FIRST EDITION

POCKET GUIDE ON ECG FOR NURSES

POCKET GUIDE ON ECG FOR NURSES

Pocket Guide on ECG for Nurses

Medical Surgical Nursing Department Apollo College of Nursing Chennai

Pocket Guide on ECG for Nurses

2011 with authors
A.Lizy Sonia, Dr.Latha Venkatesan

First edition: 2011 All rights reserved

No part of this publication may be reproduced or transmitted in any form or by any means, electronic, mechanical, photocopy, recording, translated or any information storage and retrieval system, without permission in writing from the publisher. This book has been published in faith that the material provided by authors/ contributors is original. Every effort is made to ensure accuracy of material, but publisher, printer and author/ editor will not be held responsible for any inadvertent errors. In case of any dispute, all legal matters to be settled under Chennai Jurisdiction only.

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Preface
The finest gift that is ever known Is the presence of a wave in the ECG shown If those waves goes to a stand still The heart of the loved ones will shrill Utilizing your expert knowledge and skill You can identify and prevent an impending drill Vimala Edwards

Pocket guide on ECG is a simple comprehensive ECG learning guide that teaches the art and science of electrocardiogram (ECG) interpretation. ECG guide covers most of the basic concepts needed to interpret an ECG. This includes topics on electrophysiology, leads, normal ECG, abnormalities and arrhythmias. The evolution of this text began with an ECG workshop that was part of the curriculum for the undergraduate and postgraduate nursing students at Apollo College of Nursing. The central aim of this book is to unra vel the clinical intricacies of practice in this field. This guide deliberately focuses on the skills required by nurses caring for cardiac patients in a hospital setting. This guide is specially designed for the nursing students who are beginners and are not experience with ECG reading before; it will serve as an introduction to basic electrocardiogram (ECG) interpretation. It is not a textbook and does not include all the theory and rationale that underpins the various skills. This guide can be used for self study, designed to be small enough to carry around especially when in clinical practice.

The targets for this book are the students with no prior experience in ECG interpretation. It may serve as a review for the experienced person. The learning process is given as a sequence of steps for easy understanding.We hope that you find this guide useful, stimulating and challenging. Each chapter discuss a particular topic, written by an enthusiastic subject specialist. Critical exercises with ECG tracings complement towards the end of this guide.

CONTENTS
1. 2. 3. 4. 5.

Introduction ECG Basics ECG in patients with Myocardial infarction ECG in patients with atrial arrhythmias ECG in patients with ventricular arrhythmias ECG in patients with heart block Index Reference

6.

Chapter-1
INTRODUCTION
LEARNING OBJECTIVES: After studying this chapter, the reader will be able to define ECG list down the uses of ECG

ELECTROCARDIOGRAM The electrocardiogram, as the name suggests, is a record of the electrical activity of the heart. Electrocardiography is the practice of measuring and recording the electricity in the heart. ECG stands for two different words: electrocardiogram and electrocardiograph. The abbreviation ECG is also interchangeable with EKG. EKG was the abbreviation for people who spelled "cardio" with a 'k'. ECG is short for electrocardiogram. Electro- refers to

electricity, -cardio- refers to the heart, and gram refers to a recording. Therefore, the electrocardiogram is a recording of the heart's electrical activity. Electrocardiography is a simple investigation to perform, but accurate interpretation can be challenging. The electrocardiogram provides a graphic record of the electrical activity of the heart. Each cardiac cell generates an action potential as it becomes depolarized and then repolarized during a normal cycle. Depolarization of cardiac cells proceeds in an orderly fashion in the normal situation beginning in the sinus node, and then spreading sequentially through the atria, AV node, and ventricles. The electrical signal spreads through the heart as a wave front of depolarization. This wave front results in a minute electrical field that can be detected at the body's surface as an electrocardiogram. EKG monitoring is becoming more common in both inpatient and outpatient care settings. Nurses are asked to be responsible for cardiac patients, including monitoring and interpreting cardiac dysrhythmias. They must develop critical thinking skills that help them evaluate the significance of these dysrhythmias. A thorough understanding of cardiac

anatomy, physiology and properties can provide a framework for understanding and interpreting cardiac rhythms.

INTRODUCTION The most comprehensive work on human electrocardiogram was done by Willem Einthoven in 1903. He was awarded the Nobel Prize for this in 1924. ECG remains the most basic, non invasive, simple, fairly informative and routine modality of investigation in all cardiac evaluation. There is no substitute to the ECG with respect to studying disorders that

manifest as changes in the electrical activity of the heart. For examples in conditions like heart blocks, bundle branch blocks, arrhythmias, myocardial infarctions, etc., no other investigation can give information that the ECG can provide with such clarity and accuracy.

DEFINITION OF ECG

It is defined as a graphic presentation of the electrical potentials generated in the heart on a paper by surface electrodes. The electrical events are displayed as waveforms in different planes.

USES OF ECG

Atrial and /or ventricular hypertrophy Myocardial ischemia and infarction. It is a gold standard for diagnosis and management of arrhythmias. Conduction disturbance [heart blocks] Myocardial and pericardial diseases. Effects of drugs, electrolytes, poisons on the heart. Detection of efficacy of various cardiac intervention procedures i.e. angioplasty, bypass surgery.

Increased use in pacemaker functioning /dysfunctioning. Diagnoses asymptomatic coronary artery disease.

INTRODUCTION

Holters monitoring is used to relate symptoms with ECG and signal averaged ECG to determine prognosis of arrhythmias.

