18323168 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 gynaeDr Bashir associate professor MedicineDr Udaman neurologistDr Patnaik HOD orthoDr Tin swe aye paeds

From RT to LtProfessor Dr Datuk rajagopal NDr Bashir associate professor medicineDr Urala HOD gynaeDr Nagi reddy tamma HOD-opthomologyDr Setharamarao Prof ortho

ELECTROGRAPHY MADE EASY

ULTIMATE AIM TO HELP PATIENTS

ECG machine

Limb and chest leadsWhen 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 chestSo in reality we see only 10 chest leads.

Position of limb and chest leads

Four limb leads

Six chest leadsV1- 4th intercostal space to the right of sternumV2- 4th intercostal space to the left of sternumV3- halfway between V2 and V4V4- 5th intercostal space in the left mid-clavicular lineV5- 5th intercostal space in the left anterior axillary lineV6- 5th intercostal space in the left mid axillary line

Horizontal plane - the six chest leads6.5

Colour codes given by AHA

ECG Paper: Dimensions5 mm1 mm0.1 mV0.04 sec0.2 secSpeed = rateVoltage ~Mass

ECG paper and timingECG paper speed =25mm/secVoltage calibration 1 mV = 1cm

ECG paper - standard calibrationseach small square = 1mmeach large square = 5mm

Timings1 small square = 0.04sec1 large square = 0.2sec25 small squares = 1sec5 large squares = 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 paper5 Large squares = 1 secondTime1 Large square = 0.2 second1 Small square = 0.04 second2 Large squares = 1 cm6.1

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 scaleNormal amplitude10 mm/mVHalf amplitude5 mm/mVDouble amplitude20 mm/mV

ECG WAVESYou 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 ECGNormal Intervals:PR 0.12-0.20sQRS duration

Simplified normal Position of leads on ECG graphLead 1# upward PQRS Lead 2# upward PQRS Lead 3# upward PQRSLead AVR#downward or negative PQRSLead AVL# upward PQRSLead AVF# upwards PQRS

Simplified normal Position of leads on ECG graphChest lead V1# negative or downward PQRSChest leads V2-V3-V4-V5-V6 all are upright from base line .The R wave slowly increasing in height from V1 to V6.So in normal ECG you see only AVR and V1 as negative or downward defelections as shown in next slide.

Normal ECG

Slide 13

P-waveNormal P wave length from beginning of P wave to end of P wave is 2 and a half small square.Height of P wave from base line or isoelectric line is also 2 and a half small square.

P-waveNormal valuesup in all leads except AVR.Duration. < 2.5 mm.Amplitude. < 2.5 mm.

Abnormalities1. Inverted P-waveJunctional rhythm.2. Wide P-wave (P- mitrale)LAE3. Peaked P-wave (P-pulmonale)RAE4. Saw-tooth appearanceAtrial flutter5. Absent normal P waveAtrial fibrillation

P wave height 2 and half small squares ,width also 2 and half small square

Shape of P waveThe upward limb and downward limbs of P wave are equal.Summit or apex of P wave is slightly rounded.

P pulmonale & P mitraleP pulmonale-Summit or apex of P wave becomes arrow like pointed or pyramid shape,the height also becomes more than two small squares from base line.P waves best seen in lead 2 and V1.

P pulmonale & P mitraleP mitrale- the apex or summit of p wave may become notched .the notch should be at least more than one small square.Duration of P becomes more than two and a half small squares.

Left Atrial EnlargementCriteria

P wave duration in II >than 2 and half small squares with notched p waveorNegative 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

Atrial fibrillationP waves thrown into number of small abnormal P waves before each QRS complexThe duration of R-R interval variesThe amplitude of R-R variesAbnormal P waves dont resemble one another.

Atrial flutterThe 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.

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

Paroxysmal atrial tachycardiaThe 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.

NORMAL P-R INTERVAL

PR intervaltime 0.12 seconds to 0.2 seconds.

