ELECTROCARDIOGRAPHY

(ECG)
 His Bundle Electrogram

◼ A catheter containing ring electrodes at

its tip is passed through a vein to the right
side of heart & manipulated into a
position close to tricuspid valve.

◼ Electrical events in AV node , bundle of

His & purkinje fibres can be studied
◼ Normal HBE :
➢ A deflection → activation of AV node
➢ H spike → transmission of impulse
through His bundle.
➢ V deflection → ventricular depolarisation
Uses of HBE
◼ Useful in pateints with heart blocks
◼ Simultaneously record ECG also
◼ PA interval: beginning of P wave to A
deflection in His bundle electrocardiogram
◼ Indicates conduction time from SA node to
AV node
◼ Duration : 27msec
◼ AH interval : interval from AV node to Bundle
of His- 92msec
◼ HV interval : from Bundle of His & its
branches till ventricular depolarisation
(43msec)
CLINICAL APPLICATIONS
OF ECG
◼ Is an important tool in the diagnosis,
prognosis & planning treatment in most of
the cardiac disorders.
◼ The important applied aspects which need
special mention are:
Cardiac arrhythmias (Heart blocks,
atrial & ventricular arrhythmias).
Myocardial infarction, ischaemia.
Hypertrophy of cardiac chambers.
Regular sinus rhythm :

60-100 bpm
◼ SA node- pacemaker
◼ P wave followed by QRS complex
◼ Waves, Intervals, segments – normal duration
and voltage.
 CARDIAC ARRHYTHMIAS
◼ Refers to disruption of the normal cardiac rhythm.

◼ SINUS ARRHYTHMIA :
➢ Normal sinus rhythm except for the R-R interval
(heart rate) which varies in a set pattern.
 SINUS ARRHYTHMIA

◼ HR increases during inspiration & decreases

during expiration
◼ Normal phenomenon due to fluctuation in
parasympathetic output to heart
◼ During inspiration impulses in vagi from stretch
receptors in lung inhibit cardioinhibitory area
◼ →decreases vagal tone → increases heart rate
◼ SINUS TACHYCARDIA : normal sinus rhythm
except for increased HR (HR>100).
Normally… exercise.
Fever, hyperthyroidism, as a reflex response to
lowered BP.
◼ SINUS BRADYCARDIA : normal sinus
rhythm except for decreased HR (<60bpm).
Seen in trained athletes..
Abnormal : hypothyroidism,..
Conductive system of Heart
Flow of Cardiac Electrical
Activity

SA node Atrial muscle

Internodal Atrial muscle

conducting
fibers

AV node (slow)

Purkinje fiber Ventricular muscle

conducting system
HEART BLOCKS
◼ Refers to slowing down/ blockage of
cardiac impulse conduction (from SA
node) along the cardiac conductive
pathway.
 HEART BLOCKS
(Conduction disturbances)

◼ SA nodal block
◼ Atrioventricular block
- nodal block
- infranodal block
◼ Bundle branch block
◼ Fascicular block
 SA nodal block

◼ Blockage of impulse conduction from SA node

to Atria.
◼ Occurs suddenly & initially heart stops. After an
interval of 2 cardiac cycles, AV node becomes
pacemaker & heart starts functioning again. (AV
nodal rhythm).
◼ Marked bradycardia, dizziness & syncope (Sick
Sinus Syndrome).
SA nodal block

◼ Absent P wave, normal QRS, slow HR.

◼ Elderly, in patients recovering from coronary
artery occlusion.
Atrioventricular block
Causes:
◼ Ischemia of AV node / AV bundle

◼ Compression of AV bundle by scar tissue

◼ Inflammation of AV bundle- myocarditis

caused by rheumatic fever

◼ Extreme stimulation by vagus

 Atrioventricular Block
◼ Incomplete heart block:
- first degree
-second degree heart block

◼ Complete heart block (third degree heart

block)
◼ First degree AV nodal block :
➢ Slowing down of conduction at the level of AV
node.
➢ Though all the atrial impulses reach the
ventricles but the PR interval is abnormally
long ie., >0.2 sec.
◼ Second degree AV nodal block :
➢ Not all atrial impulses are conducted to ventricles.
➢ ..one ventricular contraction after every 2, 3 or 4
atrial contractions : 2:1, 3:1 or 4:1 block. (Mobitz
type II block)
Second degree AV nodal block :

➢ Wenckebach phenomenon (Mobitz type I block)

: progressive lengthening of PR interval in
successive beats & finally failure of one impulse
to be transmitted.
◼ Third degree (complete) heart block:
➢ No impulse from atria pass to ventricles.
➢ Ventricles starts beating at their own rhythm (40
bpm) : idioventricular rhythm.
➢ Atria : 72 bpm.
➢ ECG : complete dissociation between P waves &
QRS complexes : Atrioventricular dissociation.
◼ Third degree (complete) heart block:
➢ Is caused by septal MI, damage to His during
surgical repair of congenital septal defects.

