17-12-2024

LEARNING OBJECTIVES
At the end of the session, the Phase I student must be able to;

1. Identify and explain the physiological basis of ECG changes during

sinus arrhythmias, atrial fibrillation and ventricular fibrillation.
2. Explain the pathophysiology of different types of heart block
3. Understand the physiological basis of ECG changes during Heart
CLINICAL APPLICATIONS OF block
ELECTROCARDIOGRAPHY Dr Neetha Shastry
FMMC
4. Understand the physiological basis of ECG changes during
PY5.6: Describe abnormal ECG, arrythmias, heart block and myocardial Infarction Myocardial infarction.
DR NEETHA S 2

1 2

Cardiac Arrhythmias

Myocardial infarction

Effect of changes in the ionic composition of blood on ECG

CARDIAC ARHYTHMIAS
DR NEETHA S 3 DR NEETHA S 4

3 4

Regularly irregular rhythm – sinus arrhythmia(normal)

BRADYARRHYTHMIAS
Small decreases in RR interval ( HR) during inspiration, small
increases in RR interval (HR) during expiration

SAN
Arrhythmias – abnormal rhythms
Bradyarrhythmias – sustained abnormal rhythms at a rate slower
than normal sinus rate
Tachyarrhythmias – sustained abnormal rhythms at a rate faster
than normal sinus rate Atrial
Muscle
Extra systoles – occasionally occurring extra beats due to
abnormal premature excitation arising in a focus outside the SAN

Ventricular
DR NEETHA S 5 Muscle 6
PhysioCentral: [Link]/hnharsha

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BRADYARRHYTHMIAS BRADYARRHYTHMIAS

SAN SAN
King Sinus is dead
Long live King Atrium!
Atrial escape

Atrial Atrial
Muscle Muscle

Ventricular Ventricular
PhysioCentral: [Link]/hnharsha Muscle 7 Muscle 8
PhysioCentral: [Link]/hnharsha

7 8

BRADYARRHYTHMIAS BRADYARRHYTHMIAS Sustained escape rhythms in the event of sinus

failure
Types
 Atrial
 40 to 50/min
SAN  Abnormal P
 Normal QRS, T
 Junctional (nodal)
 40 to 50/min
 Absent P
Atrial
King Sinus is dead Muscle  Normal QRS, T
Long live King Ventricle!  Ventricular
Ventricular  Normal P
escape
 30 /min
Ventricular  Abnormal QRS, T
Muscle
PhysioCentral: [Link]/hnharsha  P – QRS dissociation
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9 10

TACHYARRHYTHMIAS ATRIAL TACHYARRHYTHMIAS

A focus outside the SAN becomes Atrial tachycardia
abnormally excitable – discharges at  150 – 250 /min
a rate hifher than the normal SAN  Abnormal P waves @ >150/min
rate and “takes over” the pacing
 Normal QRS
 At rates > 200, AV block
“Ectopic pacemakers” Atrial flutter
 Atrial
 > 250 /min
 Junctional
 Saw tooth like P waves
 Ventricular
 Normal QRS but with incomplete (2:1 or 3:1
conduction)
Atrial fibrillation
 Chaotic uncordinated atrial depolarization
 Absent / “fibrillatory” P waves
 Normal QRS at variable rate

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ATRIAL TACHYCARDIA ATRIAL FLUTTER

AV node conducts impulses to the ventricles at a ratio of 2:1, 3:1, 4:1, or greater

Rate: Atrial: 250–350 bpm; ventricular: variable

Rhythm: Atrial: regular; ventricular: variable
P Waves: Flutter waves have a saw-toothed appearance
PR interval: Variable
QRS: Usually normal (0.06–0.10 sec), but may appear widened if flutter waves are
buried in QRS
DR NEETHA S 13 DR NEETHA S 14

13 14

VENTRICULAR TACHYARRHYTHMIAS
ATRIAL FIBRILLATION Ventricular tachycardia
>150
No P waves
Abnormal, broad but regular QRS
complexes
No identifiable T wave

Rate: Atrial:300-500 bpm; ventricular: 100-180bpm

Rhythm: Irregular Ventricular fibrillation
P Waves: No true P waves; fibrillatory, chaotic atrial activity Chaotic uncordinated ventricular
PR Interval: None depolarization
QRS: Normal (0.06–0.10 sec) Irregular fibrillatory baseline
DR NEETHA S 15 No QRS complexes

15 16

VENTRICULAR FIBRILLATION

Chaotic electrical activity occurs with no ventricular depolarization or contraction

Rate: Indeterminate
Rhythm: Chaotic
P Waves: None
PR Interval: None
QRS: None
CONDUCTION BLOCKS
DR NEETHA S 17 DR NEETHA S 18

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SA NODAL BLOCK
▪Impulse from the sinus node is blocked before it enters the atrial
Heart blocks refer to the slowing down or blockage of cardiac impulse muscle.
(generated from SA node) along the cardiac conductive pathway. ▪Sudden cessation of P waves, with resultant standstill of the atria.

