IVMS-CV-Introduction to EKG Intepretation

Introduction to EKG InterpretationMarc Imhotep Cray, M.D.Professor of Basic Medical SciencesCompanion Study Resource :MicroEKG ManualVideo Education:12 Lead ECG Placement Part I12 Lead ECG Placement Part IIThe ElectrocardiogramPropagation of Electrical Activity Through the HeartThe Cardiac Action PotentialGeneration of the Cardiac PacemakerThe ElectrocardiogramCardiac VectorsElectrical Conductivity in the Heart3Within the atria and ventricles myocardial cells are connected by gap junctions.Gap junctions allow the cardiac action potential to propagate from cell to cell through a low resistance pathway.IVMS © 1999-2009Electrical Conductivity in the HeartElectrical activity can pass from cell to cell in the atria and ventricles.The atria and ventricles are electrically isolated by the hearts fibrous skeleton the Annulus fibrosus.The heart has specialized electrically active cells in addition to contractile myocardium.These cells form the Sinatorial (SA) node, Atrioventricular (AV) node, Bundle of His and Purkinje FibresElectrical activity normally originates in the SA node.The AV node forms the only site of electrical connection between the atria and ventricles. 4IVMS © 1999-2009Specialized Conductive Tissue in the Heart5IVMS © 1999-2009AutorhythmicitySome heart cells (SA, AV node and Purkinje) show automaticity, the ability to generate a heart beat.These cells have an intrinsic rhythmicity which generates a pacemaker potential.The heart does not require nerve or hormonal input to beat.The heart transplant patients the nerves are severed but the heart beats on.6IVMS © 1999-2009Propagation of the Cardiac Action Potential7Action potential (AP) starts at SA node.AP conducted through atrial muscle, interatrial band and internodal pathways.The AP is delayed at the AV node before entering the Bundle of His. Conduction through the Bundle of His and Purkinje fibres is extremely rapid.The ventricles depolarise from endo to epicardium and from apex to base.IVMS © 1999-2009The Cardiac Action Potential8The cardiac action potential has several distinct phases.The cardiac action potential is different in the ventricles, atria and conductive tissue.Cells in the specialised electoral pathways of the heart are spontaneously active and show automaticity.These cells do not have a true resting membrane potential.IVMS © 1999-2009Cardiac versusSkeletal Muscle AP9IVMS © 1999-2009The Phases of the Ventricular AP10The rapid depolarization is due to the opening of voltage gated Na+channels.Inactivation of the Na+channels and opening of slow Ca2+channels produces the plateau. During the cardiac AP K+conductance falls. Repolarization occurs by a return of the Ca2+and K+permeability to resting values.IVMS © 1999-2009Mechanism of the Pacemaker Potential11The rapid depolarization phase of the AP in cardiac pacemaker cells is due to opening of slow Ca2+channels.Repolsarisation after the AP is due to opening of K+channels.Spontaneous depolarization is produced by a progressive fall in the K+permeability combined with an inward current if(the nature of ifis still under investigation).IVMS © 1999-2009Cardiac PacemakersThe sinoatrial has the fastest pacemaker potential (~90-100 beats/min) and is the normal pacemakerThe atrioventricular node is the next fastest (~40-60 beats/min) followed by cells in the bundle of His (15-30).The fastest pacemaker normally drives the heart and suppresses other pasemakers (overdrive suppression).A beat generated outside the normal pacemaker is an ectopicbeat.The site that generates an ectopic beat is known as an ectopic focus(foci pl.) or ectopic pacemaker. 12IVMS © 1999-2009Neural Control of Heart Rate13Noradrenaline (NA) from sympathetic nerves and circulating adrenaline, increase the heart rate and enhances conduction of the AP. Acetylcholine (ACh) released from parasympathetic nerves reduces the heart rate and conduction across the AV node. IVMS © 1999-2009Neural Control of Heart RateAgents that alter heart rate are chronotropic.Positive chronotropic agents increase heart rate.Adrenaline and NA act onb-adrenergic receptors on the heart.Isoprenaline (isoproterenol) is b-adrenergic agonist which increases heart rate.Propranolol is a b-adrenergic antagonist that blocks the actions of adrenaline, NA and isoprenaline.Adrenergic stimulation increases the Na+and Ca2+permeability of cardiac cells, hypopolarising them and increasing the pacemaker potential rise. At rest the heart is under week sympathetic tone.14IVMS © 1999-2009Neural Control of Heart RateAgents