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The. ECG. Made Easy. EIGHTH EDITION. John R. Hampton. DM MA DPhil FRCP FFPM FESC. Emeritus Professor of Cardiology. University of Nottingham, UK. 𝗣𝗗𝗙 | A true medical classic should be novel, stimulate thought and discussion, transcend both specialty and experience, and most importantly be moreish. John R. Hampton-The ECG Made Easy-Churchill Livingstone ().pdf. Ashraf Alqudwa. Figure The structure of [M(N2S2)]. The ECG Made Easy For.

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Library of Congress Cataloging-in- Publication Data. ECG interpretation made incredibly easy!. —. 5th ed. p. ; cm. Includes bibliographical references and index . With significant hypertrophy 92 Abnormalities of P waves, QRS complexes and T waves left ventricle, depolarization of The ECG Made Easy 8th. For forty years The ECG Made Easy has been regarded as one of best introductory guides to the ECG. With over half a million sales and.

A description of the ST segments and T waves. However, you must think about all the findings every time you interpret an ECG. The interpretation of an ECG indicates whether the record is normal or abnormal: Figures 1.

Lead V1 is positioned over the right ventricle, and lead V6 over the left ventricle. Recognizing the limits of normality is one of the main difficulties of ECG interpretation. If the first deflection is downward, it is a Q wave. Any upward deflection is an R wave. A downward deflection after an R wave is an S wave.

When the wave spreads away from a lead, the deflection is predominantly downward. The conduction of this wave front can be delayed or blocked at any point.

However, conduction problems are simple to analyse, provided you keep the wiring diagram of the heart constantly in mind Fig. We can think of conduction problems in the order in which the depolarization wave normally spreads: Remember in all that follows that we are assuming depolarization begins in the normal way in the SA node. The rhythm of the heart is best interpreted from whichever ECG lead shows the P wave most clearly.

This is usually, but not always, lead II or lead V1. First degree heart block is not in itself important, but it may be a sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturbances.

There may be alternate conducted and nonconducted atrial beats or one conducted atrial beat and then two or three nonconducted beats , giving twice or three or four times as many P waves as QRS complexes. It is important to remember that, as with any other rhythm, a P wave may only show itself as a distortion of a T wave Fig.

There are three variations of this: There may be progressive lengthening of the PR interval and then failure of conduction of an atrial beat, followed by a conducted beat with a shorter PR interval and then a repetition of this cycle. Most beats are conducted with a constant PR interval, but occasionally there is atrial First degree heart block Fig.

The Wenckebach phenomenon is usually benign, but Mobitz type 2 block and 2: You have to look at the PR interval in all the leads to see that there is no consistency. Complete heart block may occur as an acute phenomenon in patients with myocardial infarction when it is usually transient or it may be chronic, usually due to fibrosis around the bundle of His.

It may also be caused by the block of both bundle branches. The extra time taken for depolarization of the whole of the ventricular muscle causes widening of the QRS complex. In the normal heart, the time taken for the depolarization wave to spread from the interventricular septum to the furthest part of the ventricles is less than ms, represented by three small squares of ECG paper.

If the QRS complex duration is greater than ms, then conduction within the ventricles must have occurred by an abnormal, and therefore slower, pathway.

A wide QRS complex can therefore indicate bundle branch block, but widening also occurs if depolarization begins within the ventricular muscle itself see Ch. However, remember that in sinus rhythm with bundle branch block, normal P waves are present with a constant PR interval.

We shall see that this is not the case with rhythms beginning in the ventricles.

Block of both bundle branches has the same effect as block of the His bundle, and causes complete third degree heart block. Left bundle branch block LBBB is always an indication of heart disease, usually of the left ventricle. It is important to recognize when bundle branch block is present, because LBBB prevents any further interpretation of the cardiogram, and RBBB can make interpretation difficult. Remember see Ch. The right ventricle therefore depolarizes after the left.

It is seldom of significance, and can be considered to be a normal variant. Excitation then spreads to the left ventricle, causing an S wave in lead V1 and an R wave in lead V6 Fig. It takes longer than in a normal heart for excitation to reach the right ventricle because 44 Conduction and its problems Conduction in right bundle branch block: The right ventricle is depolarized before the left, so despite the smaller muscle mass there is an R wave in lead V1 and an S wave often appearing only as a notch in lead V6 Fig.

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Remember that any upward deflection, however 2Problems in the right and left bundle branches 45 Conduction in right bundle branch block: Subsequent depolarization of the left ventricle causes an S wave in lead V1 and another R wave in lead V6 Fig. Conduction in left bundle branch block: The depolarization wave therefore spreads into the ventricles by three pathways Fig.

