basic ecg interpretation

Gippsland Basic ECG Package 2006 / 2009 / 2010 / 2014 of 74

GIPPSLAND HEALTH SERVICES CONSORTIUM

BASIC ECG INTERPRETATION

LEARNING PACKAGE http://www.heartfoundationjm.org/p/ServicesAboutHeart.htm

NAME________________________________________

HEALTH SERVICE / DEPARTMENT________________________

Edited by: Michelle Shanahan 2006 Reviewed: September 2006, March 2009, May 2010, July 2014

Approved by the Gippsland Region Nurse Educators Group May 2010 Acknowledgements to Gippsland Health Service Consortium Members for input

GRCE Points 5

http://www.heartfoundationjm.org/p/ServicesAboutHeart.htm


Table of Contents Aim ........................................................................................................................................................... 5 Target Population ..................................................................................................................................... 5 Package Format ....................................................................................................................................... 5 Objectives ................................................................................................................................................. 5 MODULE ONE ......................................................................................................................................... 6

Anatomy and Physiology of the Heart .................................................................................................. 6 Atria ...................................................................................................................................................... 6 Ventricles .............................................................................................................................................. 6 Structure of the Heart Diagram ............................................................................................................. 7 The Layers of the Heart ........................................................................................................................ 8

Endocardium ..................................................................................................................................... 8 Myocardium....................................................................................................................................... 8 Epicardium ........................................................................................................................................ 8

Valves ................................................................................................................................................... 9 Atrioventricular Valves ...................................................................................................................... 9 Valvular Diagrams ........................................................................................................................... 10

Coronary Blood Supply ....................................................................................................................... 11 Cardiac Veins ..................................................................................................................................... 12 Conductive System of the Heart ......................................................................................................... 13 Depolarisation ..................................................................................................................................... 14 Repolarisation ..................................................................................................................................... 14 Pacemakers of the heart .................................................................................................................... 14 Test - Module One .......................................................................................................................... 15

MODULE TWO ....................................................................................................................................... 16 The Electrical Events of the Cardiac Cycle ........................................................................................ 16 The P wave ......................................................................................................................................... 17 QRS Complex ..................................................................................................................................... 17 The T wave ......................................................................................................................................... 17 Intervals .............................................................................................................................................. 18

PR Interval ...................................................................................................................................... 18 QRS Interval.................................................................................................................................... 18 ST segment ..................................................................................................................................... 18

Test- Module Two ............................................................................................................................... 19 Module Three ......................................................................................................................................... 20

Rate Calculation ................................................................................................................................. 20 ECG Paper ......................................................................................................................................... 20

Horizontal plane .............................................................................................................................. 20 Vertical plane .................................................................................................................................. 20

Detecting normal sinus rhythm ........................................................................................................... 21 Lead placement and recording the 12 lead ECG ........................................................................... 21 The limb leads ................................................................................................................................. 21 Standard Leads ............................................................................................................................... 21 Augmented leads ............................................................................................................................ 22 Chest leads ..................................................................................................................................... 22 Placement of chest leads ................................................................................................................ 22

Grouping Of Leads ............................................................................................................................. 24 Leads are grouped together and reflect a particular wall of the heart. ........................................... 24

Recording an ECG.............................................................................................................................. 25 Test – Module Three .......................................................................................................................... 26

Module Four ........................................................................................................................................... 27 The normal 12 Lead ECG ................................................................................................................... 27 Rules for ECG Interpretation .............................................................................................................. 29

3 Checks: ........................................................................................................................................ 29 Interpretation: .................................................................................................................................. 29

Examples of Normal Electrocardiographs .......................................................................................... 30 Test – Module Four ............................................................................................................................ 31

Module Five ............................................................................................................................................ 32 Angina ................................................................................................................................................. 32 ECG Changes ..................................................................................................................................... 32 Symptoms ........................................................................................................................................... 32 An example of an ECG showing ST depression with unstable Angina .............................................. 33 Acute Coronary Syndrome ................................................................................................................. 33 Test – Module Five ............................................................................................................................. 34


Module Six .............................................................................................................................................. 35 Acute Myocardial Infarction ................................................................................................................ 35 Pathophysiology ................................................................................................................................. 35 Symptoms ........................................................................................................................................... 35 ST Segment Infarction (STEMI) ECG Criteria .................................................................................... 35 Anterior Wall Infarction ....................................................................................................................... 37 Inferior wall infarction .......................................................................................................................... 38 Right ventricular (RV) infarction .......................................................................................................... 39 ECG using right sided leads ............................................................................................................... 39 Non ST Elevation AMI (non-STEMI)................................................................................................... 40 Posterior wall infarction ...................................................................................................................... 41 The Mirror Test in reading Posterior Infarction ECG .......................................................................... 42

Application of the Mirror Test .......................................................................................................... 42 Reciprocal ECG Changes .................................................................................................................... 422

Test – Module Six ............................................................................................................................. 433 Module Seven ...................................................................................................................................... 444

Atrio-Ventricular (AV) Blocks ............................................................................................................ 444 Causes of AV blocks include: ........................................................................................................... 444 Types ................................................................................................................................................ 444 First Degree AV Block ...................................................................................................................... 444 Second Degree AV Block ................................................................................................................. 455 Type I Second Degree AV Block ...................................................................................................... 455 Clinical Implications .......................................................................................................................... 455 Type II second degree AV Block ...................................................................................................... 466 ECG Recognition .............................................................................................................................. 466 Treatment ......................................................................................................................................... 466 Third Degree AV Block (Complete Heart Block) .............................................................................. 477

Clinical Implications ...................................................................................................................... 477 Treatment ...................................................................................................................................... 477

Test – Module Seven ........................................................................................................................ 488 Module Eight .......................................................................................................................................... 49

Rhythms Associated with Cardiac Arrest ........................................................................................... 49 Ventricular Tachycardia ...................................................................................................................... 49 ECG Recognition ................................................................................................................................ 49 Clinical Implications ............................................................................................................................ 49 Treatment ........................................................................................................................................... 49

Conscious VT ................................................................................................................................. 49 Unconscious VT .............................................................................................................................. 49

Ventricular Fibrillation ....................................................................................................................... 500 ECG Recognition ............................................................................................................................ 50 Clinical Implications ........................................................................................................................ 50 Treatment ........................................................................................................................................ 50

Defibrillation ........................................................................................................................................ 51 Asystole .............................................................................................................................................. 52

Clinical Implications ........................................................................................................................ 52 ECG Recognition ............................................................................................................................ 52 Treatment ........................................................................................................................................ 52

Pulseless Electrical Activity (PEA) ...................................................................................................... 53 Clinical Implications ........................................................................................................................ 53 Treatment ........................................................................................................................................ 53

Bradydysrhythmias ............................................................................................................................. 54 Treatment ........................................................................................................................................ 54

Test – Module Eight ............................................................................................................................ 56 Module Nine ........................................................................................................................................... 57

Bundle Branch Blocks ........................................................................................................................ 57 Right Bundle Branch Block ................................................................................................................. 58

ECG Criteria for RBBB .................................................................................................................... 58 Left Bundle Branch Block ................................................................................................................... 59

ECG Criteria for LBBB .................................................................................................................... 59 Test – Module Nine ............................................................................................................................ 60

Module Ten ............................................................................................................................................ 61 Atrial Dysrhythmia............................................................................................................................... 61

Premature Atrial Contractions (PAC) .............................................................................................. 61 Clinical Implications ........................................................................................................................ 61

Atrial Flutter ........................................................................................................................................ 62


Clinical Implications ............................................................................................................................ 62 ECG Recognition ................................................................................................................................ 62 Atrial Fibrillation (AF) .......................................................................................................................... 63

Clinical Implications ........................................................................................................................ 63 ECG Recognition ............................................................................................................................ 63

Supra Ventricular Tachycardia (SVT) ................................................................................................. 64 Clinical Implications ........................................................................................................................ 64 ECG Recognition ............................................................................................................................ 64

Premature Ventricular Complexes (PVC) ........................................................................................... 65 Clinical Implications ........................................................................................................................ 65 Ventricular Bigeminy ....................................................................................................................... 65 ECG Recognition ............................................................................................................................ 65

Test – Module 10 ................................................................................................................................ 67 Method of Rhythm Analysis & ECG Interpretation ............................................................................. 69

1. Measurements (usually made in Lead II): ................................................................................... 69 2. Rhythm Analysis ......................................................................................................................... 69 3. Conduction Analysis ................................................................................................................... 69 4. Waveform Description ................................................................................................................. 70 5. ECG Interpretation ...................................................................................................................... 70 6. Comparison with previous ECG .................................................................................................. 70

Where to go now!!!.............................................................................................................................71 References ......................................................................................................................................... 71


Aim

The aim of the package is to enable to learner to develop a basic understanding of normal and abnormal cardiac rhythms, as well as the ECG changes associated with myocardial ischaemia, infarction and cardiac arrests.