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 syndrome2. Long PR interval First degree heart block

Short P-R intervalShort P-R interval seen in WPW syndrome or pre- excitation syndrome or LG syndromeP-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.

Lengthening of P-R intervalOccurs 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 .

Q WAVESQ waves

Normal Q wave

Abnormal Q wavesThe duration or width of Q waves becomes more than one small square on ECG graph.The depth of Q wave becomes more than 25% of R wave.The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy.

Q wave in MI

Q wave in septal hypertrophy

QRS COMPLEXQRS duration8 mm some say >10 mm chest leads (in at least one of chest leads).

QRS complexNormal valuesDuration: < 2.5 mm.Morphology: progression from Short R and deep S (r/s) in V1 to tall R and short S in V6 with small Q in V5-6.Abnormalities:1. Wide QRS complex Bundle branch block.Ventricular rhythm.

2. Tall R in V1RVH.RBBB.Posterior MI.WPW syndrome. 3. abnormal Q wave [ > 25% of R wave]MI.Hypertrophic cardiomyopathy.Normal variant.

Small voltage QRSDefined as < 5 mm peak-to-peak in all limb leads or

Normal upward progression of R wave from V1 to V6V1V2V3V4V5V6The R wave in the precordial leads must grow from V1 to at least V4

J pointThe term J point means Junctional point at the end of S wave between S wave and beginning of S-T segment.

J pointQSST

L V H-Voltage CriteriaIn adult with normal chest wallSV1+RV5 >35 mmorSV1 >20 mmor 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 hypertrophyNormally 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

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

Right Ventricular HypertrophyWILL SHOW ASRight axis deviation (RAD)Precordial leadsIn V1, R wave > S waveIn V6, S wave > R waveUsual manifestation is pulmonary disease orcongenital heart disease

Right Ventricular Hypertrophy

Right ventricular hypertrophyRight 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 HypertrophyOther 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 HypertrophyTrue 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 counter-clockwise rotation of the heart. This can be seen with abnormal chest shape.

Right Ventricular HypertrophyTall R wave in V1Right axis deviationRight atrial enlargementDown sloping ST depressions in V1-V3 ( RV strain pattern)

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:

Right 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 RBBBST/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 & MIIf 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 RBBBRBBB 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 RBBBis 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 seeECG 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 LBBBSo 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 LBBBLBBB 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 patternCannot diagnose the presence of MI with LBBB

Partial / Incomplete LBBBis 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- SEGMENT

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

NORMAL CONCAVITY OF S-T SEGMENTIt 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 squareAcute MI.Prinzmetal angina.Acute pericarditis.Early repolarizationST depression:More than one small squareIschemia.Ventricular strain.BBB.Hypokalemia.Digoxin effect.

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 segmentConcavity lost and convexity appear facing upwards.

Diagnostic criteria for AMIQ wave duration of more than 0.04 secondsQ wave depth of more than 25% of ensuing r waveST elevation in leads facing infarct (or depression in opposite leads)Deep T wave inversion overlying and adjacent to infarctCardiac 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.MyocarditisVentricular strainBBB.Hypokalemia.Digoxin effect.

QT- interval Definition: Time interval between beginning of QRS 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 to R interval -

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

QT Interval- Should be < 1/2 preceding R to R interval -QT interval65 - 90 bpm

QT Interval- Should be < 1/2 preceding R to R interval -QT interval65 - 90 bpmNormal QTc = 0.46 sec

Atrioventricular (AV) Heart Block

Classification of AV Heart Blocks

DegreeAV Conduction Pattern1St Degree BlockUniformly prolonged PR interval2nd Degree, Mobitz Type IProgressive PR interval prolongation2nd Degree, Mobitz Type IISudden conduction failure3rd Degree BlockNo AV conduction

AV BlocksFirst DegreeProlonged AV conduction timePR interval > 0.20 seconds

1st Degree AV BlockProlongation of the PR interval, which is constantAll P waves are conducted