The cardiac axis see Ch. Because the left ventricle contains more muscle than the right, it has more influence on the cardiac axis Fig. If the anterior fascicle of the left bundle branch fails to conduct, the left ventricle has to be depolarized through the posterior fascicle, and so the cardiac axis rotates upwards Fig.

When the right bundle branch is blocked, the cardiac axis usually remains normal, because there is normal depolarization of the left ventricle with its large muscle mass Fig. If the right bundle branch and both fascicles of the left bundle branch are blocked, complete heart block occurs just as if the main His bundle had failed to conduct.

Relief of symptoms always comes first. However, some general points can be made about the action that might be taken if the ECG shows conduction abnormalities. When depolarization begins in the SA node the heart is said to be in sinus rhythm. Depolarization can, however, begin in other places. When attempting to analyse a cardiac rhythm remember: The keys to rhythm abnormalities are: Look for the lead in which they are most obvious.

The stars in the figures in this chapter indicate the part of the heart where the activation sequence began. The SA node normally has the highest frequency of discharge. Therefore the rate of contraction of the ventricles will equal the rate of discharge of the SA node. The rate of discharge of the SA node is influenced by the vagus nerves, and also by reflexes originating in the lungs.

Although Figure 3. In the supraventricular 58 The rhythm of the heart Division of abnormal rhythms into supraventricular and ventricular Fig. In ventricular rhythms, on the other hand, the depolarization wave spreads through the ventricles by an abnormal and slower pathway, via the Purkinje fibres Fig.

The QRS complex is therefore wide and is abnormally shaped. Repolarization is also abnormal, so the T wave is also of abnormal shape. Abnormal rhythms arising in the atrial muscle, the junctional region or the ventricular muscle can be categorized as: The QRS complex is therefore normal, and is the same whether depolarization was initiated by Spread of the depolarization wave in supraventricular rhythms Fig.

However, the protective mechanisms must normally be inactive if competition between normal and abnormal sites of spontaneous depolarization is to be avoided.

This is achieved by the secondary sites having a lower intrinsic frequency of depolarization than the SA node. The heart is controlled by whichever site is spontaneously depolarizing most frequently: Escape rhythms are not primary disorders, but are the response to problems higher in the conducting pathway.

They are commonly seen in the acute phase of a heart attack, when they may be associated with sinus bradycardia. It is important not to try to suppress an escape rhythm, because without it the heart might stop altogether. Atrial escape beats can occur singly. Ventricular escape rhythms can occur without complete heart block, and ventricular escape beats can be single Fig.

The rhythm of the heart can occasionally be controlled by a ventricular focus with an intrinsic frequency of discharge faster than that seen in complete heart block.

Although the appearance of the ECG is similar to that of ventricular tachycardia described later , accelerated idioventricular rhythm is benign and should not be treated. The ECG appearance of an extrasystole arising in the atrial muscle, the junctional or nodal region, or the ventricular muscle, is the same as that of the corresponding escape beat — the difference is that an extrasystole comes early and an escape beat comes late.

Atrial extrasystoles have abnormal P waves Fig.

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In a junctional extrasystole there is Accelerated idioventricular rhythm Fig. The QRS complexes of atrial and junctional extrasystoles are, of course, the same as those of sinus rhythm. Ventricular extrasystoles, however, have abnormal QRS complexes, which are typically wide and can be of almost any shape Fig. Ventricular extrasystoles are common, and are usually of no importance. However, when they occur early in the T wave of a preceding beat they can induce ventricular fibrillation see p.

It may, however, not be as easy as this, particularly if a beat of supraventricular origin is conducted abnormally to the ventricles 64 The rhythm of the heart R on T phenomenon: Ventricular extrasystole Fig. It is advisable to get into the habit of asking five questions every time an ECG is being analysed: Does an early QRS complex follow an early P wave? If so, it must be an atrial extrasystole. Can a P wave be seen anywhere? A junctional extrasystole may cause the appearance of a P wave very close to, and even after, the QRS complex because excitation is conducted both to the atria and to the ventricles.

Is the QRS complex the same shape throughout i. Supraventricular beats look the same as each other; ventricular beats may look different from each other. Is the T wave the same way up as in the normal beat? In supraventricular beats, it is the same way up; in ventricular beats, it is inverted.

Does the next P wave after the extrasystole appear at an expected time? The effects of both supraventricular and ventricular extrasystoles on the following P wave are as follows: The criteria already described can be used to decide the origin of the arrhythmia, and as before the most important thing is to try to identify a P wave.

The difference between this sort of atrioventricular block and second degree heart block is that in atrioventricular block 66 The rhythm of the heart No P wave Expected P waveP Ventricular extrasystole Fig. When atrial tachycardia or atrial flutter is associated with 2: Any arrhythmia should be identified from the lead in which P waves can most easily be seen. In the record in Figure 3.

