ECG SLU elective Review Cards Learn The Heart website

Question 1

Left Bundle Branch Block

Answer 1

QRS > 120 msec
Absence of Q waves in leads I, V5, and V6
Monomorphic R wave in I, V5, and V6
ST and T wave displacement opposite major QRS deflection.

Question 2

Simple LBBB diagnosis

Answer 2

QRS > 120 msec with a downward deflected QRS on V1.

Question 3

Simple RBBB diagnosis

Answer 3

QRS >120 msec with an upward deflected QRS on V1

Question 4

Incomplete LBBB

Answer 4

QRS between 100-199 msec with other positive LBBB criteria.

Question 5

Rate dependent LBBB

Answer 5

Caused by myocardial ischemia or refractoriness of LBBB at faster heart rates. Difficult to distinguish from ventricular tachycardia, both have wide QRS complex.

Question 6

Sgarbossa Criteria

Answer 6

Use to diagnose acute myocardial infarction with LBBB present. Need 3 points, criteria 3 is in debate so either 1 or 2 suffice to diagnose acute myocardial infarction with LBBB.

1) ST elevation > 1 mm and concordant with QRS complex. (5 points)
2) ST depression > 1 mm in leads V1, V2, or V3. (3 points)
3) ST elevation > 5 mm discordant with QRS. (2 points)

Question 7

Right Bundle Branch Block

Answer 7

QRS > 120 msec
rSR’ bunny ear pattern in anterior precordial leads (V1-V3)
Slurred S waves in leads I, aVL, and frequently V5 and V6.

Question 8

Additional ECG abnormalities often seen with RBBB

Answer 8

TWI and ST depressions in V1-V3. This makes is hard to see myocardial ischemia in anterior precordial leads, MI are easy to see unlike LBBB.

Question 9

Ashman beat

Answer 9

A variation of RBBB, a premature atrial contraction or supraventricular beat that happens during right bundle refractory period.

Question 10

Left Anterior Fascicular Block

Answer 10

LAD
qR complex in lead I and aVL
rS complex in lead II, III, and aVF.

Question 11

Quick diagnosis of LAFB

Answer 11

Determine left axis deviation. Then look for upward QRS in lead I and downward in lead aVF and lead II. An rS complex in lead III.

Question 12

Old inferior wall MI and LAFB

Answer 12

Old inferior MI can not be diagnosed in setting of LAFB due to the inferior Q waves present from the LAFB.

Question 13

Left Posterior Fascicular Block

Answer 13

RAD
qR complex in lead II, III, and aVF
rS complex in lead I and aVL
ABSENCE of right atrial enlargement and/or RVH.

Question 14

Bifascicular Block

Answer 14

RBBB + LAFB/LPFB. Indicate significant conduction disease and are at higher risk of higher degree blocks. Usually leading to symptomatic bradycardia requiring pacemaker implantation.

Question 15

Lev’s disease

Answer 15

Also known as Lenegre-Lev syndrome or senile degeneration of the conduction system. Presents as an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. Most commonly seen in the elderly. Associated with Stokes-Adams attacks, involving temporary LOC 2/2 marked bradycardia.

Question 16

Trifascicular Block

Answer 16

RBBB + LAFB/LPFB + First degree AV block. A trifascicular block is a precursor to complete heart block. Does not need immediate treatment, but up to 50% will progress and need permanent pacemaker.

Question 17

First Degree AV Block

Answer 17

PR > 200. Due to slow conduction through AV node. Delaying the time it takes for SA node impulse to reach the ventricles, thus the increase in the PR interval. No treatment, but should avoid AV nodal blockers.

Question 18

Second Degree AV Block Type I

Answer 18

Also called Wenckebach or Mobitz Type I AV block. Increasing delay in AV nodal conduction until failure of a P wave conduction through AV node.

Question 19

Second Degree AV Block Type II

Answer 19

Also known as Mobitz Type II AV block. AV node becomes completely refractory to conduction on intermittent bases. Equal PR intervals with predictable drop in QRS in a 2:1 or 3:1 pattern. This indicates significant conduction disease of His-Purkinje system, it is irreversible. Due to increased risk of progression to complete third degree block, patients receive permanent pacemakers.

Question 20

2:1 AV Block

Answer 20

A form of second degree AV nodal block with every other P wave conducting through AV node and reaching ventricles. Can be hard to determine if from second degree type I or II.

Question 21

Ways to distinguish 2:1 AV nodal Block

Answer 21

Remember type I is a nodal issue, type II is infranodal, the problem is with His-Purkinje system.
Carotid sinus massage or Adenosine (slow AV node conduction). Gives more time for AV node to recover and can unmask PR prolongations.
Atropine, enhances AV nodal conduction and could eliminate second degree type I AV nodal block (this is the type due to AV nodal delay). Exercise would work via the same mechanism.

