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Current of Injury in ECG

Flow of current from damaged area to normal area of heart between heart beats is called current of injury

Damaged area (semi-viable)

Remains depolarized (negative outwards)

Vector of injury current points towards normal part of heart (positive)

Base of vector lies in damaged area of the heart (negative)

Causes

Ischemia (most common cause)

O2lack, Co2accumulation, nutrients deficiency →depression of Na+/ K+Pump

Mechanical trauma

Ruptures the cell membranes

Infections

Ruptures the cell membranes

Damaged myocardium (permanently -ve) will affect the pattern of repolarization

Injury current represents the mean recordable repolarization vector (incomplete ‘T wave’ vector)

Repolarization is not complete so ‘T wave’ will not come to base line

Injury current Positive or negative

Depends upon the relation between current of injury vector and +ve electrode of the respective lead

Injured myocardium

Produces injury currents →ST segment shift on ECG

Infarcted(dead) myocardium

does not generate electrical activity →SignificantQ waves on ECG

Normal myocardium suffering from mild ischemia

Repolarization starts early in ischemic area →T wave vector shifts → change in T wave morphology

Arrhythmia

Irregular heart beat

Normal Sinus Rhythm (NSR)

Rhythm generated by SA nodeat a rate of 60 to 100beats per minute with sequential inscriptionof P–QRS–T waves at regular intervals

Sinus Tachycardia

Normal sinus rhythm with heart rate more than 100 beats per minute

Causes

Exercise, emotions, fever, hyperthyroidism etc

ECG finding

Decreased RR interval < 0.6 seconds (< 3 large squares)

Sinus Bradycardia

Normal sinus rhythm with heart rate less than 60 beats per minute

Causes

Sleep, Athletes, drugs (beta blockers) etc

ECG findings

Increased RR interval > 1.0 seconds (> 5 large squares)

Sinus Arrhythmia

Fluctuation in heart rate with phases of respiration

Increase during inspiration

Decrease during expiration

A normal phenomenon

Mediated by parasympathetic system

Decreased sinus arrhythmia may lead to rhythm problems

Cause

Inhibition of cardioinhibitory area

Stimulation of stretch receptors in lungs

Afferents through vagal nerve to cardioinhibitory area

Spillover of signals from respiratory center to vasomotor center

ECG findings

Variable RR intervals (heart rate variability)

Heart Blocks

Blockage of impulse conduction

Intra-atrialblocks

Atrioventricular blocks

Intraventricular blocks

Intra-atrialblocks

Sinus arrest (sick sinus syndrome)

SA node fails to generate an impulse

Sino-atrialblock

Impulse is generated but it is blocked to enter the atria

A complete cycle (P-QRS-T) is missed

SA node resumes pacing or any other potential pacemaker takes over

Incomplete heart blocks

First degree heart block

PR interval more than 0.2 seconds

Second degree heart block

Gradual lengthening of PR interval until blocking the impulse –Wenckebachphenomenon

Intermittent conduction of impulse from atria to ventricles –Mobitz phenomenon

P : QRS = 2 : 1 or 3 : 2 or 3 : 1 etc

Complete heart block

Third degree heart block

Total blockade of impulse conduction from atria to ventricles

Atrioventricular dissociation

Ventricles escape

Idioventricular rhythm

Atria pace at their own rhythm

Stokes-Adams syndrome

Intermittent complete AV block

Due to border line ischemia of conductive system

Fainting due to lack of blood supple to brain

Ventricular escape after about 5-30 seconds due to overdrive suppression

Right bundle branch block

Left bundle branch block

Electrical alternans

Conduction block in terminal purkijefibers

The pacemaker of heart

When SA node fails

Ectopic pacemakers take over

Present in conducting fibers

Atrial ectopic focus

Inherent rate -60 to 80 per minute

AV nodal (junctional) ectopic focus

Inherent rate -40 to 60 per minute

Ventricular ectopic focus

Inherent rate -15 to 40 per minute

Escape beat

Response of ectopic pacemakers to pause in cardiac electrical activity from SA node

Escape beats

Atrial escape beat

Nodal (junctional) escape beat

Ventricular escape beat

Escape rhythm

Atrial escape rhythm

Atrial ectopic focus (60-80 beats/min)

Nodal (junctional) escape rhythm

Junctional ectopic focus (40-60 beats/min)

Ventricular escape rhythm

Ventricular ectopic focus (15-40 beats/min)

Pathologic & irritable pacemakers

Ectopic pacemakers present in conducting system

Ectopic pacemakers in cardiac muscle cells

Pathologic and irritable pacemakers lead to arrhythmias with heart rates over 150 per minute

Premature contractions

A contraction that appears before its expected time from an irritableectopic focus

Also called extrasystole or premature beat

Premature atrial contraction

Premature nodal or junctional contraction

Premature ventricle contraction (PVC)

Irritable ectopic foci

Occasional discharge leads to Premature contractions

Repetitive discharge leads to Paroxysmal tachycardias, flutter or fibrillation

Paroxysmal tachycardia

Heart rate from 150 to 250 per minute

Sudden attack of tachycardia

Tachycardia abolishes by itself

Cause

Pacing from irritable ectopic foci

Re-entry mechanism

Paroxysmal tachycardia

Atrial

Nodal

Ventricular tachycardia -run of PVCs

Flutter

Heart rate from 250 to 350 per minute

Cause

re-entry (circus movement)

Multiple irritable ectopic foci

Fibrillation

Hear rate from 350 to 450 per minute

Cause

re-entry (circus movement)

Multiple irritable ectopic foci

Flutter & Fibrillation

Flutter

Atrial

ventricular

Fibrillation

Atrial

Ventricular

Ventricular fibrillation

A serious emergency

Many areas of ventricles contract simultaneously

Rate on ECG 350-450 per minute

Ventricles can’t pump blood

Leads to death if not treated

Cause

Electric shock

PVC (R on T phenomenon)

Treatment

Electroshock (cardioversion)

Ventricles are thrown into refractoriness

New impulse generates at SA node

Cardiopulmonary resuscitation (CPR)

Re-entry (Circus movements)

Propagation of cardiac impulse continuously within a closed circuit

Prerequisites for re-entry

Long pathway

dilated heart

Low velocity of conduction

Ischemia, conduction blockade, increased ECF K+

Shortened refractory period

Epinephrine, repetitive electric stimulation

Chain reaction mechanism

A mechanism to develop ventricular fibrillation

Simultaneous appearance of refractory and excitable areas

Division of impulses

Establishment of re-entry circuits

Vicious circle of impulse formation & patches of refractory areas

CLINICAL USE OF ECG

Heart rate

Rhythm

Infarction

Hypertrophy

Axis deviation

Electrolyte imbalance

Drug toxicity

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