CLINICAL APPLICATION

OF ECG
DR DIPTI BANIA
• ECG is an indispensable tool in the diagnosis, prognosis and planning treatment in most of the
cardiac disorders. The important applied aspects which need special mention are:
• • Cardiac arrhythmias,
• Myocardial infarction,
• Hypertrophy of various cardiac chambers and
• Effects on ECG of changes in the ionic composition of blood.

• Cardiac arrhythmias
• Cardiac arrhythmias refers to disruption of the normal cardiac rhythm.
The normal cardiac rhythm implies a regular sinus rhythm with a normal
cardiac rate, between 60 and 100 beats/min (average 72 beats/min). Sinus
rhythm is said to be present when the SA node is pacemaker, and each P
wave is followed by a normal QRS complex, the P–R and Q–T intervals are
normal, and R–R interval is regular. Cardiac arrhythmias may be
discussed as:
• • Abnormal sinus rhythm,
• • Conduction disturbances (heart blocks) and
• • Ectopic cardiac rhythm.
Abnormal sinus rhythm
Sinus arrhythmia
• Sinus arrhythmia is characterized by a normal sinus rhythm
except for the R–R interval (cardiac rate) which varies in a set
pattern.
• Sinus arrhythmia is usually, but not always synchronized with
respiration. Usually, heart rate increases during inspiration and
decreases during expiration, as a result of variations in vagal
tone that affect the SA node.
.During inspiration, impulses from lung stretch receptors
carried by vagii inhibit cardioinhibitory area (vagal centre) in
the medulla, resulting decrease in tonic vagal discharge (vagal
tone) and rise in heart rate
Sinus arrhythmia is common in children and in endurance
athletes with slow heart rates.
Electrocardiogram tracings showing:A, normal sinus rhythm; B, sinus arrhythmia; C, sinus
tachycardia; and D, sinus bradycardia.
• Sinus tachycardia
• • Sinus tachycardia is characterized by a normal sinus rhythm except
for increased heart rate (i.e. decreased but regular R–R interval).
Tachycardia is labelled when heart rate is more than 100 beats/min.
• • Sinus tachycardia is a normal response to exercise and is also
associated with fever, hyperthyroidism and as a reflex response to low
arterial pressure.
• Fever. The heart rate increases by 10 beats/min for each degree
Fahrenheit (18 beats/min/°C) rise in body temperature up to 105 oF
(40.5 oC); with further rise in body temperature, heart rate may
decrease due to debility of heart muscle. Tachycardia in fever occurs
due to increase in metabolic rate of SA node which directly increases its
excitability.
• Sympathetic activity. Factors which increase sympathetic activity also
lead to tachycardia, e.g. hypovolemic shock (as a reflex response to low
arterial pressure), exercise, hyperthyroidism.
Sinus bradycardia
• Sinus bradycardia is characterized by a normal sinus rhythm except for
decreased heart rate (i.e. increased but regular R–R interval). Bradycardia
is labelled when heart rate becomes less than 60 beats/min.
• Sinus bradycardia is more commonly seen in highly trained endurance
athletes due to increased vagal lone, sometimes it may be abnormal.

Carotid sinus syndrome.

In patients with carotid sinus syndrome, the baroreceptors present in
carotid sinus are very sensitive, even mild pressure on the neck elicits
strong baroreceptor reflex to cause bradycardia, sometimes heart may
stop for 5–10 s.
Sick sinus syndrome
• Sick sinus syndrome refers to a condition characterized by marked
bradycardia accompanied by dizziness and syncope.
• Causes of sick sinus syndrome include:
Impaired impulse generation in the SA node leading to Sinus bradycardia that
does not improve with sympathetic stimulation or vagal inhibition.

• SA nodal block and Sinus arrest, i.e. complete stoppage of sinus discharge.

