1.

atrial arrhythmia:

atrial fibrillation:

-Because 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.

-the QRS complexes that are produced when an atrial action potential does reach the
ventricles will occur in an “irregularly irregular” manner.

-This means an ECG showing atrial fibrillation will have no visible P waves and an
irregularly irregular QRS complex.

2.Atrial flutter:

-Atrial rate not as fast as atrial fibrillation.“sawtooth” pattern of the P waves.A

narrow complex tachycardia at a ventricular rate of exactly 150 bpm is very
commonly atrial flutter.

-regularity of the QRS complexes

3. Multifocal atrial tachycardia:

MAT multifocal atrial tachycardia different p waves.at least three.

Sinus Arrhythmia:

sinus arrhythmia is a variation of the P-P interval, from one beat to the next, of
at least 0.12 seconds, or 120 milliseconds.

Sinus Bradycardia:

normal upright P wave in lead II ― sinus P wave ― preceding every QRS complex.

Sinus Tachycardia:

normal upright P wave in lead II preceding every QRS complex

2:Ventricular arrhythmia:

Ventricular fibrillation:

It occurs when the ventricular rate exceeds 400.

Ventricular Tachycardia:

wide QRS complex heart rhythm

-different QRS morphologies — one with a right bundle branch block morphology and
one with a left bundle branch block morphology.
Polymorphic VT (Torsades de Pointes) is a form of VT with multiple QRS morphologies

-Polymorphic VT (Torsades de Pointes) is a form of VT with multiple QRS

morphologies.

-R to S interval greater than 100 ms in any one precordial lead

-Sometimes explained as the absence of a “RS complex,” concordance simply means

“all up” or “all down.”

-If AV dissociation is present, the diagnosis is VT. AV dissociation occurs when P

waves, representing atrial depolarization, are seen at different rates than the QRS
complexes.

-See the PP interval when in sinus rhythm then march out the P waves within the
wide QRS complex to find the AV dissociation that is present, confirming the
diagnosis of VT.

-VT is frequently either in a right bundle branch block (upright in V1) or a left
bundle branch block pattern (downward in V1).

see concordance present in the precordial leads (V1-V6)

-3.chamber enlargement:

left atrial enlargement:

-When left atrial enlargement occurs, it takes longer for cardiac action potentials
to travel through the atrial myocardium; thus, the P wave also lengthens.

-diagnosing LAE on a 12-lead ECG is as follows:

1.The length of the P wave in lead II is greater than 120 milliseconds

OR
2.The downward deflection of the P wave in lead V1 is greater than 40
milliseconds in length, with greater than 1 millimeter negative deflection (< -1 mm
in amplitude)

-the amplitude of the P wave is exaggerated due to the close proximity of the
hypertrophied right atrial myocardium to the SA node.

right atrial enlargement:

-The P wave amplitude in lead II > 2.5 mm, or

The upward deflection of the P wave in lead V1 > 1.5 mm in amplitude.

Left Ventricular Hypertrophy (LVH):

larger mass of myocardium for electrical activation to pass through; thus the
amplitude of the QRS complex, representing ventricular depolarization, is
increased.

-abnormally thickened.electrical activity takes longer.LVH with QRS widening

-similar mechanisms that can result in abnormal ST segments or T waves. This is

referred to as “LVH with strain” or “LVH with repolarization abnormality.”

-p depolarization atrium qrs depolarization ventricular st repolarization

-The typical pattern with LVH includes deviation of the ST segment in the opposite
direction of the QRS complex (discordance), and a typical T wave inversion pattern
is present

Right Ventricular Hypertrophy:

-due to chronic pressure overload.RVH is diagnosed on ECG in the presence of a R/S

ratio of greater than 1 in lead V1 in the absence of other causes, or if the R wave
in lead V1 is

greater than 7 millimeters tall.

-Strain causes ST segment depression and asymmetric T wave inversions in leads V1

to V3.

4.conduction abnormalities:

-right bundle branch block:

The ECG criteria for a right bundle branch block include the following:

QRS duration greater than 120 milliseconds

rsR’ “bunny ear” pattern in the anterior precordial leads (leads V1-V3)
Slurred S waves in leads I, aVL and frequently V5 and V6

-Remember that T wave inversions and ST segment depression are normal in leads V1
to V3 in the presence of a right bundle branch block; thus, myocardial ischemia
technically cannot be

easily determined in these leads.

unlike in the presence of a left bundle branch block, myocardial ischemia and
infarction can easily be detected on ECG when a RBBB is present.

-ECG displaying a right bundle branch block with an anterior ST segment elevation
MI

-There are times when a QRS complex may appear in a RBBB pattern intermittently.

-A typical “bunny ear” pattern is not always present in a RBBB, as the R or the R’
may be very small
-The QRS morphology criteria to diagnose VT with a RBBB include the following:

A monophasic R or biphasic qR complex in V1

An RSR’ or “bunny ear” pattern present in V1 or V2, with the R peak higher in
amplitude than the R’ peak (see image below)
A rS complex in lead V6 (favors VT)

The QRS morphology criteria to diagnose VT with a RBBB include the following:

-Left Bundle Branch Block (LBBB):

The ECG criteria for a left bundle branch block include:

QRS duration greater than 120 milliseconds

Absence of Q wave in leads I, V5 and V6
Monomorphic R wave in I, V5 and V6
ST and T wave displacement opposite to the major deflection of the QRS complex.
-If the QRS complex is widened and downwardly deflected in lead V1, a left bundle
branch block is present.
- If the QRS complex is widened and upwardly deflected in lead V1, a right bundle
branch block is present.
-The ECG strip below shows normal sinus rhythm, then atrial fibrillation with a
rapid ventricular response develops. With the faster heart rate, the QRS complex
morphology changes to that
of a LBBB. As sinus rhythm restores, and the ventricular rate slows, the QRS
morphology returns to normal.

