ecg basics & cardicac physiology

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ECG BASICS ECG BASICS & & PHYSIOLOGY PHYSIOLOGY OF OF HEART HEART SUBHANJAN DAS SUBHANJAN DAS

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Page 1: Ecg basics & cardicac physiology

ECG BASICSECG BASICS&&

PHYSIOLOGYPHYSIOLOGYOFOF

HEARTHEARTSUBHANJAN DASSUBHANJAN DAS

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Heart is a pumping Heart is a pumping organorgan

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How heart keeps How heart keeps pumping?pumping?

1.special structure of cardiac muscle1.special structure of cardiac muscle syncytial naturesyncytial nature both resting membrane potential & both resting membrane potential &

action potential are different form action potential are different form skeletal muscleskeletal muscle

2.auto rhythmicity of heart2.auto rhythmicity of heart

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Action potential of heart Action potential of heart musclemuscle

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Factors affecting action Factors affecting action potentialpotential

1 K+ concentration1 K+ concentration 2 Ca++ concentration2 Ca++ concentration 3Na+ concentration3Na+ concentration 4 temperature4 temperature

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Excitation contraction Excitation contraction couplingcoupling

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Excitation contraction Excitation contraction couplingcoupling

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Duration of contractionDuration of contraction

Atria 0.2secAtria 0.2sec Ventricle 0.3 secVentricle 0.3 sec Normally contraction time is 40% of Normally contraction time is 40% of

cardiac cycle. When heart rate cardiac cycle. When heart rate increases 3 times it is 65% of increases 3 times it is 65% of cardiac cycle.cardiac cycle.

Relaxation decreasesRelaxation decreases Ventricular filling decreasesVentricular filling decreases

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Cardiac cycleCardiac cycle

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Atrial systoleAtrial systole

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IMCIMC

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ejection phaseejection phase

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IMRIMR

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Heart soundsHeart sounds

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Regulation of pumpingRegulation of pumping

1Frank Starling mechanism1Frank Starling mechanism 2 autonomic innervation2 autonomic innervation Within physiological limit heart Within physiological limit heart

pumps all the blood that comes to it pumps all the blood that comes to it without allowing excessive pooling without allowing excessive pooling of blood in the veins of blood in the veins

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Parasympathetic Parasympathetic innervationinnervation

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Effects of autonomic Effects of autonomic stimulationstimulation

Chronotropic effect Chronotropic effect Dromotropic effectDromotropic effect Bathmotropic effectBathmotropic effect Inotropic effectInotropic effect

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Effects of autonomic Effects of autonomic stimulationstimulation

Sympathetic stimulation: HR can go Sympathetic stimulation: HR can go upto 250 bpm in young individual.upto 250 bpm in young individual.

Parasympathetic stimulation: HR Parasympathetic stimulation: HR can go down to zero. Although vagal can go down to zero. Although vagal escape follows.escape follows.

Both Sympathetic and Both Sympathetic and parasympathetic system maintain a parasympathetic system maintain a low level firing at resting condition.low level firing at resting condition.

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Energy considerationsEnergy considerations Source: oxidative respirationSource: oxidative respiration FA- biggest sourceFA- biggest source glucose/ lactate also usedglucose/ lactate also used Energy efficiency max 20-25%, rest Energy efficiency max 20-25%, rest

is converted to heat (HF: 5-10% )is converted to heat (HF: 5-10% ) Expenditure increases when Expenditure increases when ventricles are ventricles are

dialateddialated BP is elevatedBP is elevatedEnergy expenditure is measured by Energy expenditure is measured by

oxygen comsumptionoxygen comsumption

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Special conductive Special conductive systemsystem

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Rate of discharge Rate of discharge

SA node 70-80 bpmSA node 70-80 bpm AVnode 40-60 bpmAVnode 40-60 bpm AV bundle 15-40 bpmAV bundle 15-40 bpm

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Autorhythmicity of SA Autorhythmicity of SA nodenode

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Autorhythmicity of SA Autorhythmicity of SA nodenode

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Autorhythmicity of SA Autorhythmicity of SA nodenode

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Autorhythmicity of SA Autorhythmicity of SA nodenode

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Autorhythmicity of SA Autorhythmicity of SA nodenode

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Special conductive Special conductive systemsystem

Nodal delayNodal delay .09sec AV node.09sec AV node .04 sec penetrating .04 sec penetrating

portionportion Additional .03 sec Additional .03 sec

internodal pathwayinternodal pathway

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Ectopic pacemakerEctopic pacemaker

Heart blockHeart block Stokes Adams syndromeStokes Adams syndrome

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ECGECG

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Heart muscle wraps around heart Heart muscle wraps around heart like a double spiral with a fibrous like a double spiral with a fibrous septa between the spiral layers.septa between the spiral layers.