• Treatment, when the condition causes severe symptoms, consists of

implantation of artificial pacemaker. Sinus node dysfunction accounts for over
half of the pacemaker implants.
Pacemakers are the electronic devices that sense and pace the activity of the
chambers of the heart by programming in most physiological way to maintain
the cardiac output.
The artificial pacemakers are the stimulators planted underneath the skin and
electrodes are usually connected to right ventricles to provide rhythmical
impulses to ventricles.
Conduction disturbances (heart blocks)
Heart blocks refer to slowing down or blockage of cardiac impulse (generated from
SA node) along the cardiac conductive pathway.
Conduction blockage may occur as:
• SA nodal block,
• AV nodal block and
• Bundle branch block.
SA nodal block
• SA nodal block or the so-called SA block is characterized by the blockage of
impulse conduction from SA node to atria.
• It occurs in the elderly and in patients recovering from coronary artery occlusion.
• It occurs suddenly and initially the heart stops (i.e. neither atria nor ventricles
contract for a while). After an interval of approximately two cardiac cycles, the AV
node becomes the pacemaker, and the heart starts functioning again. This is called
AV nodal rhythm.
• SA block may manifest as sick sinus syndrome .
• AV nodal rhythm also called junctional rhythm is characterized by inverted P wave
and normal QRS complex, and the rate is slower than sinus rhythm.
AV nodal rhythm seen in SA node blockage
• AV nodal block.
• AV nodal blockage may occur as incomplete heart block (which includes
first-degree and second-degree heart blocks) or complete heart block
(third-degree heart block). AV nodal blockages are associated with
following conditions:
• • Coronary insufficiency can cause AV nodal ischaemia.
• • Compression of AV node by scar tissue or by calcification.
• • Inflammation of AV node results due to myocarditis can depress
conduction of impulse from atria to ventricles.
• • Vagal excitation results due to strong stimulation of baroreceptors in
carotid sinus syndrome.
• First-degree AV nodal block.
• First-degree AV nodal (or heart) block is characterized by slowing of
conduction at the level of AV node. Though all the atrial impulses reach
the ventricles but the PR interval is abnormally long, i.e. more than 0.21
s ,but seldom increases more than 0.30 s.
• Second-degree AV nodal block.
• In second-degree AV nodal block not all atrial impulses are conducted to ventricles. It is usually associated
with organic heart diseases. Consequently, there may be one ventricular contraction after every 2, 3 or 4
atrial contractions producing the so-called 2:1, 3:1 or 4:1 block (constant block).
• Other forms of second degree heart blocks are:
• • Wenckebach phenomenon (mobitz type I block).
• It is characterized by a progressive lengthening of the P–R interval in successive beats and finally a failure
of one impulse to be transmitted.
• • Periodic block (mobitz type II).
• It is characterized by an occasional failure of conduction that results in an atrial to ventricular rate of for
example 6:5 or 8:7. The P–R interval is constant.
• Third-degree (complete) AV nodal block.
• • In third-degree complete AV block, no impulse from atria can pass to the ventricles.
• • Therefore, ventricles start beating at their own rhythm (about 40 beats/min) called idioventricular rhythm.
• • The atria, however, continues to beat at the normal sinus rhythm of about 72 beats/min. Thus, ECG shows
that there is complete dissociation between P waves and QRS complexes called atrioventricular dissociation.
• • Third-degree block is caused by organic heart diseases, septal myocardial infarction and damage to bundle
of His during surgical repair of congenital interventricular septal defects.
• • Third-degree block may be associated with prolonged ventricular standstill (asystole) until a ventricular
focus begins firing. The asystole, lasting for a minute may result in cerebral ischaemia producing dizziness
and fainting (syncope), the condition is termed Stokes–Adams’ syndrome. Even death may also occur due to
prolonged cerebral ischaemia.
• Treatment. Mostly these patients are provided with artificial pacemakers.
Various types of AV nodal blocks:A, normal sinus rhythm; B, first-degree AV block; C, second-degree AV block
(2:1); D, 3:1 block; and E, complete AV block (third degree).
Bundle branch block
• Bundle branch block refers to conduction blocks in one or more branches of the
bundle of His.
• In this condition, excitation passes normally down the bundle on the intact side and
then sweeps back through the muscle to activate the ventricle on the blocked side.
• Therefore, the ventricular rate is normal, but the QRS complexes are prolonged
(beyond 0.12 s) and deformed The characteristic features of the branch involved are:
Right bundle branch block (RBBB) may occur in otherwise healthy individuals or
secondary to chronic pulmonary disease. The activation of right ventricle is delayed and
ECG may show features of RAD .
• Left bundle branch block (LBBB) is usually associated with organic heart disease. It is
best diagnosed using left precordial leads
• Hemiblock or fascicular block refers to block in either anterior or posterior fascicle of
LBB. Left anterior hemiblock (LAH) produces abnormal LAD in ECG, whereas left
posterior hemiblock (LPH) produces abnormal RAD.
• Bifascicular block, i.e. RBBB with LAH or LPH is not uncommon.
• Trifascicular block, i.e. RBBB with LAH and LPH may also occur.

