By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associate Professor Medicine Email drbashir123@gmail.com

From Right to Left Dr.Smitha associate prof gynae Dr Bashir associate professor Medicine Dr Udaman neurologist Dr Patnaik HOD ortho Dr Tin swe aye paeds

From RT to Lt Professor Dr Datuk rajagopal N Dr Bashir associate professor medicine Dr Urala HOD gynae Dr Nagi reddy tamma HODopthomology Dr Setharamarao Prof ortho

ULTIMATE

AIM TO HELP PATIENTS

When

an ECG is taken we put 4 limb leads or electrodes with different colour codes on upper and lower limbs one each at wrists and ankles by applying some jelly for close contact. We also put six chest leads at specific areas over the chest So in reality we see only 10 chest leads.

Four limb leads

Six chest leads V1- 4th intercostal space to the right of sternum V2- 4th intercostal space to the left of sternum V3- halfway between V2 and V4 V4- 5th intercostal space in the left mid-clavicular line V5- 5th intercostal space in the left anterior axillary line V6- 5th intercostal space in the left mid axillary line

ECG paper speed Voltage calibration 1 mV

= 25mm/sec = 1cm

ECG paper - standard calibrations each small square = 1mm each large square = 5mm Timings 1 small square 1 large square 25 small squares 5 large squares = = = = 0.04sec 0.2sec 1sec 1sec

After

applying these leads on different positions then these leads are connected to a connector and then to ECG machine. The speed of machine kept usually 25mm/second.calibration or standardization done while machine is switched on.

The

first step while reading ECG is to look for standardization is properly done. Look for this mark and see that this mark exactly covers two big squares on graph.

Normal amplitude 10 mm/mV

Half amplitude 5 mm/mV

Double amplitude 20 mm/mV

You

will see then base line or isoelectric line that is in line with P-Q interval and beginning of S-T segment. From this line first positive deflection will arise as P wave then other waves as shown in next slide. Small negative deflections Q wave and S wave also arise from this line.

Normal Intervals: PR 0.12-0.20s QRS duration than 0.2 seconds. This you will see in all leads and is same fixed lengthening .

Slide 44

Q

waves 25% of R wave] MI. Hypertrophic cardiomyopathy. Normal variant.

Defined

as < 5 mm peak-to-peak in all limb leads or 35 mm or SV1 >20 mm or RV6 >20 mm

Left ventricular hypertrophy-Voltage Criteria Count

small squares of downward R wave in V1 plus small squares of R wave in V5 . If it comes to more than 35 small squares then it is suggestive of LVH.

Normally

you see R wave is downward deflection in V1.but if you see upward R wave in V1 then it is suggestive of RVH etc.

WILL

SHOW AS Right axis deviation (RAD) Precordial leads In V1, R wave > S wave In V6, S wave > R wave Usual manifestation is pulmonary disease or congenital heart disease

Right

ventricular hypertrophy (RVH) increases the height of the R wave in V1. And R wave in V1 greater than 7 boxes in height, or larger than the S wave, is suspicious for RVH. Other findings are necessary to confirm the ECG diagnosis.

Other

findings in RVH include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordial (V4-V6). The T wave is inverted in V1 (and often in V2).

True

posterior infarction may also cause a tall R wave in V1, but the T wave is usually upright, and there is usually some evidence of inferior infarction (ST-T changes or Qs in II, III, and F).

A

large R wave in V1, when not accompanied by evidence of infarction, nor by evidence of RVH (right axis, inverted T wave in V1), may be benign counterclockwise rotation of the heart. This can be seen with abnormal chest shape.

Tall

R wave in V1

Right

axis deviation Right atrial enlargement Down sloping ST depressions in V1-V3 ( RV strain pattern)

(1)

QRS duration exceeds 0.12 seconds or 2 and half small squares roughly in V1 and may also see it in V2. (2) RSR complex in V1 may extend to V2.

ST/T

must be opposite in direction to the terminal QRS(is secondary to the block and does not mean primary ST/T changes).

It

you meet all above criteria it is then complete right bundle branch block. In incomplete bundle branch block the duration of QRS will be within normal limits.

If

abnormal Q waves are present they will not be masked by the RBBB pattern. This is because there is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can still be seen.

RBBB

is seen in : (1) occasional normal subjects (2) pulmonary embolus (3) coronary artery disease (4) ASD (5) active Carditis (6) RV diastolic overload

is

diagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and a half small squares.

ECG

characteristics of a typical RBBB showing wide QRS complexes with a terminal R wave in lead V1 and slurred S wave in lead V6. Also you see R wave has become upright in V1.QRS duration has also increased making it complete RBBB.