Chapter-2

NORMAL ECG
LEARNING OBJECTIVES: After studying this chapter, the reader will be able to
Discuss the electrical activity of the heart

Describe the electrode and lead system Identify the orientation of different leads

ELECTRICAL ACTIVITY OF THE HEART

The heart muscle possesses an intrinsic property of impulse formation and conduction. The sino atrial node is a natural pacemaker, generates the electrical potentials regularly due to its inherent property. The electrical potential generated in the heart (e.g. SA node), propagates, through the specialised conducting tissues in a waveform in a coordinated manner to produce an ECG complex consisting of P-QRS-T during one beat of the heart. Conducting System of Heart Sinoatrial node Atrioventricular node Bundle of his Purkinje fibers Fig. 2.1. Conducting System of Heart NORMAL ECG ECG Complex

An ECG complex (P QRS-T complex) indicates the total electrical events that occur during one beat. The P wave represents the atrial depolarisation and repolarisation of atria. The QRS-T complex represents ventricular activation (depolarisation) and recovery (repolarisation). The ECG complex records electrical impulses from the heart as deflections or waveforms on the graph paper. Normally, an individual cell is excitable but its activity does not reach to the surface because of a weak electrical potential; but cumulative effect of a group or group of cells can make electrical potential reproducible on the surface as resultant electrical force or potential which is recorded as deflections or waves The ECG complex involves two processes:

Atrial events Ventricular events Activation of atria (atrial events)

Normally, the SA node (a natural pacemaker) situated in the upper part of the right atrium generates impulses spontaneously and regularly. The electrical impulses from the SA node travel through three conducting pathways (anterior, middle and posterior intermodal pathways) to the atrioventricular (AV) node. These pathways transmit the electrical impulses to the atria muscle cells which get activated (depolarised) in an organised fashion to produce a P wave on the ECG.

Activation of ventricles (Ventricular events)

From the SA node, the impulses reach AV node where a slight physiological delay occurs. Now the impulse enters bundle of His which splits in to two conducting pathways i.e. right and left bundle branches. The right bundle branch conducts impulses to the right ventricle via a special network of conducting fibres called purkinje fibres.

NORMAL ECG

The left bundle branch further divides in to anterior and posterior fascicles which conduct the impulses to the anterior and posterior portions of the left ventricle via the purkinje system respectively. The ventricular activation (depolarisation) produces QRS. The recovery of left ventricle (repolarisation) is represented by ST segment and the T wave.

Fig. 2.2. Conducting System of Heart THE ELECTRODE AND LEAD SYSTEM

The Electrode: The ECG lead system consists of 5 electrodes; four for the limbs and one for the chest which is moved at different positions on the precordium. The lead system: A 12 lead surface ECG is standard and conventional method to record the electrical activity of the heart from 12 different views in two planes i.e. frontal and horizontal.

The two planes of 12 leads are Frontal plane leads include leads I, II, III, aVR, aVL and aVF. Horizontal plane leads include V1 to V6

NORMAL ECG

12 leads are classified into two lead systems as Limb leads(bipolar and unipolar) Chest electrodes and chest leads

Limb leads (bipolar and unipolar) The bipolar leads require two electrodes at a record the tracing; one act as a positive and the other as a negative electrode. The bipolar limb leads I, II and III. The same bipolar leads are used to form the unipolar limb leads i.e. aVR, aVL and aVF, where the letter a stands for augmented which means the electrical forces in these leads are enlarged in response to electrically created negative centre. The letter v stands for unipolar. These leads need one electrode for recording, hence called unipolar leads. This electrode is positive (+) with reference to electrically created negative centre in the machine which augments the electrical forces. Chest electrodes and chest leads: The chest leads are also unipolar leads where either a chest electrodes is moved at six different positions or six different chest electrodes are placed at different positions These leads are designated by the letter V as V1, V2, V3, V4, V5 and V6. The placement of electrodes as follows: V1- fourth intercostal space, right sternal border. V2 fourth intercostal space, left sternal border. V3 midway between V2-V4 V4- fifth intercostal space, left midclavicular line V5- fifth intercostals space, anterior axillary line V6- fifth intercostal space, mid axillary line. Fig. 2.3. Placement of chest leads NORMAL ECG

The same lead system can be used on the right side in a case of dextrocardia or to record right sided events in a case with pulmonary embolism, right ventricular infarction or right ventricular hypertrophy. Lead axis The theoretical line joining the two electrodes of a lead oriented in any particular direction is called axis of that lead or lead axis. This is different from electrical axis of the heart. ORIENTATION OF DIFFERENT LEADS

The 12 leads ECG consists of three limb leads (I, II, III), three unipolar leads (aVR, aVL and aVF) and six chest leads (V1-V6). The orientation of the ECG leads to the heart is as follows: Leads II, III and aVF are oriented to inferior surface of the heart i.e. they represent electrical events of inferior surface. Leads I and aVL are oriented to high and superior left lateral wall The lead aVR is a cavitary lead i.e. records all the negative waves (negative P-QRS T complex) Leads V1-V6 are oriented to anterior wall of the heart; leads V1-V4 are called anterioseptal leads, leads V5-V6 called apical leads V3-V4 called transition leads or interventricular septum leads. The electrocardiographic paper The electrocardigraphic [ECG] paper is a graph paper with horizontal and vertical lines at 1mm distance that intersect to form small and large squares respectively. Vertical measurement reflects voltage and horizontal measurement reflects time. Each small square is equal to 1mm, 0.04 second in time and 0.1mV in height. Each large square is bounded by a heavier or dark line, consists of 5 small squares [5mm], reflects 0.5Mv [height] and 0.2 second in duration. After every 5 big squares, the dark line extends on to the white upper border of the

NORMAL ECG

Fig. 2.4. The fundamentals of electrocardiographic paper Speed of the paper The ECG paper runs at a speed of 25mm per second. A faster speed of 50mm/sec may occasionally be employed to visualise wave deflections. Heart rate Heart rate (beats/min) on ECG implies ventricular rate which means the number of QRS in one minute. Normally, each QRS complex is preceded by P wave, hence heart rate also refers to atrial rate (the number of P waves/min), therefore, normally if each P wave is conducted and followed by a QRS, then atrial and ventricular rates are same.

