Rate in beats/min = 60/interval between two beats in seconds

A handy shortcut is:

Heart rate (beats/min) = 1500/R-R interval (mm)
1500/20 = 75 b/min

Heart block Heart block results when

conduction between the atria and
ventricles is altered. This often occurs
at the AV node which has a low safety
factor.

First degree - prolonged PR interval only. The normal PR

interval is 0.12 to 0.21 seconds. A PR interval >0.21 would be
classified as first degree block.
Usually this block is above His bundle

Second degree - some P waves are not followed by QRS.

Often has a regular sequence, i.e., 2:1 or 3:2.
The first number is the number of P waves present and the
second is the number of QRSs.
What is this?

Mobitz I (Wenckebach) the PR progressively lengthens

with one P wave for every QRS until a beat is dropped.
Usually the block is above His bundle.
This is common in coronary patients and is caused by
increased vagal tone and usually eventually disappears with
no problems

Mobitz II the PR is constant but with occasional dropped

beats. This is a more serious arrhythmia because the injury is
probably in fast conducting tissue below the His bundle which
is not under vagal control.

This is unambiguously Mobitz II

It is a dangerous arrhythmia because
the heart may suddenly start beating
very slowly or even stop.

Complete heart block. Since there is no conduction

down the AV node pathway atria and ventricles beat
regularly but at different rates.

Slow ventricular rate

Usually treated with pacemaker
May be temporary or intermittent.
Can be induced by drugs that cause increased vagotonia

WPW: Normally conducting

cardiac muscle bridges the gap
between atria and ventricles.
The accessory pathway activates the
ventricle before normal activation
via the AV node.

The PR interval is <0.12 sec

Delta waves are usually present

Can get retrograde conduction causing reentry and a

tachyarrhythmia.
If accessory pathway has short antegrade refractory
period, can allow the ventricle to beat too fast with atrial
fibrillation

Fig 3

Sinus Tachycardia >100b/min

1. Normal P waves
Normal sinus rhythm

2. Normal or shortened PR
interval
3. QRS and T vectors are normal
4. ST segments are normal

Sinus tachycardia

5. RR interval short <15mm

1500/100 = 15

Sinus bradycardia

Fig 3

Sinus Bradycardia <60b/min

Normal sinus rhythm

1. P waves are present and all

are followed by a QRS
2. Normal and constant PR
interval
3. QRS and T vectors are
normal

Sinus tachycardia

4. ST segments are normal

5. RR interval long >25mm
1500/60 = 25

Sinus bradycardia

Premature ventricular contraction (PVC)

1. Arises from ectopic focus in ventricles
2. Early QRS not preceded by a P wave (see fig 4)
3. Will have an unusual QRS shape
a) odd vector
b) prolonged QRS duration

Premature ventricular contraction (PVC)

1. Arises from ectopic focus in ventricles
2. Early QRS not preceded by a P wave (see fig 4)
3. Will have an unusual QRS shape
a) odd vector
b) prolonged QRS duration
4. A compensatory pause

Multifocal PVCs.
Two separate foci are originating PVCs
Irritable ventricle
IF all PVC are identical it is from one ectopic site (Unifocal).

Premature atrial contraction (PAC)

1. Arises from an ectopic focus in the atria.
2. Will have an identifiable P wave but the shape of the
P wave may be altered
3. May have a normal QRS
4. May have a compensatory pause

The compensatory pause

is lacking because the SA
node was reset.
The rhythm has been
shifted.

The QRS may be altered

if some of the ventricle is
still in its refractory
period.

Atrial fibrillation
1. Irregularly irregular
2. No P waves

The AV node keeps the

ventricular rate low
May be treated with drugs
to depress AV conduction
and slow the ventricular
rhythm: Beta blockers,
calcium channel blockers

Common: will occur in

about 1/3 of the population
Not a serious arrhythmia
unless in WPW

Electrical reentry can

cause fibrillations and
tachycardias.

Ventricular tachycardia (Fig 9)

1. Regularly occurring rhythm originating from a regular
ventricular ectopic focus.
2. QRS morphology is usually like a PVC

Because the cardiac output is very low it usually produces

myocardial ischemia and often progresses to ventricular
fibrillation

Ventricular fibrillation (VF)

1. Thought to be a reentrant excitation of the ventricles;
premature impulse may arise during vulnerable period
2. Irregular baseline with no identifiable waves

3. No cardiac output. Usually the cause of "sudden death"

4. May be the result of ischemia, lightning strike,
electrocution, chest trauma, or drugs
5. Requires CPR and electrical difibrillation. Patients do
not spontaneously recover.

Extended phase two cause long QT syndrome.

12 blocks

Q-T interval is ratedependent and is an index

of the duration of phase 2
in the ventricular AP
12 x 40 = 480 ms

Long QT syndrome
1. Prolonged duration of phase 2 causes an early
afterdepolarization. That can trigger an early action
potential causing a reentrant tachycardia
2. Patients may experience attacks of VT with torsades
de pointes - a waxing and waning of the QRS
morphology (as if circling around a point).

3. Long QT is induced by some drugs and can be due to

genetic abnormalities in some potassium and calcium
channels. At present 5 separate genetic defects have been
identified which cause long QT

14 STEPS TO ASSURE A SUCCESSFUL READING AND

UNDERSTANDING OF AN UNKNOWN ECG
1. Is the ventricular rhythm regular?
2. Are there P waves?
3. Is the atrial rhythm regular?
4. Is there one P wave for each QRS?
5. What are the atrial and ventricular rates?
6. What is the P-R interval?
7. Is the P-R interval constant?
8. Are there extra or premature beats?
9. What is the QRS duration?
10. Does the QRS morphology indicate presence of a conduction
defect?
11. What is the mean electrical QRS axis?
12. What is the mean electrical P wave axis?
13. Is there S-T segment deviation?
14. Are there pathologic Q waves?

Fig 12 a summary of heart blocks.

Fig 13 a summary of other arrhythmias.

 A nivel molecular, el mecanismo de las arritmias son heterogeneas, pero

el mecanismo comn ha sido identificado en el disparo de las arritmias
como cambios en el potencial de membrana, transporte de iones y manejo
intracelular del calcio. Por muchos aos se conoce que hay un mal
manejo de Ca++ con sobrecarga del relculo sarcoplasmtico (RS)
generando la liberacin espontanea de Ca++ por el receptor de ryanodine
(RyR) y una depolarizacin por corriente de ingreso a travs de un
intercambiador sodio-calcio
Esos espontaneos eventos conocidos postdepolarizacin retardada dispara
las arritmias. La postdepolarizacin temprana otro curso de las arritmias,
ocurre durante la injuria de reperfusiny son causados por potenciales de
accin (PA) prolongados permitiendo el ingreso excesivo de Ca++ por
los canles tipo L, adems la reperfusin induce el incremento de (Ca++)i,
induciendo la repolarizacin heterogenea. El mal manejo de RS del Ca++
esta implicado en la patogenesis de la alternancia del PA, ondas en
espiral, fibrilacin ventricular ( Circulac 21.07.08.)