Note: HBE is useful for detailed analysis of the site of block when there is a defect in
• Ectopic cardiac rhythm
• Ectopic cardiac rhythm refers to abnormal cardiac excitation
produced either by an ectopic focus or a re-entry phenomenon.
Ectopic cardiac rhythm includes the following conditions:
• A. Atrial arrhythmias
• 1. Atrial extra systole,
2. Paroxysmal atrial tachycardia,
3. Atrial flutter and
4. Atrial fibrillation.

• B. Ventricular arrhythmias
1. Ventricular extrasystole,
2. Paroxysmal ventricular tachycardia and 3. Ventricular
fibrillation.
• Mechanisms of development of cardiac arrhythmias
• Cardiac arrhythmias may result from ectopic foci of excitation and/or re- entry mechanism.
• 1. Ectopic foci of excitation
• Under normal circumstances, SA node acts as a pacemaker since its rate of
rhythmic discharge is more rapid than the rate of discharge of other parts of
conduction system and myocardium of heart. However, in certain abnormal
conditions, the His–Purkinje fibres or the myocardial fibres become
hyperexcitable and discharge spontaneously. In these conditions, increased
automaticity of the heart is said to be present. The site in the heart which
becomes hyperexcitable is called an ectopic focus which may behave as:
• • Single discharge. When the irritable ectopic focus discharges once, an extra
systole or premature beat is caused before the next normal beat. Depending upon
the site of ectopic focus the premature beat may be atrial, nodal or ventricular.
• • Repetitive discharge. If the ectopic focus discharge impulses repeatedly at a
rate higher than that of SA node, the tachycardia with very high rate
(tachyarrhythmias) results. Depending upon the rate and rhythm and the site of
ectopic focus, the tachyarrhythmias are named as:
• • Paroxysmal tachycardia (atrial, nodal and ventricular),
• • Atrial flutter,
• Atrial fibrillation and
• 2. Re-entry mechanism
• Re-entry mechanism or the circus movement refers to a phenomenon in which the wave
of excitation propagates repeatedly (continuously) within a closed circuit. It is a more
common cause of tachyarrhythmias. Re-entry of excitation wave is known to occur under
two situations: (1) in the presence of transient block in the conduction pathway and (2) in
the presence of an abnormal extra bundle of conducting tissue called bundle of Kent.
• Re-entry due to transient block in the conduction system
• • Normally, during depolarization of a ring of cardiac tissue, the impulse spreads in both
directions of the ring and the tissue behind each branch of the impulse is refractory and
thus the impulse cannot go down the other side.
• • When there is a transient block on one side, the impulse can go down on the other side
of ring , because this portion is not depolarized and so not refractory.
• • If the transient block is worn off, the impulse from retrograde direction is conducted
through this (previously blocked) area and then continues to circle indefinitely. This
phenomenon is called circus movement or re-entry phenomenon .
• • The site of re-entry keeps on producing impulses continuously. If the re-entry is in AV
node, the re-entrant activity depolarizes the atrium and the resulting atrial beat is called
an echo beat. In addition, the re- entrant activity in the node propagates back down to
ventricles producing paroxysmal nodal tachycardia. The re-entrant activity can also
become established in atrial muscle fibres (producing atrial tachycardias, flutter or
fibrillation) and in ventricular muscle fibres (producing ventricular tachycardia or
Re-entry phenomenon or circus movements, a cause of cardiac arrhythmias; A, normal
depolarization of a ring cardiac tissue; B, spread of wave of excitation in presence of transient
block; and C, circus movement.
• Re-entrant activity in the presence of bundle of kent
• • Bundle of Kent is an abnormal extra bundle of conducting tissues
present in some individuals. This bundle connects the atria and
ventricles directly, so the conduction is very rapid than through the
regular conductive system.
• • If a transient block develops in the normal conductive system, the
impulse from SA node reaches the ventricle through the bundle of
• Kent and produces excitation. If the blockage in the normal conduction
system wears off, then the excitation wave from the ventricle travels in
the opposite direction and re-enter the AV node and a circus movement
is established .
• This re-entrant activity produces echo beat in atria and nodal
paroxysmal tachycardia or the so-called supraventricular tachycardia.
• • The nodal paroxysmal tachycardia occurring in patients with bundle of
Kent is called Wolff–Parkinson–White syndrome, producing short PR
interval, prolonged slurred QRS deflection but normal PJ interval (start
