ARRHYTHMIAS

ARRHYTHMIA (DYSRHYTHMIA)

Abnormality in rhythm

ECG

Depolarization

Process of electrical activation

of the heart muscle cells.

Repolarization
Reverse electrical process to
return the heart muscle cells to
their initial state after depolarization

Normal ECG tracing

Normal Pacemaker Rates

MECHANISIMS FOR
ARRHYTHMIA GENESIS

Re-Entry
2 Limbs
Area of slow conduction
Each limb different refractory period

Automaticity
Repetitive firing of a single focus

A.

Enhanced automaticity
(Ie. B-agonists)

B.

Abnormal automaticity
(Ie. MI, Electrolyte, Disturbance, CLD, Hypoxia,
Pulmonary infection, Cardiac stimulants, Acute
alcohol ingestion)

MECHANISIMS FOR
ARRHYTHMIA GENESIS

Triggered Arrhythmias

Prolonged QT syndrome
Torsade de pointes

How to Identify Arrhythmias

TREAT THE PATIENT NOT THE MONITOR

All rhythm interpretation must be

correlated with the clinical
observation and condition of the
patient.

ECG Analysis

1st Question:
Is there a normal looking
QRS complex?
No QRS complex:
-Asystole
-Ventricular fibrillation

Ventricular Asystole

Total absence of ventricular

activity.
No depolarization
no
ventricular contraction
Treatment: Epinephrine

Ventricular Fibrillation

Chaotic ventricular rhythm

Multiple areas within the ventricles display
marked variation in depolarization and
repolarization.
No cardiac output
Most common mechanism of cardiac arrest
from myocardial ischemia or infarction.
Coarse VF usually indicates recent onset
of VF; can be readily corrected by prompt
defibrilation.
Fine VF approaches asystole; often means
considerable delay since collapse;
successful resuscitation more difficult.

ECG criteria of VF

No normal looking QRS

complexes.
Rate: very rapid; too
disorganized to count.
Rhythm: irregular; no QRS
complex, ST segment, p waves
and T waves.

Ventricular Fibrillation

Ventricular Fibrillation

Ventricular Tachycardia

3 or more beats of ventricular origin in

succession at a rate > 100 per min.
No normal looking QRS.
QRS width > 0.12 sec.; morphology
bizaare.
p waves not recognized in rapid VT.
Rhythm regular or irregular
ST segment and T wave usually opposite in
polarity to the QRS.
May be well tolerated or associated with
grave, life-threatening hemodynamic
compromise.

Ventricular Tachycardia

Ventricular Tachycardia

Torsades de Pointes

VT with constantly changing QRS.

Name derived from the fact that its
electrical activity appears to be twisted into
a helix.
Causes: Drug toxicity, idiosyncratic reaction
to type IA antiarrhythmic drugs (Quinidine,
Procainamide, Disopyramide) or any
agents that prolong the QT interval (normal
QT > 40 secs.), hypokalemia,
hypomagnesemia and bradycardias.
Treatment: -DC offending agents
-MgSo4
-Overdrive pacing

Premature ventricular
contraction

Depolarization arising in either ventricles

before the next expected sinus beat.
May be unifocal or multifocal.
ECG criteria:
- QRS not normal looking;
(wide to > 0.12 sec.)
- Rhythm irregular
- p waves:
- sinus p waves usually
obscured by the QRS, ST
segment or T wave of the PVC.
- retrograde p wave may occur

Premature ventricular
contraction

Premature ventricular
contraction

Premature ventricular
contraction

Variants of PVCs

Ventricular Bigeminy
Ventricular Trigeminy
Ventricular Quadrigeminy
Couplet
Triplet
Uniform or Unifocal
Multiform or Multifocal
Interpolated PVC
R on T Phenomenon
Fusion (Dressler) Beats

Ventricular Bigeminy

If every other beat is a PVC

Ventricular trigeminy

If every 3rd beat is a PVC

Couplet

Two PVCs (uniform or

multiform) in a row.

Uniform or Unifocal PVCs

PVCs are identical in shape

Originate from a single ectopic
focus.

Multiform or Multifocal PVCs

PVCs look different in the same

ECG lead
Usually originate from different
ectopic sites, but sometimes fire
from a single site and are
conducted along different routes
in the ventricles.

Interpolated PVC

A PVC is sandwiched between

2 normal sinus beats and does
not significantly interrupt the
underlying rhythm.

R on T Phenomenon

A PVC that occurs on or near

the peak of previous T wave.
This is the vulnerable period
during ventricular repolarization
when PVCs may predispose to
ventricular tachycardia or
ventricular fibrillation.

Fusion (Dressler) Beats

A PVC fires at the same time

that a normally conducted QRS
complex occurs.

PVC Treatment

Isolated or non-VT PVCs

- Rarely treated except for
needed symptomatic relief.
PVCs in acute MI
- Need to aggressively treat
the ischemia or infarction.
- Antiarrhythmic agents.

ECG Analysis

2nd Question
-Is there a p wave?