Target Population

Any health care professional who is unfamiliar with the concepts used in deciphering ECG’s and wishes to gain a better understanding of basic ECG interpretation.

Package Format

The learning package is presented in self-paced modules. At the conclusion of each module there is a self-test, either in the form of multiple choice questions or ECG’s to interpret. An answer guide is available from your educator to obtain feedback and hence maximize your learning.

Objectives

By the completion of this learning package the learner will have a greater understanding of the anatomy and physiology of the conduction system of the heart. By the completion of this learning package the learner will be able to measure

a heart rate from a rhythm strip PR interval QRS duration

By the completion of this learning package the learner will be able to Recognize and understand basic rhythms Identify additional rhythm events such as PVC’s & PAC’s Identify rhythm events from atria, AV junction and ventricles

By the completion of this learning package the learner will be able to Identify normal conduction pathway Identify that there is a conduction abnormality

By the completion of this learning package the learner will be able to Carefully analyze a 12 lead ECG for abnormalities in the order which they appear:

P waves, QRS complexes, ST segments, T waves and U waves if present.

By the completion of this learning package the learner will be able to Interpret an ECG as normal or abnormal List abnormalities found on the ECG Identify rhythm abnormalities Identify ST – T wave abnormalities Identify ECG changes associated with angina Identify ECG changes associated with Inferior MI Identify ECG changes associated with Anterior MI Identify ECG changes associated with a past MI Identify conduction abnormalities such as bundle branch block


MODULE ONE

ANATOMY AND PHYSIOLOGY OF THE HEART

The heart is a muscular organ which weighs approximately 300 grams and is located within the mediastinum between the lungs. It is made up of four chambers, two atria and two ventricles, which beat independently.

ATRIA

The two upper chambers are the atria. The left and right atria are separated by the intra atrial septum, and should beat simultaneously. The right atria, upon contraction, sends blood to the right ventricle and the left atria sends blood to the left ventricle.

VENTRICLES

The two lower chambers are the ventricles. These are higher pressure chambers than the atria and are separated by thick intraventricular septum. Blood is ejected from the right ventricle and travels to the lungs to be oxygenated and the blood from the left ventricle is transported throughout the body via the aorta. The blood enters the right atrium via the Superior Vena Cava from the top of the body or the Inferior Vena Cava if returning from the lower half of the body. See following page for diagrams of the Structure of the Heart


STRUCTURE OF THE HEART DIAGRAMS www.chelation.co.uk/ gfx/heart.jpg

http://media.wiley.com/assets/8/01/0-7645-5422-0_0901.jpg



THE LAYERS OF THE HEART

ENDOCARDIUM

This is the inner layer of the heart. It is made up of endothelial tissue and covers the valves and chordae tendinae. The endocardium is continuous with the lining of the great vessels of the heart, creating a smooth walled and enclosed circulatory system.

MYOCARDIUM

The myocardium is the middle and thickest layer of the heart. It is made up of cardiac muscle, whose thickness varies from one heart chamber to another. The muscle tissue consists of striated fibre cells, separated by intercalated disks so that electrical impulses can move easily and rapidly from cell to cell. This is referred to as the syncytial nature of cardiac muscle.

http://www.heartfoundationjm.org/v/Deco/ServicesAboutHumanHeartHeartWall.jpg

EPICARDIUM OR PERICARDIUM

The epicardium or pericardium is the outer layer and is a double walled membranous sac. It encloses the heart with the inner wall termed the visceral layer and the outer wall the parietal layer. The visceral and parietal pericardia are separated by a fluid-containing space called the pericardial cavity. The pericardial fluid (10 – 30ml) lubricates the membranes allowing them to slide over one another with a minimum of friction as the heart beats. It also helps prevent displacement of the heart during gravitational acceleration or deceleration and provides a physical barrier against inflammation and infection

Fibrous Pericardium

Serous Pericardium (parietal layer)

Space

Serous pericardium (visceral layer: epicardium)

PERICARDIUM

MYOCARDIUM (muscle layer)

ENDOCARDIUM



VALVES Forward blood flow through the heart is controlled by valves. There are four valves situated in the heart, two atrioventricular and two semilunar valves, all of which open and close passively, in response to where the pressure upon them is generated. For example the valves close when backward pressure from the blood is exerted on them. Conversely they open when they sense a forward pressure gradient. The valves are connected to the heart by chordae tendinae which further connect to muscular extensions of the myocardium called papillary muscles.

ATRIOVENTRICULAR VALVES

1. Tricuspid Valve Three leaflets Lies between the right atrium and the right ventricle

2. Mitral Valve Two leaflets Lies between the left atrium and left ventricle

Semilunar valves

1. Pulmonic Valve

Two leaflets Lies between the right ventricle and the pulmonary artery

2. Aortic Valve Two leaflets Lies between the left ventricle and the aorta

See following page for Valvular Diagrams


VALVULAR DIAGRAMS http://www.heartfoundationjm.org/p/ServicesAboutHeart.htm


http://www.biosbcc.net/b100cardio/images/FG21_06B.jpg

Close-up of the mitral valve

This close-up of the two leaflets of the Mitral Valve shows the chordae tendinae nicely. The chordae are connected to the myocardium of the left ventricle by large muscular bundles called papillary muscle. This chordae/papillary muscle structure helps to maintain valve geometry during ventricular contraction to reduce regurgitation back through the valve. Blood flows out towards the viewer in this picture.





CORONARY BLOOD SUPPLY

CORONARY ARTERIES Due to its high demand for oxygen, the heart has its own blood supply. The right and left coronary arteries originate behind the cusps of the aorta. The right coronary artery (RCA) supplies

the right side of the heart the posterior septum the sino-atrial (SA) node in 60% of people the atrio-ventricular (AV) node in 90% of people

The left coronary artery further divides into the left anterior descending (LAD) and the circumflex branch. The LAD travels down the anterior portion of the left ventricle and the circumflex wraps around the side of the left ventricle and down the posterior portion of the left heart. The LAD supplies

the left ventricle the anterior septum the anterior papillary muscles

The circumflex branch supplies

the lateral and posterior portion of the left heart the sino-atrial (SA) node of 40% of people the atrio-ventricular (AV) node in 10% of people

http://www.cardiologist.uk.com/images/heart.jpg

http://www.cardiologist.uk.com/images/heart.jpg


CORONARY VEINS After passing through an extensive capillary network, blood from the coronary arteries drains into the cardiac veins, which travel alongside the arteries. The three main cardiac veins form a single drainage system which empties the deoxygenated blood into the right atrium at the coronary sinus (just above the tricuspid valve).

http://www.ajronline.org/cgi/content-nw/full/177/6/1447/FIG1

Fig. 1A. — Major epicardial coronary veins. Drawing in frontal projection shows that anterior interventricular (AIV) and obtuse marginal (OMV) veins drain into great cardiac vein (GCV). Oblique vein of Marshall (VM) drains into coronary sinus (CS) at level of venous valve of Vieussens, marking point of transition of coronary sinus and great cardiac vein in mid atrioventricular groove. Posterior interventricular vein (PIV) joins coronary sinus near ostium to right atrium.

Reference for this section McCance K. & Huether, S. (2014) Pathophysiology: The biologic basis for disease in adults and children. (7

th ed.) St Louis:Mosby

http://www.ajronline.org/content/vol177/issue6/images/large/12_AB0364_01A.jpeg



CONDUCTIVE SYSTEM OF THE HEART Before the heart can contract it must be stimulated. The stimulus must be delivered quickly and efficiently to all areas of the myocardium. In order to achieve these two functions the heart relies on firstly Self Excitation and secondly Rapid Conduction via specialized conductive pathways. Automatically, and at regular intervals, an electrical impulse arises in the sino-atrial (SA) node. The impulse travels through pathways in the right and left atrium called internodal pathways until it reaches the atrio-ventricular (AV) node, located between the right atrium and the right ventricle. The impulse is delayed in the AV node momentarily to allow time for the atria to contract. The impulse then travels though the Bundle of His and then down the right and left bundle branches. The impulse then spreads down through the myocardium via the purkinje fibres. Ventricular contraction then occurs.

1. For the impulse to move quickly though the heart muscle it must travel down specialized conductive pathways.

2. If there is a blockage in an area of the conductive system then the impulse will travel through the heart much more slowly.