Junctional tachycardia: Junctional nodal tachycardia Fig. The QRS complexes have essentially the same shape as those of the junctional tachycardia Junctional nodal tachycardia If the area around the AV node depolarizes frequently, the P waves may be seen very close to the QRS complexes, or may not be seen at all Fig.

The QRS complex is of normal shape because, as with the other supraventricular arrhythmias, the ventricles are activated via the His bundle in the normal way. The lead ECG in Figure 3. Carotid sinus pressure activates a reflex that leads to vagal stimulation of the SA and AV nodes. This causes a reduction in the frequency of discharge of the SA node, and an increase in the delay of conduction in the AV node. It is the latter which is important in the diagnosis and treatment of arrhythmias.

Carotid sinus pressure completely abolishes some supraventricular arrhythmias, and slows the ventricular rate in others, but it has no effect on ventricular arrhythmias. Excitation has to spread by an abnormal path through the ventricular muscle, and the QRS complex is therefore wide and abnormal.

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Wide and abnormal complexes are seen in all 12 leads of the standard ECG Fig. Remember that wide and abnormal complexes are also seen with bundle branch block Fig. If a patient with an acute myocardial infarction has broad complex tachycardia it will almost always be ventricular tachycardia.

However, a patient with episodes of broad complex tachycardia but without an infarction could have ventricular tachycardia, or supraventricular tachycardia with bundle branch block or the Wolff—Parkinson—White syndrome see p. Under such circumstances the following points may be helpful: Finding P waves and seeing how they relate to the QRS complexes is always the key to identifying arrhythmias.

Always look carefully at a full lead ECG. If possible, compare the QRS complex during the tachycardia with that during sinus rhythm. If the patient has bundle branch block when in sinus rhythm, the 75 Sinus rhythm with left bundle branch block Fig. QRS complex during the tachycardia will have the same shape as during normal rhythm.

If the QRS complex is wider than four small squares ms , the rhythm will probably be ventricular in origin. Left axis deviation during the tachycardia usually indicates a ventricular origin, as does any change of axis compared with a record taken during sinus rhythm. If during the tachycardia the QRS complex is very irregular, the rhythm is probably atrial fibrillation with bundle branch block see below. Fibrillation can occur in the atrial or ventricular muscle.

At times there may be flutter-like waves for 2—3 s. The AV node is continuously bombarded with depolarization waves of varying strength, and depolarization spreads at irregular intervals down the His bundle. However, these waves are irregular, and the ventricles therefore contract irregularly. Because conduction into and through the ventricles is by the normal route, each QRS complex is of normal shape.

In a lead record, fibrillation waves can often be seen much better in some leads than in others Fig. Lead II: Atrial fibrillation Fig. As the patient will usually have lost consciousness by the time you have realized that the change in the ECG pattern is not just due to a loose connection, the diagnosis is easy. The accessory bundles form a direct connection between the atrium and the ventricle, usually on the left side of the heart, and in these bundles there is no AV node to delay conduction.

The second part of the QRS complex is normal, as conduction through the His bundle catches up with the pre-excitation. Ventricular fibrillation Fig. Depolarization can spread down the His bundle and back up the accessory pathway, and so reactivate the atrium. It is not possible to distinguish enhanced automaticity from re-entry tachycardia on standard ECGs, but fortunately this differentiation has no practical importance.

Although this book is not intended to discuss therapy in detail, it seems appropriate to outline some simple approaches to patient management that logically follow interpretation of an ECG recording: For fast or slow sinus rhythm, treat the underlying cause, not the rhythm itself.

Extrasystoles rarely need treatment. In patients with acute heart failure or low blood pressure due to tachycardia, DC cardioversion should be considered early on. Patients with any bradycardia that is affecting the circulation can be treated with atropine, but if this is ineffective they will need temporary or permanent pacing Fig.

The first treatment for any abnormal tachycardia is carotid sinus pressure. This should be performed with the ECG running, and may help make the diagnosis: Narrow complex tachycardias should be treated initially with adenosine.

Wide complex tachycardias should be treated initially with lidocaine. However, in cases of difficulty it is helpful to ask the following questions, referring to Table 3. Is the abnormality occasional or sustained? Are there any P waves? Are there as many QRS complexes as P waves? Are the ventricles contracting regularly or irregularly? Is the QRS complex of normal shape? What is the ventricular rate?

Table 3. Then ask the following questions — always in the same sequence: Are there any abnormalities of the P wave? What is the direction of the cardiac axis? Is the QRS complex of normal duration?