(1)Prolonged

QRS complexes, greater than 0.12 seconds or roughly 2 and half small squares in all leads almost. (2)Wide, notched QRS (M shaped) V5, V6 (3)Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV) (4)In V2, V3 small r wave may be seen due to activation of para septal region

So

look in all leads for QRS duration to make it complete LBBB or incomplete LBBB as u did in RBBB. Look in V5 and V6 for M shaped pattern at summit or apex of R wave. Look for any changes as S-T depression and T wave in inversion if any.

LBBB

is seen in : (1) Always indicative of organic heart disease (2) Found in ischemic heart disease (3) Found in hypertension. MI should not be diagnosed in the presence of LBBB Q waves are masked by LBBB pattern Cannot diagnose the presence of MI with LBBB

is

diagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and half small squares.

it's isoelectric. [i.e. at same level of PR or PQ segment at least in the beginning]

It

then gradually slopes upwards making concavity upwards and not going more than one small square upwards from isoelectric line or one small square below isoelectric line. In MI this concavity may get lost and become convex upwards called coving of S-T segment.

ST elevation: More than one small square1.

ST depression: More than one small square

Acute MI. Prinzmetal angina. Acute pericarditis. Early repolarization

Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect.

Slide 11

Slide 12

Concavity

lost and convexity appear facing

upwards.

Normal values. 1.amplitude: < 10mm in the chest leads. Abnormalities: 1. Peaked T-wave: Hyper-acute MI. Hyperkalemia. Normal variant

. 2. T- inversion:

Ischemia. Myocardial infarction. Myocarditis Ventricular strain BBB. Hypokalemia. Digoxin effect.

Definition: Time interval between beginning ofQRS complex to the end of T wave. Normally: At normal HR: QT 11mm (0.44 sec)

Abnormalities:

Prolonged QT interval: hypocalcemia and congenital long QT syndrome. Short QT interval: hypercalcemia.

Degree 1 Degree BlockSt

AV Conduction Pattern Uniformly prolonged PR interval Progressive PR interval prolongation Sudden conduction failure No AV conduction

2nd Degree, Mobitz Type I 2nd Degree, Mobitz Type II 3rd Degree Block

First

Degree

Prolonged AV conduction time PR interval > 0.20 seconds

prolonged PR interval

Second

Degree

Definition More Ps than QRSs Every QRS caused by a P

There

is intermittent failure of the supraventricular impulse to be conducted to the ventricles of the P waves are not followed by a QRS complex.The conduction ratio (P/QRS ratio) may be set at 2:1,3:1,3:2,4:3,and so forth

Some

Types Type I Wenckebach phenomenon

Type II Fixed or Classical

ECG

findings 1.Progressive lengthening of the PR interval until a P wave is blocked

ECG findings

1.Intermittent or unexpected blocked P waves you dont know when QRS drops 2.P-R intervals may be normal or prolonged,but they remain constant 4. A long rhythm strip may help

Mobitz type I or Winckebach Mobitz type II

Characteristics Atrial rate > Ventricular rate QRS usually longer than 0.12 sec Usually 4:3 or 3:2 conduction ratio (P:QRS ratio)

Definition: Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave will be constant for each QRS . EKG Characteristics:Atrial and ventricular rate is irregular. P Wave: Present in two, three or four to one conduction with the QRS. PR Interval constant for each P wave prior to the QRS. QRS may or may not be within normal limits.

Sudden appearance of a single, nonconducted sinus P wave...

Two or more consecutive nonconducted sinus P waves

Characteristics Atrioventricular dissociation Regular P-P and R-R but without association between the two Atrial rate > Ventricular rate QRS > 0.12 sec

P

waves are not conducted to the ventricles because of block at the AV node. The P waves are indicated below and show no relation to the QRS complexes. They 'probe' every part of the ventricular cycle but are never conducted.

The P wave bears no relation to the

QRS complexes, and the PR intervals are completely variable

30 AV Block

AV dissociation atria and ventricles beating on their own no relation between Ps & QRSs Atrial rate is different from ventricular ventricular rate: 30-60 bpm Rhythm is regular for both QRS can be narrow or wide depends on site of pacemaker!