HTTP://MEDSTAT.MED.UTAH.EDU/KW/ECG/MML/ECG_CCS.GIF

http://medstat.med.utah.edu/kw/ecg/mml/ecg_ccs.gif


DEPOLARISATION The initial spread of the impulse through a muscle is known as depolarisation. The impulse causes ion changes to alter in the cell, allowing extracellular sodium to rush into the cell and potassium to move out. In turn this electrical change results in cellular contraction or systole.

REPOLARISATION

This is when the sodium - potassium pump on the cell membranes realigns the electrolytes, causing the cells to relax and return to their resting state, otherwise known as diastole. On the ECG both depolarisation (systole) and repolarisation (diastole) are distinguishable.

PACEMAKERS OF THE HEART

The primary pacemaker of the heart is the sinoatrial (SA) node. It normally discharges impulses at a rate of 60-100 times per minute, but is capable of producing up to a person’s maximal heart rate, which is calculated at approximately 220 minus the person’s age. Should the SA node fail to fire, the Bundle of His fibres, situated in the atrio-ventricular nodal region can discharge at a rate of 40-60 times per minute. Failing this, the purkinje fibres deep in the bundle branches take over the pacing of the heart, but are only capable of eliciting a heart rate of 15-40 beats per minute. Because the SA node normally discharges at the fastest rate, it is the pacemaker responsible for optimal heart rate control, hence the term ―normal sinus rhythm‖.

Reference for this section

Wagner G (2008). Marriott’s Practical Electrocardiography. (11th ed.) Sydney:Lippincott, Williams & Wilkins


TEST - MODULE ONE

1) The heart comprises a. two atria and two ventricles b. four atria and four ventricles c. two atria and one ventricle d. one atria and two ventricles

2) The middle layer of the heart is a. epicardium b. endocardium c. sub endocardium d. myocardium

3) The mitral valve separates the

a. right atria and ventricle b. left atria and ventricle c. the right and left atria d. the right and left ventricle

4) The left ventricle’s blood is supplied by the a. right coronary artery b. the circumflex artery c. the left anterior descending artery d. the femoral artery

5) The initial spread of electrical impulse through the heart is known as

a. repolarisation b. automaticity c. depolarisation d. diastole


MODULE TWO

THE ELECTRICAL EVENTS OF THE CARDIAC CYCLE Each beat of the heart is represented on the ECG by three main deflections:

P Wave QRS Complex T Wave

http://199.33.141.196/faculty/webpages/stodd/oceanweb/bio2/bio2lectures/Lecture3/img029.jpg

REMEMBER Each of these deflections represents either depolarisation or repolarisation of both the atria and ventricles. Please note that even though the atria do engage in a relaxation period (repolarisation), electrically the impulse this generates is too small to be evidenced on the actual ECG.

I I

II



THE P WAVE

This represents atrial depolarisation and begins as soon as the impulse leaves the sinus node and initiates atrial contraction. The P wave is gently rounded in shape and is usually about 2-3mm in height (2 to 3 little boxes). See next module for explanation of paper speed

QRS COMPLEX

The QRS complex represents ventricular depolarisation and may have various components, depending on which lead of the ECG is recorded.

q wave – the initial negative deflection preceding an r wave r wave – the first positive deflection s wave – the negative deflection following the r wave. The amplitude or height of

the QRS complex should be greater than 5mm and less than 20mm. In order to measure amplitude both negative and positive deflection should be added together.

Duration and width represents the time the impulse takes to pass over the ventricles. This should not exceed 0.12 seconds (or 3 little boxes).

THE T WAVE

The T wave results from the repolarisation or diastole of the ventricles. The T wave should be rounded and symmetrical, with the wave beginning to form from the isoelectric line, i.e. the baseline. Towards the end of the T wave is an area called the vulnerable period. A stimulus generated at this time, either intrinsically or extrinsically, may result in ventricular fibrillation; an abnormal rhythm which left untreated is fatal.

Approximate location of the vulnerable period. (Conover, 1996)


INTERVALS

PR INTERVAL

The distance from beginning of the P wave to the beginning of the QRS complex is referred to as the PR interval. It represents the length of time it takes for the impulse to travel from the atria to the ventricles. The normal PR interval is between 0.12 and 0.20 seconds (3 - 5 little boxes).

QRS INTERVAL

As stated on the previous page this should not exceed 0.12 seconds (3 little boxes)

ST SEGMENT

The ST segment is the interval that occurs between the end of the QRS complex and the beginning of the T wave. It represents the end of depolarisation and the beginning of repolarisation. It should be isoelectric, which means flat on the baseline. Elevation or depression of the ST segment may indicate an abnormality of the myocardial tissue due to injury or ischaemia.

http://www.ce5.com/EKG.gif

Reference for this section

Wagner G (2008). Marriott’s Practical Electrocardiography. (11th ed.) Sydney:Lippincott Williams & Wilkins



TEST- MODULE TWO 1) The P wave represents

a) atrial depolarization b) ventricular depolarisation c) atrial diastole d) ventricular systole

2) Ventricular diastole is represented by the

a) P wave b) T wave c) QRS wave d) R wave

3) The normal PR interval is

a) 0.04 seconds b) 0.12 – 0.20 seconds c) 0.20 – 0.24 seconds d) 0.16 - 0.20 seconds

4) The width of a normal QRS complex should be

a) greater than 0.12 seconds b) less than 0.12 seconds c) equal to 0.20 seconds d) 0.12 – 0.20 seconds

5) The size and height of a normal P wave is a) 3-4 mm in height and gently rounded b) 2-3 mm in height and gently rounded c) 2-3 mm in height and slightly pointed d) 3-4 mm in height and slightly pointed


MODULE THREE

RATE CALCULATION There are several methods for calculating heart rate. However the most reliable method, even in the setting of an irregular rhythm is to calculate the number of cycles in six seconds and multiply that number by ten. 1. Choose a place to start and count 30 large squares (= 6 seconds). 2. Count the number of R waves in that period. 3. Multiply that number by 10 to give you the rate for one minute.

ECG PAPER

HORIZONTAL PLANE

Time is measured on the horizontal plane. Each small square on the ECG paper is equal to 1mm in length and represents 0.04 seconds. The large squares (5 small squares) are therefore 5mm in length and equal 0.20 seconds in time.

Important These horizontal plane measures are accurate only for standardized ECG paper speed which is 25mm/second.

VERTICAL PLANE

Amplitude (height) or voltage is measured on the vertical plane. Each small square on the ECG paper is equivalent to 1mm in height and ten of the small squares (ie.10mm) are equivalent to one millivolt or two large squares. This is standard calibration. 15 Large boxes (in length) are equivalent to a 3 second time strip

http://www.monroecc.edu/depts/pstc/backup/ekggraph.gif



DETECTING NORMAL SINUS RHYTHM The normal cardiac rhythm is called sinus rhythm because it is formed by electrical impulses formed within the SA node. The features of a normal rate and rhythm are Rate 60-100bpm Rhythm Regular Components P wave, followed by QRS complex followed by T wave, with normal

intervals.

LEAD PLACEMENT AND RECORDING THE 12 LEAD ECG

Depolarisation (i.e. ion alterations) of the cardiac cells causes contraction of the heart muscle. These electrical changes set up an electrical field which can be recorded from electrodes which are placed on the body. The 12 lead ECG views these impulses from twelve different angles, despite attaching only 10 leads to the patient. The twelve recording leads are separated into two groups; the limbs leads and the chest leads.

THE LIMB LEADS

These are further divided into: Standard Leads Augmented Leads

STANDARD LEADS

These leads are bipolar because they pick up electrical messages at two places spontaneously. They have two electrodes, one negative and one positive. The limb leads are made up of the following:

Lead I right arm negative to left arm positive Lead II right arm negative to left leg positive Lead III left arm negative to left leg positive

The axes of the three bipolar leads forms Einthoven’s triangle.

Right Arm Left Arm Left Leg

www.cvphysiology.com/ Arrhythmias/A013a.htm

Einthoven's triangle is formed by the axes of the three bipolar limb leads, 1, 11, and 111.

http://www.cvphysiology.com/Arrhythmias/A013a.htm


The diagram shows the placement of the positive and negative electrodes for each lead.

AUGMENTED LEADS

As these leads pick up impulses at only one point, they are known as unipolar. The ECG machine calculates the three leads of AVR, AVL and AVF, using the three limb leads. The three unipolar leads are as follows: AVR records the impulse that is transmitted from a point in the heart to the Right Arm AVL records the impulse that is transmitted from a point in the heart to the Left Arm AVF records an impulse that is transmitted from a point in the heart to the Left Foot The lead attached to the right leg is an earth lead only. In reference to unipolar leads, the V stands for unipolar and the A stands for augmented, meaning that the ECG machine also augments or increases the size of these low voltage leads.

