monophasic
R < R1
A-V Dissociation, Fusion, and Capture Beats in VT
E
F
ECTOPY
C
FUSION
CAPTURE
Wide QRS Tachycardia
Narrow QRS
Wide QRS - BBB
(Aberrant conduction)
Wide QRS - Preexcitation
(Conduction via AP)
Wide QRS - VT
Wide QRS Tachycardia
Wide QRS Tachycardia may be of Ventricular or Supraventricular origin.
The main features of this wide QRS tachycardia that differentiate between ventricular
and supraventricular origin are the presence of P waves and AV dissociation.
Ventricular
tachycardia
a) Abnormal and wide QRS complexes with secondary ST segment and T wave changes
b) A ventricular rate usually between 140 and 200 beats/min
c) A regular or slightly irregular rhythm
d) Abrupt onset and termination
e) AV dissociation
f) Capture beats
g) Fusion beats
Idioventricular Rhythm
Torsade de pointes
Polymorphous ventricular tachycardia
•This is a form of VT where there is usually no difficulty in recognising its
ventricular origin.
•wide QRS complexes with multiple morphologies
•changing R - R intervals
•the axis seems to twist about the isoelectric line
•it is important to recognise this pattern as there are a number of reversible
causes
•heart block
•hypokalaemia or hypomagnesaemia
•drugs (e.g. tricyclic antidepressant overdose)
•congenital long QT syndromes
•other causes of long QT (e.g. IHD)
Conduction blocks
Conduction blocks
First Degree AV Block
AV block is defined by PR intervals greater than 200 ms.
This may be caused by : drugs, such as digoxin;
excessive vagal tone
ischemia or
intrinsic disease in the AV junction or
bundle branch system
Second Degree AV Block: Type I Mobitz
Second Degree AV Block: Type I Mobitz
The 3 rules of “classic AV Wenckebach” are:
1) decreasing RR intervals until pause
2) the pause is less than preceding 2 RR intervals
3) the RR interval after the pause is greater than the RR interval just prior to
pause.
Second Degree AV Block: Type I Mobitz
Progressive PR segment prolongation prior to dropped QRS complex.
Second Degree AV Block: Type II Mobitz
P waves
Dropped QRS
wave with
prolonged RR
High Grade AV block
AV conduction ratio 3:1 or higher
Complete Heart Block
Complete Heart Block
a) P waves are not conducted to the ventricles because of block at the AV node.
The P waves are indicated below and show no relation to the QRS complexes.
They 'probe' every part of the ventricular cycle but are never
conducted.
b) The ventricles are depolarized by a ventricular escape rhythm
Junctional Rhythm
Junctional Rhythm
HEMIBLOCKS
Left Anterior Hemiblock (LAH)
a)
Displacement of the mean QRS axis in the frontal plane to between –300 and –900
( abnormal Left axis deviation )
b) A qR complex ( or an R ) in I and aVL, an rS in II, III and aVF
c)
Normal or slightly prolonged QRS
Left Posterior Hemiblock
Left posterior fascicular block (posterior hemiblock, LPH) may be difficult to diagnose
without prior ECGs. The QRS axis shifts substantially rightward. An axis of over +120,
with no evidence of RVH or anterior infarction, is presumed LPH.
RS in I and aVL and a qR in Inferior leads are suggestive.
Bundle Branch Blocks
Left Bundle Branch Block
Left Bundle Branch Block
a) QRS duration > 0.12 secs
b) Absence of “Q” waves in I,V5 & V6
c) Presence of a broad monophasic R in leads I, V5 & V6 which is usually notched
d) Displacement of ST segment and T wave in the opposite direction to the major
deflection of the QRS
e) Broad deep QS in V1
f) Delay of onset of the intrinsicoid deflection (R peak time) in V5 and V6
delayed intrinsicoid
deflection
Left Bundle Branch Block
a) QRS duration > 0.12 secs
b) Absence of “Q” waves in I,V5 & V6
c) Presence of a broad monophasic R in leads I, V5 & V6 which is usually notched
d) Displacement of ST segment and T wave in the opposite direction to the major
deflection of the QRS
e) Broad deep QS in V1
f) Delay of onset of the intrinsicoid deflection (R peak time) in V5 and V6
Right Bundle Branch Block
a) Prolongation of QRS > 0.12 secs
b) Secondary R (R’) in the right precordial leads with the R’ > than the initial R (rsR’)
c) Delayed intrinsicoid deflection in the right precordial leads
d) Wide S wave in leads I, V5 & V6
RBBB complicating Inferior Wall MI
Bifascicular block
RBBB
L
A
H
Normal
PR
interval
Intraventricular conduction block involving a RBBB with a division of the Left
Bundle (either LAH or LPH) may be considered as a Bifascicular Block
Trifascicular
Block
A nice example of trifascicular block: Lead V1 shows RBBB; Lead II is mostly
negative with an rS morphology suggesting left anterior fascicular block. Since
Mobitz type II 2nd degree AV block is more often located in the bundle branch
system, the only location left for this block is the left posterior division of the left
bundle. Therefore all three ventricular conduction pathways are diseased.