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

First Degree Blockprolonged PR interval

Analyze the Rhythm

AV BlocksSecond DegreeDefinitionMore Ps than QRSsEvery QRS caused by a P

Second-Degree AV Block

There is intermittent failure of the supraventricular impulse to be conducted to the ventricles

Some 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

Second Degree

TypesType IWenckebach phenomenon

Type IIFixed 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

Pattern Repeats.PRI = .24 secPRI = .36 secPRI = .40 secQRS is dropped

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

Pause4:3 Wenckebach (conduction ratio may not be constant)2nd degree AV Block (Mobitz I also called Wenckebach):

Type II Second-Degree AVBlock:Mobitz Type II ECG findings

1.Intermittent or unexpected blocked P waves you dont know when QRS drops2.P-R intervals may be normal or prolonged,but they remain constant4. A long rhythm strip may help

Second Degree AV BlockMobitz type I or WinckebachMobitz type II

Type 1 (Wenckebach)Progressive prolongation of the PR interval until a P wave is not conducted.Constant PR interval with unexpected intermittent failure to conductType 2

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 systemNon-conducted sinus impulses2:1 block3:1 blockPRI is CONSTANT

Analyze the Rhythm

Second Degree Mobitz

CharacteristicsAtrial rate > Ventricular rateQRS usually longer than 0.12 secUsually 4:3 or 3:2 conduction ratio (P:QRS ratio)

Analyze the Rhythm

Mobitz IIDefinition: 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 IISudden appearance of a single, non-conducted sinus P wave...

Advanced Second-Degree AV BlockTwo or more consecutive nonconducted sinus P waves

Complete AV Block

CharacteristicsAtrioventricular dissociationRegular P-P and R-R but without association between the twoAtrial rate > Ventricular rateQRS > 0.12 sec

3rd Degree (Complete) AV BlockEKG Characteristics:No relationship between P waves and QRS complexesRelatively constant PP intervals and RR intervalsGreater 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 prognosisTreatment: usually requires pacemakerQRS intervalsP-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 BlockAV dissociationatria and ventricles beating on their ownno relation between Ps & QRSsAtrial rate is different from ventricularventricular rate: 30-60 bpmRhythm is regular for bothQRS can be narrow or widedepends on site of pacemaker!

Key pointsWenckebachlook for group beating & changing PRMobitz IIlook for reg. atrial rhythm & consistent PR3o blockatrial & 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 IIIS wave in lead III > lead II

QR pattern in lead I and AVL,with small Q waveNo other causes of left axis deviation

Left Anterior Hemiblock (LAHB): Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and IIILPIFLASFLBB1.2.Lead IIILead ILead AVF

Left Posterior Fascicular Block

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

Left Posterior Hemiblock (LPHB): Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF.Notes on (LPHB): QRS is normal width unless BBB is presentIf LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71%LPIFLASFLBB1.2.Lead IIILead ILead AVF

Bifascicular Bundle Branch Block RBBB with either left anterior or left posterior fascicular blockDiagnostic criteria1.Prolongation of the QRS duration to 0.12 second or longer2.RSR pattern in lead V1,with the R being broad and slurred3.Wide,slurred S wave in leads I,V5 and V64.Left axis or right axis deviation

Trifascicular Block

The combination of RBBB, LAFB and long PR interval

Implies that conduction is delayed in the third fascicle

Indications For Implantation of Permanent Pacing in Acquired AV Blocks

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

Cardiac PacemakersDefinitionDelivers artificial stimulus to heartCauses depolarization and contractionUsesBradyarrhythmiasAsystoleTachyarrhythmias (overdrive pacing)

Cardiac PacemakersTypesFixedFires at constant rateCan discharge on T-waveVery rareDemandSenses patients rhythmFires only if no activity sensed after preset interval (escape interval)Transcutaneous vs Transvenous vs Implanted

Cardiac Pacemakers

Cardiac PacemakersDemand Pacemaker TypesVentricularFires ventriclesAtrialFires atriaAtria fire ventriclesRequires intact AV conduction