CHEST LEADS

There are six chest leads, V1-V6. Again V represents unipolar, hence the impulse that is recorded is transmitted from a point in the heart to that lead only.

Did you know? The chest leads are also commonly referred to as precordial leads.

PLACEMENT OF CHEST LEADS

V1 4th intercostal space, right sternal border V2 4th intercostal space, left sternal border V3 directly between V2 and V4 V4 5th intercostal space, midclavicular line V5 on the same plane as V4, anterior axillary line V6 on the same plane as V4, mid axillary line


http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/images/6_lead_placement.gif

Electrode sites for the chest leads.

The precordial leads are on the patient’s right from V1 at the right sternal

border to V6 at the left midaxillary line.

http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/images/6_lead_placement.gif


GROUPING OF LEADS

LEADS ARE GROUPED TOGETHER FOR ASSESSMENT OF THE ECG, AND REFLECT A PARTICULAR WALL OF THE HEART.

Anterior leads V3, V4 Anteroseptal leads V1, V2, V3, V4 Lateral leads V5, V6, AVL, Lead I Inferior leads II, III, AVF Posterior leads V1, V2 (indirect)

http://www.anaesthetist.com/icu/organs/heart/ecg/images/leads.jpg

http://www.publicsafety.net/image/precord_view.gif




RECORDING AN ECG 1. Ensure correct placement of chest leads. If a serial ECG is required it is a good idea

to mark the spots where the electrodes have been placed to maintain consistency of graphs. Alternatively, the electrodes can be left in place

2. Limb leads may be placed on the wrist and angle, or the arm, shoulder or thigh. 3. Avoid placing leads over hairy, sweaty or bony prominences. 4. Remove anything which may cause interference and hence reduce the quality of the

ECG. These include removing any metal objects from the person’s body such as a watch, as well as turning off anything electrically powered in close proximity of the person, e.g. IV pumps.

5. Ask the patient to breathe quietly and perhaps hold their breath while you record the

ECG. Also ensure that the patient is warm, relaxed and comfortable to avoid tremors and fidgeting.

6. Label the ECG with name, DOB, time, reason for ECG, and including any symptoms

the patient may have, such as SOB, diaphoresis, chest pain and where, and rated in severity out of 10.


TEST – MODULE THREE 1) Each small square on the ECG paper is equal to

a) 0.05 seconds b) 0.05 mm

c) 0.04 mm d) 0.04 seconds

2. The standard leads are

a) unipolar b) bipolar c) augmented d) negative

3. In regards to chest leads the V stands for

a) augmented b) standard c) unipolar d) bipolar

4.) The axes of the three bipolar leads form

a) Einthoven triangle b) Einthoven’s square c) Einthoven’s triad d) Einthoven’s circle

5. The lead attached to the right lower limb is

a) a chest lead b) AVR c) AVL d) an earthing lead

6. How many chest leads are there?

a) five b) six c) four d) twelve


MODULE FOUR

THE NORMAL 12 LEAD ECG The normal electrocardiogram is composed of a P wave, a QRS complex and a T wave. The P wave represents atrial depolarization, the QRS represents ventricular depolarization and the T wave reflects the phase of rapid repolarisation of the ventricles. If electrical currents generated in the cardiac cells flow towards an electrode, a positive or upright deflection will be recorded on the ECG paper. Conversely if the current flows away from the electrode then the resultant deflection on the ECG will be negative or downward. In the standard 12 lead ECG the individual recordings for each lead may seem different but this is only because they are recorded from different positions on the body, from different angles. All these different recording angles are employed to arrive at a true picture of what is really happening with the heart. Atrial depolarisation spreads from the SA node in the top right hand corner of the right atrium through both atria and down to the AV node. It travels in leftward and inferior direction, essentially towards the left foot. The current passes through the AV node, bundle of his and both ventricular walls at the same time, but the impulse traverses the right ventricular wall first because it is so much thinner than the left. The septum is normally depolarised from left to right then both ventricles are subsequently depolarised. As the left ventricle has a much thicker muscle mass, most of the electrical forces are picked up from there, and that is the actual deflection that is seen on an ECG. Therefore most electrical impulses travel in a downward leftward direction.

Normal deflections of the leads Lead I

positive P wave none or small q wave (due to septal depolarisation) positive r wave positive t wave

Lead II

positive P wave positive r wave may have an s wave


Lead III positive P wave (can be flat or biphasic or negative) positive r wave S wave deeper than the r wave (due to left sided depolarisation)

AVL

same as lead I as they record from the same position AVF

similar to lead III as it is in a similar position AVR

negative P wave negative QRS complex (s) wave negative t wave

Chest leads V1

negative P wave (may be positive) small r wave due to both septal and right ventricular forces. When right ventricular

activation is still beginning the dominant leftward force of the left ventricle produces a deep s wave.

V2

positive P wave slightly bigger r wave

V3

more r wave progression, usually biphasic V4

mainly positive with a smaller s wave V5

totally positive as a r wave progression continues V6

totally positive (no s wave)


RULES FOR ECG INTERPRETATION

3 CHECKS:

1. Look at AVR. It should be negative 2. Calibration mark at beginning of ECG should be 2 large boxes high (= 10 mm or 1

mV, i.e. the standard calibration) 3. Speed of paper should be 25 mm per second

INTERPRETATION:

1. Diagnose, using the rhythm strip (lead II gives best picture of all deflections) 2. Check r wave progression across anterior (chest) leads 3. Look at leads in groups, i.e. the groups which reflect a particular wall of the heart 4. Look at ST segments, t wave and check for the presence of pathological Q waves. 5. Make your final diagnosis.


EXAMPLES OF NORMAL ELECTROCARDIOGRAPHS

http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson9/#RVMI

http://cardiology.ucsf.edu/ep/Imagesheart/normalecg.jpg




TEST – MODULE FOUR

1) If electrical currents flow towards an electrode the deflection on the ECG paper will be a. negative b. isoelectric c. positive d. downward

2) Normal sinus rhythm originates from the

a. SA node b. AV node c. bundle of his d. purkinje fibres

3) On a normal 12 lead ECG AVR should be

a. positive b. totally negative c. show R wave progression d. biphasic

4) In lead V6 the R wave should be totally

a. negative b. biphasic c. downward d. positive

5) Lead II, III and AVF represent what wall of the heart?

a. inferior b. posterior c. lateral d. anterior


MODULE FIVE

ANGINA Angina is a reversible condition in which the myocardial oxygen demand temporarily exceeds the oxygen supply. The major symptom of angina is chest pain, but it is often associated with shortness of breath, sweating, nausea. Angina results from the narrowing of the coronary arteries. This may be permanent due to structural abnormality such as atherosclerosis or transient due to spasm of the artery wall. As arterial flow is decreased the myocardial tissue’s need for oxygen and nutrients continues. The same work of pumping blood must be accomplished with less available energy and oxygen. The tissue that depends on the blood supply becomes ischaemic as it continues to function with less oxygenated blood.

ECG CHANGES

ST Segment depression usually greater than 0.5 mm (1/2 a little box) in 2 or more leads

T wave flattening or inversion The ST segment depression can be widespread over the ECG leads indicating 3 vessel involvement or it can be specific to one area of the heart. Widespread ST segment elevation suggests spasm of the coronary arteries and not myocardial infarct. http://www.med.umich.edu

SYMPTOMS

pain due to lactic acid formation (anaerobic metabolism) associated breathlessness diaphoresis dizziness

Most people with chronic angina feel the pain when they exercise, also with some emotions, i.e. anxiety, fear, which constrict the arteries and increase heart rate (sympathetic control).


AN EXAMPLE OF AN ECG SHOWING ST DEPRESSION WITH UNSTABLE ANGINA http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson9/#RVMI

ACUTE CORONARY SYNDROME (ACS)

ACS encompasses any patient’s presentation of chest pain of cardiac origin. It is classified into three categories: High risk, Intermediate risk and Low risk.

High risk would encompass the ST elevation MI or prolonged chest pain,

Intermediate would encompass what we know as unstable angina, where the pain has resolved but they have other risk factors,

Low risk would be pain but few risk factors. Follow http://www.heartfoundation.com.au/downloads/NHF_ACS_chart0506.pdf to see the algorithm from the Heart Foundation regarding treatment and risk factors of each category.