Bundle Branch
SA Nodal Block AV Nodal Block
Block

DR NEETHA S 19 DR NEETHA S 20

19 20

ATRIOVENTRICULAR BLOCK Heart

Blocks
Causes:
▪Ischemia of the A-V node or A-V bundle fibers
Incomplete Complete
▪Compression of the A-V bundle
▪Inflammation of the A-V node or A-V bundle
▪Extreme stimulation of the heart by the vagus nerves First Third
degree Degree
Incomplete AV Complete Second
Nodal Block AV Nodal Block Degree
DR NEETHA S 21 DR NEETHA S 22

21 22

FIRST DEGREE HEART BLOCK

PR interval
0.16s First-degree block is defined as,
delay of conduction

RR interval
from the atria to the ventricles but not
0.24s
actual blockage of conduction.

I degree Heart Block - Prolonged PR interval > 0.21s DR NEETHA S 23 DR NEETHA S 24

23 24

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SECOND DEGREE HEART BLOCK – MOBITZ TYPE I

Wenckebach Phenomenon:
Progressive increase in PR interval until a P wave fails to be conducted
PR interval
0.16s
Clinically seen in,
• Acute inferior MI
• Digitalis toxicity

RR interval
0.24s

II - Mobitz type I - progressive increase in PR interval

until a P wave fails to be conducted DR NEETHA S 25 DR NEETHA S 26

25 26

SECOND DEGREE HEART BLOCK – MOBITZ TYPE II COMPLETE A-V BLOCK (THIRD-DEGREE BLOCK).
No impulse from atria can pass to the ventricles.

Ventricles start beating at their own rhythm (about 40 beats/min) -

-- Idioventricular rhythm
PR interval
0.16s
Atria continue to beat at the normal sinus rhythm of 72 beats/min.

ECG: Complete dissociation between P waves and QRS complexes

II - Mobitz type II - normal PR interval in conducted beats atrioventricular dissociation
But some P waves are not conducted DR NEETHA S 27 DR NEETHA S 28

27 28

STOKES-ADAMS SYNDROME—VENTRICULAR ESCAPE.

In case of AV nodal blocks-

Each time A-V conduction ceases, the ventricles start their own
impulse.

Do not start their own beating until after a delay of 5 to 30

seconds.

DR NEETHA S 29 DR NEETHA S 30

29 30

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Brain cannot remain active for more than 4 to 7 seconds without blood supply

AV block
Loss of consciousness a few seconds after complete block occurs
(heart does not pump any blood for 5 - 30 s, until the ventricles “escape.”)
ventricular
Purkinje system beyond the escape. Following “ESCAPE”, the slowly beating ventricles restore the blood supply to
block Discharge rhythmically
at a rate of 15 to 40 the brain - rapid recovery from the faint.
times/min & act as the
pacemaker of the ventricles.
Periodic fainting spells are known as :

The Purkinje system does not begin to emit its intrinsic rhythmical
impulses for 5 to 20 seconds. Stokes-Adams syndrome.
DR NEETHA S 31 DR NEETHA S 32

31 32

WOLFF-PARKINSON-WHITE SYNDROME
Accessory pathway (Bundle of Kent) between atria and ventricles

Electrical impulses are rapidly conducted to the ventricles.

• Rate: Depends on rate of underlying rhythm
These rapid impulses slur the initial portion of the QRS; the slurred • Rhythm: Regular unless associated with A-fib
effect is called a delta wave. • P Waves: Normal (upright and uniform) unless A-fib is present
• PR Interval: Short (<0.12 sec) if P wave is present
• QRS: Wide (>0.10 sec);
• delta wave present
DR NEETHA S 33 DR NEETHA S 34

33 34

CORONARY CIRCULATION - APPLIED ASPECTS

Myocardial ischemia
Hypoxia of myocardium due to inadequate blood supply
“relative inadequacy” – worsened by exercise
Reduces functional effectiveness of myocardium
If severe may lead to ischemic necrosis (death) of myocardial cells
Accumulation of metabolic products may be responsible for
ECG CHANGES IN MYOCARDIAL stimulation of pain fibers - angina

INFARCTION
DR NEETHA S 35 DR NEETHA S 36

35 36

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ECG changes in leads facing the infarcted wall ECG changes in reciprocal leads

