Basic:

Rate:

QTc
QT interval to heart rate.
Faster heart beats Faster ventricles
repolarize Shorter QT interval.
I.e., normal QT varies with heart rate.
For each heart rate, calculate an adjusted QT
interval, called the:

Intervals:

corrected QT (QTc)

PR
0.12 - 0.20 seconds (3 - 5 boxes)
< 0.12 s

0.12-0.20 s

> 0.20 s

High NE/E states

Wolff-Parkinson-White

Normal

AV nodal
blocks

WPW syndrome
(delta-wave)

1st Degree AV Block

Normal ; < 0.44 s

Long QT : > 0.44 s

Tip: QT > half RR interval long.

QRS
0.04 - 0.12 seconds. (1 - 3 boxes)
< 0.10 s

0.10-0.12 s
> 0.12 s
Incomplete
BBB
Normal Bundle Branch
PVC
Block (BBB) Ventricular rhythm
Incomplete bundle
branch block

3rd degree AV block

with ventricular escape
rhythm

A prolonged QT may predispose a type of

ventricular tachycardia called Torsades de
Pointes. Causes include drugs, electrolyte
abnormalities, CNS disease, post-MI, and
congenital heart disease.

Heart Arrhythmias
1. Sinus Rhythms
Sinus Tachycardia
Sinus Bradycardia

Rate: > 100 bpm

Rate: < 60 bpm

2. Premature Contraction / Beats

Contour of P, PR interval, timing differ from normal
Atrial
pulse from SA node and QRS will be narrow (0.04 (PACs)
0.12 s) (normal impulse conduction in ventricles)
Ventri- Wide and bizarre QRS complex(es).
a. Uniform : look alike,
cular
(PVCs) b. Multiform : look different
3. Supraventricular Arrhythmias
a. Atrial Fibrillation (AF)
No normal P waves, Flutter wave. (No organized
atrial depolarization, impulses are not from sinus),
atrial activity is chaotic (irregular rate). Common, affects 2-4%, up to 5-10% if > 80 years old.
Due to multiple reentry between LA and RA.
b. Paroxysmal SupraventricularTachycardia (PSVT)
HR suddenly speeds up, often due to PAC and the P
waves are lost. Due to reentry in AV node.
c. Atrial Flutter
No P waves, saw tooth pattern at 250 - 350 bpm.
Only some impulses conduct through AV node (usually
every other impulse). Due to reentry in RA with every
2nd, 3rd or 4th impulse generate a QRS (others are blocked in AV node as node repolarizes).
4. Ventricular Arrhythmias
a. Ventricular Fibrillation
Completely abnormal. Ventricular cells are excitable and depolarizing randomly. Causes rapid
drop in CO and death
b. Ventricular Tachycardia
Impulse originates in ventricles (no P waves, wide QRS).
Due to reentry in ventricle.
5. AV Junctional Blocks
a. 1st Degree AV Block
PR Interval: > 0.20 s, Prolonged
conduction delay in the AV node or Bundle of His.
b. 2nd Degree AV Block, Type I (Mobitz I/ Wenckebach)
PR interval progressively lengthens, then
impulse is completely blocked (P wave not
followed by QRS). Each atrial impulse causes
longer delay in AV node until one impulse (usually 3rd or 4th) fails to conduct to AV node.
c. 2nd Degree AV Block, Type II / Mobitz II
Occasional P waves are completely blocked
(P wave not followed by QRS). Conduction is
all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His.
d. 3rd Degree AV Block
P waves are completely blocked in the AV
junction; QRS originate independently from below

the junction. (Ventricles pacemaker: around 30-45 bpm, conduction through ventricles is
inefficient and the QRS will be wide and bizarre.)

Axis
Axis refers to the mean QRS axis (or vector) during
ventricular depolarization. An abnormal axis can
suggest disease such as pulmonary hypertension from
a pulmonary embolism.
The QRS axis is determined by overlying a circle,in the
frontal plane. By convention, the degrees of the circle
are as shown. A quick way to determine the QRS axis
is to look at the QRS complexes in leads I and II.
QRS Complexes
I (L) II (R)
Axis
+
+
normal
+
left axis deviation
+
right axis deviation
right superior axis deviation
Diagnosing a Myocardial Infarction (MI)
One way to diagnose an acute MI is to look for elevation of the
ST segment.
MI Location
MI
Lead
Anterior V1 - V4
Lateral
I, aVL, V5 - V6
Types of MI:
Inferior
II, III aVF
ST (Transmural / Q wave)
Non-ST (Subendocardial / Non-Q-wave)
Ischemia ST depression, peaked T-waves, then T-wave ST depression & T-wave inversion
inversion
Infarct
ST elevation & appearance of Q-waves
Fibrosis
ST and T-waves normalize, Q-waves persist
ST normalize, but T-wave inversion persists

Heart Hypertrophy
Left atrial enlargement (LAE)

P wave - atrial depolarization

II : P > 0.04 s (1 box) between
notched peaks, or
V1 : P Neg. deflection > 1 x1 box

Cause : LVH from hypertension.

Right atrial enlargement (RAE)

II
: P >2.5mm, or
V1/V2 : P >1.5mm

Cause : RVH from pulmonary hypertension

Left ventricular hypertrophy (LVH)

R in V5 (or V6) + S in V1 (or V2) > 35 mm,

or avL: R > 13 mm
Cause: hypertension.

Right ventricular hypertrophy (RVH)

R wave is normally small in V1, V2 because

RV does not have a lot of muscle mass. But
in RVH the R wave is tall in V1, V2.
Right axis deviation, and V1 : R >7mm tall

Cause: left heart failure.

Bundle Branch Blocks (BBB)

QRS complex widen because when the
conduction pathway is blocked it will take longer for the electrical signal to pass throughout the
ventricles.

Left Bundle Branch Blocks (LBBB)

V1-V2 : Broad, deep S waves / W wave

Right Bundle Branch Blocks (RBBB)

V1-V2 : Rabbit Ears
/ M wave

Bifascicular block = RBBB + left bundle hemiblock, manifest as an axis deviation, eg LAD in the case
of left ant. hemiblock. Trifascicular block = bifascicular block + 1st degree heart block.