NB: You may see Non STEMI and STEMI now written as Non STEACS and STEACS – which is ST

elevation Acute Coronary Syndrome.


http://www.heartfoundation.com.au/downloads/NHF_ACS_chart0506.pdf


TEST – MODULE FIVE 1) Angina results from

a. widening of the coronary arteries b. narrowing of the coronary arteries c. increased arterial flow d. increased oxygen to the heart

2) Angina is

a. transient and reversible b. results in permanent scarring c. stops the heart d. can only happen once in a person’s life

3) The primary ECG change seen with angina is

a. ST elevation b. T wave elevation c. ST depression d. absence of p waves

4) The most common symptom associated with angina is

a. feeling tired b. pain in legs c. chest pain d. headache

5) What is another ECG change that may be seen in angina?

a. long PR interval b. T wave elevation c. no P waves d. T wave flattening or inversion


MODULE SIX

ACUTE MYOCARDIAL INFARCTION (AMI) AMI is a life threatening condition characterized by the formation of localized necrotic areas within the myocardium. Myocardial infarction usually follows the sudden cessation of blood flow and therefore oxygen supply to the heart muscle.

PATHOPHYSIOLOGY

Is complete or nearly complete occlusion of a coronary vessel by severe chronic atherosclerotic plaque with a superimposed thrombus formation.

SYMPTOMS

chest pain, which may radiate to arms, jaw, shoulder or back diaphoresis dizziness shortness of breath nausea and vomiting feeling of impending doom

ST SEGMENT INFARCTION (STEMI) ECG CRITERIA

Initially persistent ST segment elevation of o ≥ 2 mm (2 little boxes) in 2 or more chest leads or o ≥ 1 mm in 2 or more limb leads

followed by T wave inversion Q waves will later develop and are permanent

During a myocardial infarction the initial ECG change is ST segment elevation in the group of leads reflecting the affected surface of the myocardium.

The evolution of ST segment changes in acute myocardial infarction (An explanation follows)


javascript:showPic('../../mml/ecg_evol.gif',370,305)


Normal appearances in a lead, which by the QRS morphology clearly lies over the L ventricle

Within hours of the clinical onset of infarction there is ST segment deviation. At this stage no QRS changes or T wave changes have occurred. Although such a pattern is frequently spoken of loosely, as following ―acute infarction‖, no definitive evidence of infarction is shown. There is evidence of myocardial damage, demonstrating an unstable situation. In the vast majority of cases evolutionary changes of infarction follow. Occasionally the record returns to normal.

Within hours to days the R wave voltage has fallen and abnormal Q waves have appeared. These changes are sufficient to prove the occurrence of infarction. In addition T wave inversion has appeared and the ST elevation becomes less pronounced.

Within one or more weeks the S-T segment changes revert completely to normal. The R wave voltage remains reduced and the abnormal Q waves persist. Deep symmetrical


T wave inversion may develop at this stage. In some patients this pattern remains permanently, in others it progresses to the appearance in the next figure.

Months after the clinical infarction the T waves, as above, may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist

ANTERIOR WALL INFARCTION An infarction of the anterior wall of the heart results from the occlusion of the left anterior descending coronary artery or one of its branches. The following ECG is an example of an antero-lateral myocardial infarction Notice the ST elevation in the Limb leads as well as in most of the chest leads

http://members.evansville.net/ict/ekg-ami-antlat-500.jpg



INFERIOR WALL INFARCTION

In order for the inferior wall to become infarcted, the circumflex or the right coronary artery must be occluded. The following ECG is an example of an inferior myocardial infarction Some of you may have noted the ST elevation in V1 This is due to myocardial infarction of the R ventricle Remember the R ventricle is fed by both the circumflex and right coronary artery.


RIGHT VENTRICULAR (RV) INFARCTION

Right ventricular infarcts are reflected in lead V4R. Hence in order to determine this it is first necessary to do another ECG with right sided leads.

ECG USING RIGHT SIDED LEADS

V1 (becomes V2R) and V2 (essentially becomes V1R) are placed in the usual position. When doing the ECG, placement mirrors a normal ECG V3R directly between V2R (where V1 would normally be) and V4R V4R = mid clavicular line, 5th intercostal space on the right side of the chest V5R = on the same plane as V4R, anterior axillary line, on the right side of the chest V6R = on the same plane as V4R, mid axillary line, on the right side of the chest RV infarcts happen in the setting of inferior wall infarction, when the occlusion is in the right coronary artery. As RV infarcts carry a poorer prognosis than an inferior infarction alone, it is important, in the setting of an inferior AMI to perform right sided leads in order to determine if a RV infarct is also present to avoid possible mismanagement.

ST elevation, ≥ 2mm, in right chest leads, especially V4R (see below)




NON ST ELEVATION AMI (NON-STEMI) The diagnosis of a non-STEMI infarct can only truly be made when there is a characteristic rise in the levels of serum troponin and creatine-kinase-MB, in association with transient non-specific findings on their ECG. These changes may include ST depression or T wave abnormalities without the evolution of Q waves, or both. Whilst non-STEMI’s result in smaller infarct size, people do have a higher incidence of post infarction angina and rate of reoccurrence than those who have STEMI’s.

Although it is tempting to localize the non-Q MI by the particular

leads showing ST-T changes, this is probably only valid for the ST

segment elevation pattern

Evolving ST-T changes may include any of the following patterns:

o Convex downward ST segment depression only (common).

o Convex upwards or straight ST segment elevation only

(uncommon)

o Symmetrical T wave inversion only (common)

o Combinations of above changes




POSTERIOR WALL INFARCTION

There are no leads directly over the true posterior wall. The changes are reflected in the leads on the opposite wall, ie V1 to V3. Therefore these changes are seen back to front or as a mirror image. Instead of an abnormal Q wave, there is a tall, broad initial R wave. Also instead of ST segment elevation resulting from an injury current traveling away from the electrode, there is ST segment depression resulting from injury current traveling toward the electrode. The t wave is upright rather than inverted. As with right ventricular infarcts, posterior infarcts often accompany inferior wall infarctions. In the acute stage ST depression is usually evident in V3 and V4, giving way to an R wave in V1 as the infarct progresses. This ECG is an example of an Acute infero-posterior MI (note tall R waves V1-3,

marked ST depression V1-3, ST elevation in II, III, aVF)


ECG changes are seen in anterior precordial leads V1-3, but are the

mirror image of anteroseptal MI

Increased R wave amplitude and duration (i.e., a "pathologic R

wave" is a mirror image of a pathologic Q)

R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)

Hyperacute ST-T wave changes: i.e., ST depression and large,

inverted T waves in V1-3

Late normalization of ST-T with symmetrical upright T waves in

V1-3



THE MIRROR TEST IN READING POSTERIOR INFARCTION ECG

APPLICATION OF THE MIRROR TEST

The anterior precordial leads (V1, V2, V3) provide a mirror- image view of the posterior wall of the left ventricle.

Thus, the tall R waves and ST depression, that is seen in V1, V2, and V3 look like Q waves and coved ST elevation when the Mirror Test is performed.

If this was an actual paper ECG tracing, you would flip the page over, rotate it 180° & hold it up to the light

Thus, the purpose of the Mirror Test is to facilitate recognition of ECG changes that might represent acute posterior MI.

RECIPROCOL ECG CHANGES

ST segment depression occurring in the leads opposite or distal to the affected wall or region is referred to as reciprocal ECG changes. For example in the setting of an acute anterior infarct, accompanying ST depression may be seen in the inferior leads. Generally ST depression mirrors the degree of ST elevation occurring. Whilst the exact mechanism of reciprocal changes is not understood there are several thoughts. Firstly it may be a sign of ischaemia on the opposite wall; or it simply may be an electrographic phenomena. It is however universally accepted that these types of infarcts carry a worse prognosis.

Reference for this section Davey P (2008) ECG at a Glance Chichester: Wiley & Sons


TEST – MODULE SIX 1) An ensuing acute myocardial infarction is most often characterized by

a. ST depression ≥ 0.5 mm in 2 or more limb leads b. ST elevation of ≥ 2mm in 2 or more chest leads c. long ST interval d. short PR interval

2) Q waves form as a result of

a. angina b. non-STEMI c. STEMI d. chest pain

3) An anterior AMI results from occlusion of the LAD or one of its branches. Which

leads would it be most evident? a. V3, V4 b. AVL, Lead I, V5, V6 c. Lead II, III and AVF d. V7, V8 and V9

4) Right ventricular infarctions are common in the setting of

a. atrial fibrillation b. anterior infarctions c. angina d. inferior infarctions

5) ST segment depression occurring in the leads opposite the affected wall are

referred to as a. recent changes b. reciprocal changes c. evolving changes d. permanent changes

6) What leads directly represent the posterior wall of the heart?

a. all leads b. V3, V4 c. none d. II, III, AVF


MODULE SEVEN

ATRIO-VENTRICULAR (AV) BLOCKS AV, or heart blocks, occurs when a transmission of an impulse through the heart is blocked at the AV node.

