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The ECG criteria for a left bundle branch block (LBBB) include:

1) QRS duration of > 120 milliseconds.


2) Absence of Q wave in leads I, V5, and V6.
3) Monomorphic R wave in I, V5, and V6.
4) ST and T wave displacement opposite to the major deflection of the QRS complex.
Note: If the QRS duration is between 100-119 milliseconds with criteria 2, 3, and 4 of the above,
an incomplete left bundle branch block is present.
The ECG criteria for a right bundle branch block include:
1) QRS duration of > 120 milliseconds
2) rsR' "bunny ear" pattern in precordial leads
3) Slurred S waves in leads I, V5, and V6.

The criteria to diagnose a LAFB is as follows:


1. Left axis deviation of at least -45 degrees
2. The presence of a qR complex in lead I and a rS complex in lead III.
3. Usually a rS complex in lead II and aVF as well (not always).
qR complex: Small Q waves with tall R waves

The criteria to diagnose a LPFB is as follows:


1) Right axis deviation of 90 to 180 degrees
2) The presence of a qR complex in lead III and a rS complex in lead I.
3) Absence of RAE and RVH.
RAE: right atrial enlargement

Right atrial enlargement produces a peaked P wave (P pulmonale) with amplitude:

> 2.5 mm in the inferior leads (II, III and AVF)

> 1.5 mm in V1 and V2

A bifascicular block is defined by the combination of a right bundle branch block and a left
anterior (or posterior) fascicular block

A trifascicular block is the combination of a right bundle branch block, left anterior or posterior
fascicular block and a first degree AV block (prolonged PR interval)
A first degree AV block is indicated on the ECG by a prolonged PR interval. The PR interval is
normally 0.12-0.20 seconds. A PR interval consistently longer than 0.20 seconds (greater than 5
small boxes) indicates a 1st degree AV block. Note: there is a 1:1 ratio between P waves and
QRS complexes in 1st degree AV block, unlike 2nd and 3rd degree AV nodal block.

In second degree AV nodal block (a.k.a. Wenckebach block or Mobitz Type I AV block),
varying failure of conduction through the AV node occurs such that some P waves may
not be followed by a QRS complex. Unlike 1st degree AV nodal block, a 1:1 P wave to
QRS complex ratio is not maintained. Second degree type I AV block is specifically
characterized by increasing delay of AV nodal conduction until a P wave fails to conduct
through the AV node. This is seen as progressive PR interval prolongation with each
beat until a P wave is not conducted.
Second degree type 1: 1:1,5:2
Second degree type 2: 1:2:1:2 lebih berat penanganannya.
2:1 AV block is a form of second degree AV nodal block and occurs when every other P wave is
not conducted through the AV node to get to the ventricles and thus every other P wave is NOT
followed by a QRS complex. (seperti second degree type 2).

Complete heart block (a.ka. third degree AV nodal block) occurs when NO action potentials
conduct through the AV node. This results in the P waves (atrial depolarizations) being
completely unrelated to the QRS complexes (ventricular depolarizations). So the P waves occur
at one rate and the QRS complexes at another. This is termed AV dissociation.

Ischemic heart disease

The ECG findings of an acute AWMI (anterior wall myocard infark) include:
1) ST segment elevation in the anterior leads (V3 and V4) and sometimes in septal
and lateral leads depending on the extent of the myocardial infarction. This ST elevation
is concave downward and frequently overwhelms the T wave. This is called
"tombstoning" due to the similarity to the shape of a tombstone.
2) Reciprocal ST segment depression in the inferior leads (II, III and aVF).
The ECG findings of an old anterior wall myocardial infarction include:

1) Loss of anterior forces leaving Q waves in leads V1 and V2. This is related to "poor R
wave progression" or PRWP, however different.
Note: To distinctly say that an old anterior wall myocardial infarction is present on the ECG,
there must be no identifiable R wave in lead V1 and usually V2 as well. If there is an R
wave in V1 or V2, the term PRWP can be used, but not an old anterior wall myocardial
infarction.
2) Rarely, persistent ST elevation may be seen in V1 and/or V2 indicating a left ventricular
aneurysm which is a known complication of a myocardial infarction.