-Sgarbossa criteria, and they are listed below.

ST segment elevation > 1 mm and in the same direction (concordant) with the QRS
complex = 5 points
ST segment depression > 1 mm in leads V1, V2 or V3 = 3 points
ST segment elevation > 5 mm and in the opposite direction (discordant) with the QRS
= 2 points

A score of 3 points is required to diagnose an acute MI. Criteria #3 is under

debate as to its usefulness; therefore, either
essentially required. This
patient just made 1 mm ST segment elevation in
elevation in V6 — an ECG indeed from a patient
descending thrombosis.
criteria 1 or criteria 2 are
lead V5 and about 0.5 mm ST
with an acute left anterior

-Third-Degree Atrioventricular (AV) 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) ― meaning the P waves occur at one rate and
the QRS complexes at
another. This is termed “AV dissociation.”
4.Ischemic Heart Disease:

Posterior Wall Myocardial Infarction (MI).

The ECG findings of a posterior wall myocardial infarction are different than the
typical ST segment elevation seen in other myocardial infarctions.

The ECG findings of an acute posterior wall MI include the following:

ST segment depression (not elevation) in the septal and anterior precordial leads
(V1-V4). This occurs because these ECG leads will see the MI backwards; the leads
are placed anteriorly,
but the myocardial injury is posterior.
A R/S wave ratio greater than 1 in leads V1 or V2.
ST elevation in the posterior leads of a posterior ECG (leads V7-V9). Suspicion for
a posterior MI must remain high, especially if inferior ST segment elevation is
also present.
ST segment elevation in the inferior leads (II, III and aVF) if an inferior MI is
also present.

An inferior wall myocardial infarction:

An inferior wall myocardial infarction — also known as IWMI, or inferior MI, or

inferior ST segment elevation MI, or inferior STEMI — occurs when inferior
myocardial tissue supplied by the

right coronary artery, or RCA, is injured due to thrombosis of that vessel.

ST segment elevation in the inferior leads (II, III and aVF)

Reciprocal ST segment depression in the lateral and/or high lateral leads (I, aVL,
V5 and V6)
Note: If the reciprocal ST segment depressions are not present, consider
alternative causes of ST segment elevation, such as pericarditis.
An inferior MI can have multiple potential complications and can be fatal.

-Anterior Wall ST Segment Elevation MI:

An anterior wall myocardial infarction — also known as anterior wall MI, or AWMI,
or anterior ST segment elevation MI, or anterior STEMI — occurs when anterior
myocardial tissue usually

ST segment elevation in the anterior leads (V3 and V4) at the J point and sometimes
in the septal or lateral leads, depending on the extent of the MI. This ST segment
elevation is concave

downward and frequently overwhelms the T wave.

Reciprocal ST segment depression in the inferior leads (II, III and aVF).

See the full 12-lead ECG example below and a few more at the bottom.

The ECG findings of an old anterior wall MI include the loss of anterior forces,
leaving Q waves in leads V1 and V2. This is a cause of poor R wave progression, or
PRWP.
To distinctly say that an old anterior wall MI 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 poor R wave progression, but not old anterior wall MI, can be used.

On rare occasions, persistent ST segment elevation may be seen in V1 and/or V2,

indicating a ventricular aneurysm — a known complication of a myocardial
infarction. Visit Left Ventricular

Aneurysm ECG Review or Left Ventricular Aneurysm Topic Review. An example of an old
anterior myocardial infarction with a left ventricular aneurysm is below.

6.miscellaneous:

-Atrial Septal Defect (ASD):

An atrial septal defect should show a right bundle branch block, or RBBB ―
sometimes incomplete ― on ECG.

-Hypercalcemia:

The ECG findings of hypercalcemia include:

A shortened QT interval
A shortened ST segment
Osborne Waves

-Hypocalcemia:

A prolonged QT interval
A lengthened ST segment

There are many causes of a prolonged QT interval on the ECG, including genetic long
QT syndrome, electrolyte abnormalities and medications.

-Hyperkalemia:

Hyperkalemia can cause life-threatening arrhythmia.

Peaked T waves best seen in the precordial leads, shortened QT interval and, at
times, ST segment depression

Widening of the QRS complex (usually potassium level ≥ 6.5 mEq/L). This frequently
appears as “non-specific intraventricular conduction delay,” characterized by a
widened QRS complex of

greater than 120 milliseconds that does not meet the criteria for a left or right
bundle branch block. Frequently, an IVCD will look like a LBBB in lead V1 with a rS
complex or monomorphic

S wave, and it appears like a RBBB in leads I and V6 with a broad, slurred S wave.

If you see an IVCD, think of hyperkalemia.

Decreased amplitude of the P waves, an increase in the PR interval and bradycardia
in the form of atrioventricular blocks occur as the potassium level exceeds 7.0
mEq/L

-Absence of the P waves and eventually a “sine wave” pattern, as seen below, which
is frequently a fatal rhythm.

- calcium is “cardioprotective” instant reversal of all hyperkalemic ECG changes

within seconds of administration is experienced

-therefore, other therapy such bicarbonate or insulin is needed to do this. Calcium

administration can be fatal when digoxin toxicity is causing hyperkalemia and
should be avoided.

-Hypokalemia:

The typical ECG findings of hypokalemia (low potassium level) include:

U wave that occurs just after the T wave and is usually of smaller amplitude than
the T wave.
flattening of the T wave.
ST depression on occasion, which can mimic ischemia.