NORMAL ECG Calculation of heart rate: Heart rate calculation depends on the regularity and irregularity of rhythm. If rhythm is regular, then heart rate is calculated by the:

The 1500 method: on ECG, one second is marked by a dark line on upper white border; comprises of 25 small squares; hence in one minute, there are 1500 (25x60) small squares. Count the QRS complexes or P waves in 12 such dark lines (time markers) and multiply it by 5 to get heart rate per minute, or count down in between 10 or 30 such lines and multiply it by 6 or 2 respectively to get heart rate. The R-R method : Divide 1500 by number of small squares counted in- between two consecutive QRS complexes to get the heart rate; for example, if there are 20 small squares in- between two successive R-R complexes, then heart rate is 1500/20 =75/min

If rhythm is irregular, then heart rate is calculated by six second method.

Six second method: Count the number of QRS within 6 seconds (within 30 big squares or within 6 dark lines representing the time marker.) and multiply the number obtained by 10 to get the approximate heart rate in one minute. This method is used in patients of atrial fibrillation to know the ventricular rate.

FUNDAMENTALS OF ECG

Normal electrocardiogram To define normalcy in electrocardiography is not only difficult but impossible task because of so many normal variations and physiological conditions affecting the ECG Conventionally, it is better to say that electrocardiogram is within normal limits rather than a normal electrocardiogram.

NORMAL ECG

The normal electrocardiogram means: Normal heart rate (60-100 bpm), sinus rhythm, normal QRS axis and a normal PQRS T complex provided the electrodes placement and ECG recording has been done under proper conditions. Components of an ECG complex:

Normally an ECG complex consists of: Waveforms: P-QRS-TU Segments : PR and ST Junction : QRS- T junction The normal P wave It is produced by atrial depolarisation, best seen in leads I, II, III and aVF. It is usually upright in all leads except aVR where it is always inverted. It can be inverted in leads III and aVL. P wave may be normally biphasic i.e. have both upward or positive and downward or negative reflection) in lead V1 and sometimes in V2.

The characteristic of P wave: Shape : upright Height : < 2.5mm Duration 0.08 to 0.10 sec but not > 0.11 sec in any circumstance Visibility best seen in leads I, II, aVF.

NORMAL ECG The normal QRS It is produced by ventricular depolarisation, is positive in all leads except aVR and is equiphasic (R=S) in leads V3 and V4. The characteristics of QRS complex: Width or duration of QRS is 0.04 to 0.10 sec, but should not exceed 0.11 sec in any lead normally. The VAT (ventricular activation time) is measured from the beginning of Q wave to top of the R wave, is 0.03 sec in right oriented leads V1-V2 and 0.05 sec in left oriented leads.(V5-V6) A transition complex consisting of an R and a S wave of equal amplitude, is normally seen in V3 or V4. The S wave The S wave is second negative deflection in QRS complex, produced by depolarisation of basal portion of the heart. Normally, as R wave progresses in height from V1-V6, the S wave decreases in depth from V1-V6, hence, it is Z. The normal T wave The normal T wave is a positive deflection representing the ventricular repolarisation. The T wave amplitude diminishes with age. The characteristics of normal T wave: It is an upright deflection in all leads except aVR. It has a blunt apex and follows QRS complex after ST segment. It is inscribed in the same direction as QRS complex.

NORMAL ECG The U wave The normal U wave is small, shallow, rounded upward deflection inscribed after the T wave and indicates delayed ventricular repolarisation. Normally it is best seen in leads V3 V4. The normal ECG intervals 1) The P-R interval: It is measured from the beginning of P wave to the beginning of Q wave is not seen. The normal characteristics of normal P-R interval are: Duration is 0.12 to 0.20 sec at normal heart rate. Varies with heart rate .at a heart rate of 60/min, the P-R interval of 0.22 sec is normal. It is normally short (<0.12 sec) in infants.

2) The QRS interval: It is measured from the beginning of QRS to its end point called J point. It actually represents the time taken by the depolarisation of the septum and ventricles from endocardial to epicardial surface. The characteristics are same as characteristics of QRS complex.

3) The QT interval : The interval between the beginning of QRS to the end of T wave is called QT interval. It represents the total activation of ventricles (depolarisation cum repolarisation). It varies with heart rate for which it is called corrected QT (QTc) interval.

Normal range of QTc = 0.35 to 0.4 sec Normal QTC; it is, <0.40 sec in males and <0.45 sec in females.

4) The QU interval : It is measured from the beginning of Q wave to the end of U wave provided U wave is seen.

NORMAL ECG

5) The P-P interval : It is the interval between two successive P waves. It is measured from the beginning of first p wave to the beginning of next p wave. It is used to calculate atrial rate similar to R-R method used to calculate ventricular rate i.e. 1500 /R-R OR P-P interval provided heart rate is regular. The clinical importance lies when atrial rate is different than ventricular rates. 6) The R-R interval: It is measured between two successive R waves i.e. measured from the beginning of one R wave to the beginning of next R wave. It is used to calculate ventricular rate. Slight variation in R-R interval may occur due to respiratory sinus arrhythmia. Irregular R-R intervals indicate disturbance in ventricular rhythm or irregular ventricular disturbance. Normal segments: PR segment: It is the distance between the end of the P wave to the beginning of QRS complex normally, it is isoelectric, hence it is used as baseline to evaluate the deviation of ST segment. The ST segment:

It is the distance from the end of S wave to the beginning of T wave The TP segment: It is the portion of tracing between the end of T wave and the beginning of the next P wave. The R-S junction: The R-S junction is called J point at which QRS ends with S wave returning to the baseline and ST segment starts.