1. ST-segment elevation (>2mm in 2 contiguous leads) 1. ST-segment depression

2. Inverted T-wave/ peaked T-wave ( early sign of MI) 2. Tall and upright T-wave

3. Deep & wide Q-wave ( >0.04s, >25% of height of R-wave)

2
1

1 2
3
DR NEETHA S 37
Reciprocal leads: Leads opposite to infarcted area DR NEETHA S 38

37 38

Clinically all the changes do not appear simultaneously

Progression of MI and ECG changes Progression of MI and ECG changes

I. ST segment changes III. Q-wave changes

• Within few hours to days of ischemia: • Appears after a week
Elevation of ST-segment • Gradually deepens and remains permanent
• Within 2-3 weeks of ishemia
ST-segment returns to baseline

II. T-wave changes

• Tall peaked T waves – within few hours
• Inverted T-wave – 2-3 days
• Gradually becomes flat and then upright – 2-3 months
DR NEETHA S 39 DR NEETHA S 40

39 40

Tall, peaked T-wave; ST- segment Elevation Minutes to Hours

ST- segment Elevation; Slow inversion of T-wave 24-48 hours

Progression of MI

ST- segment normalizes, T-wave deeply 96 hours

inverted, Appearance of Q-wave

T-wave gradually returns to normal, Q-wave

fully developed
Weeks-Months ELECTROPHYSIOLOGY OF ECG
CHANGES IN MI
DR NEETHA S 41 DR NEETHA S 42

41 42

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QUICK RECAP NORMAL MYOCARDIAL AREA AT REST

Depolarisation towards +ve electrode
Polarised state.
Or Positive deflection
Replarisation away from +ve electrode
Inside negative with reference to outside and (RMP)

Depolarisation away from +ve electrode

Or Negative deflection
Replarisation towards +ve electrode

DR NEETHA S 43 DR NEETHA S 44

43 44

INJURY CURRENT INJURY CURRENT CONTINUED

Definition: Injury current is the electrical current that flows between
the damaged (infarcted) area of the heart and the surrounding
healthy tissue. Because these damaged cells are partially depolarized, there is a
difference in charge between the infarcted (partially depolarized)
cells and the surrounding healthy (polarized) cells.
Cause: This occurs because the damaged heart muscle cells remain
partially depolarized (partially charged) while the surrounding
healthy cells are normally polarized (neutral or positively This difference in charge causes an electrical current to flow from
charged). the injured area to the healthy area.

In the infarcted area, the heart muscle cells instead of returning to This is reflected as ST segment elevation in ECG.
the fully polarized (negatively charged) resting state, these cells
stay in a partially depolarized state, where the interior is less
negative (more positive) than it should be.
DR NEETHA S 45 DR NEETHA S 46

45 46

PHYSIOLOGICAL BASIS OF ECG CHANGES IN ACUTE

MYOCARDIAL INFARCTION ECG CHANGES IN MYOCARDIAL INFARCTION
Partial or total depolarization of the injured muscle all the time.
Myocardial infarction
Ischemic death of myocardial cells – death of myocardial cells
Current flows between the pathologically depolarized and the normally due to lack of oxygen (lack of blood supply)
polarized areas, even between heartbeats.
Several changes seen during infarction
Defects in repolarization
This is called a current of injury OR Injury Current Loss of –ve membrane potential
Ischaemic area Persistent depolarization
Replacement of myocardial tissue by fibrotic tissue (non-excitable)
DR NEETHA S 47 DR NEETHA S 52

47 52

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Ischaemia

Less negative RMP- depolarized state

↓ O2 supply

↓ ATP
Ischemic cells repolarize faster compared to
↓ activity of Na+-K+ATPase normal cells
pump

↑ extracellular K+
Conduction velocity is reduced
Less negative RMP-
depolarized state

Inactivation of VGNaC
DR NEETHA S 53 DR NEETHA S 58

53 58

HYPERKALAEMIA
▪Tall & Peaked T waves

▪PR interval, QT interval : Normal

EFFECT OF CHANGES IN THE IONIC

COMPOSITION OF BLOOD ON ECG
DR NEETHA S 59 DR NEETHA S 60

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HYPOKALEMIA HYPOCALCEMIA
▪PR interval is prolonged ▪prolongation of the ST segment
▪U waves become prominent ▪consequently, the QT interval is also increased.

▪ST segment is depressed

▪Late T wave inversion may occur in the precordial leads.

DR NEETHA S 61 DR NEETHA S 62

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HYPERCALCEMIA

The heart relaxes less during diastole and eventually stops in

systole (calcium rigor).

THANK YOU
DR NEETHA S 63 DR NEETHA S 64

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