CAUSES OF AV BLOCKS INCLUDE:

infection AMI drugs, such as digoxin and quinidine

TYPES

First degree AV block Second degree AV block, type 1 and 2 Third degree AV block (complete heart block)

FIRST DEGREE AV BLOCK

First degree heart block is defined as a PR interval that is prolonged (0.20 or more) and does not change from beat to beat. There is a delay of conduction through the AV node due to:

coronary disease rheumatic disease hyperthyroidism normal variation ageing

All beats, however, are conducted as normal to the ventricles. Hence the person is asymptomatic and does not require any treatment.

Did you know? About 10% of people with an acute inferior AMI develop a 1st degree heart block. Of these 30% will go on to develop a 2nd or 3rd degree AV block.

http://en.wikipedia.org/wiki/ECG



SECOND DEGREE AV BLOCK

Defined as when one or more, but not all, atrial impulses fail to reach the ventricles because of impaired conduction through the AV node. There are two types of second degree block, Type I and Type II.

TYPE I SECOND DEGREE AV BLOCK

This is also known as Wenckebach, or less frequently as Mobitz I. In classic AV Wenckebach the PR interval lengthens until finally one P wave is not conducted (ie does not result in a QRS), which produces a pause. After the pause the sequence repeats itself. It is often associated with digitalis intoxication, inferior AMI, acute myocarditis or the period immediately following open-heart surgery.

CLINICAL IMPLICATIONS

As most beats are conducted through to the ventricles, usually this condition is clinically benign.

ECG RECOGNITION

Normal or near normal PR interval that gradually lengthens with each beat until finally an impulse fails to reach the ventricles and a beat is dropped.

After the dropped beat the PR interval reverts back to normal and the process starts again.

Cyclic in nature Normal width QRS complexes




TYPE II SECOND DEGREE AV BLOCK

This block is occasionally also referred to as Mobitz II. It is more sinister than Type I as the blockage is within or below the level of the bundle of His. If left untreated it frequently goes onto complete heart block.

ECG RECOGNITION

Usually the PR interval is normal or near normal Some p waves are not conducted through to the ventricles, often as frequently

as every second beat QRS complex is often broad (greater than 0.12 seconds)

TREATMENT

Generally as soon as this rhythm is recognized temporary cardiac pacing is instituted, followed by the insertion of a permanent pacemaker.


http://www.txai.org/edu/irregular/bradycardias.htm




THIRD DEGREE AV BLOCK (COMPLETE HEART BLOCK)

Complete heart block is diagnosed when no atrial impulses are conducted to the ventricles. Therefore the ventricles engender their intrinsic own rate. The ECG strip has a typical pattern, where P waves are evenly spread across the ECG strip, and so are the QRS’s, but neither are connected to each other.


In complete heart block the rate of the ventricles is dependent upon the level of the lesion. The lower down the lesion, the slower and less dependable the ventricular rate.

TREATMENT

Complete heart block usually requires temporary and frequently permanent pacing. If there is a delay in pacing being available the person may benefit from an intravenous isoprenaline infusion, which enhances AV conduction.

Reference for this section Hampton J (2013) The ECG in Practice (6

th ed). Sydney: Churchill Livingstone


HTTP://WWW.TXAI.ORG/EDU/IRREGULAR/BRADYCARDIAS.HTM




TEST – MODULE SEVEN 1) Heart blocks occur when the transmission of an impulse is blocked at the

a. SA node b. bundle branches c. AV node d. bundle of his

2) First degree AV block occurs when the PR interval is

a. greater than 0.20 seconds b. less than 0.20 second c. equal to 0.20 second d. none of the above

3) Second degree AV block (type I) is also known as

a. Einthoven’s block b. Wenckebach c. complete heart block d. Mobitz Type 11

4) In Type II second degree block the PR interval is frequently

a. lengthened b. normal or near normal c. short d. undetectable

5) When there is no association between P waves and QRS complexes the disorder

is known as a. first degree heart block b. SA node block c. second degree heart block d. complete heart block


MODULE EIGHT

RHYTHMS ASSOCIATED WITH CARDIAC ARREST Cardiac arrest is defined as the cessation of cardiac function resulting in the loss of effective cardiac output which, if left untreated will cause brain tissue damage and ultimately death.

VENTRICULAR TACHYCARDIA

This life threatening dysrhythmia indicates the presence of significant underlying cardiac disease and occurs most commonly in the setting of acute myocardial infarction and coronary artery disease. It also occurs in people with cardiomyopathy mitral valve prolapse, or altered ion levels, especially potassium and magnesium.

ECG RECOGNITION

Four or more consecutive premature ventricular contractions Essentially regular Rate 110-250 beats per minute no associated p wave, as the complexes originate in the ventricles QRS complexes are wide and bizarre in appearance


People with VT may be conscious, initially, but left untreated will often be rendered unconscious, and rapidly progress to ventricular fibrillation and ultimately death.

TREATMENT

CONSCIOUS VT

Amiodarone, usually as an infusion of up to 15 mg/kg for 24 hours &/Or Lignocaine 1-1.5mg/kg IVI stat, potentially followed by a lignocaine infusion

UNCONSCIOUS VT

Direct Current Reversion (DCR): o Monophasic defibrillation of 1 x 360 Joules & 360 J for all subsequent

shocks o Biphasic defibrillation of 1x 200 Joules & 200 J for all subsequent

shocks Once reverted, an infusion of lignocaine or amiodarone is usually commenced.

HTTP://WWW.TXAI.ORG/EDU/IRREGULAR/VENTRICULAR_TACHYARRHYTHMIAS.HTM

http://www.txai.org/edu/irregular/ventricular_tachyarrhythmias.htm


VENTRICULAR FIBRILLATION

Ventricular fibrillation is defined as chaotic depolarisation of individual myocardial muscle fibres which do not produce an effective ventricular contraction, therefore the heart does not pump and no pulses are felt.

ECG RECOGNITION

Irregular, chaotic undulations No clear-cut ventricular complexes


Rapid loss of consciousness, with no detectable pulse or blood pressure is inevitable with VF. Left untreated all people with VF will die

TREATMENT

Direct Current Reversion (DCR): o Monophasic defibrillation of 1 x 360 Joules & 360 J for all subsequent

shocks o Biphasic defibrillation of 1 x 200 Joules & 200 J for all subsequent

shocks

1mg IVI of Adrenaline may be required in an effort to increase the electrical activity within the heart and hence make the heart more responsive to defibrillation.

HTTP://WWW.TXAI.ORG/EDU/IRREGULAR/VENTRICULAR_TACHYARRHYTHMIAS.HTM



DEFIBRILLATION

Transthoracic cardioversion delivers electrical energy to the heart by means of metal paddles or pads placed on the intact chest or placed directly on the heart when the chest is opened, such as during cardiac surgery. This procedure depolarises the excitable myocardium, thereby interrupting re-entrant circuits and discharging automatic pacemaker foci to establish electrical homogeneity. In other words, it temporarily ceases all electrical activity in the heart muscle in order to allow the SA node to resume its pacemaker role. Sinus rhythm is restored if the sinus node is the first pacemaker to fire after the electrical shock. Sternum Apex At V2 Right of the sternum At V6 mid axilla Paddle Positions:


ASYSTOLE

Asystole is recognized by an absence of any electrical activity at all in the myocardium.


A heart in asystole has no electrical impulse initiated and hence is incapable of any mechanical activity. At this point the person is clinically dead.

ECG RECOGNITION

An essentially flat line on the ECG signal There may be odd undulations but no discernible complexes

TREATMENT

Cardiopulmonary Resuscitation (CPR) Adrenaline 1mg IVI stat, repeat every 4 minutes.


PULSELESS ELECTRICAL ACTIVITY (PEA)

PEA is also referred to as Electromechanical Dissociation (EMD). It is defined as normal ECG tracings on the cardiac monitor, but there is actually an absence of any cardiac function (contractions). Hence the ECG may show sinus rhythm but the heart will not be beating and therefore there will be no pulses. The person will be in an arrested state.


PEA is often caused by compression on the heart due to such things as cardiac tamponade, tension pneumothorax or pulmonary embolus. In the case of severe hypovolaemia the heart, whilst it still has the electrical and mechanical capability to pump blood there is not enough circulating volume for the heart to eject any stroke volume. Again this ultimately results in PEA.

TREATMENT

CPR Adrenaline 1mg IVI every 4 minutes Identify and treat cause


BRADYDYSRHYTHMIAS Slow rhythms such as sinus bradycardia and complete heart block may cause a cardiac arrest. In the ECG strip below, the SA node has failed (no P waves visible) and the rate is in the mid 30’s, indicating that the ventricles have engendered their own rate. This type of bradydysrhythmia is also termed idioventricular rhythm (ie rhythm within the ventricle). Note the wide, bizarre QRS’s

AGONAL RHYTHM Agonal rhythms are sometimes known as dying heart rhythm. These rhythms are associated with the lowest pacemaker in the Purkinjes firing at a very slow rate. This rhythm can be treated with adrenaline but if left untreated, is a precursor of asystole.