➢ May be associated with prolonged ventricular

standstill (asystole) until a ventricular focus
begins firing. This may result in cerebral
ischaemia → dizziness & fainting(syncope) :
STOKES- ADAMS SYNDROME.
BUNDLE BRANCH BLOCK
◼ Conduction blocks in one / more branches of
bundle of His.
◼ Depolarisation pass through bundle on intact side
◼ Then sweep back through the muscle to activate
ventricle on blocked side
◼ ventricular rate is normal
◼ QRS complex is prolonged.
◼ RBBB : healthy/ sec. to chronic pulmonary
disease. ECG: RAD.

◼ LBBB : heart disease. ECG : LAD

BUNDLE BRANCH BLOCK
Fascicular block
◼ Block occurs in anterior /posterior fascicle of
left bundle branch

◼ Localised by His bundle ECG

TREATMENT
◼ SA nodal block , 2nd degree AV block &
complete heart block - implantation of
electronic cardiac pacemakers with tip
positioned in rt ventricle
◼ Pace maker is set to fire impulses at a normal
rate
◼ A battery operated electrical stimulator is kept
beneath the skin
◼ Electrodes are connected to rt ventricle
◼ Battery replaced every 5 years
◼ Demand pace makers: fire impulses when
patient’s own pace maker slows

◼ Dual chamber pace makers :

◼ Pace makers in atria & ventricle maintaining
normal AV synchrony
 ECTOPIC CARDIAC RHYTHM

◼ Refers to abnormal cardiac excitation produced either

by an ectopic focus or a re-entry phenomenon.

Atrial arrhythmias Ventricular arrhythmias

- Extrasystole - Extrasystole
- Paroxysmal atrial - Paroxysmal ventricular
tachycardia tachycardia
- Atrial flutter - Ventricular fibillation
- Atrial fibillation
 MECHANISM
◼ Ectopic foci of excitation:

Normally, SA node : pacemaker.

Abnormal, His- Purkinje fibres or myocardial
fibres become hyperexcitable & discharge
spontaneously.
The site in the heart which becomes
hyperexcitable : ectopic focus
--- single discharge → extrasystole/ premature
beat.
--- repetitive discharge → Paroxysmal atrial
tachycardia , atrial flutter or ventricular fibrillation.
Ectopic foci : causes
◼ Ischemia /hypoxia
◼ Increased levels of catecholamines
◼ Certain drugs : nicotine , caffeine
◼ Calcified plaques
 MECHANISM

◼ Re-entry Phenomenon / Circus movement :

➢ Refers to a phenomenon in which the wave of
excitation propagates repeatedly within a closed
circuit.
➢ Occurs under 2 situations:
✓ Presence of transcient block in the conduction
pathway.
✓ presence of abnormal extra bundle of
conducting tissue called BUNDLE OF KENT.
Reentry phenomenon/ circus
movement
Reentry phenomenon
◼ If there is a transcient block on one side or a
portion of conducting system the impulse can
go down through normal side
◼ If the block then wears off impulse may
conduct in the retrograde direction in the
previously blocked side
◼ Then it moves back to origin & descend again
establishing a circus movement
Atrial premature beat/atrial
extrasystole
◼ Irritable focus in atria discharges once
◼ A beat occurs before expected normal beat
◼ Abnormal P wave & normal QRS & T waves
◼ Small pause between extrasystole & next
normal beat
ATRIAL TACHYCARDIA
Atrial Tachycardia: 140-220 beats/min

PAT : occurs in paroxysms, begins suddenly & lasts for few seconds.
 ATRIAL FLUTTER

Atrial flutter : 220-350bpm

Commonly due to circus movt in rt atria
ECG: Saw toothed pattern of flutter
waves
AV node cannot conduct >230 impulses
/min
Usually associated with 2:1 or 3:1 block
 ATRIAL FIBRILLATION

Atrial fibrillation: irregular, rapid rate(350-500bpm).