Trifascicular Block
RBBB- rsR’ in V1,V2
LA
H
qR
in I,
aVL
rS
in
II,II
I
aVF
a) PR prolongation
b) RBBB with a left anterior hemiblock (LAH) or left posterior hemiblock (LPH)
OR Left Bundle Branch Block
Trifascicular Block
Right Atrial Enlargement
high pointed P wave ³ 2,5 mm in II and/or aVF
high P wave in V1 or V2; positive part > then 1,5 mm
Frontal plane P wave vector > + 75º
Left Atrial Enlargement
Left atrial vectors travel posteriorly, leftward, and inferiorly and are reflected in the mid
and late portions of the P wave. Left atrial enlargement causes an increase in the
duration (time) of the vectors, but does not usually result in any significant shift of the
axis of the P wave. This results in a broad, notched P wave in leads I and II, frequently with accompanying slurring of the terminal portion of the P wave. The distance
between the two peaks of the notched P wave is usually longer ttotal duration of greater
than 0.12 seconds. Usually, the voltage (amplitude) of the P wave increases only
slightly.
Left Atrial Enlargement with RVH
Left atrial enlargement and right ventricular hypertrophy have developed secondary to
mitral stenosis causing fixed pulmonary hypertension
RVH: Right Axis Deviation > 1100 or
R/S ratio in V1 >1
R in V1 +S in V5 or 6>11mm
R in V1 >7mm
S in V1 <2mm
rSR’ in V1 >10mm
Left Ventricular Hypertrophy
> 35mm
> 26mm
Limb leads: R in lead I + S in lead III > 25 mm OR R in aVL > 11mm OR
R in aVF >20mm OR
S in aVR >14
Precordial leads: R in V5 or V6 >26mm OR R in V5 or V6 + S in V1 > 35mm OR
largest R +largest S >45mm
Supporting criteria: ST segment depression and T wave inversion in left precordial
leads and in leads where QRS is upright (LV strain pattern).
Ven
tric
ula
r
Hy
per
tro
phy
Left Ventricular Hypertrophy
LVH strain pattern
LV
Strain
Pattern
A) LVH only
B) LVH with
Strain pattern
The ST segment is depressed and the T wave is inverted. Note too that the R wave
has become even taller.
Acute
pulmonary
embolus
S1 Q3 T3
The following often transient, changes may be seen in a large pulmonary embolus
• S1Q3T3 pattern ( a classic finding, not frequently seen )
• Prominent S wave in lead I
• Q wave and inverted T wave in lead III
Acute
• Sinus tachycardia
• T wave inversion in leads V1 - V3
pulmonary
• Right Bundle Branch Block
embolus
• low amplitude deflections
Chronic Obstructive Pulmonary Disease
a)
P waves >2.5mm in II, III, aVF with a axis of > 700 in frontal plane
b) Lead I sign with an isoelectric P and a QRS amplitude < 1.5mm
c)
QRS amplitude < 5mm in all limb leads
d) R/S ratio of <1 in V5 and V6
e)
S1S2S3 Syndrome with an R/S ratio of <1 in leads I, II and III
Digitalis toxicity
a)
ST segment depression
b) Decreased amplitude of T wave which may be biphasic
c)
Shortening of QT interval
d) Increased amplitude of U wave
“U”
Digitalis Effect on Rhythm and Conduction
EKG in Heart Transplant
a) Two sets of P waves
b) RBBB – complete or incomplete
c) Left anterior or posterior hemiblock
d) ST segment and T wave elevation as in pericarditis, although transient
e) Bradyarrhythmias, atrial, junctional or ventricular arrhythmias
Hypocalcemia
a)
Prolongation of QTc interval secondary to an increased duration of the ST segment
with no change in the duration of the T wave ( morphology of “T” may alter peaked or flattening or inversion). Similar changes may be seen only with
hypothermia.
b) QTc is directly proportional to the ionic calcium level and seldom exceeds
140msec. If QTc is > 140 msec, consider other associated abnormalities.
Hypokalemia
a)
b)
c)
d)
e)
ST segment depression,
Decreased T wave amplitude
Prominent U wave
Prolongatiuon of QRS and P wave changes
Cardiac Arrhythmias and AV blocks may occur
Hyperkalemia
The following changes may be seen in hyperkalemia
• wide, tall and tented T waves
• wide QRS
• atrial fibrillation
• ventricular fibrillation
Advanced Hyperkalaemia
Marked widening of the QRS duration combined with tall, peaked T waves are
suggestive of advanced hyperkalemia.
Note the absence of P waves, suggesting a junctional rhythm, but in hyperkalemia the
atrial muscle may be paralyzed while still in sinus rhythm.
The sinus impulse conducts to the AV node through internodal tracts without activating
the atrial muscle.
Neurogenic T waves (Osborne waves)
a)
Large , upright or deeply inverted T waves
b) Prominent U waves
c)
Prolongation of QTc interval
d) Abnormal Q waves, diffuse ST elevation or depression may also be seen
e)
mimic ischemic changes
Acute Pericarditis
a) Diffuse ST segment elevation and T wave inversion in all leads
b) PR segment depression (>0.8mm) in all leads except aVR and occasionally V1.
In aVR it is always elevated. These changes are attributed to subepicardial atrial injury
c) Low voltage QRS complexes & electrical alternans (with significant pericardial
effusion)
Low Voltage EKG
a) Uniform Reduction of QRS voltage in all leads
b) ST segment and T wave changes
DEXTROCARDIA
DEXTROCARDIA
DEXTROCARDIA
Left vs Right sided leads in Dextrocardia
Demand Pacing
Limb Lead Reversal
Note upright QRS complex and P wave in lead aVR with inverted QRS in leads I and
aVL.