of P wave to end of QRS complex).
Re-entry phenomenon in the presence of bundle of Kent (A) and electrocardiogram record in a patient
with bundle of Kent showing short PR interval, wide and slurred. QRS complex with normal PJ interval
(Wolff- Parkinson-White (WPW) syndrome) (C) and Lown-Ganong- Levine (LGL) syndrome (D).
• Salient features of cardiac arrhythmias
• Extra systole
• Extra systole (premature beat, premature contraction or ectopic beat) refers to the contraction of the
heart prior to the time that normal contraction would have been expected. It is caused by some
ectopic focus in the atria or ventricles and thus the premature beat may be atrial or ventricular.
• Causes of extra systole: The main cause of ectopic foci is mechanical irritation, which occurs due to
ischaemia of local area of heart, calcified plaques, cardiac catheterization and local toxic irritation
caused by drugs, nicotine, caffeine, etc.
• Atrial extra systole (premature beat)
• Cause. Atrial premature beat is caused by an ectopic focus in the atrium which becomes pacemaker
for one beat. Atrial premature beats may occur frequently in healthy persons. In athletes, lack of
sleep, increased consumption of coffee, smoking etc.
• ECG appearance .of atrial premature beat is characterized by: A premature P wave occurs early and
has an aberrant configuration and an abnormal short PR interval because of the different path of atrial
depolarization.
• • QRS complex and T wave are normal.
• • Interval between premature beat and next succeeding beat is slightly prolonged called
compensatory pause.
• • The subsequent cardiac rhythm is shifted and reset, because the premature beat discharges the SA
node, which then repolarizes and fires after the normal interval.
• Significance. Since atrial extra systole occurs normally, the patient may or may not be aware of an
occasional irregularity in the cardiac rhythm.
Electrocardiographic recording extrasystole: A, normal ECG; B, ECG with atrial premature
beat (atrial extra systole); and C, ECG with ventricular premature beat.
• Ventricular extra systole
• Cause. Ventricular extra systoles can arise from any portion of the ventricular
myocardium and occasionally occur in otherwise healthy individuals. Frequently
ventricular premature beats occur with many forms of heart disease, especially coronary
artery disease (because ischaemia increases the irritability of the myocardium).
• ECG appearance of ventricular premature beat is characterized by ,
• • Absence of P wave preceding the QRS complex.
• • QRS complex is prolonged and bizarre shaped because of the slow spread of the
impulse from the ectopic focus through the ventricular muscle to the rest of the
ventricle.
• • T wave is usually oppositely directed from the QRS complex.
• • Compensatory pause is often long. Since retrograde transmission of depolarization to
the atria usually does not occur with premature ventricular beat, so, the atrial rate
remains unaltered. The atrial depolarization that follows the premature ventricular beat
arrives while the AV node is still refractory and, therefore, it is not conducted to the
ventricles, creating a pause in the ventricular rhythm.
• This pause is usually fully compensatory so that R–R interval of the beat preceding the
premature ventricular beat interval together equals two normal cycle lengths. Thus, the
ventricular premature beats do not interrupt the regular discharge of the SA node,
• The beat following ventricular premature beat is usually stronger
than the normal because of the added stroke volume and thus usually
detected by the patient.
• Interpolated beats. When the patient’s sinus rhythm is slow, in that case
a premature ventricular beat may occur without altering the normal R–R
interval. Such a premature ventricular beat is termed an interpolated
beat.

• Pulse deficit.
• Ventricles contract ahead of time in atrial and ventricular premature
beats. Sometimes by that time ventricles are not filled with blood and
stroke volume output during the contraction is therefore decreased or
even absent. During such a contraction, pulse wave passing to periphery
may be so weak that it is not felt at the radial artery. A deficit in the
• Atrial arrhythmias
• • Atrial tachycardia occurs when an atrial site (outside the SA
node) becomes the dominant pacemaker. It is characterized by
very regular rates ranging from 140 to 220 beats/min. Atrial
tachycardia may be caused by overindulgence in caffeine,
nicotine or alcohol and may also occur during anxiety attack.
• Paroxysmal atrial tachycardia (PAT) as the name indicates occurs
in paroxysms, which usually begin suddenly and lasts for few
seconds. PAT may result from discharge of a single ectopic site
or a re-entry phenomenon .

