ECG ECG is invented by William Einthoven in 1901ECG is a graphic record of the

electrical activity of heart over time captured and externally recorded by skin electrodes. The spread of impulse through the heart produces weak electrical current through the entire body, which can be detected & amplified by the ECG machine & recorded on calibrated graph paper.

Purpose of ECG To diagnose arrhythmia To study the cardiac functions – rate, rhythm & axis To diagnose cardiac disease condition- MI , injury, ischemia & hypertrophy To detect electrolyte imbalance To evaluate pacemaker function, and response to medications To obtain baseline recording before, during and a medical procedure.

Lead ECGFor standard 12 lead ECG , 10 electrodes are placed in the body[6 on the chest and 4 on the limbs]. The limb electrodes give the first 6 leads:- lead I, II, III, aVR, aVL and aVF. Other 6 electrodes form procordial chest lead V1- V 6

V1 - 4th intercostal space - right margin of sternum V2 - 4th intercostal space - left margin of sternum V3 - linear midpoint between V2 and V4 V4 - 5th intercostal space at the mid clavicular line V5 - horizontally adjacent to V4 at anterior axillary line V6 - horizontally adjacent to V5 at mid-axillary line

LEADSA lead is a record of electrical activity between two electrodes. Each lead records the average current flow at a specific time in a portion of the heart.

Unipolar lead: aVR, aVL, aVF, v1- v6(lead with single positive electrode)Bipolar lead I, II, II( consists of two electrodes of opposite polarity +/-)Leads allow viewing heart’s electrical activity in two different planes. Frontal and horizontal. Also there are three types of leads

6 standard limb leads : record electrical activity in the frontal plane, 3 bipolar leads and 3 unipolar leads. They are formed by 3 electrodes placed on the Rt arm, Lt arm, and Lt leg. The line joining the axes of the 3 electrodes gives EINTHOVEN TRIANGLE, with heart at the centre.

1. LEAD I – records the electrical potential between left arm (+) and Rt arm (-) electrodes[views the lateral surface of left ventricle]

2. LEAD II – records electrical potential between left leg(+) and Rt arm(-) electrodes.[views the inferior surface of the left ventricle]

3. LEAD III – records the electrical potential between left leg(+) and left arm(-) electrodes. [views the inferior surface of the left ventricle]

6 precordial leads: record the electrical activity in the horizontal plane.

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Leads aVR, aVL, and aVF are augmented limb leads. They are derived from the same three electrodes as leads I, II, and III. Lead aVR or "augmented vector right" has the positive electrode (white) on the right arm.

The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm.

Lead aVL or "augmented vector left" has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm.

Lead aVF or "augmented vector foot" has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg.

aVR – views the heart from right shoulder, views the base of the heart.

aVL- views the heart from left shoulder, views the lateral wall of the heart. aVF – views the heart from left foot, oriented to inferior surface left ventricle.

Leads• Wave of depolarization travelling towards a positive electrode causes an upward deflection

on the ECG• Wave of depolarization travelling away from a positive electrode causes a downward

deflection on the ECG• Biphasic Wave

Duration P wave : <0.11sec PR interval: 0.12-0.2sec QRS complex: 0.04- 0.1sec QT interval:o.43sec (women) Segment – strait line between waves Interval – wave plus a segment

1. P-Wave Depolarization of atrial muscle and the spread of electrical impulse throughout the right

and left atria.NORMAL CHARACTERISTICS OF THE P-WAVE

It is small & smoothly rounded. Low voltage (2-3mm in amplitude) Duration : 0.11sec Positive in leads I, II, aVF, and V2 – V6 May be positive, negative, or biphasic in leads III, aVL, and V1.

Abnormal P Waves P – Pulmonale- Tall Peaked, Right atrial enlargement secondary to pulmonary HTN

(COPD) P-Mitrale- Broad notched, LA enlargement secondary to mitral valve disease

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QRS Complex

1st Negative deflection = Q Wave[ septal depolarisation] 1st Positive deflection = R wave Negative deflection after R wave = S wave Positive deflection after R wave = R Prime(R’) Negative deflection after S wave = S Prime

Depolarization of ventricles Since ventricles has larger muscle mass – QRS amplitude is much larger than P wave. Amplitude as high as 25mm Duration with Normal Conduction <o.1 sec. Amplitudes >25mm can mean chamber enlargement as in ventricular hypertrophy

Increased Amplitude LVH

S (V1 or V2) + R (V5 or V6) ≥35mm Largest (R+S) in precordial leads ≥45mm R wave in aVL ≥11mm

Eg:- in HTN, AS, AR, MR or Coarctation of aortaRVH

R/S ratio in V1 or V2 >1

Posterior wall MI, COPD, TS.