Question 22

Third Degree AV Block

Answer 22

A complete heart block. No action potentials are conducting through AV node. Results in complete disassociation of P and QRS complexes, with atria and ventricle contracting at their intrinsic rhythms. P waves at a rate of 60-100 with QRS complexes at a rate of 30-40.

Question 23

High Grade AV nodal Block

Answer 23

A type of 3rd degree heart block with occasional P wave conduction through AV node and generate an associated QRS.

Question 24

Digoxin effect on ECG

Answer 24

Classic digoxin effect appears as a downsloping ST segment depression also known as the “reverse tick” or “reverse check” sign.

Question 25

Digoxin Arrhythmias

Answer 25

Classic arrhythmias seen during digoxin toxicity include atrial tachycardia with a 2:1 conduction, bidirectional ventricular tachycardia and atrial fibrillation with a slow ventricular response.

Question 26

Sinus Tachycardia

Answer 26

Indicated on ECG with normal upright P wave in leads II with NSR and atrial rate of 100 with ventricular rate of 100. A dissociation between the two rates indicates an AV dissociation

Question 27

Differential diagnosis for sinus tachycardia

Answer 27

1) Exercise
2) Anemia
3) Dehydration or shock
4) Fevers/sepsis/infection
5) Hypoxia
6) Chronic pulmonary disease
7) Hyperthyroidism
8) Pheochromocytoma
9) Medications/stimulants
10) Decompensated congestive heart failure
11) Pulmonary embolus

Question 28

Sinus Bradycardia

Answer 28

Normal upright P wave in lead II, NSR, at a rate of less than 60 bpm.

Question 29

Causes of sinus bradycardia

Answer 29

1) AV blockers
2) Heightened vagal tone (eg well trained athletes)
3) Sick sinus syndrome
4) Hypothyroidism
5) Hypothermia
6) OSA
7) Hypoglycemia

Question 30

Sinus Arrhythmia

Answer 30

Refers to changing sinus node rate with respiratory cycle. Common in young healthy individuals and has no clinical significance. The heart rate increases with inspiration, due to Bainbridge Reflex and decreases with expiration. On ECG a PP interval variation of at least 0.12 secs (120 msec).

Question 31

Bainbridge Reflex

Answer 31

Heart rate increase in response to increased atrial pressure. A compensatory mechanism since increased right atrial pressures frequently result from elevated left heart pressures from decreased cardiac output.
The Bainbridge reflex acts in opposition of the carotid reflex

Question 32

Carotid baroreceptor reflex

Answer 32

Increase in heart rate with decreased tension on baroreceptors in hypotension or hypovolemia.

Question 33

Premature Atrial Contractions

Answer 33

Due to a focus in atrium generating an action potential before the next scheduled SA node action potential. PAC have four characteristics.

1) Premature.
2) Ectopic, thus P wave morphology will be different from normal.
3) Narrow complex, PACs come from atrium and will travel through AV node leading to normal conduction and spread through ventricles. Note that PVC are wide complex.
4) Compensatory pause after PAC, the atrial action potential sends the SA node into a refractory period.

Question 34

Atrial Fibrillation

Answer 34

Due rapid firing AP within the pulmonary veins or atrium in a chaotic manner. Results in a very fast atrial rate (400-600 bpm). On ECG, no P waves, instead coarse fibrillatory waves from the fast and low amplitude atrial AP firing. The irregular entry of atrial AP through AV node leads to the “irregularly irregular” pattern, with ventricular rate between 100-200.

Question 35

Irregular irregular rhythms

Answer 35

1) Atrial fibrillation
2) Atrial flutter with variable conduction
3) Multifocal Atrial Tachycardia.

Question 36

Atrial Flutter

Answer 36

Due to “re-entrant circuit” causing a repeated loop of electrical activity depolarizing the atrium at a rate of about 250-350 bpm. Produces characteristic “sawtooth” pattern of P waves. Usually every other P waves gets through producing a ventricular rate of about 150 bpm with regular RR intervals if there is no variable conduction.
A narrow complex tachycardia at a ventricular rate of exactly 150 bpm is often atrial flutter.