NORMAL SINUS RHYTHM

Ventricular and atrial rate: 60 -100 [adult] Ventricular and atrial rhythm: Regular QRS shape and duration: usually normal. P wave : normal and consistent shape; always in front of the QRS PR interval : Consistent interval between 0.12 and 0.20 sec P:QRS ratio :1:1 Fig. 2.5. Normal Sinus Rhythm

Chapter-3
ECG IN PATIENTS WITH MYOCARDIAL INFARCTION

LEARNING OBJECTIVES: After studying this chapter, the reader will be able to Define myocardial infarction
Discuss the risk factors

Identify the ECG changes Describe the collaborative management Myocardial infarction DEFINITION is most

commonly due to occlusion of a coronary Myocardial infarction commonly known as a heart attack is the interruption of artery following the rupture of a vulnerable blood supply to a part of the heart, causing heart cells to die. atherosclerotic plaque, which is an unstable collection of lipids and macrophages in the wall of an artery. Ischemia is left untreated for a sufficient period of time, can cause damage or death (infarction) of myocardium.

Fig. 3.1. Occlusion of coronary arteries in heart ECG IN PATIENTS WITH MYOCARDIAL INFARCTION

RISK FACTORS

Modifiable risk factors include

Diabetes (with or without insulin resistance) most important risk factor Tobacco smoking Hyperlipoproteinemia especially high LDL and Low HDL High Triglycerides High blood pressure Family history of ischemic heart disease (IHD) Obesity (defined by a body mass index of more than 30 kg/m, or waist-hip ratio). Age: Men at age 45 Women at age 55 A first-degree male relative (brother, father) who suffered a coronary vascular event at or before age 55 or has a first-degree female relative (mother, sister) who suffered a coronary vascular event at age 65 or younger.

High homocysteine insufficient due to insufficient intakes of vitamins B2, B6, B12 and folic acid

Stress High quantities of alcohol Males are more at risk than females.

Non-modifiable risk factors include Age Sex Family history of an early heart attack (before the age of 60) Socioeconomic factors Unmarried cohabitation oral contraceptive pills Periodontitis ECG IN PATIENTS WITH MYOCARDIAL INFARCTION Basic types of acute myocardial infarction

Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply.

Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. Clinically, a myocardial infarction can be sub classified based on ECG changes as ST elevation MI (STEMI) Non-ST elevation MI (non-STEMI)

A 2007 consensus document classifies myocardial infarction into five main types:

Type 1 Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection. Type 2 Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension.

Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood

Type 4 Associated with coronary angioplasty or stents: Type 4a Myocardial infarction associated with PCI Type 4b Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy.

Type 5 Myocardial infarction associated with CABG A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation, totally occluding the artery and preventing blood flow downstream. ECG IN PATIENTS WITH MYOCARDIAL INFARCTION SUMMARY OF ECG CHANGES IN CAD, ISCHEMIA AND MI

EKG Markers of underlying CAD Left Ventricular Hypertrophy ST segment changes T Wave changes Diagnostic Q Waves in 2 contiguous leads Left Bundle Branch Block or other conduction changes Deep symmetric T-wave inversion General EKG Changes suggestive of Ischemia General EKG Changes suggestive of acute MI Electrocardiogram may be completely normal ST Elevation or ST depression Over 1 mm ST changes that are transient with New left ventricular strain pattern New Left Bundle Branch Block Q Waves (.04 sec and 1/3 height of R Wave)

symptoms Summed ST deviation (sum of affected leads) >2.5 mm Occurs in multiple precordial leads Left main coronary artery stenosis marker aVR ST segment elevation > V1 ST segment elevation Anterior MI Anatomic Distribution EKG Changes Lead V3 to lead V4 Distribution Left Coronary Artery: LAD-Diagonal branch Findings: Lateral MI Anatomic Distribution ST segment elevation in leads V5, V6, I, AVL ST segment depression in leads V1, V2, V3 Distribution Left Coronary Artery: Circumflex branch Posterior Infarction Anatomic Distribution Lead V1 to Lead V4 ST depression Distribution Left Coronary Artery: Circumflex Right Coronary Artery: Posterior descending

Unless isolated in Lead III T Wave inversion Unless isolated to Lead III or Lead V1 ST-T elevation (>1mm in limb or precordial leads) Must have >=2 concordant leads with changes ST depression in Lead V1, Lead V2 (Posterior MI) Hyperacute T Waves (over 50% of preceding Septal MI Anatomic Distribution Electrocardiogram Changes Lead V1 to lead V2 Distribution Left Coronary Artery: LAD-Septal Branch Findings: Inferior MI Anatomic Distribution Lead II, Lead III, and Lead aVF Distribution Right Coronary Artery: Posterior descending branch Complications RV Infarction Anatomic Distribution Lead V4R (Lead V4 placed on Right chest) Distribution Right Coronary Artery: Proximal branches Complications Diagnosis >1mm ST Elevation in V4R Suspect in Inferior MI

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION STEMI ST elevation in contiguous leads T waves flattening T wave inversion Develop new Q waves ST segments classically normalize Persistent ST elevation with development of an LV aneurysm NSTEMI Widespread ST depression ST-T changes

Fig. 3.2. Sequence of changes seen during evolution of myocardial infarction In the early stages of acute myocardial infarction the electrocardiogram may be normal or near normal; less than half of patients with acute myocardial infarction have clear diagnostic changes on their first trace. About 10% of patients with a proved acute myocardial infarction (on the basis of clinical history and enzymatic markers) fail to develop ST segment elevation or depression. Hyperacute T waves The earliest signs of acute myocardial infarction are subtle and include increased T wave amplitude over the affected area. T waves become more prominent, symmetrical, and pointed (hyperacute). Hyperacute T waves are most evident in the anterior chest leads and are more readily visible when an old electrocardiogram is available for comparison.