T - Wave

Represents the repolarisation of the ventricles Same direction as predominant QRS

NORMAL T waves :- T wave not normally more than 5 mm(in any limb leads) and or 10mm ( in any precordial lead)T wave is normally positive in leads I, II, III, V2 to V6, and negative in lead aVRT wave is +ve in aVL and aVF, but may be negative if QRS complex is <6mm in height and may be positive or negative in leads III & V1.

Abnormalities – usually inversion with BBB, hypertrophy or AMI Negative T waves suggests myocardial infarction. Tall pointed (peaked) T wave – in hyperkalemia Not normally taller than 5mm in any limb lead or 10 mm in any precordial lead 2/3rd height of R wave

PR Interval

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P +PR interval Represents repolarisation of Rt and Lt atria & the spread of impulse through AV node,

Bundle of His, Rt and Lt bundle branches & the purkinjee fibres 0.12 to 0.2 sec is the duration long PR interval is seen in 1st degree AV block, drug toxicity, hypercalcemia,

hypothermia, PR intervals are all the same and always followed by QRS increased vagal stimulation (i.e. IWMI)

Q’s (Pathologic)

Look for presence of pathologic “Q”s Size DOES matter Wider than 0.03 sec (1 small box) >33% height of the “R” wave Any Q (or QS) in V1 + V2 or V3

ST Segment

Time between completion of depolarization and onset of repolarisation Normally isoelectric & gently blends into upslope of T wave Point where ST takes off from QRS= J point Plays important role in diagnosis of ischemic heart disease. Abnormal ST elevation – early depolarisation

- Myocardial infarction if ST elevation is > 1mm(limb leads) and >2 mm in precordial leads

- Ventricular aneurysms- Acute pericarditis- Hyperkalemia, hypothermia- Left ventricular hypertrophy, LBBB

ST segment depression – hyperventilation, myocardial ischemia (depression of >1mm)- RVH, LVH- Drug effect – digitalis cause a depression of ST segment(DIG CLIP)- Hypokalemia

QT Interval Beginning of QRS to end of T Wave Normal variations with HR and gender Abnormalities

o Prolonged – commonly from drugs like Procanamide or Quinidine or electrolyte imbalance

o Increased opportunity for R on T, ventricular re-entry arrhythmias and sudden death

ST Segment Displacement

Elevation

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Early Repolarisation Ischemic Heart Dx Ventricular aneurysm Acute Pericarditis LVH or LBBB Hyperkalemia Hypothermia

Depression

Normal Variants Loose lead Hyperventilation Ischemic Heart Dx RVH, LVH, MVP Drug effect Hypokalemia

E.C.G. -- Reading - 7 steps

1. Calculate heart rate- number of QRS complexes in one minute i.e. - ___________1500______________________

no. of small squares in between two R waves. or ____________300_________________________

no. of large squares in between two R waves.

if rhythm is irregular .count the QRS complexes in a 6 second strip and multiply that with 10.

2. Check the P-P interval and RR interval regularity.3. Determine the QRS duration( n <0.12 sec in duration)4. Determine whether the QRS shape if not consistent, then identify the shapes5. Identify the P wave ; is there a Pwave infront of every QRS, and P wave shape6. Determine atrial rate, atrial rhythm7. Determine if PR interval is consistent, irregular, or regularly irregular8. P:QRS ratio

Determining Axis

Impulse toward electrode = Positive Impulse away from electrode = Negative The more directly toward or away the greater the amplitude either positive or negative

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Axis DeviationLeads I and aVF divides the heart into 4 quadrants. These leads can be used to quickly estimate electrical axis. In leads I and aVF QRS complexis normally positive , if in either the leads it is negative , then axis deviation is present

Normal Axis = 60 Degrees (0-90) Further counter clockwise than 0 = Left Axis Deviation[ -1 to – 900]current flows to left of

normalCauses - it can be normal variant in young & thin individuals

o Due to mechanical shift associated with inspiration or emphysemao RVH, dextrocardia, & left posterior hemiblock

Further clockwise than 90 = Right Axis Deviation[+90 to +1800] current flows to right of normalCauses – it can be normal variant particularly in older individuals & obesity

o Mechanical shift associated with aspiration, high diaphragm caused by pregnancy, ascitis, abdominal tumour

o Left anterior hemiblocko Hyperkalemiao RVH, dextrocardia• > -30 Marked LAD• >-120 Marked RAD