• ECG appearance of PAT is characterized by an inverted P wave

before each QRS complex, and this P wave is partially
superimposed on to the normal T wave of the preceding beat .
• Atrial flutter is said to occur with atrial rates of 220–350 beats/min. During atrial flutter, AV node is
unable to transmit all of the atrial impulses and therefore the ventricular rate may be half, one-
third or one-fourth of the atrial rates. Like atrial tachycardia, atrial flutter may result either from a
single ectopic focus or a re-entry phenomenon.
• ECG appearance in atrial flutter: the P wave is strong and QRS-T complex follows once after two P
waves or three P waves (2:1 or 3:1 rhythm).
• • Atrial fibrillation is characterized by a totally irregular, rapid rate (350–500 beats/min). In it, there
occurs contraction of only small portion of the atrial musculature at one time because large
portion of the atria are still in refractory period. Ventricular rate is completely irregular because
only a fraction of the atrial impulses that reach the AV node are transmitted to the ventricles.
• ECG appearance is characterized by: Small irregular oscillations called F waves. There are no
recognizable P waves
• • R–R interval is irregularly irregular QRS complex and T wave are normal because the impulses
that are transmitted through the AV node are conducted normally through the ventricles.
• Causes. Atrial fibrillations are frequently associated with enlarged atria secondary to AV valve
diseases.
• Treatment. Atrial fibrillations can be converted back to normal rhythm by
cardioversion/defibrillation. A strong single electric shock of alternating current is passed through
the heart for a fraction of second. All action potential stop and heart remains quiescent for few
seconds (3– 5 s) or refractoriness of heart. After that it begins to beat with normal rhythm.
• Complications. Long-term fibrillation is associated with thrombi in the atrial appendages.
• Nodal arrhythmia
• Nodal paroxysmal tachycardia
• is similar to atrial tachycardia and may be indistinguishable on ECG. They are called
supraventricular tachycardia ECG appearance: almost normal QRS–T complexes, but P
wave is either totally missing or obscured, but can be distinguished from the
paroxysmal ventricular tachycardia by HBE. In supraventricular tachycardia, there is
a His bundle (H) deflection whereas in ventricular tachycardia, there is none.

• Wolff–Parkinson–White syndrome also known as accelerated AV conduction refers to

occurrence of repeated attacks of nodal paroxysmal tachycardia due to presence of
bundle of Kent. The bundle of Kent is aberrant musculature or nodal tissue which
connects the atria and ventricles directly. This bundle conducts more rapidly than the
slowly conducting AV node, and one ventricle is excited early. The presence of bundle
of Kent rapidly establishes re-entry phenomenon (circus movement) in prone patients
(see page 265).