with negative chronotropic actions slow the heart.Acetylcholine acts on M-cholinergic (muscarinic) receptors on the heart.Methacholine, carbachol (carbamylcholine) and muscarin are pharmacological stimulants of muscarinic receptors.Atropine is a muscarinic antagonist that blocks the actions of ACh and other muscarinic receptor agonistsACh increases K+permeability of cardiac cell hyperpolarising them and reducing the rise in the pacemaker potentialAt rest the heart is under parasympathetic tone which slows the natural rhythm of the heart.15IVMS © 1999-2009Resting Autonomic Control of Heart Rate16At rest heart rate is under both sympathetic and parasympathetic tone.Normally the parasympathetic inhibition of rate is larger than the sympathetic stimulation.IVMS © 1999-2009Some Other Agents.Nifedipine and Verapamil are calcium channel blocking agents that reduce heart rate.Increased extracellular K+(hyperkalaemia): hyperpolarises cardiac myocytes, shortens the AP and slows the heart. Arrhythmia or heart block is often produced with fibrillation at higher levels. Only a 5-10mM rise in extracellular K+can cause death.Excessive extracellular Ca2+(hypercalcaemia) can produce spastic contractions of the heart.Reduced Ca2+(hypocalcaemia) concentrations inhibit heart contraction and can trigger ectopic foci.17IVMS © 1999-2009The Electrocardiogram (EKG/ECG)18Pwave is due to atrial depolarisation. The QRScomplex is due to ventricular depolarisation.Twave is Ventricular repolarisation.U wave is often seen in hypokalaemia. An atrial T wave is occasionally seen in complete heart blockIVMS © 1999-2009EKG Intervals19P-R interval: delay between atial and ventricular depolarisation.QRS: time for ventricular depolarisation.Q-T:Duration of electrical systole.IVMS © 1999-2009Normal EKG IntervalsP-R interval is normally 0.12-0.20 sec, most of this time is delay at the AV node. An increased P-R interval (>0.28 sec) is characteristic of 1stdegree heart block.QRS complex normally lasts less than 0.10 sec. Increased width of the complex is a characteristic of defects in the branch bundles or Purkinje fibres i.e. branch bundle block.Q-T interval varies inversely with heart rate.20IVMS © 1999-2009Extracellular Action Potential21IVMS © 1999-2009The Cardiac Vector22The Heart is a three dimensional object so the mean axis of polarity in the heart exists as a vector.A vector has both an orientation and a magnitude. Both the direction and magnitude of the cardiac vector change during the heart beat.IVMS © 1999-2009The Cardiac Vector23IVMS © 1999-2009EKG Limb Leads24IVMS © 1999-200925IVMS © 1999-2009Normal EKG recorded on the Bipolar Limb Leads26IVMS © 1999-2009Uses of the EKGHeart RateConduction in the heartArrhythmias Direction of the cardiac vectorDamage to the heart muscleProvides NO (direct) information about pumping or mechanical events in the heart.27IVMS © 1999-2009EKG Interpretationhttp://www.pana.org/Power%20Point%20Presentations/12-lead%20EKG%20Interpretation.pdfThe Basics •PQRST•Rate•Rhythm•Axis•Intervals•Ischemia29IVMS © 1999-2009PQRST waves30Name the wavesPTQRName the intervalsPRQTIVMS © 1999-2009PQRST waves31Name the wavesName the intervalsPTSRPRQTIVMS © 1999-2009Rate –The Paper32Measure the rate by the distance between QRS complexes3001501007560Or look at the right upper corner for the rate or look at the monitor for the rateIVMS © 1999-2009Rate –The Paper33What are the time intervals between lines?0.2 sec200 msec0.04 sec40 msecNormal paper speed is 25 mm/secIVMS © 1999-2009Rhythm Questions•Is this sinus rhythm?•Are there P waves present?–If not…Atrial fibrillation•Is this sinus rhythm?–P before every QRS–PR interval the same for every beat–PR less than 0.2 sec (one big box)•Not sinus rhythm…–AV block–Tachydysrhythmia–Bradydysrhythmia34IVMS © 1999-2009Is this sinus rhythm?1.P in front of every QRS?2.PR interval >0.12 and < 0.20 sec?3.P upright in I, II, and III?