Key points

Wenckebach look for group beating & changing PR Mobitz II look for reg. atrial rhythm & consistent PR 3o block atrial & ventricular rhythm regular rate is different!!! no consistent PR

Left axis deviation , usually -45 to -90 degrees QRS duration usually lead III S wave in lead III > lead II QR pattern in lead I and AVL,with small Q wave No other causes of left axis deviation

Right

axis deviation QR pattern in inferior leads (II,III,AVF) small q wave RS patter in lead lead I and AVL(small R with deep S)

RBBB with either left anterior or left posterior fascicular block Diagnostic criteria 1.Prolongation of the QRS duration to 0.12 second or longer 2.RSR pattern in lead V1,with the R being broad and slurred 3.Wide,slurred S wave in leads I,V5 and V6 4.Left axis or right axis deviation

The

combination of RBBB, LAFB and long PR interval that conduction is delayed in the third fascicle

Implies

1.Third-degree AV block, Bradycardia with symptoms Asystole e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy) 2.Second-degree AV block with symptomatic bradycardia

Definition Delivers artificial stimulus to heart Causes depolarization and contraction

Uses Bradyarrhythmias Asystole Tachyarrhythmias (overdrive pacing)

Types Fixed

Fires at constant rate Can discharge on T-wave Very rare Senses patients rhythm Fires only if no activity sensed after preset interval (escape interval)

Demand

Transcutaneous vs Transvenous vs Implanted

Demand

Pacemaker Types

Ventricular Fires ventricles AtrialFires atria Atria fire ventricles Requires intact AV conduction

Demand

Pacemaker Types

Atrial Synchronous Senses atria Fires ventricles AV SequentialTwo electrodes Fires atria/ventricles in sequence

Problems Failure to capture No response to pacemaker artifact Bradycardia may result Cause: high threshold Management Increase amps on temporary pacemaker Treat as symptomatic bradycardia

Problems Failure to sense Spike follows QRS within escape interval May cause R-on-T phenomenon Management Increase sensitivity Attempt to override permanent pacer with temporary Be prepared to manage VF

AICD Automated

Implanted CardioDefibrillator

Uses Tachyarrhythmias Malignant

arrhythmias

VT VF

Programmed

at insertion to deliver predetermined therapies with a set order and number of therapies including: pacing overdrive pacing cardioversion with increasing energies defibrillation with increasing energies standby mode

Effect of standby mode on Paramedic treatments

Potential

Complications

Fails to deliver therapies as intendedworst complication requires Paramedic intervention broken or malfunctioning lead parameters for delivery are not specific enough parameters for delivery are not specific enough and device senses a reset may be shut off (not standby mode) with donut-magnet

Delivers therapies when NOT appropriate

Continues to deliver shocks

Sinus Exit Block Due

to abnormal function of SA node MI, drugs, hypoxia, vagal tone Impulse blocked from leaving SA node usually transient Produces 1 missed cycle can confuse with sinus pause or arrest

Sinus block

r

d

d

dQ

ur u r ur d d

Junctional Premature Beat single

or Bundle of His area of the condunction system Retrograde P waves immediately preceding the QRS

ectopic beat that originates in the AV node

Retrograde P waves immediately following the QRS Absent P waves (buried in the QRS)

Rhythm Rate:

40 to 60 beats/minute (atrial and ventricular) Rhythm: regular atrial and ventricular rhythm P wave: usually inverted, may be upright; may precede, follow or be hidden in the QRS complex; may be absent PR interval: not measurable or less than .20 sec.

Rhythm

Frequent

PVCs Multiform PVCs Runs of consecutive PVCs R on T phenomenon PVC that falls on a T wave PVC during acute MI

Uniform

Multiform PVC rhythm patterns Bigeminy PVC occurs every other complex Couplets 2 PVCs in a row Trigeminy Two PVCs for every three complexes

Ventricular tachycardia (VTach)3

or more PVCs in a row at a rate of 120 to 200 bts/min-1 Ventricular fibrillation (VFib) No visible P or QRS complexes. Waves appear as fibrillating waves

Type

of VT known as twisting of the points. Usually seen in those with prolonged QT intervals caused by

Paper

Speed: 25 mm/ sec 60 seconds / minute 60 X 25 = 1500 mm / minute

OR Take

6 sec strip (30 large boxes) Count the P/R waves X 10

Premature

Beats: PVC

Widened QRS, not associated with

preceding P wave Usually does not disrupt P-wave regularity T wave is inverted after PVC Followed by compensatory ventricular pause

Name

Conduction

PR-Int

R-R Rhythm

1:

P=R

> .20

Regular

2:Mobitz P > R I 2:Mobitz P > R II 3: P>R

Progressive Irregular Constant Grossly Irregular Regular Regular(20-40 bpm)

What

is the mechanism?

Problems in impulse formation?

(automaticity or ectopic foci) Problems in impulse conductivity? (block or re-entry) Where

is the origin?