Cardiac PacemakersDemand Pacemaker TypesAtrial SynchronousSenses atriaFires ventriclesAV SequentialTwo electrodesFires atria/ventricles in sequence

Cardiac PacemakersProblemsFailure to captureNo response to pacemaker artifactBradycardia may resultCause: high thresholdManagementIncrease amps on temporary pacemakerTreat as symptomatic bradycardia

Cardiac PacemakersProblemsFailure to senseSpike follows QRS within escape intervalMay cause R-on-T phenomenonManagementIncrease sensitivityAttempt to override permanent pacer with temporaryBe prepared to manage VF

Implanted DefibrillatorsAICDAutomated Implanted Cardio-DefibrillatorUsesTachyarrhythmiasMalignant arrhythmiasVTVF

Implanted DefibrillatorsProgrammed at insertion to deliver predetermined therapies with a set order and number of therapies including:pacingoverdrive pacingcardioversion with increasing energiesdefibrillation with increasing energiesstandby modeEffect of standby mode on Paramedic treatments

Implanted DefibrillatorsPotential ComplicationsFails to deliver therapies as intendedworst complicationrequires Paramedic interventionDelivers therapies when NOT appropriatebroken or malfunctioning leadparameters for delivery are not specific enoughContinues to deliver shocksparameters for delivery are not specific enough and device senses a resetmay be shut off (not standby mode) with donut-magnet

Sinus Exit BlockDue to abnormal function of SA nodeMI, drugs, hypoxia, vagal toneImpulse blocked from leaving SA nodeusually transientProduces 1 missed cyclecan confuse with sinus pause or arrest

Sinus block

ARRTHYMIAS AND ECTOPIC BEATS

normal ("sinus") beatssinus 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" beatQRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normalAtrial Escape BeatRecognizing and Naming Beats & Rhythms

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 beatJunctional Escape BeatQRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normalRecognizing and Naming Beats & Rhythms

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 ventriclesQRS 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 beatVentricular Escape Beatthere is no p wave, indicating that the beat did not originate anywhere in the atriaRecognizing and Naming Beats & Rhythms

Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryThe Re-Entry Mechanism of Ectopic Beats & RhythmsElectrical ImpulseCardiac Conduction TissueTissues 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

Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryPremature Beat ImpulseCardiac Conduction Tissue1. 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 Repolarizing Tissue (long refractory period)The Re-Entry Mechanism of Ectopic Beats & Rhythms

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 Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueThe Re-Entry Mechanism of Ectopic Beats & Rhythms

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

Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueThe Re-Entry Mechanism of Ectopic Beats & Rhythms

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

Recognizing and Naming Beats & RhythmsCharacteristics 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 PVCsInterpolated PVC note the sinus rhythm is undisturbedThe classic PVC note the compensatory pause

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 FibrillationRecognizing and Naming Beats & Rhythmssinus beatsUnconverted V-tach r V-fib V-tachR on T phenomenontimeThe sooner defibrillation takes place, the increased likelihood of survival

Recognizing and Naming Beats & RhythmsNotes 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

Recognizing and Naming Beats & RhythmsPremature Atrial Contractions (PACs): An ectopic focus in the atria discharges causing an early beat The P-wave of the PAC will not look like a normal sinus P-wave (different morphology) QRS is narrow and normal looking because ventricular depolarization is normal PACs may not activate the myocardium if it is still refractory (non-conducted PACs) PACs may be benign: caused by stress, alcohol, caffeine, and tobacco PACs may also be caused by ischemia, acute MIs, d electrolytes, atrial hypertrophy PACs may also precede PSVTPACNon conducted PACNon conducted PAC distorting a T-wave

Premature Junctional Contractions (PJCs): An ectopic focus in or around the AV junction discharges causing an early beat The beat has no P-wave QRS is narrow and normal looking because ventricular depolarization is normal PJCs are usually benign and require not treatment unless they initiate a more serious rhythmRecognizing and Naming Beats & RhythmsPJC