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION

Fig. 3.3. ECG changes in anterior myocardial infarction Anterior MI Yellow indicates V1, V2, V3, V4 Anterior infarct with ST elevation Left Anterior Descending Artery (LAD) V1 and V2 may also indicate septal involvement which extends from front to the back of the heart along the septum LBBB RBBB 2nd Degree Type2Complete Heart block

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION Inferior MI Blue indicates leads- Inferior II, III, AVF Inferior Infarct with ST elevations Right Coronary Artery (RCA) 1st degree Heart Block 2nd degree Type 1, 2 3rd degree Block N/V common, Brady

Fig. 3.4. ECG changes in inferior myocardial infarction

Lateral MI Red indicates leads I, AVL, V5, V6. Lateral infarcts with ST ELEVATION Left Circumflex artery Rarely by itself Usually in combo.

Fig. 3.5. ECG changes in lateral myocardial infarction

Posterior MI Green indicates leads V1, V2 Posterior Infarct with ST Depressions and/ tall R wave RCA and/or LCX Artery Understand Reciprocal changes The posterior aspect of the heart is viewed as a mirror image and therefore depressions versus elevations indicate MI Rarely by itself usually in combo

Fig. 3.6. ECG changes in posterior myocardial infarction

Sub Endocardial infarcts

No color for Sub Endocardial infarcts since they are not transmural Look for diffuse or localized changes and non Q wave abnormalities T-wave inversions ST segment depression

Fig. 3.7. ECG changes in sub endocardial infarction

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION

A combination of infarctions Anterolateral yellow and red Inferoposterior blue and green Anteroseptal yellow and green

Fig. 3.8. ECG changes in combination of infarction

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION The WHO criteria a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention is diagnostic of MI.

COLLABORATIVE MANAGEMENT

Prevention of MI in patients with atherosclerosis Strict blood pressure management Lifestyle changes, Smoking cessation Regular exercise,

A sensible diet for patients with heart disease Limitation of alcohol intake. Long-term medications post-MI, The consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. Anti platelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin

Beta blocker therapy such as metoprolol or carvedilol should be commenced for those with left ventricular dysfunction and/or continuing cardiac ischemia.

ACE inhibitor therapy should be commenced 2448 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct and/or evidence of left ventricular dysfunction to prevent the development of heart failure, and decrease ventricular remodelling post-MI.

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION Statin therapy their LDL lowering effects plaque stabilization and multiple other ("pleiotropic") effects The aldosterone antagonist agent epiderenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction,. Spironolactone is another option that is sometimes preferable to eplerenone due to cost. Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI. due to electrical stabilization and the prevention of ventricular fibrillation. Blood donation may reduce the risk of heart disease for men Heparin to people who have heart conditions like unstable angina and some forms of heart attack reduces the risk of having another heart attack. (Cochrane review) An MI is a medical emergency and treatment attempts to salvage as much myocardium as possible and to prevent further complications, thus the phrase "time is muscle".

Fig. 3.9. Treatment of acute coronary syndrome

ECG IN PATIENTS WITH MYOCARDIAL INFARCTION The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. Indications for thrombolytic treatment ST elevation >1 mm in two contiguous limb leads or >2 mm in two contiguous chest leads

Posterior myocardial infarction Left bundle branch block

ST segment depression or enzymatic changes are not indications for thrombolytic treatment

Fig. 3.10. Acute medical management of unstable angina and NSTEMI

Chapter-4
ECG IN PATIENTS WITH ATRIAL ARRHYTHMIAS
LEARNING OBJECTIVES: After studying this chapter, the reader will be able to Define various atrial dysrhythmias
Discuss the causes of atrial dysrhythmias List the types of atrial dysrhythmias

Identify the ECG changes in various types

DESCRIPTION

Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart. These disorders can cause disturbances of the heart rate, the heart rhythm, or both. Dysrhythmias may initially be evidenced by the hemodynamic effect they cause (e.g. A change in conduction may change the pumping action of the heart and cause decreased blood pressure). Cardiac monitoring is now used in wide range of hospital, clinic and home settings. Prompt assessment of dysrhythmias and the patients response to the rhythm is critical. CAUSES Cardiac Conditions Accessory pathways Cardiomyopathy Conduction defects Heart failure Myocardial cell degeneration Myocardial infarction Valve disease Acid-base Imbalance Alcohol Caffeine, tobacco Connective tissue disorders Drug effects (e.g., antidysrhythmias drugs, stimulants, - adrenergic blockers) or toxicity Electric shock Electrolyte imbalance (e.g., hypokalemia, hypocalcaemia) Emotional crisis

Other Conditions

Herbal supplements. Hypoxia, shock Metabolic conditions

Types of Dysrhythmias Sinus Node Dysrhythmias Atrial Dysrhythmias Junctional Dysrhythmias Ventricular Dysrhythmias Conduction Abnormalities

TYPES OF ATRIAL DYSRHYTHMIAS

PREMATURE ATRIAL COMPLEX

Definition A premature atrial complex is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node. Causes Alcohol Caffeine Nicotine Anxiety or Emotional stress Physical fatigue Hypokalemia