Atria, Junction, Ventricles?

Normal Left

Electrical Axis:

(Lead I + / aVF +)

Axis Deviation:

Lead I + / aVF Pregnancy, LV hypertrophy etc

Right

Axis Deviation:

Lead I - / aVF + Emphysema, RV hypertrophy etc.

Both

I and aVF are Check to see if leads are transposed (- vs +) Indicates: Emphysema Hyperkalemia VTach

RCA: LCA: LAD:

Inferior myocardium Lateral myocardium

II, III, aVF I, aVL, V5, V6

Anterior/Septal myocardium V1-V4

Uniformed/Multiformed Couplets/Salvos/Runs Bigeminy/Trigeminy/Quadrageminy

Rate:

101-250 beats/min regular

Rhythm: P

waves: absent interval: none

PR

QRS

duration: > 0.12 sec. often difficult to differentiate between QRS and T wave Note: Monomorphic - same shape and amplitude

Rate:

150-300 beats/min regular or irregular

Rhythm: P

waves: none interval: none

PR

QRS

duration: > 0.12 sec. gradual alteration in amplitude and direction of the QRS complexes

Rate:

CNO as no discernible complexes rapid and chaotic

Rhythm: P

waves: none interval: none duration: none Note: Fine vs. coarse?

PR

QRS

Rate:

none none

Rhythm: P

waves: none interval: not measurable duration: absent

PR

QRS

The

absence of a detectable pulse and blood

pressure Presence

of electrical activity of the heart as

evidenced by ECG rhythm, but not VF or VT

ventricular bigeminy The

ECG trace below shows ventricular bigeminy, in which every other beat is a ventricular ectopic beat. These beats are premature, wider, and larger than the sinus beats.

ventricular bigeminy

ventricular trigeminy; The

occurrence of more than one type of ventricular ectopic impulse morphology is evidence of multifocal ventricular ectopics. In this example, the ventricular ectopic beats are both wide and premature, but differ considerably in shape

ventricular trigeminy

ventricular trigeminy

To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG.12-Lead ECG

Rhythm Strip

One way to diagnose an acute MI is to look for elevation of the ST segment.

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

If you see changes in leads V1 - V4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

Do you think this person is having a myocardial infarction. If so, where?

Yes, this person is having an acute anterior wall myocardial infarction.

Now, where do you think this person is having a myocardial infarction?

This is an inferior MI. Note the ST elevation in leads II, III and aVF.

How about now?

This persons MI involves both the anterior wall (V2V4) and the lateral wall (V5-V6, I, and aVL)!

ST segment elevation over area of damage ST depression in leads opposite infarction Pathological Q waves Reduced R waves Inverted T waves

Inferior - underneath Anterior - front Lateral - left side Posterior - back

Leads II, III and avF look UP from below to the inferior surface of the left ventricle Mostly perfused by the Right Coronary Artery

II III aVF

The front of the heart viewing the left ventricle and the septum Leads V2, V3 and V4 look towards this surface Mostly fed by the Left Anterior Descending branch of the Left artery

V2 V3 V4

The left sided wall of the left ventricle Leads V5 and V6, I and avL look at this surface Mostly fed by the Circumflex branch of the left artery

Posterior wall infarcts are rare Posterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changes Blood supply predominantly from the Right Coronary Artery

RIGHT

LEFT

Inferior II, III, AVF

Antero-Septal V1,V2, V3,V4

Posterior V1, V2, V3

Lateral I, AVL, V5, V6

The ST segment lies above the isoelectric line: Represents

myocardial injury It is the hallmark of Myocardial Infarction The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas Other causes to be ruled out include pericarditis and ventricular aneurysm

Less than 12 hours

ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction (Quinn, 1996) The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal Usually occurs within a few hours of infarction May vary in severity from 1mm to tombstone elevation

24 - 48 hours from the onset of a myocardial infarction ST segment elevation is less (coming back to baseline). T waves are inverting. Pathological Q waves are developing (>2mm)

Isoelectric

ST segments T waves upright. Pathological Q waves. May take months or weeks.

Changes

occurring on the opposite side of the myocardium that is infarcting

Commonly

ST depression and deep T wave

inversion History of chest pain typical of MI Other autonomic nervous symptoms present Biochemistry results required to diagnose MI Q-waves may or may not form on the ECG

Ventricular Strain Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment.

Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom)

Widened

QRS (> 0.12 sec, or 3 small

squares) Two R waves appear R and R in V5 and V6, and sometimes Lead I, AVL. Have predominately negative QRS in V1, V2, V3 (reciprocal changes).