Inferior myocard infark


The ECG findings of an acute inferior myocardial infarction include:
1) ST segment elevation in the inferior leads (II, III, and aVF).
2) Reciprocal ST segment depression in the lateral and/or high lateral leads (I, aVL, V5 and V6).
Note: If the reciprocal ST depressions are not present, consider alternative causes of ST
segment elevation such as pericarditis.
The findings of an old inferior myocardial infarction on the ECG are pathologic Q wave in the
inferior leads. In general, if the Q wave is wider than 0.04 ms (one small box) or at least 1/3 the
height of the QRS complex, then inferior Q waves are thought to represent an old myocardial
infarction.

Posterior MI

The ECG findings on an acute posterior wall MI include:


1) ST segment depression (not elevation) in the septal and anterior precordial leads (V1 to
V4). This occurs since these ECG leads will see the MI backwards (since the leads are
placed anteriorly, but the myocardial injury is posterior).
2) The ratio of the R wave to the S wave in leads V1 or V2 is > 1.
3) ST elevation in the posterior leads of a posterior ECG (leads V7 to V9). Suspicion for a
posterior MI must remain high, especially if inferior ST elevation is also present.
4) ST elevation in the inferior leads (II, III, and aVF) may be seen if an inferior MI is also
present.

Biasanya barengan dengan MI (karena branch koronernya sama2 share.

Atrial Aritmia
Sinus tachycardia is indicated on ECG with a normal upright P wave in lead II preceding every
QRS complex (indicating that the pacemaker is coming from the sinus node and not elsewhere
in the atria) with an atrial rate of greater than 100 per minute. Usually the ventricular rate
(indicated by the QRS complex rate), is also greater than 100 since in most cases the P wave
conducts through the AV node to the ventricles to produce a QRS complex in a 1:1 fashion

differential diagnosis for sinus tachycardia includes:


1) Exercise
2) Anemia
3) Dehydration or shock
4) Fever/sepsis/infection
5) Hypoxia
6) Chronic pulmonary disease
7) Hyperthyroidism
8) Pheochromocytoma
9) Medications/stimulants
10) Decompensated congestive heart failure
11) Pulmonary embolus
Sinus bradycardia occurs on an ECG when there is a normal upright P wave in lead II (sinus P
wave) preceding every QRS complex with a ventricular rate of less than 60 beats per minute.

Sinus bradikardia
Causes of sinus bradycardia include:
1. AV blocking medications (beta-blockers, non-dihydropyridine calcium channel blockers,
digoxin).
2. Heightened vagal tone (i.e. well trained athlete)
3. Sick sinus syndrome
4. Hypothyroidism
5. Hypothermia
6. Obstructive sleep apnea
7. Hypoglycemia
Sinus aritmia

The sinus node rate can change with inspiration and expiration, especially in younger people.
The heart rate speeds up with inspiration (due to the Bainbridge reflex) and decreases with
expiration. The ECG criteria to diagnose sinus arrhythmia is a variation of the PP interval from
one beat to the next of at least 0.12 seconds or 120 milliseconds. Sinus arrhythmia, if not in a
young person and not occurring with respiration, may be a sign of sick sinus syndrome (SSS).

Premature Atrial Contraction (PAC)


There are four main characteristics of PACs:
1) They are premature. That is they occur earlier than you would expect if you were
to measure the previous P to P intervals.
2) They are ectopic. Meaning originating outside of the SA node. Thus the P wave
morphology would be different than the normal sinus P wave.

Atrial fibrilasi
Atrial fibrillation occurs when action potentials fire very rapidly within the pulmonary veins or
atrium in a chaotic manner. The result is a VERY fast atrial rate (about 400-600 beats per
minute). Since the atrial rate is so fast and the action potentials produced are of such low
amplitude, P waves will NOT be seen on the ECG in patients with atrial fibrillation. At
times, the P wave activity can be seen as coarse fibrillatory waves and the term coarse atrial
fibrillation is used, although there is no clinical significance to this finding.
The atrial action potentials all attempt to conduct through the AV node, however the AV node
becomes intermittently refractory and will only allow a certain number of atrial action potentials
to reach the ventricles. This is why the ventricular rate is NOT also 400-600, but rather
around 100-200 beats per minute. The degree to which action potentials can cross the AV
node to the ventricles is variable and reduced by AV blocking medications.
Since the AV node is intermittently (not regularly) refractory, the QRS complexes that are
produced when an atrial action potential does reach the ventricles will occur in an irregularly
irregular manner as there is no pattern to their frequency. This is commonly described as
varying RR intervals.
Thus an ECG showing atrial fibrillation will have NO visible P waves and an irregularly
irregular QRS complex. The ventricular rate is frequently fast unless the patient is on AV
node blocking drugs (such as beta-blockers or non-dihydropyridine calcium channel
blockers).