•Yes to all 3 indicates sinus rhythm35IVMS © 1999-2009The AV Blocks•1stDegree AVB–PR interval fixed–PR interval > 200 msec36IVMS © 1999-2009The AV Blocks•Type 1 Second Degree Block–Wenkebach–Watch for grouped beating–PR lengthens–RR shortens–Dropped beat37IVMS © 1999-2009The AV Blocks•Type 2 Second Degree Block–PR interval fixed–P without QRS –Dropped beat often in a fixed ratio38IVMS © 1999-2009The AV Blocks•Third Degree Block–AV dissociation–Escape beat•AV nodal –rate normal–Narrow complex•Junctional –rate 40-60’s–Narrow complex•Ventricular –rate 30-40’s–Wide complex, bizarre shape39IVMS © 1999-2009Fill in the table with the correct rhythmsNarrowWideRegularIrregular40IVMS © 1999-2009Filled in the Table41NarrowWideRegularSinus rhythmSupraventricular tachy (SVT)Re-entrant tachycardia (WPW)Ventricular tachycardiaSVT with BBBSVT with aberrancyIrregularAtrial fibrillation (AF)Multifocal Atrial Tachy (MAT)AF with BBBAF with aberrancyTorsade du PointesIVMS © 1999-200942The Normal Axis-30°to 90°-30°90°IVMS © 1999-2009The Axis –Lead I430°IVMS © 1999-200944The Axis –Lead II60°IVMS © 1999-200945The Axis –Lead III120°IVMS © 1999-200946The Axis –Lead aVF90°IVMS © 1999-200947The Axis –Lead aVL-30°IVMS © 1999-200948The Axis –Lead aVR-150°IVMS © 1999-2009490°I60°II120°III90°aVF-30°aVL-150°aVRThe AxisIVMS © 1999-2009How to find the axis…•Find the most isoelectric limb lead (R=S)•The mean axis is perpendicular to this lead. •If the QRS is positive then the axis is in that direction.•If the QRS is negative then the axis is away from that lead.50IVMS © 1999-2009Axis Practice –What is the axis?51Most isoelectric lead?Lead aVFPositive or negative?PositiveaVF is 90°The axis is perpendicular to thisand is 0°IVMS © 1999-200952Axis Practice –What is the axis?Most isoelectric lead?Positive or negative?and is -30°Lead IIPositiveII is +60°The axis is perpendicular to thisIVMS © 1999-200953Axis Practice –What is the axis?Positive or negative?Lead aVRNegativeaVR is -150°The axis is perpendicular to thisMost isoelectric lead?and is -60°Intervals54PR intervalNormal range0.12 to 0.20 secQT intervalNormal range<.45 secQT intervalThe normal QT interval will vary with heart rate and a corrected score is the most accurate measure.55QTc = QT ÷preceding RR interval RR intervalIVMS © 1999-2009Bundle Branch Blocks•Left (LBBB)•Right (RBBB)•Left Anterior Fascicular Block (LAFB)•Left Posterior Fascicular Block (LPFB)56IVMS © 1999-2009Wide QRS = Bundle Branch Block•RBBB–Rabbit ears in V1–Tall R in V6 with slurred S–Normal or right axis (90 to 110)•LBBB–V1 –small R and deep, wide S–V6 –Tall, wide, slurred R–Normal or left axis (-30 to -90)57IVMS © 1999-2009Fascicular Blocks•LAFB–Left axis (-30 to -90)–I and aVL = small Q–II, III, aVF = small R and deep S–q1r3•LPFB–Right axis (110 to 180)–I, aVL, V5-6 = no Q, small R, deep S–II, III, aVF = small Q, tall R–q3r158IVMS © 1999-2009Ischemia or Infarction•ST segment = depression Infarction•ST segment = elevation Ischemia59IVMS © 1999-2009Where do you see EKG changes for the following areas of ischemia?•Anterior•Septal•Anteroseptal•Inferior•Lateral•Posterior•Right ventricular60IVMS © 1999-2009Anterior Ischemia•ST segment elevation–V3 and V4•Reciprocal changes (ST depression)–II, III, AVF61IVMS © 1999-2009Septal Ischemia•ST segment elevation–V1 and V262IVMS © 1999-2009Anteroseptal•ST segment elevation–V1 through V4•Reciprocal changes (ST depression)–II, III, AVF63IVMS © 1999-2009Inferior Ischemia•ST segment elevation–II, III, aVF•Reciprocal changes (ST depression)–V1 through V464IVMS © 1999-2009Lateral Ischemia•ST segment elevation–I, aVL, V5 and V6•Often associated with anterior ischemia•Reciprocal changes (ST depression)–II, III, AVF65IVMS © 1999-2009Posterior Ischemia•Easy to miss!•Tall R wave in V1 and V2•ST segment depression in V1 through V4•If you hold the EKG up to a bright light and turn it over you will see the classic ST elevation. 66IVMS © 1999-2009Right Ventricular •ST segment elevation–II, III, aVF•Tall R –II, III, aVF•Reciprocal changes (ST depression)–I and aVL–Check right sided leads•Expect hypotension with nitroglycerine or morphine67IVMS © 1999-2009Which coronary artery?68IVMS © 1999-2009IVMS © 1999-200969High Yield Data and ECG TracingsIVMS © 1999-200970IVMS © 1999-200971IVMS © 1999-200972IVMS © 1999-200973IVMS © 1999-200974IVMS © 1999-200975IVMS © 1999-200976IVMS © 1999-200977IVMS © 1999-200978Resources for Further StudyIVMS © 1999-200979Electrocardiogram, EKG, or ECG–Explanation of what an ECG is, who needs one, what to expect during one, etc. Written by the National Heart Lung and Blood Institute (a division of the NIH)University of Maryland School of Medicine Emergency Medicine Interest Group–Introduction to EKG's as written by a medical student and a cardiologistECG in 100 steps: SlideshowECG Lead Placement–A teaching guide "designed for student nurses who know nothing at all about Cardiology"ECGpedia: Course for interpretation of ECG12-lead ECG librarySimulation tool to demonstrate and study the relation between the electric activity of the heart and the ECGMinnesota ECG CodeopenECGproject -help develop an open ECG solutionEKG Review: Arrhythmias–A guide to reading ECG's written by a college (not medical school) professor