Arrhythmias identifyed by the absence

or abnormal appearance of p waves
- Atrial fibrillation
- Atria flutter

Atrial Fibrillation

No discernible p wave; fibrillatory

waves may be seen
May result from multiple areas of
reentry within the atria
Atrial electrical activity is rapid at
around 400 700 per min.
Ventricular rhythm is irregularly
irregular
May be associated with Sick Sinus
Syndrome, hypoxia, increased atrial
pressure, pericarditis and many other
conditions.
Usualy the result of some underlying
form of heart disease.

Atrial Fibrillation

Atrial Fibrillation- Treatment

Rate Control (Diltiazem,

Verapamil, Beta blockers,
Digitalis)
Chemical Cardioversion (With
Procainamide or Quinidine)
Electrical Cardioversion

Atrial Flutter

P waves occur rapidly with a

characteristic sawtooth appearance.
Result of reentry circuit within the atria
A physiologic block at the AV node is
common (i.e. 2:1 AV conduction)
Atrial rate approximately 300 per min.
(220-350 per min.)
Atrial rhythm is regular
Ventricular rhythm may be regular or
irregular
Seen in mitral or tricuspid valvular
heart disease, acute or chronic cor
pulmonale and coronary heart disease

Atrial Flutter

Atrial Flutter - Treatment

Cardioversion (if with

hemodynamic compromise)
Pharmacologic therapy
-Diltiazem, Verapamil, Beta
blocker, Digitalis

Wandering Atrial Pacemaker

Wandering Pacemaker

Paroxymal Atrial Tachycardia

Paroxysmal Atrial Tachycardia

Multifocal Atrial Tachycardia ( MAT)

Irregular atrial rhythm irregular

ventricular rhythm
Atrial rate 100 180 / min.
Varying P-P interval
Varying P-R interval
Varying R-R interval
3 consecutive P waves of different
morphology at a rate >100/min. in a
single lead.

Multifocal Atrial Tachycardia

Junctional Complexes

Conducting tissue near the AV

node has taken over the
pacemaker function of the heart
Heart rate is slow at 40-60 beats
per min.
Inverted but narrow QRS
complexes
Retrogrede p waves often seen
in leads II and III

Junctional Rhythm

Idioventricular Rhythm

Rate: 30 40 /min.
No P waves
Widened QRS complexes
Abnormal ST segments and
secondary T wave changes

Idioventricular Rhythms

Accelerated Idioventricular Rhythm

ECG analysis

3rd Question
- what is the relationship
between the p waves and the
QRS complexes?Normally, every QRS in the
normal ECG is preceded by a p
wave .

Heart Blocks

Rhythms caused by altered

conduction through the AV
node.

1o Heart Block (1o AV block)

A delay in the passage of the

impulse from atria to ventricles;
delay usually occurs at the AV
node but may be infranodal.
PR interval is prolonged to >
0.20 sec.
Treatment usually unnecessary
when it occurs without
symptoms.

1o Heart Block (1o AV block)

1o Heart Block (1o AV block)

2o Heart Block (2o AV block)

Some impulses are conducted

and others are blocked
2 types
-Type 1, 2o AV block
(Wenckebach)
-Type 2, 2o AV block

Type 1, 2o AV block (Wenckebach)

Almost always occurs at the level of

the AV node
Often due to increased
parasympathetic tone or to drug
effect (Digitalis, Propanolol or
Verapamil)
Usually transient
Prognosis good
Characterized by a progressive
prolongation of the PR interval
before a dropped beat

Type 1, 2o AV block
(Wenckebach)

Type 1, 2o AV block
(Wenckebach)

2 AVB, Mobitz Type II

PR interval is normal or sl.

Prolonged
PR interval is usually fixed and
constant
Dropped beat in a regular
interval
Block mostly occurs at the level
of the bundle branches

2 AV Block (Mobitz II)

2 AV Block (2:1 Block)

Third Degree AB block

(3AVB)

R-R interval constant

P-P interval constant
P-R interval variable
Dissociation of Atrial and
Ventricular depolarizations

A-V Dissociation

Complete A-V Block

Sinus Arrhythmia

Usually a sinus rhythm with a rate that

varies with respiration (Respiratory
sinus arrhythmia)
Usually benign
P P interval gradually increase and
decrease. Difference of longest and
shortest P P interval is 0.16 sec.
PR interval is constant
Each P wave is followed by a QRS
complex

Sinus Arrhythmia

Sinus Arrhythmia

Abnormalities in Heart rate

Sinus Bradycardia
Sinus Tachycardia

Sinus Bradycardia

Heart rate < 60 per min.

Each P is followed by a QRS complex
PR interval is fixed and constant
Decrease in the rate of atrial depolarization due to
slowing of the SA node
May be due to sinus node disease, increase
parasympathetic tone or drug effects (Digitalis,
Propanolol or Verapamil)

Sinus Bradycardia

Sinus Bradycardia

Sinus Tachycardia

Heart rate > 100 beats per min.

Each P wave is followed by a QRS
complex
Characterized by an increase in
the rate of discharge of the SA
node
Secondary to multiple factors:
exercise, anxiety, fever,
hypovolemia, etc.

Sinus Tachycardia

Sinus Tachycardia

Premature Atrial Contractions

Premature depolarization
p morphology different from
regular P waves
The interval between the sinus P
waves preceding and following a
PAC is less than twice the
normal P-P interval (non fully
compensatory pause)

Premature Atrial Contraction

Premature Nodal Beats

Thank You