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Flow of currentFlow of current

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leadsleads

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Other leadsOther leads Chest leads 6 in no.Chest leads 6 in no. + pole connected to chest, -ve to all 3 + pole connected to chest, -ve to all 3

limbslimbs Infrequently 7Infrequently 7th th & 8 & 8thth chest leads & chest leads &

esophageal leads used.esophageal leads used. aVR- Rt +veaVR- Rt +ve aVF- Lt leg +veaVF- Lt leg +ve aVL- Lt arm +veaVL- Lt arm +ve Recording of V1 V2 upside down as it is Recording of V1 V2 upside down as it is

more closer to base rather than apexmore closer to base rather than apex

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Axis of leadsAxis of leads

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Vector Vector

Instantaneous mean vector:Instantaneous mean vector:

At any given instance the total amount At any given instance the total amount of current flowing in the heart is of current flowing in the heart is represented in magnitude and represented in magnitude and direction by the vector. Current direction by the vector. Current flows from DEPOLARISED to flows from DEPOLARISED to POLARISED area i.e. NEGATIVE to POLARISED area i.e. NEGATIVE to POSITIVE POSITIVE

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Vector analysisVector analysis

Closer the angle higher is the Closer the angle higher is the componentcomponent

+ve vector: reading above the +ve vector: reading above the baselinebaseline

- ve vector: reading below the - ve vector: reading below the baselinebaseline

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Mean vectorMean vector

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Axis deviationAxis deviation

1Normal:1Normal:

20degree to left, 100 degree to right20degree to left, 100 degree to right

Lt RtLt Rt

Expiration InspirationExpiration Inspiration

Supine StandingSupine Standing

Fat Tall/ leanFat Tall/ lean

2Hypertrophy / conduction block2Hypertrophy / conduction block

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Left Deviation : Left Deviation : pathologicalpathological

HypertensionHypertension Aortic valve stenosisAortic valve stenosis RegurgitationRegurgitation LBBBLBBB

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LBBB Left Deviation LBBB Left Deviation

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Right DeviationRight Deviation

Pulmonary stenosisPulmonary stenosis Fallots tetralogyFallots tetralogy VSDVSD Pulmonary hypertensionPulmonary hypertension RBBBRBBB

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Right DeviationRight Deviation

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Vector analysis: axis Vector analysis: axis deviationdeviation

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High voltage ECGHigh voltage ECG

Normally peak of R to bottom of S: Normally peak of R to bottom of S: 0.5 to 2 mv0.5 to 2 mv

Abnormally large: summation of all 3 Abnormally large: summation of all 3 leads >4mvleads >4mv

Cause :hypertrophyCause :hypertrophy

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Low voltage ECGLow voltage ECG

1 decreased current production1 decreased current production

low muscle mass: common in old low muscle mass: common in old MI propagation also slowed- MI propagation also slowed- prolongationprolongation

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2 reduced conduction2 reduced conduction A. pericardial effusionA. pericardial effusion B. pulmonary emphysemaB. pulmonary emphysema 3 flow in AP axis3 flow in AP axis

rotation of axisrotation of axis

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Prolonged QRS complexProlonged QRS complex Normal : 0.06- 0.08 secNormal : 0.06- 0.08 sec Hpertrophy or dilatation of ventricles: Hpertrophy or dilatation of ventricles:

conduction prolonged .09- .12secconduction prolonged .09- .12sec

Prolongation in BBB- propagation Prolongation in BBB- propagation through muscle:through muscle:

>.09 sec abnormal>.09 sec abnormal>.12- almost certain to be pathological >.12- almost certain to be pathological

block in ventricular conduction systemblock in ventricular conduction system>.14 – complete block>.14 – complete block

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Bizzare QRS complexBizzare QRS complex

1 scar tissue 1 scar tissue 2 Multiple block2 Multiple block

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Current of injuryCurrent of injury

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Current of injuryCurrent of injury

Injured area: depolarised- emits –Ve Injured area: depolarised- emits –Ve charge.charge.

Injury: mechanical/ infection/ Injury: mechanical/ infection/ ischemiaischemia

As the area remains continuously As the area remains continuously depolarised a current flow in the depolarised a current flow in the ventricle even before QRS starts. This ventricle even before QRS starts. This is Current of injury.is Current of injury.

Axis deviation also presentAxis deviation also present

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Current of injuryCurrent of injury J pointJ point

No current flows when the ventricles No current flows when the ventricles are fully depolarised. So the iso are fully depolarised. So the iso electric point is seen at the end of QRS electric point is seen at the end of QRS complex.this is called J point.complex.this is called J point.

ST segment shiftST segment shift

As the Current of injury is present the As the Current of injury is present the TP segment is shifted. But in common TP segment is shifted. But in common practice it is considered TP is in iso practice it is considered TP is in iso electric line. So this phenomenon is electric line. So this phenomenon is usually termed as ST segment shiftusually termed as ST segment shift

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Current of injuryCurrent of injury

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Current of injuryCurrent of injury

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T WAVE ABNORMALITYT WAVE ABNORMALITY

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Arrhythmias Arrhythmias

1 tachycardia 1 tachycardia

>100bpm, normal but shorter waves>100bpm, normal but shorter waves

Causes:Causes:

Temperature- 10beats/degree F upto Temperature- 10beats/degree F upto 105degree 105degree

Sympathetic stimulationSympathetic stimulation

toxicitytoxicity

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2 bradycardia:2 bradycardia:

<60 bpm<60 bpm

Athletes, carotid sinus syndromeAthletes, carotid sinus syndrome

Due to increased vagal stimulationDue to increased vagal stimulation

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Sinus arrhythmiaSinus arrhythmia

Can result from any circulatory reflex Can result from any circulatory reflex that alters the strength of the that alters the strength of the autonomic signal to SA nodeautonomic signal to SA node

Respiratory type results from spill over Respiratory type results from spill over of signals from the medullary of signals from the medullary respiratory centre to vasomotor centre.respiratory centre to vasomotor centre.

