ECG Made Easy by Dr Bashir Ahmed Dar Associate Professor Medicine Chinkipora Sopore Kashmir

ECG BASICSBy Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associate Professor Medicine Email [email protected]

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

ELECTROGRAPHY MADE EASY

ULTIMATE

AIM TO HELP PATIENTS

ECG machine

Limb and chest leads 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.

Position of limb and 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

Horizontal plane - the six chest leadsLA RA V1 V2 V3 V4 V5 V6 V5 V4 V1 V2 V3 LV RV V6

6.5

Colour codes given by AHA

ECG Paper: Dimensions5 mm 1 mm

Voltage ~Mass

0.1 mV

0.04 sec 0.2 sec

Speed = rate

ECG paper and timing

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.

ECG paper1 Small square = 0.04 second 1 Large square = 0.2 second 5 Large squares = 1 second

2 Large squares = 1 cm

Time

6.1

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.

STANDARDISATION ECG amplitude scale

Normal amplitude 10 mm/mV

Half amplitude 5 mm/mV

Double amplitude 20 mm/mV

ECG WAVES 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.

ECG WAVES

The Normal ECG

Normal Intervals: PR 0.12-0.20s QRS duration than 2 and half small squares with notched p wave or Negative component of biphasic P wave in V1 1 small box in area

Right Atrial EnlargementCriteria P wave height in II >2 and half small squares and are also tall and peaked. or Positive component of biphasic P wave in V1 > 1 small box in area

Slide 15

Atrial fibrillationP

waves thrown into number of small abnormal P waves before each QRS complex The duration of R-R interval varies The amplitude of R-R varies Abnormal P waves dont resemble one another.

Slide 41

Atrial flutter The

P waves thrown into number of abnormal P waves before each QRS complex. But these abnormal P waves almost resemble one another and are more prominent like saw tooth appearance.

Slide 40

Junctional rhythm In

Junctional rhythm the P waves may be absent or inverted.in next slide u can see these inverted P waves.

Slide 43

Paroxysmal atrial tachycardia The

P and T waves you cant make out separately The P and T waves are merged in one The R-R intervals do not vary but remain constant and same. The heart rate being very high around 150 and higher.

Slide 39

NORMAL P-R INTERVAL PR

interval seconds.

time 0.12 seconds to 0.2

That

is three small squares to five small squares.

PR intervalDefinition: the time interval between beginning of P-wave to beginning of QRS complex. Normal PR interval 3-5mm or 3-5 small squares on ECG graph (0.12-0.2 sec) Abnormalities 1. Short PR interval WPW syndrome 2. Long PR interval First degree heart block

Short P-R interval Short

P-R interval seen in WPW syndrome or preexcitation syndrome or LG syndrome P-R interval is less than three small squares. The beginning of R wave slopes gradually up and is slightly widened called Delta wave. There may be S-T changes also like ST depression and T wave inversion.

Slide 17

Lengthening of P-R interval Occurs

in first degree heart block. The P-R interval is more than 5 small squares or > than 0.2 seconds. This you will see in all leads and is same fixed lengthening .

Slide 44

Q WAVESQ

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

Small voltage QRS 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.

LEFT VENTRICULAR HYPERTROPHY

Right ventricular hypertrophy 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.

Dominant or upward R wave in V1 Causes RBBB Chronic

lung disease, PE Posterior MI WPW Type A Dextrocardia Duchenne muscular dystrophy

Right Ventricular Hypertrophy 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

Right ventricular hypertrophy 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.

Right Ventricular Hypertrophy 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).

Right Ventricular Hypertrophy 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).

Right Ventricular HypertrophyA

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.

Although there is no widely accepted criteria for detecting the presence of RVH, any combination of the following EKG features is suggestive of its presence: Tall

Right Ventricular Hypertrophy

R wave in V1

Right

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

Right Ventricular Hypertrophy

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

ECG criteria for RBBB (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.

ECG criteria for RBBB 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.

RBBB & MI 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.

Significance of RBBB RBBB

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

Partial / Incomplete RBBB 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.

In next slide you will see 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.

ECG criteria for LBBB (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

ECG criteria for LBBB 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.

Significance of LBBB 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

Partial / Incomplete 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.

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

NORMAL CONCAVITY OF S-T SEGMENT 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.

AbnormalitiesST 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

Stress test ECG note the ST Depression

Note the arrows pointing ST depression

ST depression & Troponin T positive is NON STEMI

Coving of S-T segment Concavity

lost and convexity appear facing

upwards.

Diagnostic criteria for AMI Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias

Abnormalities of ST- segment

Q waves in myocardial infarction

T-waveNormal 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.

