Baylor Ecg

Front 1

Normal QRS axis

Back 1

downward & to the left (-30 to +90)

QRS is (+) in I & aVF

Front 2

Inferior leads

Back 2

II, III, aVF

They point inferiorly and reflect inferior LV wall pathology

Front 3

Lateral leads

Back 3

I and aVL

They point laterally and reflect lateral LV wall pathology

Front 4

aVR orientation

Back 4

points away from the heart orientation in the chest

All Standard ECG Leads have Positive QRS except aVR

Front 5

septal (or anteroseptal) leads

Back 5

V1, V2

Front 6

anterior leads

Back 6

V3, V4

Front 7

lateral leads

Back 7

V5, V6

Front 8

QRS Interval is effected by

Back 8

Bundle Branches
Purkinje Fibers
Myocardium

Front 9

PR Interval is effected by

Back 9

AV Node
His Bundle

Front 10

Abnormal P wave is caused by

Back 10

Ectopic atrial rhythm

Front 11

Long PR Interval is caused by

Back 11

AV Block

Front 12

Short PR Interval is caused by

Back 12

Accessory tract

Front 13

Wide QRS interval is caused by

Back 13

Bundle branch block
Dilated ventricles

Front 14

QRS Axis ranges

Back 14

Normal =– 30 to + 90
Left = – 30 to – 90
Right = +90 to 180
Indeterminate = -90 to 180 (Extreme axis deviation either to the left or right)

Front 15

Systematic Evaluation of 12 lead ECG (11 things to check)

Back 15

1. Rhythm
2. Rate
3. QRS axis
4. P wave morphology
5. P-R interval
6. QRS interval
7. QT interval
8. Chamber enlargement: LVH, RVH
9. Pathologic Q waves
10. ST and T wave changes
11. Precordial R wave progression

Front 16

ECG Time:
1 small box =
1 large box =

Back 16

0.04 sec (40msec)
0.2sec (200msec)

Front 17

Left atrial enlargement shown by

Back 17

Bifid or notched P wave in lead II

Front 18

Right atrial enlargement shown by

Back 18

Tall P wave > 2.5 mm in lead II

Front 19

Normal PR interval

Back 19

PR 0.12 - 0.20 seconds (from beginning of P wave to beginning of R wave

Front 20

Causes of prologed PR interval

Back 20

Block in the AV node delays AV conduction

Beta blockers
Calcium channel blockers
digoxin
amiodarone
clonidine
Calcification of conduction system due to Lev's or Lenegre's disease

Front 21

WPW ECG Triad

Back 21

Short PR interval
Wide QRS
Delta Wave (beginning of the R wave kind of slurs upwards)

Caused by an accessory path between atria and ventricles

Front 22

Right Bundle Branch block shown by

Back 22

RSR' in V1 and V2
QRS is prolonged >0.12sec

Front 23

Left Bundle Branch block shown by

Back 23

RSR' in V5 and V6
QRS is prolonged >0.12sec

Front 24

ECG presentation of left ventricle hypertrophy

Back 24

Identical to LBBB, differentiated due to clinical manifestation of heart failure

RVH also resembles RBBB

Front 25

QTc

Back 25

QT divided by the square root of the RR interval in seconds (to correct for shorter QT at faster heart rates)

Normal range from 360 to 440 msec

Front 26

Causes of prolonged QT interval

Back 26

1. Drugs:
A. Anti-arrhythmics (class IA, IC, III)
B. Anti-psychotics
C. Tricyclic Anti-Depresants
D. Antifungals

2. Electrolyte abnormalities: low K, Mg or Ca

Congenital abnormalities

Front 27

Torsades de Pointes

Back 27

Polymorphic ventricular tachycardia

Complication of Long QT syndrome

Front 28

delta wave is seen when

Back 28

there is anterograde conduction from atria to ventricle through an accessory pathway

Front 29

Left ventricular hypertrophy voltage criteria

Back 29

R Wave in V5 or V6 AND
S Wave in V1 or V2 > 35 mm.

Front 30

Dx of LVH

Back 30

Most sensitive is echo.