• Lown–Ganong–Levine syndrome It is characterized by attacks of paroxysmal

supraventricular tachycardia, usual nodal tachycardia in individuals with short PR
intervals and normal QRS complexes. In this condition, depolarization presumably
passes from the atria to the ventricles via an aberrant bundle that bypasses the AV
node but enters the intraventricular conducting system distal to node
• Paroxysmal ventricular tachycardia occurs when a ventricular site
discharges rapidly and repetitively, usually as a result of re-entry
phenomenon. Alterations in vagal tone (by carotid sinus massage or
Valsalva manoeuvre) do not affect ventricular tachycardia because the
ventricles do not receive any efferent vagal innervation.
• Causes. Ventricular tachycardias are usually associated with serious
heart disease or drug toxicity.
• ECG appearance is characterized by• Wide, bizarre QRS complexes that
occur at rapid rate and
• • P waves are usually indistinguishable. Significance. Ventricular
tachycardia is more serious because cardiac output is decreased,
sustained ventricular tachycardia can be a life- threatening when it
degenerates into ventricular fibrillation.
Electrocardiographic record in ventricular arrhythmias: A, normal; B, paroxysmal
ventricular tachycardia; and C, ventricular fibrillation.
• Ventricular fibrillation occurs when small segments of ventricular myocardium show rapid,
irregular ineffective contractions. In this condition, cardiac output is zero and so the
peripheral pulse is absent. ECG is must to differentiate ventricular fibrillation from the
cardiac standstill.
• Causes. Ventricular fibrillation is very common during electric shock and during
ischaemia of conductive system. Other causes are coronary occlusion, trauma to heart,
chloroform anaesthesia and improper handling of heart during cardiac surgery.
• ECG appearance is characterized by:
• Undulating waves of varying frequency and amplitude. The voltage of the ECG waves in
ventricular fibrillation is about 0.2-0.5 mV or less.
• • Ventricular premature beats are usually seen as the precipitating cause, one of which
falls on the vulnerable period of the T wave (i.e. the interval near the peak of T wave
when the ventricle is partially repolarized). A premature beat during the vulnerable
period produces fibrillation because the chances of re-entry occurring are more.
• Significance. Ventricular fibrillation is the most common cause of sudden death in
patients with myocardial infarcts.
• Treatment. Cardiopulmonary resuscitation must be started immediately to prevent
tissue death.
• Immediate electric or electronic defibrillation (cardioversion) should be performed.
• • T cardioversion/defibrillation is done by applying electrodes directly to two sides of the
heart or on the chest wall using 110 volts of 60 cycles at alternating current for 0.1 s or
• Techniques for evaluation of arrhythmia
• 1. Electrocardiographic monitoring is the ideal way of establishing a correlation between symptoms
and a rhythm disturbance, but this is not always easy because symptoms are usually sporadic.
• • When episodes of arrhythmia are infrequent, then continuous 24-h monitoring may be helpful.
• • Exercise testing may be helpful if symptoms are associated with stress or exertion.
• 2. Heart rate variability (HRV) refers to beat to beat variation of heart rate.
• The R–R interval variations during resting condition represents a fine tuning of beat to beat control
mechanisms. HRV reflects fluctuations rather than absolute levels of sympathetic and
parasympathetic impulse. The analysis of beat to beat variation in heart rate is used to investigate
sympathovagal imbalance, i.e. integrity of autonomic activity and vulnerability to various
cardiovascular disorder resulting from autonomic imbalance.
• HRV is recorded by ECG lead II on Polyrite D system and its time domain and frequency domain
variables are analyzed.
• 3. Electrophysiological testing is intracardiac, electrocardiographic recordings is useful in diagnosis
and management of complex arrhythmia.
• 4. Autonomic testing is an important component of evaluation in patients with recurrent syncope.
Autonomic testing can be done by simple Head up tilt test (HUT), also called as Tilt Table Test.
• 5. Tilt table testing is based on the fact that in upright posture, there is venous pooling in lower
limbs that reflexly increases heart rate and vasoconstriction (compensatory mechanism). Head-up-
tilt-testing can identify the syncope due to vasovagal /autonomic imbalance.
• Treatment of arrhythmia
• 1. Mechanical Measures are used to interrupt the attack. These include: Valsalva manoeuver and
carotid sinus massage. These manoeuvers stimulate the vagus nerve, delays A–V conduction and
block the re-entry mechanism, and ultimately terminating arrhythmia.
• 2. Anti Arrhythmic Drugs have limited efficiency due to frequent side effects. Broadly
antiarrhythmic drugs are divided into four classes based on their electropharmacological
actions:
• • Class I agents block membrane sodium channels, thus slowing conduction and prolonging
the refractoriness. These include: Quinine and procainamide.