QT- intervalDefinition: 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.

QT Interval - Should be < 1/2 preceding R toR interval -

QT Interval - Should be < 1/2 preceding R toR interval -

QT interval

QT Interval - Should be < 1/2 preceding R toR interval -

QT interval

QT Interval - Should be < 1/2 preceding R toR interval R R

QT interval

QT Interval - Should be < 1/2 preceding R toR interval R R

QT interval

QT Interval - Should be < 1/2 preceding R toR interval R R

QT interval

QT Interval - Should be < 1/2 preceding R toR interval 65 - 90 bpmR R

QT interval

QT Interval - Should be < 1/2 preceding R toR interval 65 - 90 bpmR R

QT interval

Normal QTc = 0.46 sec

Atrioventricular (AV) Heart Block

Classification of AV Heart BlocksDegree 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

AV Blocks First

Degree

Prolonged AV conduction time PR interval > 0.20 seconds

1st Degree AV Block

Prolongation of the PR interval, which is constant All P waves are conducted

1st degree AV Block: Regular Rhythm PRI > .20 seconds or 5 small squares and is CONSTANT Usually does not require treatment

PRI > .20 seconds

First Degree Block

prolonged PR interval

Analyze the Rhythm

AV Blocks Second

Degree

Definition More Ps than QRSs Every QRS caused by a P

Second-Degree AV Block 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

Second Degree Types Type I Wenckebach phenomenon

Type II Fixed or Classical

Type I Second-Degree AV Block: Wenckebach Phenomenon ECG

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

2nd degree AV Block (Mobitz I also called Wenckebach):

Irregular Rhythm PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse) PRI is NOT CONSTANT

PRI = .24 sec

PRI = .36 sec

PRI = .40 sec

QRS is dropped

Pause 4:3 Wenckebach (conduction ratio may not be constant) Pattern Repeats.

Type II Second-Degree AV Block: Mobitz Type II

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

Second Degree AV Block

Mobitz type I or Winckebach Mobitz type II

Type 1 (Wenckebach)Progressive prolongation of the PR interval until a P wave is not conducted.

Type 2

Constant PR interval with unexpected intermittent failure to conduct

Mobitz Type I

MOBITZ TYPE 1

2nd degree AV Block (Mobitz II): Irregular Rhythm QRS complexes may be somewhat wide (greater than .12 seconds) Non-conducted sinus impulses appear at unexpected irregular intervals PRI may be normal or prolonged but is CONSTANT and fixed Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart block (3rd degree block) Its appearance in the setting of an acute MI identifies a high risk patient Cause: anterioseptal MI, Treatment: may require pacemaker in the case of fibrotic conduction system

PRI is CONSTANT

Non-conducted sinus impulses

2:1 block

3:1 block

Analyze the Rhythm

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

Analyze the Rhythm

Mobitz II

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.

Mobitz Type II

Mobitz Type II

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

Advanced Second-Degree AV Block

Two or more consecutive nonconducted sinus P waves

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

3rd Degree (Complete) AV Block

EKG Characteristics:

No relationship between P waves and QRS complexes Relatively constant PP intervals and RR intervals Greater number of P waves than QRS complexes

Complete heart blockP

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.

3rd degree AV Block (Complete Heart Block): Irregular Rhythm QRS complexes may be narrow or broad depending on the level of the block Atria and ventricles beat independent of one another (AV dissociation) QRSs have their own rhythm, P-waves have their own rhythm May be caused by inferior MI and its presence worsens the prognosis Treatment: usually requires pacemaker

QRS intervals

P-wave intervals note how the P-waves sometimes distort QRS complexes or T-waves

Third-Degree (Complete) AV Block

Third-Degree (Complete) AV Block

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 Anterior Fascicular Block

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

LBB LPIF

Lead I

Left Anterior Hemiblock (LAHB):2. Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and III

1.

LASF

2.

Lead III

Lead AVF

Left Posterior Fascicular Block 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)

LBB LPIF

Lead I

Left Posterior Hemiblock (LPHB):2. Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF.

1.

