ADVANCED ECG INTERPRETATION

Sanal Salim
Educator

Presentation outline
Normal cardiac rhythm
How to define Cardiac arrhythmia
What are the mechanism of arrhythmias
Types of cardiac arrhythmias
Relation of arrhythmias with ECG

Anatomy of heart

Conduction system of heart

Arrhythmias

Cardiac arrhythmia, also known as cardiac

dysrhythmia or irregular heartbeat, is a group of
conditions in which the heartbeat is irregular, too
fast, or too slow.

NORMAL CARIDAC RHYTHM

CRITERIA

Heart rate =60-100b/mts

Heart beat originate from SA node
Passage through normal conduction pathway
Pass with normal velocity

VELOCITY
Moderate speed through atrium
Slow in AV Node
High speed through bundle of
his and purkinje fibres

Normal Rhythm

Classification
>100/mts

<60/mts

TACCHYARRYTHMIA

>350
250-300
150-250

100-150

 Paroxysmal arrhythmia appears suddenly and

quickly disappears
Fibrillation in atrium =Atrial fib
Fibrillation in Ventricle =VF

BRADYARRYTHMIA

II.CLASSIFICATION
DEPENDING ON THE SITE OF ORIGIN

SINUS ARRYTHMIA
Rhythm originating from SA node
ATRIAL ARRYTHMA
Rhythm originating from Atrial tissue
JUNCTIONAL ARRYTHMIA/NODAL ARRYTHMIA
Rhythm originating from AV NODE

All the three are originating from an area above the

ventricle so refer as SUPRAVENTRICULAR

TACCHYARRYTHMIAS

 VENTRICULLAR ARRYTHMIAS
Rhythm originating from ventricle

MECHANISM OF CARDIAC
ARRYTHMIA

INCREASED AUTOMATICITY
Automaticity- Property of myocardium to
depolarize spontaneously
Normally -Ca++ influx helps in depolarization

K++ dependent repolarization

In case of sympathetic over activity
(catecholamine/epinehrine, non epinephrine) leads
to increased Ca++ influx -----increased
automaticity

PHENOMENON OF RE-ENTRY
CIRCUS MOVEMENT
Cardiac impulse moves around a dead area inn
rapid circular manner and it keeps throwing cardiac
impulses to rest of tissue which leads to taccky
arrhythmias

Sinus arrhythmias-Physiological
sinus arrhythmias

 Vagus exert inhibitory effect on SA node

Inspiration=vagus inhibited i.e. its cannot control
HR
Expiration=vagus stimulated i.e. it inhibit SA node
and decreases HR

R-R DECREASE IN INSPIRATION

INCREASE IN EXPIRATION

SINUS TACHYCARDIA

 CAUSES: ECERCISE, FEVER ,T3,T4

SINUS BRADYCARDIA

Slow impulse
Hypothyroidism
Athletes - Increased vagal tone

Sick Sinus Syndrome

OVER DRIVE OF HEART+ UNDERDRIVE

SA node injury-fasting and slowing of impulse

Cause

Signs and Symptoms

Usually asymptomatic
Heart disease
Moderate to extreme
stress
Excessive consumption
of stimulants like
caffeine, nicotine, and
alcohol

Risk
Reduced cardiac output

Treatment
Treatment is usually not
required unless patient is
symptomatic.

If patientis
symptomatic, find and
treat the cause.

Atrial tacchyarrythmias

Atrial tachycardia

Atria act as pacemaker

Rate -125/250/mts
Well defined multiple P wave
One P conducted to ventricle produce QRS
complex
Multiple atrial activity followed by ventricle activity

Atrial flutter

Not well defined P wave

Due to very rapid depolariztion in atria
Saw tooth pattern
Denoted as F wave

Causes

Signs and Symptoms

> 60 years old

Valve disorder (mitral)
Thickening of the heart
muscle
Ischemia
Cardiomyopathy
COPD
Emphysema

Palpitations
SOB
Anxiety
Weakness
Angina
Syncope

Medical Treatment
Cardioversion treatment of
choice

Risk
Clot formation in atria
(atria not
completely emptying)
Stroke
Pulmonary Embolism
Dramatic drop in cardiac
output

Antiarrhymics such as
procainamide to convert the
flutter

Slow the ventricular rate by using

diltiazem, verapamil, digitalis, or
beta blocker

Heparin to reduce incidence of

thrombus formation

Atrial Flutter Nursing Interventions

Assess Patient
O2 if not already given
Start IV if not already established and hang NS
Notify MD
Prepare for cardio version

Causes

Signs and Symptoms

Hypoxia
Hypertension
Congestive heart failure
Dysfunction of the sinus
node
Hyperthyroidism
Excessive alcohol or
caffeine consumption

Heart palpitations
Irregular pulse which
feels too rapid or slow,
racing, pounding or
fluttering
Dizziness or lightheadedness
Fainting
Confusion

Risk

Medical Treatment

Clot formation in atria

(atria not completely
emptying)
Stroke
Pulmonary Embolism
Dramatic drop in cardiac
output

Rate control (slow

ventricular rate to 80-100
beats/minute)
Digoxin
Beta-adrenergic blockers
Calcium channel
blockers
Antithrombotic therapy

Atrial Fibrillation Nursing

Interventions

Assess Patient
O2 if not already given
Start IV if not already established and hang NS
Notify MD
Prepare for cardioversion

 Patients with atrial arrhythmias may rapidly

transmit to ventricular arrhythmias like VT/VF
Management Terminate atrial activity / slow down
AV node i.e. transfer of impulse cannot occur

Ca++ channel blockers

Beta blockers
Digitalis( Increase the vagal activity)

Junctional arrhythmia/AV nodal

A fibrous area present b/n atria and
ventricle which act as insulator
Current pass only through AV node
AV node specialize to slow down the

conduction.
Delay in AV node for o.1 sec allow the atrium to empty
Pathology
Junctional tissue become fast/slow Leading to
tacchy/braddy arrythmia

Reason for slow passage of

impulse through AV node
AV node is full of small cells so its take long time to
pass the impulse

Cells are of small diameter ie more

resistance.