Hypermetabolic states or Atrial Ischemia, injury or Infarction Stretched atrial myocardium (as in Hyper volemia) Hypoxia Electrolyte Imbalances Chronic obstructive pulmonary disease (COPD) Hypothyroidism Coronary artery disease Valvular disease

ECG characteristics , Fig. 4.1. ECG characteristics in Pre mature atrial complex Ventricular and Atrial rate: Depends on the underlying rhythm (e.g., Sinus tachycardia) 60-100 beats/minute and irregular. Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP interval i.e. shorter than the others. This is sometimes followed by a longer than normal PP interval, but one that is less than twice the normal PP interval. This type of interval is called a Non-compensatory pause. P wave: P wave may be notched or have downward (or negative) deflection or it may be hidden in the preceding T wave. PR interval: Normally the early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20 seconds. QRS complex: Usually normal. P: QRS ratio: Usually 1:1

Clinical significance

It is usually seen in patients with heart disease. PACs are common in normal hearts. The patient may say, My heart skipped a beat. A pulse deficit (a difference between the apical and radial pulse rate) may exist. Treatment If PACs are infrequent, no treatment is necessary. If they are frequent (more than 6 per minute), this may herald a worsening disease state or the onset of more serious dysrhythmias, such as atrial fibrillation. Treatment is directed toward the cause. -Adrenergic blockers may be used e.g., Atenolol (Tenormin), Metoprolol (lopressor)

ATRIAL FLUTTER Definition

Atrial Flutter is an atrial tachy dysarhythmia identified by recurring, regular, saw tooth-shaped flutter (F wave) that originate from a single ectopic focus in the right atrial.

Fig. 4.2. Atrial flutter Clinical Association It is associated with CAD

Hypertension Mitral valve disorders Pulmonary embolus Chronic lung disease & cor pulmonale Cardio myopathy Hyperthyroidism & use of drugs such as Digoxine, Quinidine & epinephine.

Fig. 4.3. ECG showing Saw toothed P wave

Fig. 4.4. ECG characteristics in atrial flutter with a 4:1 conduction four flutter (f waves) to each QRS complex Ventricular and Atrial rate: Arial rate ranges between 250 & 400; Ventricular rate usually ranges between 75 & 150. Ventricular and atrial rhythm: The atrial rhythm is regular; the Ventricular rhythm is usually regular but may be irregular because of the change in the AV conduction P wave: Saw toothed shape. These waves are referred to as F waves PR interval: Multiple F waves may make it difficult to determine the PR interval (not measurable). QRS complex: Normal (usually) P: QRS ratio: 2:1, 3:1, or 4:1

Clinical significance High ventricular rates >100 beats/minutes loss of the atrial kick (atrial contraction reflected by a sinus P wave) that are associated with atrial flutter can cause serious signs and symptoms such as Chest pain Shortness of Breath Low blood pressure Decrease cardiac output Heart Failure Stroke (because of thrombus formation) Calcium channel blockers- verapamil (isoptin), Diltiazem (cardizen) Beta blockers- Digitalis may be administered intravenously. Sodium channel blockers- Flecainide (Tambocor), Ibutilide (Corvert), Quinidinde (Cardioquin) or Amiodarone (Cordarone) may be given to promote conversion to sinus rhythm. ATRIAL FIBRILLATION Definition

Treatment

Atrial Fibrillation causes a rapid, disorganized and uncoordinated twitching of atrial musculature (atrial contraction). It is the most common dysrhythmia that causes patients to seek medical attention. It may start and stop suddenly. or it may be chronic. It may occur for a very short time (paroxysmal)

Fig. 4.5. Atrial Fibrillation Clinical Association It is associated with Advanced Age Valvular heart disease CAD Hyper tension Cardiomyopathy Hyperthyroidism Pulmonary disease Acute moderate or heavy ingestion of alcohol (holiday heart syndrome) After math of open heart surgery Mitral valve disorders

Sometimes it occurs in people without any underlying pathophysiology (termed) lone atrial fibrillation.

Fig. 4.6. ECG showing Atrial Fibrillation ECG characteristics seen in Atrial Fibrillation

Fig. 4.7. ECG characteristics seen in Atrial Fibrillation Note: The Chaotic Fibrillatory (F) Waves Between The QRS Complexes.

Ventricular and atrial rate: Atrial rate is 300 to 600b/m. Ventricular rate is usually 120 to 200 in untreated atrial fibrillation Ventricular and atrial rhythm: Highly irregular QRS shape and duration: Usually normal, but may be abnormal. P wave: No discernible P waves; irregular undulating waves are seen and are referred to as fibrillatory or f waves. PR internal: Cannot be measured. P: QRS ratio: many: 1

Clinical Significance Atrial Fibrillation can often result in decrease in Cardiac output rapid Ventricular response, stroke (Embolised Clot), heart disease, and hypertension Treatment It depends on its cause and duration and the patients symptoms, age and co morbidities. In many patients, atrial fibrillation converts to sinus rhythm within 24 hours and

without treatment. Cardio version may be indicated for atrial fibrillation that has been present for less than 48 hours, a condition termed acute onset atrial fibrillation.
Heart Heart Disease Disease No No (or (or minimal) minimal) Heart Heart Failure Failure Amiodarone Amiodarone Dofetilide Dofetilide CAD CAD Sotalol Sotalol Amiodarone Amiodarone Dofetilide Dofetilide Disopyramide Disopyramide Procainamide Procainamide Quinidine Quinidine Amiodarone Amiodarone Yes Yes Hypertension Hypertension LVH LVH greater greater than than or or equal equal to to 1.4 1.4 cm cm Yes Yes No No Flecainide Flecainide Propafenone Propafenone Amiodarone Amiodarone Dofetilide Dofetilide Sotalol Sotalol