Atrial flutter
Atrial flutter occurs when a "reentrant circuit" is present causing a repeated loop of electrical
activity to depolarize the atrium at rate of about 250-350 beats per minute (remember the atrial
rate in atrial fibrillation is 400-600). This produces a characteristic "sawtooth" pattern of the P
waves, unlike atrial fibrillation in which the atrial rate is so fast that the P waves are not
identifiable or only coarse fibrillatory waves are seen.
the ventricular (QRS) rate will be exactly 150 beats per minute and regular.

WPW
The typical ECG finding of WPW is a short PR interval and a "delta wave". A delta wave is
slurring of the upstroke of the QRS complex.
RVH
RVH is diagnosed on ECG in the presence of a R-S ratio of > 1 in lead V1 in the absence of
other causes or if the R wave in lead V1 is > 7 mm tall
Right Atrial Enlargement (RAE)
1) The P wave amplitude in lead II greater than 2.5 millimeters
OR
2) The upward deflection of the P wave in lead V1 greater than 1.5 millimeters in
amplitude.
Right Axis Deviation
Right axis deviation occurs when the QRS axis is shifted between 90 and 180 degrees. A
number of things can result in right axis deviation which include lung disease, right sided heart
strain, right bundle branch block, and right ventricular hypertrophy. If the QRS is predominantly
downward in both leads I and aVF, then the axis is rightward.
Emboli pulmonal
sinus tachycardia, however the "S1Q3T3" (A large S wave in lead I, a Q wave in lead III, and an
inverted T wave in lead III) pattern of acute cor pulmonale is classic
Pericarditis

Stage I (acute phase): Diffuse concave upward ST segment elevation in most leads,
PR depression in most leads (may be subtle), and sometimes notching at the end of the
QRS complex.

Stage II: ST segment elevation and PR depression have resolved. T waves may be
normal or flattened.
Stage III: T waves are inverted and the ECG is otherwise normal.
Stage IV: The T waves return to the upright position thus the ECG is back to normal.
LVH
Cornell criteria: Add the R wave in aVL and the S wave in V3. If the sum is > 28 mm in
males or > 20 mm in females, then LVH is present.
Modified Cornell Criteria: Examine the R wave in aVL. If the R wave is > 12 mm in
amplitude, then LVH is present.
Sokolow-Lyon Criteria: Add the S wave in V1 plus the R wave in V5 or V6. If the sum
is > 35 mm, then LVH is present.
Romhilt-Estes LVH Point Score System:
If score = 4, then LVH present with 30-54% sensitivity. If score > 5, then LVH is present
with 83-97% specificity.
Amplitude of largest R or S in limb leads >20 mm
Amplitude of S in V1 or V2 > 30 mm
Amplitude of R in V5 or V6 > 30 mm
ST and T wave changes opposite QRS without digoxin
ST and T wave changes opposite QRS with digoxin
Left Atrial Enlargement
Left Axis Deviation
QRS duration > 90 milliseconds
Intrinsicoid deflection in V5 or V6 > 50 millisecond

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Left Atrial Enlargement

Thus the criteria for diagnosing LAE on ECG is as follows:


1) The P wave length in lead II greater than 120 milliseconds
OR
2) The downward deflection of the P wave in lead V1 greater than 40 milliseconds in
length AND greater than 1 millimeter negative deflection (less than -1 millimeter in
amplitude).
P-mitrale occurs when the depolarization of the right atrium and left atrium are both
visible in the P wave. This is seen as a notch in the P wave and occurs when the left
atrium is markedly enlarged such as in mitral valve stenosis.

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