✓ Small irregular oscillations : F waves
✓ No P waves,but QRS & T wave present with
variable intervals between 2 successive ventricular
contractions
✓ R-R interval : irregular
◼ Cause : multiple concurrently circulating
reentrant excitation waves in both atria
◼ Or discharge from multiple ectopic foci as in
ischemic heart disease, thyrotoxicosis

◼ In fibrillation, contraction of myocardial cells

is uncoordinated, irregular & pumping action
is ineffective.

13-81
 Atrial tachycardia

Atrial flutter

Atrial fibrillation
Ventricular extrasystole /premature
beat
◼ Cause: ectopic foci in ventricle
◼ Prolonged QRS with next P wave buried in it
◼ Next impulse from SA node falls in refractory
period of extrasystole→ compensatory pause
◼ Paroxysmal ventricular tachycardia :

◼ Wide. bizzare QRS complex

◼ CO is decreased, life threatening…

◼ Heart rate : 200bpm.

 Ventricular fibrillation
◼ Small segments of ventricular myocardium show
rapid, irregular ineffective contractions.
➢ Heart rate :350-500bpm
➢ CO is zero, peripheral pulse is absent.
➢ Common during electric shock, during ischaemia of
conductive system, trauma to heart, coronary
occlusion.
➢ ECG : undulating waves of varying frequency &
amplitude.
➢ CPR must be started immediately to prevent tissue
death(rate : 80-100/min, one ventilation to 5 chest
compressions)
➢ Immediate electric or electronic defibrillation should
Ventricular fibrillation
Ventricular fibrillation is life-threatening
Defibrillation
◼ A strong high voltage AC current passed
through ventricles can throw all ventricular
muscles into refractoriness simultaneously

◼ A normal rhythm follows if heart is capable of

it
Defibrillation
◼ Antiarrythmic drugs

◼ Radiofrequency catheter ablation of reentrant

pathways
 BUNDLE OF KENT
◼ Is an abnormal extra bundle of conducting
tissue present in some individuals.
◼ Connects atria and ventricles directly, so the
conduction is very rapid than through the
regular conductive system.
◼ The nodal paroxysmal tachycardia occuring in
patients with bundle of Kent is called Wolf-
Parkinson- White syndrome.
◼ ECG : short PR interval, prolonged slurred
QRS deflection.(delta waves)
Wolf Parkinson White Syndrome
MYOCARDIAL INFARCTION
◼ Refers to ischaemic necrosis of a part of
myocardium which occurs when coronary blood
ceases or reaches below a critical level
(70ml/100gm of tissue/min).

◼ ECG : Elevation of ST segment, T wave inversion

 Physiological basis of ECG changes in
acute MI

Defect in infarcted cells Current flow ECG change

1.Rapid repolarisation out of infarct ST elevation

2. Decline in resting
membrane potential into infarct ST elevation

3. Delayed depolarization out of infarct STelevation

Other changes in ECG during MI
◼ Appearance of Q waves in leads where there
were no Q waves previously or
◼ Presence of abnormal Q waves: indicates
transmural infarct

◼ Failure of progression of R wave

◼ Septal infarct → bundle branch block &

other forms of heart blocks
◼ Myocardial infarction is complicated by
development of serious ventricular arrythmias
◼ Especially ventricular fibrillation due to
reentry in first 30 min → death
Cardiac arrest
◼ Final serious abnormality of cardiac rhythm
◼ Cessation of all electrical signals in heart
◼ Can occur in anaesthesia or following severe
myocardial disease
◼ Hypoxia prevents cardiac fibres to maintain
normal electrolyte concentration differentials
across the membrane
◼ Excitability affected → loss of automatic
rhythmicity
◼ Treatment : CPR or automatic pacemaker
implantation
ECG changes in electrolyte abnormalities
◼ Low plasma level of sodium : low voltage
complexes.

◼ Hyperkalemia : lethal condition

➢ + 7mEq/L : T wave tall & peaked.
➢ 8.5 mEq/L : broad, slurred QRS,
T wave tall & slender.
➢ May result in VT/VF.
➢ Eventually, heart stops in diastole.
◼ Hypokalemia : PR interval prolonged, U waves
prominent, ST segment depressed, late T wave
inversion.

◼ Hypercalcemia: rare
◼ Increased calcium enhances cardiac contractility
◼ when large amounts of calcium is infused into
experimental animals → heart relaxes less
during diastole & eventually stops in systole
( CALCIUM RIGOR).

◼ Hypocalcemia: prolongation of ST segment and

QT interval is also increased.
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