Recognizing and Naming Beats & RhythmsMultifocal Atrial Tachycardia (MAT): Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles QRS complexes are almost identical to the sinus beats Rate is usually between 100 and 200 beats per minute The rhythm is always IRREGULAR P-waves of different morphologies (shapes) may be seen if the rhythm is slow If the rate < 100 bpm, the rhythm may be referred to as wandering pacemaker Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF Treatments: Ca++ channel blockers, b blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective)Note IRREGULAR rhythm in the tachycardiaNote different P-wave morphologies when the tachycardia begins

Recognizing and Naming Beats & RhythmsParoxysmal (of sudden onset) Supraventricular Tachycardia (PSVT): A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted normally to the ventricles (usually initiated by a PAC) QRS complexes are almost identical to the sinus beats Rate is usually between 150 and 250 beats per minute The rhythm is always REGULAR Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q) Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter May be terminated by carotid massage u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction Treatment: ablation of focus, Adenosine (d AV conduction), Ca++ Channel blockersNote REGULAR rhythm in the tachycardiaRhythm usually begins with PAC

Sinus arrest or exit block

Junctional Premature Beatsingle ectopic beat that originates in the AV node orBundle of His area of the condunction system Retrograde P waves immediately preceding the QRS

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

Junctional Escape Beat

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

Junctional Rhythm

MaligMalignant PVC patternsFrequent PVCs Multiform PVCsRuns of consecutive PVCsR on T phenomenon PVC that falls on a TwavePVC during acute MI

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

Junctional Escape Rhythm

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

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

Why 1500 / X?Paper Speed: 25 mm/ sec60 seconds / minute60 X 25 = 1500 mm / minute

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

OR

Atrial Fibrillation:

Regular IrregularPremature Beats: PVCWidened QRS, not associated with preceding P waveUsually does not disrupt P-wave regularity T wave is inverted after PVCFollowed by compensatory ventricular pause

Notice a Pattern in the PVCs?

Identifying AV Blocks: NameConductionPR-IntR-R Rhythm

Most Important Questions of ArrhythmiasWhat 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 Electrical Axis: (Lead I + / aVF +)Left Axis Deviation:Lead I + / aVF Pregnancy, LV hypertrophy etcRight 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:EmphysemaHyperkalemiaVTach

Determining Regions of CAD: ST-changes in leadsRCA: Inferior myocardiumII, III, aVFLCA: Lateral myocardiumI, aVL, V5, V6LAD: Anterior/Septal myocardiumV1-V4

Regions of the Myocardium:InferiorII, III, aVFLateralI, AVL, V5-V6Anterior / SeptalV1-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

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/minRhythm: regularP waves: absentPR interval: noneQRS duration: > 0.12 sec. often difficult to differentiate between QRS and T waveNote: Monomorphic - same shape and amplitude

Ventricular Tachycardia (VT)

V Tach

Torsades de Pointes (TdeP)Rate: 150-300 beats/minRhythm: regular or irregularP waves: nonePR interval: noneQRS 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 complexesRhythm: rapid and chaoticP waves: nonePR interval: noneQRS duration: noneNote: Fine vs. coarse?

Ventricular Fibrillation (VF)

Asystole (Cardiac Standstill)Rate: none Rhythm: noneP waves: nonePR interval: not measurableQRS duration: absent

Asystole (Cardiac Standstill)

AsystoleThe Mother of all Bradycardias

Atrial Pacemaker (Single Chamber)pacemakerCapture?

Ventricular Pacemaker (Single Chamber)pacemaker

Dual Paced Rhythmpacemaker

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 bigeminyThe 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

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.

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 (V2-V4) and the lateral wall (V5-V6, I, and aVL)!