Normal 5% variation in inspiration and Normal 5% variation in inspiration and expiration.expiration.

Deep breathing: 10%Deep breathing: 10%

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Sinoatrial blockSinoatrial block

Block in SA nodeBlock in SA node No P waveNo P wave AV nodal rhythm AV nodal rhythm Normal QRS-TNormal QRS-T Slow Slow

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AV BlocksAV Blocks

Ischemia of AV node/ bundleIschemia of AV node/ bundle Compression of bundle: scar/ Compression of bundle: scar/

calcified portioncalcified portion Inflammation of AV node/ bundleInflammation of AV node/ bundle

myocarditis/ diptheria/ rheumatic myocarditis/ diptheria/ rheumatic feverfever

Extreme vagal stimulation:Extreme vagal stimulation:

carotid sinus syndromecarotid sinus syndrome

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AV blockAV block

A.A. IncompleteIncomplete

1. first degree: prolonged PR 1. first degree: prolonged PR interval (>.20 sec). Conduction is interval (>.20 sec). Conduction is delayed but no actual blockage.delayed but no actual blockage.

May prolong upto .35-.45 secMay prolong upto .35-.45 sec

The measurement of duration The measurement of duration gives estimate of severity.gives estimate of severity.

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2. second degree2. second degree

here also PR prolonged. Some here also PR prolonged. Some beats strong enough to go through beats strong enough to go through block some are not. So for some P block some are not. So for some P wave QRS complex is present wave QRS complex is present whereas for some it is absent. whereas for some it is absent.

2:1/3:2/3:1 rhythms are present 2:1/3:2/3:1 rhythms are present sometimessometimes

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Third degreeThird degree

No impulse propagation to AV nodeNo impulse propagation to AV node Atrioventricular dissociationAtrioventricular dissociation

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Atria 100 bpm ventricle Atria 100 bpm ventricle 40 bpm40 bpm

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Bundle branch blockBundle branch block

A branch of the bundle delays A branch of the bundle delays propagationpropagation

Normal side contracts firstNormal side contracts first Duplication of 1Duplication of 1stst heart sound heart sound Prolonged QRSProlonged QRS More severe when on the left sideMore severe when on the left side

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Arborisation blockArborisation block

Purkinje fibre dysfunction due to Purkinje fibre dysfunction due to chronic myocardial damagechronic myocardial damage

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Other abnormalitiesOther abnormalities

Stokes Adams syndromeStokes Adams syndrome

Borderline ischemia of conductive Borderline ischemia of conductive tissuetissue

Electrical alternansElectrical alternans

tachycardiatachycardia

IschaemiaIschaemia

Myocarditis Myocarditis

Digitalis toxicityDigitalis toxicity

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Premature beatsPremature beats

Extrasystole & compensatory pauseExtrasystole & compensatory pauseo Local areas of ischemiaLocal areas of ischemiao Small calcified plaques at different Small calcified plaques at different

points of heart- irritatingpoints of heart- irritatingo Mechanical stimulation during cardiac Mechanical stimulation during cardiac

catheterisationcatheterisationo Toxic irritation nicotine, caffeine, drugsToxic irritation nicotine, caffeine, drugso Pulse deficite & bigeminal pulsePulse deficite & bigeminal pulse

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AV nodal/ bundle premature contractionAV nodal/ bundle premature contraction

P wave not distinct, atria & ventricles P wave not distinct, atria & ventricles depolarises at the same timedepolarises at the same time

Ventricular premature contractionVentricular premature contraction

prolonged QRS due to volume conductionprolonged QRS due to volume conduction

High voltage as one voltage depolarises High voltage as one voltage depolarises before anotherbefore another

Inverted t waveInverted t wave

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Ventricular fibrillationVentricular fibrillation Contraction of ventricular muscle mass Contraction of ventricular muscle mass

without coordination and at a high ratewithout coordination and at a high rate Some of muscle fibres contract at any Some of muscle fibres contract at any

given time and others relax so heart is given time and others relax so heart is neither in systole nor diastoleneither in systole nor diastole

Caused by reentry, facilitated by:Caused by reentry, facilitated by:

Long pathway – dilated heartLong pathway – dilated heart

Decreaesd conduction speed: high K+, Decreaesd conduction speed: high K+, ischemia, purkinje blockischemia, purkinje block

Low refractory period: repeated stimulant/ Low refractory period: repeated stimulant/ epinephrineepinephrine

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