Question 37

Counterclockwise flutter

Answer 37

Negative flutter waves in II, III, aVF

Question 38

Clockwise flutter

Answer 38

Positive flutter waves in II, III, aVF

Question 39

Multifocal Atrial Tachycardia

Answer 39

A tachycardic version of a wandering atrial pacemaker, with atrial rate > 100 bpm. MAT is due to multiple ectopic areas within atrium generating consecutive action potentials. On ECG, at least 3 P wave morphologies with NSR with ventricular rate > 100 bpm. Usually occurs in setting of severe lung disease and with exacerbation of severe lung disease.

Question 40

AV Nodal Re-entrant Tachycardia (AVNRT)

Answer 40

Most common form of paroxysmal supraventricular tachycardia in adults. AVNRT is due to re-entrant circuit in AV node itself. On ECG:

1) Narrow complex tachycardia
2) A P wave that occurs after the QRS complex (a short RP interval)
3) This tachycardia will quickly terminate with AV blocking maneuvers (carotid massage or adenosine).

Question 41

AV Re-entrant Tachycardia (AVRT)

Answer 41

Due to re-entrant circuit outside of AV node that connects atrium to ventricles. The pathway is called an “accessory pathway” or a “bypass tract.” A presence of a congenital abnormal accessory pathway is seen in WPW. On ECG

1) A narrow complex tachycardia
2) Variable findings depending on the direction of circuit and location of accessory conduction.

Question 42

Anterior Wall STEMI

Answer 42

Lack of blood supply to Anterior Wall, supplied by the left anterior descending artery (LAD). On ECG ST elevation at the J point in at least 2 contiguous lead of > 2 mm (0.2 mV) i men or 1.5 mm (0.15 mV) in women n V2-V3 and/or >1 mm in chest leads.

Question 43

Extensive anterior MI

Answer 43

Site of lesion is proximal to LAD or in left main coronary artery. The MI will extend from the anterior wall to the septal and lateral regions.

Question 44

ECG findings in old anterior wall MI

Answer 44

There is a lost of anterior forces. On ECG Q waves in leads V1 and V2 with poor R wave progression.

Question 45

Poor R wave progression

Answer 45

Normally R:S ration increases with R wave predominance in the left side precordial leads (V4-V6).

Question 46

Causes of poor R wave progression

Answer 46

1) Old anterior wall MI
2) lead misplacement (frequently in obese women)
3) LBBB or LAFB
4) LVH
5) Dextrocardia
7) Tension pneumothorax with mediastinal shift
8) Congenital Heart Disease

Question 47

Persistent ST elevation in V1 and V2

Answer 47

Consider ventricular aneurysm, a known complication of myocardial infraction.

Question 48

Inferior Wall STEMI

Answer 48

Due to infarction of tissue supplied by the right coronary artery (RCA). Can be associated with a posterior wall MI. ECG findings include ST segment elevation in the inferior leads (II, II, aVF) with reciprocal ST depressions in lateral or high lateral leads (I, aVL, V5, and V6).

Question 49

Posterior Wall MI

Answer 49

Usually supplied by the posterior descending artery (a branch of the RCA in 80% of people). ECG findings include:

1) ST depressions in septal and anterior precordial leads (V1-V4). These leads are seeing the MI backwards.
2) Ratio R:S wave in V1 or V2 > 1.
3) ST elevation in posterior leads of posterior ECG (V7-V9)
4) ST elevations consistent with inferior wall MI.

Question 50

ECG changes during ICH or s/p CEA

Answer 50

Deep TWI and QT prolongation. Mechanism is poorly understood. T wave changes can mimic Wellen’s phenomenon, however QT prolongation is specific to ICH/CEA.

Question 51

Wellens Phenomenom

Answer 51

Biphasic T waves in V1-V3 or Deep symmetric TWI in precordial lead. Indicative or severe proximal LAD stenosis. There is no ST elevation with Wellens phenomenon.

Question 52

Left Atrial Enlargement (LAE)

Answer 52

With LAE it takes longer for cardiac AP to travel through atrial myocardium, thus P wave becomes longer. On ECG;
1) P wave length in lead II > 120 msec
OR
2) Downward deflection of P wave in V1 > 40 msec (lenght) and > 1 mm in negative deflection. (Normally P wave is biphasic in V1)

Question 53

Right Atrial Enlargement (RAE)

Answer 53

With RAE the length of the P wave is not affected, since it all sits on the SA node. However the hyperthrophied right atrial myocardium that the P wave is taller (peaked). On ECG:
1) P wave amplitude in lead II > 2.5 mm
OR
2) Upward deflection of P wave in lead V1 > 1.5 mm in amplitude.

Question 54

Cornell LVH criteria

Answer 54

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.

Question 55

Right Ventricular Hyperthrophy

Answer 55

R:S ratio > 1 in lead V1
OR
R wave in V1 > 7 mm