Notes on (LPHB): QRS is normal width unless BBB is present If LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71%

LASF 2. Lead III

Lead AVF

Bifascicular Bundle Branch BlockRBBB 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

Trifascicular Block The

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

Implies

Indications For Implantation of Permanent Pacing in Acquired AV Blocks

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

Cardiac Pacemakers Definition Delivers artificial stimulus to heart Causes depolarization and contraction

Uses Bradyarrhythmias Asystole Tachyarrhythmias (overdrive pacing)

Cardiac Pacemakers 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

Cardiac Pacemakers

Cardiac Pacemakers Demand

Pacemaker Types

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

Cardiac Pacemakers Demand

Pacemaker Types

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

Cardiac Pacemakers 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

Cardiac Pacemakers 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

Implanted Defibrillators

AICD Automated

Implanted CardioDefibrillator

Uses Tachyarrhythmias Malignant

arrhythmias

VT VF

Implanted Defibrillators 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

Implanted Defibrillators 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

ARRTHYMIAS AND ECTOPIC BEATS

Recognizing and Naming Beats & RhythmsAtrial Escape Beatnormal ("sinus") beats

QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal

sinus node doesn't fire leading to a period of asystole (sick sinus syndrome)

p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. It is therefore called an "atrial" beat

Recognizing and Naming Beats & Rhythms

Junctional Escape Beat

QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal

there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. The beat is therefore called a "junctional" or a nodal beat

Recognizing and Naming Beats & RhythmsQRS is wide and much different ("bizarre") looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a ventricular beat

Ventricular Escape Beat

there is no p wave, indicating that the beat did not originate anywhere in the atria actually a "retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles

The Re-Entry Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction TissueFast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery

Tissues with these type of circuits may exist: in microscopic size in the SA node, AV node, or any type of heart tissue in a macroscopic structure such as an accessory pathway in WPW

The Re-Entry Mechanism of Ectopic Beats & Rhythms Premature Beat Impulse Cardiac Repolarizing Tissue Conduction (long refractory period) TissueFast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery

1. An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only

The Re-Entry Mechanism of Ectopic Beats & Rhythms Cardiac Conduction TissueFast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery

3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway

The Re-Entry Mechanism of Ectopic Beats & Rhythms Cardiac Conduction TissueFast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery

4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation re-enters the pathway and continues in a circular movement. This creates the re-entry circuit

Recognizing and Naming Beats & RhythmsPremature Ventricular Contractions (PVCs, VPBs, extrasystoles): A ventricular ectopic focus discharges causing an early beat Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre" QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant) In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion PVCs are sometimes described by lay people as skipped heart beats

R on T phenom em on

M u lt if o c a l P V C 's

C o m p e n s a to ry p a u s e a fte r th e o c c u ra n c e o f a P V C

Recognizing and Naming Beats & Rhythms Characteristics of PVC's PVCs dont have P-waves unless they are retrograde (may be buried in T-Wave) T-waves for PVCs are usually large and opposite in polarity to terminal QRS Wide (> .16 sec) notched PVCs may indicate a dilated hypokinetic left ventricle Every other beat being a PVC (bigeminy) may indicate coronary artery disease Some PVCs come between 2 normal sinus beats and are called interpolated PVCs

The classic PVC note the compensatory pause

Interpolated PVC note the sinus rhythm is undisturbed

Recognizing and Naming Beats & Rhythms PVC's are Dangerous When: They are frequent (> 30% of complexes) or are increasing in frequency The come close to or on top of a preceding T-wave (R on T) Three or more PVC's in a row (run of V-tach) Any PVC in the setting of an acute MI PVC's come from different foci ("multifocal" or "multiformed")These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:

Ventricular Tachycardia Ventricular FibrillationR on T phenomenon

The sooner defibrillation takes place, the increased likelihood of survival

time

sinus beats

V-tach

Unconverted V-tach r V-fib

Recognizing and Naming Beats & Rhythms Notes on V-tach: Causes of V-tach Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause) Typical V-tach patient MI with complications & extensive necrosis, EF .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)

Most Important Questions of Arrhythmias 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?

QRS AxisCheck Leads: 1 and AVF

Interpreting Axis Deviation: 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.

NW Axis (No Mans Land)Both

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

Determining Regions of CAD: ST-changes in leadsRCA: LCA: LAD:

Inferior myocardium Lateral myocardium

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

Anterior/Septal myocardium V1-V4

Regions of the Myocardium:Lateral I, AVL, V5-V6 Inferior II, III, aVF Anterior / Septal V1-V4

Sinus Arrhythmia

Sinus Arrest/Pause

Sinoatrial Exit Block

Premature Atrial Complexes (PACs)

Wandering Atrial Pacemaker (WAP)

Supraventricular Tachycardia (SVT)

Wolff-Parkinson-White Syndrome (WPW)

Atrial Flutter

Atrial Fibrillation (A-fib)

Premature Junctional Complexes (PJC)

Junctional Rhythm

Junctional Rhythm

Accelerated Junctional Rhythm

Junctional Tachycardia

Premature Ventricular Complexes (PVC's)