ECG is specific but insensitive

Front 31

Right ventricular hypertrophy is defined by

Back 31

the presence of at least one RVH
voltage criterion and right axis deviation (RAD).

Front 32

three criteria for RVH voltage

Back 32

a. Tall R wave in V1 or V2 (R wave in excess of 5 mm)
b. R wave greater than S wave in V1 or V2
c. Persistent rS QRS pattern in the precordial leads V1 to V6.

Front 33

Q waves present in a normal ECG in which leads

Back 33

leads I, aVL, aVR, V5 and V6.

Front 34

Q waves are called pathologic if

Back 34

they are wider than 0.04 second and if they are deeper than a third of the subsequent R wave.

Front 35

Pathologic Q waves indicate

Back 35

an old myocardial infarction underlying the location of the pathologic Q wave

a. Anteroseptal Q = V1 and V2
b. Anterior Q = V3 and V4
c. Lateral Q = V5 and V6 or in I and aVL.
d. Inferior Q = II, III and aVF.

Front 36

the diagnosis of an old posterior wall infarction is based on?

Back 36

the presence of tall R waves
in the anteroseptal leads V1 and V2.

Front 37

ST segment depression is most commonly due to?

Back 37

subendocardial myocardial ischemia.

Front 38

ST segment elevation can be due to:

Back 38

a. Acute myocardial infarction (AMI)
b. Acute coronary vasospasm
c. Acute pericarditis
d. Early repolarization changes
e. Transmural myocardial ischemia

Front 39

ST elevation in AMI vs acute pericarditis

Back 39

AMI = ST elevation in some leads with ST segment isoelectric or depressed in others. ST segment is convex upwards

acute pericarditis = ST segments are elevated in all ECG leads (except aVR). ST segment is concave upwards

Front 40

Normal T wave orientation

Back 40

positive or upright in all ECG leads except in aVR and V1

Front 41

Inverted T waves can be
due to

Back 41

a. Myocardial ischemia
b. LVH or RVH
c. RBBB or LBBB
d. Digoxin

Front 42

LVH effect on ST segment

Back 42

ST segment may be depressed and the T wave inverted in leads I, aVL,
V5 or V6

Front 43

RVH effect on ST segment

Back 43

ST segment may be depressed and the T wave inverted in
leads V1 and V2.

Front 44

RBBB effect on ST segment

Back 44

T wave may be inverted in V1 and V2

Front 45

LBBB effect on ST segment

Back 45

T wave may be inverted in I, aVL, V5 and V6

Front 46

Peaked T waves occur in:

Back 46

1. Myocardial ischemia
2. Acute myocardial infarction (wider base)
3. Hyperkalemia (tented = narrow based)

Front 47

Normal precordial transition point from negative QRS to positive

Back 47

V3 or V4

Front 48

Causes of Poor precordial R wave progression (QRS is still mainly negative in V5 or later)

Back 48

1. Emphysema
2. Obesity
3. Myxedema
4. Pericardial effusion
5. Diffuse myocardial disease
6. Old anterior wall myocardial infarction

Front 49

Differential diagnosis of tall R wave in V1 or V2

Back 49

1. Old posterior wall myocardial infarction
2. RVH
3. RBBB
4. WPW
5. Duchenne muscular dystrophy

Front 50

The 3 Steps in Diagnosing Any
Arrhythmia

Back 50

• Determine if the QRS complexes are narrow or wide
• Determine if the QRS complexes are regular or irregular
• Determine if P waves or evidence of atrial activity are
present

Front 51

Arrhythmia with narrow regular QRS complexes

Back 51

•Sinus tach
•Atrial tach
•Atrial flutter
•AVNRT
•AVRT

Front 52

Arrhythmia with narrow irregular QRS complexes

Back 52

•MAT
•Atrial flutter with variable conduction
•Atrial fibrillation

Front 53

Common conditions associated with sinus tachycardia

Back 53

1. fever
2. hypotension (such as in sepsis or volume depletion)
3. severe anemia
4. pain or anxiety
5. hypoxemia (from pulmonary edema, intrinsic lung disease, or pulmonary embolus)
6. severely depressed ejection fraction and/or cardiac output (as in
cardiomyopathy, large MI, valvular
disease, or pericardial effusion with
tamponade)
7. hyperthyroidism

Front 54

Charachteristics of Sinus Tachycardia

Back 54

QRS complexes are narrow
occur at regular intervals
Normal appearing P waves are visible before each QRS complex.