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

Characteristic changes in AMIST segment elevation over area of damageST depression in leads opposite infarctionPathological Q wavesReduced R wavesInverted T waves

ST elevation hyperacute phaseOccurs in the early stagesOccurs in the leads facing the infarctionSlight ST elevation may be normal in V1 or V2

Deep Q waveOnly diagnostic change of myocardial infarctionAt least 0.04 seconds in durationDepth of more than 25% of ensuing R wave

T wave changesLate changeOccurs as ST elevation is returning to normalApparent in many leads

Bundle branch blockI II IIIaVR aVL aVFV1 V2 V3V4 V5 V6I II IIIaVR aVL aVFV1 V2 V3V4 V5 V6Anterior wall MILeft bundle branch block

Sequence of changes in evolving AMI1 minute after onset1 hour or so after onsetA few hours after onsetA day or so after onsetLater changesA few months after AMIQRPQTSTRPQSTPQTSTRPSTPQTSTRPQT

Anterior infarctionAnterior infarctionLeft coronary artery

Inferior infarctionInferior infarctionRight coronary artery

Lateral infarctionLateral infarctionLeft circumflexcoronary artery

Diagnostic criteria for AMIQ wave duration of more than 0.04 secondsQ wave depth of more than 25% of ensuing r waveST elevation in leads facing infarct (or depression in opposite leads)Deep T wave inversion overlying and adjacent to infarctCardiac arrhythmias

Surfaces of the Left VentricleInferior - underneath

Anterior - front

Lateral - left side

Posterior - back

Inferior SurfaceLeads II, III and avF look UP from below to the inferior surface of the left ventricleMostly perfused by the Right Coronary Artery

Inferior Leads

IIIIIaVF

Anterior SurfaceThe front of the heart viewing the left ventricle and the septumLeads V2, V3 and V4 look towards this surfaceMostly fed by the Left Anterior Descending branch of the Left artery

Anterior Leads

V2V3V4

Lateral SurfaceThe left sided wall of the left ventricleLeads 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 SurfacePosterior wall infarcts are rarePosterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changesBlood supply predominantly from the Right Coronary Artery

Inferior II, III, AVFAntero-SeptalV1,V2, V3,V4Lateral I, AVL, V5, V6Posterior V1, V2, V3RIGHTLEFT

ST Segment Elevation

The ST segment lies above the isoelectric line:

Represents myocardial injuryIt is the hallmark of Myocardial InfarctionThe injured myocardium is slow to repolarise and remains more positively charged than the surrounding areasOther 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 hoursST 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 normalUsually occurs within a few hours of infarctionMay vary in severity from 1mm to tombstone elevation

The Fully Evolved Phase24 - 48 hours from the onset of a myocardial infarctionST segment elevation is less (coming back to baseline).T waves are inverting.Pathological Q waves are developing (>2mm)

The Chronic Stabilised PhaseIsoelectric ST segmentsT waves upright.Pathological Q waves.May take months or weeks.

Reciprocal ChangesChanges 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 MICommonly ST depression and deep T wave inversionHistory of chest pain typical of MIOther autonomic nervous symptoms presentBiochemistry results required to diagnose MIQ-waves may or may not form on the ECG

Changes in NSTEMI

Action potentials and electrophysiology++++____3.2

LVH and strain patternVentricular Strain Strain is often associated with ventricular hypertrophyCharacterized by moderate depression of the ST segment.

Sick Sinus SyndromeSinoatrial block (note the pauseis twice the P-P interval) Sinus arrest with pause of 4.4sbefore generation and conductionof a junctional escape beat Severe sinus bradycardia

Bundle Branch Block

Left Bundle Branch BlockWidened 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?

Final one

Which one is more tachycardic during this exercise test?

Any Questions?

Thanks for paying attention.

I hope you have found this session useful.