• • Class II agents are beta adrenergic blockers, which decrease automaticity, prolong AV
conduction. Examples are propranolol and metaprolol.
• • Class III agents block K+ channels and prolong repolarization and prolonging QT interval.
• • Class IV agents are calcium channel blockers, which decrease automaticity and A–V
conduction, e.g. Verapamil.
• 3. Radiofrequency Ablation:
• Cardiac catheter with electrodes attached to its tip is passed into the chambers of the heart,
and exact location of ectopic focus or accessory bundle responsible for arrhythmia is identified.
The ablation can be done by applying radiofrequency band (300–3000 kHz) with catheter tip.
Radiofrequency is particularly useful in conditions that cause supraventricular tachycardias,
Wolff–Parkinson–White syndrome and atrial flutter.
• The radiofrequency generates energy for biomedical applications like coagulation and
• Myocardial infarction
• Myocardial infarction refers to the ischaemic necrosis of a part of
myocardium which occurs when coronary blood flow ceases or is reached
below a critical level . The ECG is very useful for diagnosing and
localizing areas of myocardial infarction.
• ECG appearance.
• The ECG undergoes a series of changes following the myocardial
infarction. These changes must be recorded daily with ECG tracing for
diagnostic purpose. The hallmark of acute myocardial infarction is:
• • Elevation of ST segment in the leads overlying the area of infarct and
• • Depression of ST segment in the leads on the opposite side of area of
infarct.
• ECG appearance in old cases of myocardial infarct is characterized by:
• • ST segment returns to normal,
• • Appearance of Q wave in some of the leads in which it was not previously present and
• • An increase in the size of normal Q wave in some of the other leads.
• Physiological basis of ECG changes in acute myocardial infarction
• The alterations in ECG pattern seen in acute myocardial infarction are attributed
to injury current which flows from the affected to the unaffected part of
myocardium. This happens because of the fact that the affected part of
myocardium gets depolarized partly or completely but does not get repolarized
rapidly. The three major abnormalities that cause ECG changes (ST segment
elevation) in acute myocardial infarction are:
• 1. Decline in Resting Membrane Potential.
• The ischaemic necrosis of the myocardial fibres results in breakdown of cell
membrane producing increased K+ efflux and increase in Na+ influx. Therefore,
inside of the infarcted cells becomes less negative as compared to the unaffected
area. Therefore, during ventricular diastole, the z current flows into the infarct
from the unaffected area This results in a depression of TQ segment of the ECG
in the leads overlying the infarcted area. However, the electronic arrangement in
electrocardiographic recorders is such that TQ segment depression is recorded
as ST segment elevation.
• 2. Delayed Depolarization
• of infarcted cells causes the infarcted area to be positive relative to the
unaffected area. Therefore, current flows out of infarcted area into the
unaffected area .
• 3. Rapid Repolarization.
• The repolarization in infarcted cells occurs rapidly as compared to
unaffected area due to accelerated opening of K+ channels. Because of
the rapid repolarization in the infarct, the membrane potential of the
affected area becomes greater than that of the unaffected area.
Extracellularly, current therefore flows out of the infarct into normal
unaffected area.
• This current flow toward electrodes over the injured area, causing
increased positivity between the S and T waves of ECG. Consequently,
leads on the opposite side of the heart show ST segment depression
Electrocardiographic record in anterior wall ischaemia in lead I and II respectively: AI and
AII, normal ECG; BI and BII, ECG within few hours of ischaemia, note ST segment
elevation in lead I and depression in lead II (reciprocal); and CI and CII, ECG after several
weeks, note ST segment returns to normal and Q wave appears.
• Physiological basis of ECG changes in old cases of myocardial
infarction
• After some days or weeks of infarction, the dead myocardium
and scar tissue become electrically silent. Therefore, the
affected area becomes negative relative to the unaffected
normal myocardium during systole, and it fails to contribute
its share of positivity to the electrocardiographic complexes.
• The occurrence of Q wave in some leads (which normally lack)
and deepening of Q wave in other leads is one of the
manifestations of this negativity.
Physiological basisofECGchanges(ST segment elevation) in acute myocardial infarction: A, normal resting state; B,
decline in resting membrane potential in infarct area as compared to normal neighbouring (unaffected) region; C,
delayed depolarization of infarct area as compared to neighbouring areas; and D, rapid repolarization of infarct area
in comparison to normal neighbouring areas.
• Localization of area of myocardial infarction
• 1. Anterior myocardial infarction
• Leads showing changes of MI are LI, aVL and V3–V5
