IVMS-CV-Introduction to EKG Intepretation

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Introduction to EKG Interpretation:

Introduction to EKG Interpretation Marc Imhotep Cray, M.D. Professor of Basic Medical Sciences Companion Study Resource : MicroEKG Manual Video Education: 12 Lead ECG Placement Part I 12 Lead ECG Placement Part II

The Electrocardiogram :

The Electrocardiogram Propagation of Electrical Activity Through the Heart The Cardiac Action Potential Generation of the Cardiac Pacemaker The Electrocardiogram Cardiac Vectors

Electrical Conductivity in the Heart:

Electrical Conductivity in the Heart 3 Within 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 © 1999-2011

Electrical Conductivity in the Heart:

Electrical 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. 4 IVMS © 1999-2011

Specialized Conductive Tissue in the Heart:

Autorhythmicity:

Autorhythmicity 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. 6 IVMS © 1999-2011

Propagation of the Cardiac Action Potential:

Propagation of the Cardiac Action Potential 7 Action 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 © 1999-2011

The Cardiac Action Potential:

The Cardiac Action Potential 8 The 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 © 1999-2011

Cardiac versus Skeletal Muscle AP:

The Phases of the Ventricular AP:

The Phases of the Ventricular AP 10 The rapid depolarization is due to the opening of voltage gated Na + channels. Inactivation of the Na + channels and opening of slow Ca 2+ channels produces the plateau. During the cardiac AP K + conductance falls. Repolarization occurs by a return of the Ca 2+ and K + permeability to resting values. IVMS © 1999-2011

Mechanism of the Pacemaker Potential:

Mechanism of the Pacemaker Potential 11 The rapid depolarization phase of the AP in cardiac pacemaker cells is due to opening of slow Ca 2+ 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 i f (the nature of i f is still under investigation). IVMS © 1999-2011

Cardiac Pacemakers:

Cardiac 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 ectopic beat. The site that generates an ectopic beat is known as an ectopic focus (foci pl.) or ectopic pacemaker. 12 IVMS © 1999-2011

Neural Control of Heart Rate:

Neural Control of Heart Rate 13 Noradrenaline (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 © 1999-2011

Neural Control of Heart Rate:

Neural Control of Heart Rate Agents that alter heart rate are chronotropic . Positive chronotropic agents increase heart rate. Adrenaline and NA act on b -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 Ca 2+ permeability of cardiac cells, hypopolarising them and increasing the pacemaker potential rise . At rest the heart is under week sympathetic tone. 14 IVMS © 1999-2011

Neural Control of Heart Rate:

Neural 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. 15 IVMS © 1999-2011

Resting Autonomic Control of Heart Rate:

Resting Autonomic Control of Heart Rate 16 At rest heart rate is under both sympathetic and parasympathetic tone. Normally the parasympathetic inhibition of rate is larger than the sympathetic stimulation. IVMS © 1999-2011

Some Other Agents.:

Some 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 Ca 2+ (hypercalcaemia) can produce spastic contractions of the heart. Reduced Ca 2+ (hypocalcaemia) concentrations inhibit heart contraction and can trigger ectopic foci. 17 IVMS © 1999-2011

The Electrocardiogram (EKG/ECG):

The Electrocardiogram (EKG/ECG) 18 P wave is due to atrial depolarisation. The QRS complex is due to ventricular depolarisation. T wave is Ventricular repolarisation. U wave is often seen in hypokalaemia. An atrial T wave is occasionally seen in complete heart block IVMS © 1999-2011

EKG Intervals:

Normal EKG Intervals:

Normal 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 1 st degree 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. 20 IVMS © 1999-2011

Extracellular Action Potential:

The Cardiac Vector:

The Cardiac Vector 22 The 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 © 1999-2011

The Cardiac Vector:

EKG Limb Leads:

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Normal EKG recorded on the Bipolar Limb Leads:

Uses of the EKG:

Uses 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. 27 IVMS © 1999-2011

EKG Interpretation:

EKG Interpretation http://www.pana.org/Power%20Point%20Presentations/12-lead%20EKG%20Interpretation.pdf

The Basics :

PQRST waves:

Rate – The Paper:

Rhythm Questions:

Rhythm 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 Bradydysrhythmia 34 IVMS © 1999-2011

Is this sinus rhythm?:

The AV Blocks:

The 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 shape 39 IVMS © 1999-2011

Fill in the table with the correct rhythms:

Filled in the Table:

Filled in the Table 41 Narrow Wide Regular Sinus rhythm Supraventricular tachy (SVT) Re-entrant tachycardia (WPW) Ventricular tachycardia SVT with BBB SVT with aberrancy Irregular Atrial fibrillation (AF) Multifocal Atrial Tachy (MAT) AF with BBB AF with aberrancy Torsade du Pointes IVMS © 1999-2011

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The Axis – Lead I:

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How to find the axis…:

How 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. 50 IVMS © 1999-2011

Axis Practice – What is the axis?:

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Intervals:

QT interval:

Bundle Branch Blocks:

Wide QRS = Bundle Branch Block:

Wide 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) 57 IVMS © 1999-2011

Fascicular Blocks:

Fascicular 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 q3r1 58 IVMS © 1999-2011

Ischemia or Infarction:

Where do you see EKG changes for the following areas of ischemia?:

Anterior Ischemia:

Septal Ischemia:

Anteroseptal:

Inferior Ischemia:

Lateral Ischemia:

Posterior Ischemia:

Posterior 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. 66 IVMS © 1999-2011

Right Ventricular :

Right 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 morphine 67 IVMS © 1999-2011

Which coronary artery?:

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Resources for Further Study:

Resources for Further Study IVMS © 1999-2011 79 Electrocardiogram, 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 cardiologist ECG in 100 steps: Slideshow ECG Lead Placement – A teaching guide "designed for student nurses who know nothing at all about Cardiology" ECGpedia: Course for interpretation of ECG 12-lead ECG library Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG Minnesota ECG Code openECGproject - help develop an open ECG solution EKG Review: Arrhythmias – A guide to reading ECG's written by a college (not medical school) professor