Flecainide Flecainide Propafenone Propafenone Sotalol Sotalol

Amiodarone, , Dofetilide Amiodarone Amiodarone, Dofetilide

Disopyramide Disopyramide Procainamide Procainamide Quinidine Quinidine

Consider Consider nonpharmacological nonpharmacological options options

Disopyramide, , Procainamide, , Quinidine Disopyramide Procainamide Disopyramide, Procainamide, Quinidine

Fig. 4.8. Algorithm to Maintain Sinus Rhythm in Patients with Recurrent Paroxysmal or Persistent Atrial Fibrillation Medications Drugs such as Flecainide (Tambocor), Ibutilide (Corvert), Quinidinde (Cardioquin) or Amiodarone (Cordarone) may be given to promote conversion to sinus rthythm. Calcium channel blockers can be used e.g., verapamil (isoptin), Diltiazem (cardizen) Beta blockers e.g., Drug such as Digitalis may be administered intravenously. In addition, warfarin is indicated if the patient is at high risk for a stroke (Elderly, hypertension, heart failure). Aspirin may be substituted for warfarin for patient with contraindication to warfarin and lower risk of stroke. Pacemaker implantation or surgery is indicated for patients who are unresponsive to medications. SUMMARY OF ATRIAL ARRTHYMIAS

PATTERN

RATE&RTYTHM

P WAVE

PR INTERVAL

QRS COMPLEX

PRE MATURE ATRIAL COMPLEX ATRIAL FLUTTER

Usually 60-100 Beats /Minute & Irregular Atrial: 250-350 Beats/Minute & Regular Ventricular:> or <100 Beats /Minute & may Be Regular or Irregular Abnormal Shape Flutter(F) Waves (Saw Toothed Pattern; More Flutter Waves than QRS Complexes; may occur In 2:1, 3:1, 4:1, etc pattern Fibrillatory (F) Waves Not Measurable Normal Normal Not Measurable Normal Normal

ATRIAL FIBRILLATION

Atrial:350-600 Beats/Minute & Irregular Ventricular:>or<100 Beats/Minute &Irregular

Chapter-5
ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS
LEARNING OBJECTIVES: After studying this chapter, the reader will be able to Define Ventricular dysrhythmias List various types of Ventricular dysrhythmias
Discuss the risk factors

Identify the ECG changes

DESCRIPTION Ventricular dysrhythmias originate in the ventricular muscle or purkinje system and are considered to be more dangerous than other arrhythmias because of their potential to limit cardiac output severely. TYPES

Premature ventricular complexes Accelerated ventricular rhythm Ventricular tachycardia Ventricular flutter Ventricular fibrillation Ventricular asystole

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS PREMATURE VENTRICULAR COMPLEX Ventricular premature beats arise in one of the branches of the bundle of His, the Purkinje network or the ventricular muscle, due to Enhanced normal automaticity impulse initiation can be shifted from the sinus node to the other parts on the heart if the rate of the sinus node drops below that of the subsidiary pacemaker. Abnormal automaticity - atrial and ventricular myocardial cells that do not normally have automaticity can develop abnormal automaticity when their trans membrane resting potential is reduced. Re entry in ventricles it is a type of conduction abnormality that leads to occurrence of premature beats or sustained tachycardia rather than to block. It

occurs in the areas where the conduction velocity is abnormally slow because of ischemia, electrolyte imbalance. After depolarization after depolarization is a transient depolarization of the cell membrane that occurs at some time during or right after depolarization of an action potential.

Fig. 5.1. Normal action potential conduction

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS

Fig. 5.2. Action potential conduction of ischemia and re-entry arrhythmia

Causes Types Multifocal PVC: PVCs that are initiated from different foci appear different in contour from each other. Unifocal PVC: PVCs that appear to have same contour Ventricular Bigeminy: every other beat is a PVC Ventricular Trigeminy: every third beat is a PVC Couplets: Two consecutive PVCs Triplets/Salvo: Third consecutive PVCs ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS Hypoxia Myocardial ischemia Hypokalemia Acidosis Exercise Increased catecholamine Digitalis toxicity Caffeine and Alcohol

Criteria for diagnosis of PVC Ectopic beat occurs prematurely, before the next anticipated sinus beat The rhythm is regularly irregular The QRS complex is premature, is 0.12second or more wide and is aberrant, notched or slurred. It is associated with a T wave that usually point in a direction opposite to the main deflection of the QRS complex The premature QRS complex is not preceded by a P wave. A ventricular premature beat is often followed by a fully compensatory pause (the sum of the R-R intervals including the pre-premature beat and the post-premature beat interval equals the sum of two normal R-R intervals)

Fig. 5.3. ECG showing premature ventricular contractions

The ST segment is in opposite direction of QRS complex. P wave are absent before the ectopic beat. Multiply, ventricular premature beats that arise from a single focus show a similar shape and usually a similar coupling intervals (distance from the preceding normal QRS complex to the premature ventricular beat) in any one lead. Occasionally, a ventricular premature beat will occur simultaneously with the apex of the preceding T wave. This is R on T phenomenon. When this occurs, it may be a precursor of a ventricular tachycardia. Note: multifocal ventricular premature beat (VPB) and multiformed VPB

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS

Fig. 5.4. ECG showing R on T phenomenon Note: vulnerable period- If PCV is generated during this time ventricular fibrillation occur

Clinical associations PVC increases with aging

It is more common in people with Coronary artery disease Valve disease Hypertension Cardiomyopathy Other forms of heart disease