• • Leads showing reciprocal changes are LII, LIII and aVF. 2. Posterior
(inferior) myocardial infarction
• • Leads showing changes of MI include LII, LIII and aVF.
• • Leads showing reciprocal changes are LI, aVR, aVL and V1–V6.
• 3. Lateral myocardial infarction
• • Leads showing changes of MI include LI, aVL and V6 and
• • Leads showing reciprocal change are LII, LIII, aVF and V1.
• 4. Septal myocardial infarction
• Leads showing changes of MI are V1–V3.
• Complications
• Complications of myocardial infarction are ventricular arrhythmias which
mainly occur due to re-entrant activity during the first 30 min of
infarction, and increased automaticity after 12 h.
• Ventricular hypertrophy
• Ventricular hypertrophy occurs when the work of the ventricle is increased sufficiently. In
ventricular hypertrophy, the number of myocardial cells remains the same, but the diameter of the
individual cells increases, raising the diffusion distance for O2 and other
• metabolites.
• Left ventricular hypertrophy (LVH)
• occurs in patients with systemic hypertension or aortic valve stenosis. Right ventricular
hypertrophy (RVH) occurs in patients with pulmonary hypertension, pulmonary valve stenosis and
some congenital heart disease.
• ECG appearance
• is characterized by the following.
1. R wave. There is direct correlation between the thickness of ventricular
• wall and the height of R wave in the overlying leads. Therefore:
•InLVH,theRwaveistallinleadsI,aVL,V5 andV6 and
• • In RVH, the R wave is tall in lead III, aVR, V1 and V2.
• 2. QRS duration is increased slightly due to the increased muscle mass. It is usually less than
0.12 s, but occasionally may exceed this value.
• 3. Mean electric axis (MEA) shows ;
• • LAD in LVH and RAD in RVH.
• Effect of changes in the ionic composition of blood on electrical
activity of heart
• The electrical activity of the heart depends upon the distribution
of ions like Na+, K+ and Ca2+ in the ECF. Therefore, changes in
the ECF concentration of these ions will affect the potentials of
myocardial fibres and produce changes in the ECG as described:
• Plasma level of sodium
• Low plasma (ECF) levels of Na+ may be associated with low
voltage ECG complexes.
• Plasma levels of potassium
• Depending upon the levels of plasma K+ following ECG changes
are seen:
• 1. With normal plasma levels of K+ (4–5.5 mEq/L). The
normal ECG tracings are produced with PR interval = 0.16 s;
QRS interval = 0.06 s, QT interval = 0.4 s.
2. Hyperkalaemia, i.e. increase in plasma K+ is very dangerous
and potentially lethal condition because of its effects on heart.
Hyperkalaemia with plasma K+ ± 7.0 mEq/L, the PR and QRS
intervals are within normal limits. The T wave become tall and
peaked which is a manifestation of altered repolarization.
• In hyperkalaemia with plasma K+ levels, 8.5 mEq/L the ECG
shows
• Broad and slurred QRS complex with a QRS interval of 0.2 s
occurs due to paralysis of atria.
• T wave remains tall and slender.
• A further increase in plasma K+ levels may result in
ventricular tachycardia and ventricular fibrillation.
• As the extracellular K+ concentration increases, the resting
membrane potential of the muscle fibres decreases. Eventually
the fibres become unexcitable, and the heart stops in diastole.
• 3. Hypokalaemia, i.e. decrease in the plasma levels of potassium is a serious
condition but it is not as rapidly fatal as hyperkalaemia. It produces the following
changes in ECG
• • PR interval is prolonged,
• • U waves become prominent,
• • ST segment is depressed,
• • Late T wave inversion may occur in the precordial leads and
• • If the T and U waves merge, the apparent QT interval is often prolonged, but if
the T and U waves are separated, the true QT interval is of normal duration.
• Long QT syndrome. Long QT syndrome occurs due to genetic abnormality which
blocks one type of K+ channels KVLQT1 resulting in slow K+ efflux, prolonging
cardiac action potential and hence QT interval. The incidence of ventricular
arrhythmia and sudden death is more with prolonged QT interval.
• Normally this K+ channel (protein), in the heart is responsible for normal QT
interval, and in the stria vascularis for maintaining the high concentration of K+ in
the endolymph.
• Mutation of KVLQT1 results in long QT interval syndrome. In this syndrome
patients are deaf and also predispose to ventricular arrhythmia (because
vulnerability of heart for irregular repolarization is high). This syndrome is also
Electrocardiographic changes in relation to plasma levels of potassium: A, normal tracing (plasma K
+ 4–5.5 mEq/L); B, hyperkalaemia (plasma K + 7.0 mEq/L); C, hyperkalaemia (plasma K + 8.0
mEq/L); and D, hypokalemia (plasma K + 2.5–3.5 mEq/L).
Plasma levels of calcium
• Hypercalcaemia,
i.e. increased in extracellular Ca2+, clinically is rare if ever
high enough to affect the heart. However, when large amounts
of calcium are infused into experimental animals, the heart
relaxes less during diastole and eventually stops in systole
(calcium rigor).
• Hypocalcaemia,
i.e. decreased plasma level of Ca2+ produces prolongation of
the ST segment and consequently the QT interval is also
increased.
Thank you