TREATMENT

CPR Atropine or isoprenaline IVI Consider cardiac pacing if symptomatic

Agonal Rhythm

http://www.studentbmj.com/issues/01/12/education/ECG7.gif



It is the recommendation of the editors of this package, to ensure that information you are using is current, to access the standards for practice regarding advanced life support. Please refer to the following web site for the Australian Resuscitation Guidelines for Basic Life Support and Advanced Life Support for the most current updates. http://www.resus.org.au/ Go to policy statements and guidelines

http://www.resus.org.au/


TEST – MODULE EIGHT

1) Ventricular Tachycardia is generally defined as a. two consecutive PVC’s b. p waves followed by fast complexes c. four or more consecutive PVC’s d. rate less than 50 beats per minute

2) The first line treatment for VF or pulseless VT is

a. DCR b. amiodarone c. lignocaine d. adrenaline

3) For cardioversion to be successful which pacemaker in the heart must be the first

to fire? a. AV node b. pacing node c. bundle branches d. SA node

4) Aystole is recognised as

a. spikes on the ECG b. absence of all electrical activity on the ECG signal c. chaotic rhythm d. fast heart rate

5) A normal ECG tracing with no detectable pulse is termed

a. PEA or EMD b. PAC’s c. asystole d. VF


MODULE NINE

BUNDLE BRANCH BLOCKS Bundle Branch blocks are intraventricular conduction defects which are caused when either the right or left bundle branch is blocked (ie damaged). This causes the heart to be activated in an uneven manner. One ventricle is depolarised after the other instead of both together. Because of the delay in ventricular depolarisation, the QRS is wider than normal, ie greater than 0.12 secs

(Conover, 1996)

Anterior fascicle of LBB


RIGHT BUNDLE BRANCH BLOCK

Right bundle branch block occurs when the right bundle is blocked. This may be due to a disease process, such as an AMI (particularly an Inferior AMI), or may be a benign process. The two ventricles are activated one after the other instead of together. The septum of the left ventricle is depolarised normally and this is then followed by the right ventricle. Diagnosis is made by looking at V1 and V6. There is usually an RSR pattern, where the initial r wave represents septal depolarisation; the s wave represents left ventricular depolarisation, then the final r wave represents right ventricular activation. The notched upright V1 is reasonably classic of right bundle branch block. Looking at V6 the first part of the QRS complex is activated normally when the left ventricle is depolarised. Then the right ventricle is depolarised and as a result there is a slurred s wave in V6.

ECG CRITERIA FOR RBBB

Prolonged QRS duration (0.12 seconds or more) Triphasic complex in V1 (rSR) and V6 (qRS) T wave is usually in opposite polarity to the QRS complex Broad s waves in I and AVL

http://www.emedu.org/ecg/voz.php

The intraventricular conductive system shown through transparent walls. Note the anterior positions and similar constructions of the right bundle branch (RBB) and the anterior fascicle of the left bundle branch (LBB).



LEFT BUNDLE BRANCH BLOCK

Left bundle branch block is usually associated with heart disease. It also commonly accompanies anteroseptal myocardial infarction. Normally impulses reach the ventricle first by way of the right bundle branch after which the septum and right ventricle are depolarised. The impulse then travels across the septum of the left ventricle which is then depolarised.

ECG CRITERIA FOR LBBB

Prolonged QRS duration (0.12 seconds or more) Mainly negative and often notched complex in V1 Totally positive notched complex in Lead 1 Totally positive notched complex in V6 Terminal slurring of QRS complex due to the delayed repolarisation of the left

ventricle T wave is opposite in polarity to the QRS complex Lead I and AVL are similar to V6 in configuration

http://www.aic.cuhk.edu.hk/web8/ecg.htm

Note from editor: It may be difficult to see the notched V6 in the above ECG and we are currently on the look out for a better ECG example.



TEST – MODULE NINE

1) Bundle Branch blocks result in the ventricles being depolarised a. both together b. one after the other c. faster than normal d. has no affect on ventricular depolarisation

2) In the case of a right bundle branch block what would be seen in VI?

a. totally negative QRS complex b. no P wave c. a triphasic complex (rSR) d. T wave polarity in the same direction as the QRS complex

3) A widened QRS complex (greater than 0.12) seconds is present in

a. only left bundle branch block b. only right bundle branch block c. neither right nor left bundle branch blocks d. both right and left bundle branch blocks

4) In the case of left bundle branch block terminal slurring of the QRS complex is

due to a. delayed repolarisation of the left ventricle b. faster repolarisation of the right ventricle c. faster repolarisation of the left ventricle d. delayed repolarisation of the right ventricle

5) In both left and right bundle branch blocks the T wave is usually in the

a. same direction as the P wave b. the same direction as the QRS complex c. the opposite polarity to the QRS complex d. not present


MODULE TEN

ATRIAL DYSRHYTHMIAS

PREMATURE ATRIAL CONTRACTIONS (PAC)

When the atrial impulse originates at a point other than the sinus node, a premature atrial contraction will be the result. The ectopic focus may be anywhere in the atria. The resultant deflection is called a p prime wave. On the ECG an abnormal p wave (p prime) is seen, followed by a normal QRS and T wave. The complex is premature and therefore is closer to the preceding sinus beat than expected. The sinus node then resets itself and there is a compensatory pause before the next normal sinus beat.


Normal: emotion, caffeine and other stimulants, alcohol, tobacco Abnormal: warning sign of congestive heart failure (due to AMI) from atrial

stretch Hormonal changes, such as due to pregnancy or menopause



ATRIAL FLUTTER

Atrial flutter is caused by an ectopic focus from the atria, firing at a very fast rate, usually 300 times per minute. The AV node generally refuses to transmit all the impulses and only allows the occasional message through to the ventricles. This controls the heart rate, allowing the ventricles to fill before most contractions.



Atrial flutter may be seen in association with any of the following conditions.

Heart failure Valvular disease Pulmonary embolus Digitalis toxicity Ischaemic heart disease

ECG RECOGNITION

Flutter waves have a saw tooth configuration QRS is normal width and may be regular or irregular depending on the degree

of the AV block or wide if there is a bundle branch block also present Flutter rates are usually divisions of 300. For example

1:1 = rate of 300 beats per minute 2:1 = rate of 150 beats per minute 3:1 = rate of 100 beats per minute 4:1 = rate of 75 beats per minute



ATRIAL FIBRILLATION (AF) When many cells in the atria fire impulses haphazardly the result is disorganization of the electrical stimuli, hence the atria do not beat effectively, but rather quiver or fibrillate.


Congestive Cardiac Failure COPD Hyperthyroidism Hypertension Idiopathic

Danger of thrombus formation As the atria do not contract properly they do not fully empty. For this reason there is a greater risk of clots forming due to stasis of the blood, which may be then circulated through the body, causing a stroke or an AMI.

ECG RECOGNITION

No P waves Fibrillatory line between QRS complexes ―Irregularly irregular‖ ventricle response, as the AV node selectively chooses

impulses to go through to ventricles




SUPRA VENTRICULAR TACHYCARDIA (SVT) Supra means above, therefore an SVT is a tachycardia that originates from above the ventricles, i.e. from the atria or the AV node.


Normal heart: red wine, stimulants, pregnancy, MSG ingestion Abnormal: accessory pathway, rheumatic heart disease

ECG RECOGNITION

P waves may be abnormal, upright, inverted or very difficult to see due to rapid rate

QRS normal, but may be distorted if aberrant conduction is present rate 140-220 beats per minute Often will observe ST depression due to rapid rate (coronary arteries fill during

diastole or rest)




PREMATURE VENTRICULAR COMPLEXES (PVC)

Premature ventricular complexes are beats, or pseudo beats that originate from an ectopic focus in the ventricles. They are also known as ventricular ectopic (VE) and premature ventricular beats (PVB). PVC’s may be unifocal or multiform/multifocal. Obviously unifocal PVC keep coming from the same focus, whilst multiform or multifocal PVC’s may be from different foci or even from the same focus but depolarised in different directions.


PVC’s are present in people with normal heart. The problem with PVC’s arises when too many of them become present, as they do not represent a true effective beat. They are often more evident with recent caffeine intake, stimulants etc.

VENTRICULAR BIGEMINY

A bigeminal rhythm consists of pairs i.e. one sinus beat, one PVC, one sinus beat, one PVC, etc.