Hallmark of Infarction Transmural –death of the full thickness of myocardial wall in the area supplied by the

affected arteryST Elevation• QRS Dos not return to baseline (J-point)• 2 or more leads looking at the same wall• Acute Event[ change in ECG is acute]T Wave Inversion• Frequently bi-phasic• Same leads as ST elevation• Still in “process of infarcting”

Q Wave• Ceases to depolarize• Essentially electrically inert• Permanent

ECG changes in MIST segment depression of > 1 mm at a point 0.04 sec to the Rt of J point & is seen in 2 or more leads facing the same anatomical area of the heartT wave inversion of ischemia in full thickness of myocardium

Inferior Wall Infarction• Leads II, III and aVF

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• Reciprocal Changes in Anterior Wall• Most common Presentation is Bradycardia• Can be associated with RV InfarctionAnterior Wall Infarction• V2, V3 through V4• Loss of R Wave progression.• Reciprocal Depression in leads of inferior Wall[II, III & aVF]

Lateral wall infarction 1,avL, v5, v6 Reciprocal ST depression V1

Septal infraction V1 & V2 face the septal areaAbsence of normal R wave in V1 & V2 [ resulting QS wave]

Posterior wall MI- changes in the opposite [ ie anterior]wall of the heart can be viewed as reciprocal changesST segment depression & tall T wave in leads V1 through V4

Right ventricular infarctionSuspected when ECG changes suggesting an acute IWMI as observedST elevation of IMM or more in aVr also suggesting of RVISite of origin

Sinus node, atria, AV junction, ventricles Regularity Regular Regular irregularity (e.g., ventricular bigeminy)Irregular irregularity (e.g., atrial fibrillation)Irregular (e.g., multifocal PVCs)

DYSARRYTHMIAS

Ectopic Beats or RhythmsBeats or rhythms that originate in places other than the SA node.The ectopic focus may cause single beats or take over and pace the heart, dictating its entire rhythm.They may or may not be dangerous depending on how they affect the cardiac output Supraventricular: origin is above the ventricle, i.e., SA, atrial muscle, AV or HIS originVentricular: origin is in ventriclePremature atrial complexesPremature junctional complexes: captures the atria (retrograde) and the ventricles (ante grade). The retrograde P wave may appear before, during, or after the QRS complex; if before, the PR interval is usually short.

Sinus arrhythmias Sinus bradycardia : occurs when SA node creates an impulse at a slower than normal rate.

Rate <60 , Rhythm – regular,

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Causes :- low metabolic needs[sleep, athletic training, hypothermia], vagal stimulation, medications[ Ca channel medications,beta blocker, amiodarone], increased ICP, MI[ especially of IWMI]

Treatment : inj atropine 0.5- 1mg iv Sinus tachycardia: SA node creates an impulse @ faster than normal.Rx- calcium channel blockers, beta blockersAtrial dysrrhythmias :

Premature atrial complex : single ECG complex occurs when impulse starts in the atrium before the next normal impulse of SA node. If frequent >6 / min indicate development of more serious dysrhythmias. Causes can be caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety, hypokalemia, hypermetabolic states or atrial ischemia, injury or infraction.ECG- rate depends on underlying rhythm, rhythm is irregular due to early P waves, P waves – premature P waves maybe seen, hidden in QRS or absent. PR interval- early P wave has shorter duration but between 0.12 – 0.2 sec.

Atrial flutter : Regular atrial activity with a "clean" saw-tooth appearance. The atrial rate is usually about 300/min, but may be as slow as 150-200/min or as fast as 400-450/min. electrical cardioversion for unstable patients. If stable diltiazem, beta blockers, and digitalis can be given

Atrial fibrillation: Absent P waves;Presence of fine “fibrillatory” waves which vary in amplitude and morphology;Irregularly irregular ventricular response. Cardioversion indicated acute onset of AF patients < 48hrs onset, for those >48hrs give anticoagulants and then consider for cardioversion

Junctional dysrrythmias - Premature junctional complex: an impulse that starts in AV nodal area before the next

normal sinus impulse reaches the AV node Junctional rhythm: AV node becomes the pacemaker. These are escape rhythms. Rate 40-

60, rhythm regular, Pwave absent, after QRS or before QRS, may be inverted.Rx – same as sinus tachycardia

Atrioventricular nodal reentry tachycardia :impulse is conducted to an area in the AV node that cause the impulse to be rerouted back to the same area over and over again at a very fast rate. Each time it is conducted through this area ,it sis conducted down to the ventricles also cusing faster ventricular rate. Rate- atrial 150- 250, ventricular rate- 75- 250. Rx:- vagal maneuveres = carotid sinus massage, gag reflex, breath holding If these are ineffective give a bolus of adenosine, verapamil. then if no response go for cardioversion. If ‘p’ wave cannot be identified – supraventricular tachycardia