Always a physiological response mediated by sympathetic tone

Front 55

Characteristics of atrial tachycardia

Back 55

arises from an ectopic focus in one of the atria.

ECG that shows inverted or bizarre appearing P waves of the same morphology before each QRS

often resolves spontaneously

Front 56

Characteristics of atrial flutter

Back 56

a large reentrant circuit occurs within the atria in which a depolarization impulse circles around the atria again and again

"Saw-toothed" pattern of P-waves

Atria depolarize at ~300bpm with ~every other depolarization reaching the ventricles

Atrial flutter usually occurs in diseased or dilated atria

Front 57

Treatment of atrial flutter

Back 57

stable:
elective cardioversion or
drugs such as quinidine or amiodarone

unstable: prompt cardioversion

Second line: beta blockers to slow AV conduction

Front 58

AV Nodal Reentrant Tachycardia
(AVNRT)

Definition and treatment

Back 58

a small reentrant (“microreentrant”) circuit forms within the AV Node

terminated by slowing or blocking conduction within the AV node.

pts who become unstable or with repeated episodes may need long-term treatment

Front 59

AV Reentrant Tachycardia (AVRT)

Definition and treatment

Back 59

pts with an accessory or bypass tract (retrograde conduction through accessory tract and anterograde through AV node)

Less common than AVNRT (the two are difficult to distinguish)

Tx:
drugs to slow AV node conduction
Ablation of the bypass tract

Front 60

Multifocal Atrial Tachycardia (MAT)

Back 60

atria are depolarized from different foci => P waves are different

foci fire at different times => ventricles are depolarized at irregular intervals

Front 61

Common underlying disease of MAT

Back 61

pulmonary disease, particularly
chronic obstructive lung disease (COPD).

may be provoked by the use of sympathomimetic agents including aminophylline and inhaled beta agonists.

Front 62

ECG characteristics of MAT

Back 62

narrow QRS complexes
QRS at irregular intervals
P waves of differing morphologies are present before the QRS complexes.

Front 63

Atrial Fibrillation (physiology description)

Back 63

hundreds of different foci within the atria “fire” frequently, depolarizing the tissue immediately around the foci.

none lead to organized depolarization

Front 64

Atrial Fibrillation (ECG characteristics)

Back 64

no P waves or organized atrial activity

AV node conducts some of the impulses at irregular intervals

Front 65

Conditions that can cause atrial
fibrillation include:

Back 65

1. conditions that cause atrial distention or increased atrial pressure
2. atrial ischemia/CAD
3. toxins
4. pericarditis
5. pulmonary embolus

Front 66

Tx of A-fib

Back 66

Unstable = urgent cardioversion

Stable:
-slow the ventricular response rate by blocking the AV node
-convert the atrial fibrillation back into sinus rhythm with drugs

Front 67

Physiological causes of Ventricular Tachycardia (VT)

Back 67

autonomous foci within the ventricles that begins to spontaneously depolarize

a macroreentrant circuit, usually around ischemic tissue, scar or
aneurysm that has developed from a myocardial infarction.

Front 68

ECG charachteristics of V-Tach

Back 68

Repeated wide QRS complexes

Morphology and intervals of QRS may be irregular

Front 69

Tx of any unstable tachyarrhythmia

Back 69

cardioversion regardless of type of tachyarrhythmia

Front 70

V-Tach is defines as

Back 70

> 3 consecutive PVC’s

Front 71

Anti-arrhythmic effect of Digoxin

Back 71

blocks AVN but is not an ideal drug for acute rate control since its full
effect may take 2-3 hours

Front 72

Anti-arrhythmic effect of Amiodarone

Back 72

Tx of V-tach, A-fib, A-flutter

1month half life

Side effects = pulmonary fibrosis, thyroid dysfunction