ECG RECOGNITION

Broad QRS complex (longer than 0.12 seconds) Premature T wave in opposite direction to the QRS complex No related p wave Compensatory pause before the next complex


http://connection.lww.com/Products/morton/documents/images/Ch17/jpg/Ch17-035.jpg



TEST – MODULE TEN

1) Premature atrial contractions originate in the a. SA node b. an ectopic focus in the ventricles c. AV node d. an ectopic focus in the atria

2) Atrial flutter rates are usually in divisions of 300. Hence the rate for 2:1 would be

a. 75 beats per minute b. 150 beats per minute c. 100 beats per minute d. 300 beats per minute

3) The ventricular response in atrial fibrillation is

a. irregularly irregular b. perfectly regular c. initiated by p waves d. unable to be determined

4) SVT frequently exhibits a heart rate of

a. less than 100 beats per minute b. less than 50 beats per minute c. between 140 and 220 beats per minute d. between 50 and 100 beats per minute

5) A unifocal PVC results from

a. the same ventricular focus b. many different ventricular foci c. the same atrial focus d. many atrial foci


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METHOD OF RHYTHM ANALYSIS & ECG INTERPRETATION

This "method" is recommended when reading all 12-lead ECG's. Like the physical examination, it is desirable to follow a standardized sequence of steps in order to avoid missing subtle abnormalities in the ECG tracing, some of which may have clinical importance. All steps must be followed to ensure that if multiple abnormalities occur, all are detected. The 6 major sections in the "method" should be considered in the following order:

1. Measurements 2. Rhythm Analysis 3. Conduction Analysis 4. Waveform Description 5. ECG interpretation 6. Comparison with previous ECG (if any)

1. MEASUREMENTS (USUALLY MADE IN LEAD II):

Heart rate (state atrial and ventricular, if different)

PR interval (from beginning of P to beginning of QRS)

QRS duration (width of most representative QRS)

QT interval (from beginning of QRS to end of T)

QRS axis in frontal plane (advanced ECG module only)

2. RHYTHM ANALYSIS

State basic rhythm (e.g. "normal sinus rhythm", "atrial fibrillation", etc.)

Identify additional rhythm events if present (e.g., "PVC's", "PAC's", etc.)

Consider all rhythm events from atria, AV junction, and ventricles

3. CONDUCTION ANALYSIS

"Normal" conduction implies normal Sino-atrial (SA), atrio-ventricular (AV), and intraventricular (IV) conduction.

The following conduction abnormalities are to be identified if present:

Sino Atrial (SA) Blocks

Atrio ventricular (AV) Blocks

1st, 2nd (Type I and Type II) and 3rd degree

Intraventricular Blocks (Advanced ECG module only)

RBBB, LBBB, Fascicular Blocks, Nonspecific intraventricular conduction defects,

Wolff Parkinson White Syndrome (WPW)


4. WAVEFORM DESCRIPTION

Carefully analyze the 12-lead ECG for abnormalities in each of the waveforms in the order in which they appear: P-waves, QRS complexes, ST segments, T waves, and... Don't forget the U waves. P Waves: are they too wide, too tall, look funny (i.e., are they ectopic), etc.?

QRS complexes: look for pathologic Q waves, abnormal voltage, etc.

ST segments: look for abnormal ST elevation and/or depression.

T Waves: look for abnormally inverted T waves.

U Waves: look for prominent or inverted U waves.

5. ECG INTERPRETATION

This is the conclusion of the above analyses.

Interpret the ECG as "Normal", or "Abnormal".

Occasionally the term "borderline" is used if unsure about the significance of certain

findings.

List all abnormalities.

Examples of "abnormal" statements are: Inferior MI, probably acute Old anteroseptal MI Left ventricular hypertrophy (LVH)

6. COMPARISON WITH PREVIOUS ECG

If there is a previous ECG in the patient's file, the current ECG should be compared with it to see if any significant changes have occurred. These changes may have important implications for clinical management decisions.


WHERE TO GO NOW!!!

The best way to become proficient at reading ECG’s is to PRACTISE, PRACTISE, and PRACTISE. Every time an ECG is performed in your department take the time to read it and interpret it, discuss your findings with a more experienced colleague and you will gradually improve your skills. There are resources, such as your hospital library or the internet to access advanced ECG interpretation if you want to advance your skills further with a more in depth look at rhythm disturbances and conduction defects. To help us improve this education package please fill out the evaluation form at the end of this package.


REFERENCES

1. Conover, M. (2003) Understanding Electrocardiography. (8th ed). St Louis: Mosby

2. Davey, P. (2008) ECG at a Glance. Chichester: Wiley-Blackwell

3. Guyton, A.C. (2001) Textbook of Medical Physiology. (12th ed). Philadelphia:

W.B. Saunders Company

4. Hampton, J. (2013). The ECG in Practice. Sydney: Churchill Livingstone

5. McCance, K.L. & Huether, SE. (2013) Pathophysiology, The basis for disease in adults and children (7th ed). St Louis: Mosby

6. Wagner, G. (2008) Practical Electrocardiography. Philadelphia: Lippincott Williams & Wilkins

Web sites accessed for images used in this package: Accessed 14th October, 2005.

7. http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson9/#RVMI

8. http://connection.lww.com/Products/smeltzer10e/documents/Thumbnails/c27/t

27_019.jpg

9. http://www.txai.org/edu/irregular/bradycardias.htm

10. http://members.evansville.net/ict/ekg-ami-antlat-500.jpg

11. http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson9/

12. http://www.cardiologist.uk.com/Main/main_symptoms.htm

13. http://www.dummies.com/WileyCDA/DummiesArticle/id-1211.html

14. http://www.emedu.org/ecg/voz.php

15. http://www.vetgo.com/cardio/concepts/concsect.php?conceptkey=20104

16. http://connection.lww.com/Products/morton/documents/images/Ch17/jpg/Ch17-035.jpg

17. http://www.heartfoundationjm.org/p/ServicesAboutHeart.htm

18. http://www.chelation.co.uk/ gfx/heart.jpg

19. http://media.wiley.com/assets/8/01/0-7645-5422-0_0901.jpg

20. http://www.heartfoundationjm.org/v/Deco/ServicesAboutHumanHeartHeartWal

l.jpg


http://connection.lww.com/Products/smeltzer10e/documents/Thumbnails/c27/t27_019.jpg

http://connection.lww.com/Products/smeltzer10e/documents/Thumbnails/c27/t27_019.jpg



http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson9/

http://www.cardiologist.uk.com/Main/main_symptoms.htm

http://www.dummies.com/WileyCDA/DummiesArticle/id-1211.html


http://www.vetgo.com/cardio/concepts/concsect.php?conceptkey=20104








21. http://www.aic.cuhk.edu.hk/web8/ecg.htm

22. http://www.heartfoundationjm.org/p/ServicesAboutHeart.htm

23. http://media.wiley.com/assets/8/10/0-7645-5422-0_0902.jpg

24. http://www.biosbcc.net/b100cardio/images/FG21_06B.jpg

25. http://www.ajronline.org/cgi/content-nw/full/177/6/1447/FIG1

26. http://medstat.med.utah.edu/kw/ecg/mml/ecg_ccs.gif

27. http://199.33.141.196/faculty/webpages/stodd/oceanweb/bio2/bio2lectures/Lec

ture3/img029.jpg

28. http://www.ce5.com/EKG.gif

29. http://www.monroecc.edu/depts/pstc/backup/ekggraph.gif

30. www.cvphysiology.com/ Arrhythmias/A013a.htm

31. http://www.studentbmj.com/issues/01/12/education/ECG7.gif

32. http://www.anaesthetist.com/icu/organs/heart/ecg/images/leads.jpg

33. http://en.wikipedia.org/wiki/ECG

34. http://www.resus.org.au/

35. http://www.txai.org/edu/irregular/ventricular_tachyarrhythmias.htm

36. http://www.publicsafety.net/image/precord_view.gif

37. http://cardiology.ucsf.edu/ep/Imagesheart/normalecg.jpg






http://medstat.med.utah.edu/kw/ecg/mml/ecg_ccs.gif





http://www.cvphysiology.com/Arrhythmias/A013a.htm




http://www.resus.org.au/





Regional ECG Package Evaluation

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by ticking the appropriate box and return to Nurse Educator

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1. Overall, I found this ECG learning

package worth while

2. The way in which the learning package

was presented made it easy to

understand

3. My knowledge of this topic was

improved after completing this learning

package

4. My skills in this area have been

enhanced since completing this learning

package

5. The resources provided were sufficient

for me to answer the review questions

adequately

6. I would recommend the ECG learning

package to others

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skills acquired in my clinical practice

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basic ecg interpretation

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