Junctional bradycardias
Juctional block
Nodal block
Heart block

First degree heart block

NormallyPR interval represents the delay at AV
node
<0.20 seconds( 5 small sqaures in witdth)
Let,s assume some pathology/drugs(beta
blockers,ca channel blockers) to the patient
This results in unusual delay @ AV node

 Represented as prolonged P-R interval.

Every PR followed by QRS

2ND DEGREE HEART BLOCK

Degree of block increases
PR interval slowly increases then there is a dropped
beat, this is MOBITZ 1 TYPE SECOND DEGREE AV
BLOCK (Wenckebach)

 If the PR interval is fixed but there are dropped

beats, this is MOBITZ TYPE 2 SECOND DEGREE
HEART BLOCK

Third degree AV Block

Complete blockage
None of atrial activity conducted
As a result a new pacemaker develop in ventricle
Atria is driven by SA node
Ventricle driven by New Pacemaker
Eg : P, wave @ 80/mts
QRS

@ 40/MTS

NO CORDINATION OF ACTIVITY

Junctional tachycardia

 Normal conduction is through AV node

Some may develop pathological pathway between
atria and ventricle.
Conduction is faster than AV node and may moves
in a circular manner around results in re-entry
tachycardia

Treatment
Unilateral carotid sinus massage which inhibits AV
node and prevent circular motion of impulse

Ventricular Arrythmias
Concept
Ectopic foci present in ventricle fires rapidly
An irritable tissue(ishemic) fires automatically
Current passes through pathological pathway
rather than normal

Represented as widened QRS

Premature venrticular beat

Normal followed by PVC

Signs and Symptoms

Causes
Exercise
Stress
Caffeine
Heart disease: MI, CHF,
Cardiomyopathy, Mitral
valve prolapse
Electrolyte imbalances

Palpitations
Weakness
Dizziness
Hypotension

Risk

Treatment

Reduced cardiac output

Heart failure
May convert to V-Tach
or V-Fib

Oxygen
Treat the cause
Lidocaine is the drug of
choice,

Although procainamide is
sometimes used

Nursing Interventions for PVCs

Assess patient

O2 at 2 liters; Oxygen may abate the PVCs

Start IV if not already established and hang NS

Monitor for frequent PVCs and deterioration to

more serious rhythms

 SAME MORPHOLOGY-SINGLE ECTOPIC FOCI

 MULTIPLE FOCI

Causes

Signs and Symptoms

myocardial ischemia or
infarction
Electrolyte imbalance
Digitalis toxicity
Congestive heart failure

Chest discomfort
(angina)
Syncope
Light-headedness or
dizziness
Palpitations

Medical Treatment

Risk
Major cause of sudden
cardiac death

If there is no pulse-CPR
+ACLS protocol
Pulse++ patient is
unstable - cardiovert and
drug therapy
Amiodarone
Lidocaine
With chronic /recurrent
VT-antiarrythmics
Long term may need ICD
placed

Nursing Interventions for V-Tach

Assess your patient
If symptomatic, treatment must be aggressive and immediate
Pulse present
Oxygen
Patent IV (preferably x2)
Monitor patient very closely
Pulseless
Call Code Blue
Begin CPR
Defibrillate
Start IV if not already established and hang NS

Ventricular flutter

 In flutter one foci may firing at rate off 150-250/mts

If flutter continues mechanical failure occur to
pump
Leads to decreased CO AND coronary perfusion
If it prolongs multiple areas starts firing
Leads to VF

Ventricular Fibrillation
V-Fib (coarse and fine)
Occurs as a result of multiple weak ectopic foci in
the ventricles
No coordinated atrial or ventricular contraction
Electrical impulses initiated by multiple ventricular
sites; impulses are not transmitted through normal
conduction pathway

Causes

Signs and Symptoms

Loss of consciousness
Absent pulse

AMI
Untreated VT
Electrolyte imbalance
Hypothermia
Myocardial ischemia
Drug toxicity or
overdose

Risk

Medical treatment

Death

CPR with immediate

defibrillation
Initiate ACLS algorithm

 Assess your patient

Many things can mimic v-fib on a monitor strip
such as electric razor or shivering
You must check your patient!
Treatment must be aggressive and immediate
Start CPR/ACLS
Call a Code Blue
Defibrillate ASAP
Start IV if not already established and hang NS
Notify MD

VF PRROGRESSION

Its time to practice!!

Rhythm Identification
This rhythm strip is from a 69-year-old man
complaining of shortness of breath. Lung sounds
reveal bilateral rales. Blood pressure: 160/58.

Thank You

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