*Horizontal plane - the six chest leadsEach of the six chest leads has a fixed position. In order to place the precordial leads correctly the fourth intercostal space needs to be identified. The ribs form convenient horizontal landmarks. In order to count them, feel for the ridge with marks the junction of the manubrium and the body of the sternum. When this has been found, run the finger outwards until it reaches the second costal cartilage, which articulates with the sternum at this level. The space immediately above this is the first intercostal space. The spaces should then be counted downwards, well away from the sternum, as they are more easily felt here. V1 right sternal margin at fourth intercostal spaceV2 left sternal margin at fourth intercostal spaceV3 midway between V2 and V4V4 intersection of left midclavicular line and fifth intercostal spaceV5 intersection of left anterior axillary line with a horizontal line through V4V6 intersection of mid-axillary line with a horizontal line through V4 and V5.V1 and V2 face and lie close to the free wall of the right ventricle, V3 and V4 lie near to the interventricular septum with V4 usually at the cardiac apex, and V5 and V6 face the free wall of the left ventricle but are separated from it by a substantial distance. Together the chest leads observe changes in the anterior and lateral aspects of the heart, giving detailed information about the myocardium of the area they lie over.

ECG paperThe electrocardiogram (ECG) is a recording of the electrical activity of the heart. It records the wave of depolarisation that spreads across the heart. The ECG is recorded from two or more simultaneous points of skin contact (electrodes). When cardiac activation proceeds towards the positive contact, an upward deflection is produced on the ECG. As the activation moves away from the electrode, a downward deflection is seen. The neutral position on the ECG is known as the isoelectric line, and is where the tracing rests when there is no electrical activity in the muscle.There are many types of ECG machine, including 3, 6, and 12 channel machines. The ECG trace is printed out on paper composed of a number of 1 and 5 mm squares. The height of each complex represents the amount of electrical potential involved in each complex and an impulse of 1 mV causes a deflection of 10 mm. Horizontally each millimetre represents 0.04 second and each 5 mm represents 0.2 second.

*Rule 6The normality of QRS complexes recorded from the precordial leads is dependent on both morphological and dimensional criteria.

Diagnostic criteria for AMIMyocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis.Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves.Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.

Rule 7The ST segment should start isoelectric except in V1 and V2 where it may be elevated.Characteristic changes in AMIThe 12-lead ECG is the most useful investigation for confirming the diagnosis of acute myocardial infarction, locating the site of the infarct and monitoring the progress. It is therefore very important to know the changes that occur in this situation.The only diagnostic evidence of a completed myocardial infarction seen on the ECG are those in the QRS complexes. In the early stages changes are also seen in the ST segment and the T wave, and these can be used to assist diagnosis of myocardial infarctions. Shortly after infarction there is an elevation of the ST segment seen over the area of damage, and opposite changes are seen in the opposite leads. Several hours later pathological Q waves begin to form, and tend to persist. Later the R wave becomes reduced in size, or completely lost. Later still, the ST segment returns to normal, and at this point the T wave also decreases, eventually becoming deeply and symmetrically inverted.Although these changes occur sequentially, it is very unlikely they will all be clearly observed by the paramedic or GP. A patient can present at any stage and a progression through the ECG changes will not be seen. It is important to recognise these features as they occur rather than in association with each other. All these changes imply myocardial infarction, and will be discussed in more detail over the next few slides.

ST elevationST segment elevation usually occurs in the early stages of infarction, and may exhibit quite a dramatic change. ST elevation is often upward and concave, although it can appear convex or horizontal. These changes occur in leads facing the infarction. ST elevation is not unique to MIs and therefore is not confirming evidence. Basic requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more adjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more precordial leads for anterior infarction. You should be aware that ST elevation can be seen in leads V1 and V2 normally. However, if there is also elevation in V3 the cause is unlikely to be physiological.

Deep Q waveThe only diagnostic changes of acute myocardial infarction are changes in the QRS complexes and the development of abnormal Q waves. However, this may be a late change and so is not useful for the diagnosis of AMI in the pre-hospital situation. Remember that Q waves of more than 0.04 seconds , or 1 little square, are not generally seen in leads I, II or the precordial leads.