Ventricular Arrhythmias Premature ventricular complexes : an impulse starts in a ventricle and is conducted through the ventricles before the next normal sinus complexes. It can be bigemini, trigemini, or quadrigemini - Rate – depends on underlying rhythm- Rhythm- irregular due to early QRS, creating an R- R interval that is shorter than the

others. P-P interval may be regular- QRS shape & duration- duration 0.12 sec or more, shape is bizarre and abnormal,- Pwave- may be absent, hidden, or infront of QRS or after QRS

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- P:QRS ratio 0;1, 1l1.Rx :lidocaine Ventricular tachycardia: three or more PVCs in a row occuring at a rate exceeding 100 beats/ mt. - Rate ventricular is 100- 200 beats/ mt and atrial rate depends on underlying rhythm- Rhythm usually regular- QRS shape & duration duration is 0. 12 sec or more- P wave difficult to detect- PR interval – very irregular, if P waves are seen- P:QRS – difficult to determine, but QRS one more than P waves Rx of choice cardioversion; pulseless ventricular tachycardia: defibrillation ( immediately)Ventricular fibrillation: rate > 300, extremely irregular. Without patern, no audible heartbeat, palpable pulse, and respiration.- Rate ventricular >300/mt- Rhythm ventricular extremely irregular, without specific pattern- QRS shape & duration- irregular, undulating waves without recognizable QRS

complex- This is always characterized by the absence of an audible heart beat, a palpable pulse

& respirations. If VF is not immediately corrected, cardiac arrest and death are iminent

- Defibrillate the patient, - Eradicate the cause & administer vasoactive & antiaarrythmias drugs alternating with

defibrillationventricular asystole : flat line, CPR and emergency management necessary to keep pt alive . characterized by absent QRS complex, no heart beat, no palpable pulse & no respirationRx- CPR & emergency services- incubation & i/v- transcutaneous pacing- I/V epinephrine bolus administer &repeat at 3-5 min intervals followed by I/V

atropine 1 mg at 3- 5 min intervalPresence of AV dissociation (independent atrial activity) vs. retrograde atrial capture

Conduction abnormalities AV Block

1st Degree AV Block: All the impulses are conducted through the AV node into the ventricles at a rate slower than normal. PR interval > 0.20 sec; all P waves conduct to the ventricles. P: QRS ratio 1:12nd Degree AV Block:

Type I (Wenckebach) : occurs when all except one atrial impulses are conducted to the ventricles. Each take longer time to conduct till one impulse doesnot conduct.Progressive prolongation of PR interval before failure of an atrial impulse to be conducted

to the ventricles. P:QRS ratio 3:2, 4:3, 5:4Rhythm P_P interval is regular if the pt has a NSR, RR not regular,

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Type II (Mobitz): only some of the impulses are conducted to the ventricles. Constant PR interval followed by a sudden failure of a P wave to be conducted to the ventricle. Only some of the atrial impulses are conducted through the AV node into the ventricles.

ECG- P-P interval is regular, PR interval – constant for those Pwave just before QRS complex

Complete (3rd Degree) AV Block: third degree AV block, no atrial impulses are passed to the ventricles. Completely dissociated P wave & QRS complex each forming at its own pacemaker rhythm.

RBBBComplete RBBB has a QRS duration >0.12sTerminal R' wave in lead V1 and V 2 (usually see rSR‘ complex).ST segment depression, T wave inversion.

LBBB"Complete" LBBB" has a QRS duration >0.12sBroad or notched R waves in V5, V6, I.Lt axis deviation may be present.

Causes of dysrhythmias1. Enhanced automaticity : an abnormal condition in which cardiac cells not normally

associated with the property of automaticity begin to depolarise spontaneously. Occurs as a result of administration of epinephrine, atropine sulphate, digitalis toxicity, hypoxia, MI, hypokalemia, hypocalcemia

2. Reentry :is the propagation of an impulse through tissue already activated by that same impulse. Occurs in hyperkalemia, myocardial ischemia, anti-arrhythmic drugs

3. Escape beats : it is when SA node slows down or fails to initiate depolarisation and a lower site spontaneously producing electrical impulse.

4. Conduction disturbances: too rapid or too slow conduction. May occur after trauma, MI, electrolyte disturbances

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ECG

PRESENTATION

Presenter -Rincy Rajan MS. c Nursing I YearModerator - Madam Rachel Andrews Lecturer, CON, AIIMS

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