Treatment IV lidocaine Antiarrhythmic drugs as IV procainimide, amiodronate To reduce PVC frequency Low dose beta blockers Quinidine Disopyramide Sotalol Tocainide Moricizine Propafenone

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS ACCELERATED IDIOVENTRICULAR RHYTHM

Definition It occurs when an ectopic focus in the ventricles fires at a rate of 50 to 100 beats per minute Cause Inferior MI Reperfusion with thrombolytic therapy

ECG characteristics Pattern Accelerated Idioventricular Rhythm Rate 50 to 100 beats/min Rhythm Usually regular P wave Present but dissociated from QRS PR interval Interval Not present QRS Complex Wide and bizarre

Treatment Usually it is transient and benign and does not require treatment. Atropine can be used to increase rate of the sinus node and overdrive the ventricular rhythm Suppressive therapy may be used VENTRICULAR TACHYCARDIA Definition It is a rapid ventricular rhythm most likely due to re-entry in the ventricles, although automaticity of an ectopic focus and after depolarisations may also be mechanisms of VT

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS Types 1. Based on Duration 1. Non sustained- last <30 seconds 2. Sustained- last >30 seconds 3. Incessant- VT present most of the time 2. Based on Morphology (ECG appearance of QRS complexes) 1. Monomorphic- QRS complexes have same shape during tachycardia 2. Polymorphic- QRS complexes vary randomly in shape 3. Bidirectional alternating upright and negative QRS complexes during tachycardia

Fig. 5.5. Monomorphic- VT

ProarrhythmiaTorsaides It means Twitching of the points and describe special type of polymorphic VT in which QRS complex display continuously changing morphologies and seem to twist around the imaginary line.

Fig. 5.6. ProarrhythmiaTorsaides

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS Causes Coronary heart disease Acute ischemia and MI Cardiomyopathy Valve disease Hypertension Congenital heart disease Arrhythmogenic right ventricular dysplasia Cardiac tumours

Cardiac surgery Proarrythmic effects of many drugs

ECG Characteristics Pattern Ventricular tachycardia 100250beats/min Rate Rhythm Regular or irregular P wave Not usually present PR interval Not measurable QRS complex Wide and disorted

Treatment Immediate defibrillation Synchronized cardio version is not possible because there are no formed QRS complex If it does not convert after three shocks, continue CPR and start drug therapy Antiarrythmic drugs lidocaine, procainamide, amiodarone, or magnesium Once the rhythm has converted, maintanence therapy with IV antiarrythmic drugs is continued Implantable cardioverter defibrillator

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS

VENTRICULAR FLUTTER It is same as VT, but the rate is faster It is more dangerous because there is virtually no cardiac output

ECG Characteristics Pattern Rate Rhythm P wave PR Interval QRS Complex

Ventricular flutter

220400beats/min

Usually regular

None seen Not measurable

Very wide, regular, sine wave type of pattern

Treatment Immediate defibrillation CPR if defibrillator is not available Antiarrythmic drugs after converting the rhythm If not symptomatic, lidocaine can be used Maintenance therapy- same as for PVC VENTRICULAR FIBRILLATION

It is rapid, ineffective quivering of the ventricles. It is fatal without immediate treatment It is most frequent cause of sudden cardiac death There will be no cardiac output or palpable pulse

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS ECG characteristics

Fig. 5.6. Ventricular fibrillation

Pattern

Rate

Rhythm

P wave

PR Interval

QRS Complex

Ventricular fibrillation

Not measurable

Irregular

Absent

Not measurable

Not measurable

Treatment If severely symptomatic, cardio version can be done Defibrillation can also be used If not symptomatic, lidocaine can be used IV procainimide, amiodronate or magnesium sulphate Maintenance therapy- same as for PVC VENTRICULAR ASYSTOLE

Definition It is the absence of any ventricular rhythm; there is no QRS complex, no pulse and no cardiac output. It is always fatal unless treated immediately

ECG IN PATIENTS WITH VENTRICULAR ARRHYTHMIAS ECG characteristics Pattern Rate Rhythm P wave PR Interval QRS Complex None

Ventricular asystole None None

May be present None

Treatment Initiate CPR immediately IV epinephrine and atropine- to stimulate rhythm

SUPRAVENTRICULAR TACHYCARDIA (SVT)

Definition Supraventricular tachycardia (SVT) means that from time to time your heart beats very fast for a reason other than exercise, high fever, or stress. Types Causes Faulty electrical connections in the heart Very high levels of the heart medicine digoxin (such as Lanoxicaps or Lanoxin) or the lung medicine theophylline (such as Theochron or Uniphyl). Family history of Wolff-Parkinson-White syndrome. Lung problem such as COPD or pneumonia. Atrioventricular nodal reentrant tachycardia (AVNRT). Atrioventricular reciprocating tachycardia (AVRT), including Wolff-Parkinson-White syndrome.

Clinical features Some people with SVT have no symptoms. Others may have: Palpitations, a feeling that your heart is racing or pounding. A pounding pulse. A dizzy feeling or may feel lightheaded. Other symptoms include, near-fainting or fainting (syncope), shortness of breath, chest pain, throat tightness, and sweating. Management Medicine such as adenosine or verapamil. If the SVT is serious, electrical cardioversion can be used.

Prevention

Limit alcohol to 2 drinks a day if you are a man and 1 drink a day if you are a woman. Limit caffeine. Even decaffeinated teas or coffee can cause SVT in some people. Don't smoke. Avoid over-the-counter decongestants, herbal remedies, diet pills, and "pep" pills. Don't use illegal drugs, such as cocaine, ecstasy, or methamphetamine.