T wave inversionThe T wave is the most unstable feature of the ECG tracing and changes occur very frequently under normal circumstances, limiting their diagnostic value.Subtle changes in T waves are often the earliest signs of myocardial infarction. However, their value is limited for the reason above, but for approximately 20 to 30% of patients presenting with MI, a T wave abnormality is the only ECG sign.The T wave can be lengthened or heightened by coronary insufficiency. T wave inversion is a late change in the ECG and tends to appear as the ST elevation is returning to normal. As the ST segment returns towards the isoelectric line, the T wave also decreases in amplitude and eventually inverts. Bundle branch blockBundle branch block is the pattern produced when either the right bundle or the entire left bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle branch must be depolarised by the spread of a wave of depolarisation through ventricular muscle from the unaffected side. This is obviously a much slower process and usually the QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14 seconds (for left bundle branch block).The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction, but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (less than 0.04 seconds) in V1 to V3 which is not usually seen in anteroseptal infarction. There is also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the opposite direction to the QRS in all the precordial leads. This combination of features is diagnostic. In the rare cases where there may be doubt assume the correct interpretation is LBBB. This will make up no difference to the administration of a thrombolytic on medical direction but for the present will be accepted as a contraindication for paramedics acting autonomously (see later slide).Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in lead I, and a secondary R wave (R) in V1. As abnormal Q waves do not occur with right bundle branch block, this remains a useful sign of infarction.Sequence of changes in evolving AMIThe ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction.Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage.The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction. As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist. The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction.Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist.In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation.

Location of infarction and its relation to the ECG: anterior infarctionAs was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V16) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V26, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V16 , I, and aVL.Location of infarction and its relation to the ECG: inferior infarctionST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node. Location of infarction and its relation to the ECG: lateral infarctionOcclusion of the left circumflex artery may cause lateral infarctions.Lateral infarctions are diagnosed by ST elevation in leads I and aVL.Diagnostic criteria for AMIMyocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis.Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves.Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.

Action potentials and electrophysiologyThe heart is a hollow organ with walls made of specialised cardiac muscle. When excited, these muscles shorten, thicken and squeeze on the hollow cavities, forcing blood to flow in directions permitted by the valves (as described in the last slide).An action potential refers to the voltage changes occurring inside a cell when it is electrically depolarised, due to ionic movements into and out of the cell. Cardiac muscles can be electrically excited and show action potentials that propagate along the surface membrane, carrying excitation to all parts of the muscle. Cardiac muscle cells (cardiomyocytes) are interconnected by gap junctions, allowing action potentials to pass from one cell to the next. This ensures that the heart as a whole participates in each contraction, making the heartbeat an all or none response.The basic ventricular action potential is due to three voltage-dependent currents: sodium, potassium, and calcium. The very rapid rise of the initial spike of an action potential is due to the opening of the sodium channels, allowing sodium ions to rush into the cell from the outside, depolarising the cell further. The sodium channels then inactivate, and calcium channels activate. There is now a small flow of calcium ions flowing into the cell, balancing the small amounts of potassium ions leaking out. This results in the membrane potential being held in a suspended plateau. The potassium channels then open, and the calcium channels close, causing a rush of potassium ions out of the cell and the membrane being rapidly repolarised. The action potential does vary throughout the heart due to the presence of different ion channels. In the cells of the sino-atrial (SA node) and atrioventricular nodes (AV node) calcium channels, rather than sodium channels, are activated by membrane depolarisation, resulting in a different shape of the action potential.A recording of the electrical changes that accompany the cardiac cycle is called an electrocardiogram (ECG). Each cardiac cycle produces three distinct waves, designated P, QRS and T. It should be noted that these waves are not action potentials, they represent any electrical activity within the heart as a whole.

18323168 ecg made easy by dr bashir ahmed dar associate professor medicine chinkipora sopore kashmir

Documents

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height of p wave

normal position of leads

intercostal space

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5mmtimings1 small square

s wave

base line