Note Complexes not Contractions

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

Uniformed PVCs

R on T Phenomena

Multiformed PVCs

PVC Couplets

PVC Salvos and Runs

Bigeminy PVCs

Trigeminy PVCs

Quadrageminy PVCs

Ventricular Escape Beats

Idioventricular Rhythm

Ventricular Tachycardia (VT) 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

Ventricular Tachycardia (VT)

V Tach

Torsades de Pointes (TdeP) 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

Torsades de Pointes (TdeP)

Ventricular Fibrillation (VF) Rate:

CNO as no discernible complexes rapid and chaotic

Rhythm: P

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

PR

QRS

Ventricular Fibrillation (VF)

Ventricular Fibrillation (VF)

Asystole (Cardiac Standstill) Rate:

none none

Rhythm: P

waves: none interval: not measurable duration: absent

PR

QRS

Asystole (Cardiac Standstill)

AsystoleThe Mother of all Bradycardias

Atrial Pacemaker (Single Chamber)

pacemaker

Capture?

Ventricular Pacemaker (Single Chamber)

pacemaker

Dual Paced Rhythm

pacemaker

Pulseless Electrical Activity (PEA) 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 + = 0/0 mmHg

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

MYOCARDIAL INFARACTION

Diagnosing a MITo 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

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

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

Anterior Myocardial InfarctionIf 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.

Putting it all TogetherDo you think this person is having a myocardial infarction. If so, where?

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

Putting it all TogetherNow, where do you think this person is having a myocardial infarction?

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

Putting it all TogetherHow about now?

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

I II III

aVR aVL aVF

V1 V2 V3

V4 V5 V6

The ST segment should start isoelectric except in V1 and V2 where it may be elevated

Characteristic changes in AMI

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

ST elevation hyperacute phaseR ST P

Occurs in the early stages Occurs in the leads facing the infarction Slight ST elevation may be normal in V1 or V2

Q

Deep Q wave Only diagnostic change of myocardial infarctionST P T Q

R

At least 0.04 seconds in duration Depth of more than 25% of ensuing R wave

T wave changes Late changeR P ST

Occurs as ST elevation is returning to normal Apparent in many leadsT

Q

Bundle branch blockAnterior wall MII II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left bundle branch blockI II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Sequence of changes in evolving AMIR T P QS P Q T Q R ST P R ST

1 minute after onset

1 hour or so after onset

A few hours after onset

R P ST P T Q Q ST P T Q T

A day or so after onset

Later changes

A few months after AMI

Anterior infarctionAnterior infarctionI II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary artery

Inferior infarctionInferior infarctionI II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

Lateral infarctionLateral infarctionI II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflex coronary artery

Diagnostic criteria for AMI Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias

Surfaces of the Left Ventricle

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

Inferior Surface

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

Inferior Leads II III aVF

Anterior Surface

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

Anterior Leads V2 V3 V4

Lateral Surface

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

Lateral Leads V5, V6, I, aVL

Posterior Surface

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

ST Segment ElevationThe 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

ST-Segment Elevation

T wave inversion in an evolving MI

The ECG in ST Elevation MI

The Hyper-acute PhaseLess 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

The Fully Evolved Phase24 - 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)

The Chronic Stabilised Phase Isoelectric

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

Reciprocal Changes Changes

occurring on the opposite side of the myocardium that is infarcting

Reciprocal Changes ie S-T depression in some leads in MI

Non ST Elevation MI 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

Changes in NSTEMI

+ + + +

_ _ + + + + + _ + + _ _ + + + + + _ _ _ _ _ _

_ _ _ _ _

K

+

_ _ _ + + + + + _ + + _ + + + + + _ _ _ _ _ _ + + + + + _ _ + _ + + + + + + _ _ _ _ _ _ _ _ _ + + + +

_ _ _ _ _

K

+

+ + +

+ + _ + __ + +

+ + + + _ _ _ _ _ _ _ _ _

Action potentials and electrophysiologyRestingNa+

DepolarisedCa++

Ca Na+ in

++ in(slow)

K

+ out

Plateau

Repolarised

3.2

LVH and strain patternVentricular 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)

Channer, K. et al. BMJ 2002;324:1023-1026Copyright 2002 BMJ Publishing Group Ltd.

Examples of T wave abnormalities

Copyright 2002 BMJ Publishing Group Ltd.

Channer, K. et al. BMJ 2002;324:1023-1026

Sick Sinus SyndromeSinoatrial block (note the pause is twice the P-P interval)

Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat

Severe sinus bradycardia

Bundle Branch Block

Left Bundle Branch Block 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).

Right Bundle Branch Block

Wheres the MI?

Wheres the MI?

Wheres the MI?

Final one

Which one is more tachycardic during this exercise test?

Any Questions?

I hope you have found this session useful.