Are there any abnormalities in the QRS complex — particularly, are there any abnormal Q waves? Is the ST segment raised or depressed? Is the T wave normal? The P wave can only be normal, unusually tall or unusually broad. The QRS complex can only have three abnormalities — it can be too broad or too tall, and it may contain an abnormal Q wave. The ST segment can only be normal, elevated or depressed.

The T wave can only be the right way up or the wrong way up. Anything that causes the right atrium to become hypertrophied such as tricuspid valve stenosis or pulmonary hypertension causes the P wave to become peaked Fig.

Left atrial hypertrophy usually due to mitral stenosis causes a broad and bifid P wave Fig. Since the left ventricle does not have its usual dominant effect on the QRS shape, the complex in lead V1 becomes upright i.

There will also be a deep S wave in lead V6. Its duration is no greater than ms three small squares. In a right ventricular lead V1 , the S wave is greater than the R wave. In a left ventricular lead V5 or V6 , the height of the R wave is less than 25 mm. Left ventricular leads may show Q waves due to septal depolarization, but these are less than 1 mm across and less than 2 mm deep.

In each case, the increased width indicates that depolarization has spread through the ventricles by an abnormal and therefore slow pathway. The QRS complex in right ventricular hypertrophy Fig.

When a pulmonary embolus is suspected, look for any of the following: Peaked P waves. Right axis deviation S waves in lead I. Tall R waves in lead V1. Right bundle branch block.

Inverted T waves in lead V1 normal , spreading across to lead V2 or V3. A deep S wave will persist in lead V6. However, do not hesitate to treat the patient if the clinical picture suggests pulmonary embolism but the ECG does not show the classical pattern of right ventricular hypertrophy.

If in doubt, treat the patient with an anticoagulant. Left ventricular hypertrophy Left ventricular hypertrophy causes a tall R wave greater than 25 mm in lead V5 or V6 and a deep S wave in lead V1 or V2 Fig. With significant hypertrophy, there are also inverted T waves in leads I, VL, V5 and V6, and sometimes V4, and there may be left axis deviation. This overall direction of travel of the electrical depolarisation through the heart is known as the electrical axis.

A fundamental principle of ECG recording is that when the wave of depolarisation travels toward a recording lead this results in a positive or upward deflection. When it travels away from a recording lead this results in a negative or downward deflection. Figure 2. Six of these are recorded from the chest overlying the heart — the chest or precordial leads. Four are recorded from the limbs — the limb leads.

It is essential that each of the 10 recording electrodes is placed in its correct position, otherwise the appearance of the ECG will be changed significantly, preventing correct interpretation.

The limb leads record the ECG in the coronal plane, and so can be used to determine the electrical axis which is usually measured only in the coronal plane. A horizontal line through the heart and directed to the left exactly in the direction of lead I is conventionally labelled as the reference point of 0 degrees 0 o.

A detailed explanation of how to determine the axis is beyond the scope of this article but the principles mentioned here should help readers to understand the concepts involved. Figure 3. Transverse section of the chest showing the orientation of the six chest leads in relation to the heart Voltage and timing intervals It is conventional to record the ECG using standard measures for amplitude of the electrical signal and for the speed at which the paper moves during the recording.

This allows: Easy appreciation of heart rates and cardiac intervals and Meaningful comparison to be made between ECGs recorded on different occasions or by different ECG machines. The amplitude, or voltage, of the recorded electrical signal is expressed on an ECG in the vertical dimension and is measured in millivolts mV. On standard ECG paper 1mV is represented by a deflection of 10 mm. An increase in the amount of muscle mass, such as with left ventricular hypertrophy LVH , usually results in a larger electrical depolarisation signal, and so a larger amplitude of vertical deflection on the ECG.

An essential feature of the ECG is that the electrical activity of the heart is shown as it varies with time. In other words we can think of the ECG as a graph, plotting electrical activity on the vertical axis against time on the horizontal axis.

Standard ECG paper moves at 25 mm per second during real-time recording. This means that when looking at the printed ECG a distance of 25 mm along the horizontal axis represents 1 second in time. ECG paper is marked with a grid of small and large squares. Each small square represents 40 milliseconds ms in time along the horizontal axis and each larger square contains 5 small squares, thus representing ms.

Standard paper speeds and square markings allow easy measurement of cardiac timing intervals. Figure 4. Sample of standard ECG paper showing the scale of voltage, measured on the vertical axis, against time on the horizontal axis The normal ECG It will be clear from above that the first structure to be depolarised during normal sinus rhythm is the right atrium, closely followed by the left atrium.

So the first electrical signal on a normal ECG originates from the atria and is known as the P wave. Although there is usually only one P wave in most leads of an ECG, the P wave is in fact the sum of the electrical signals from the two atria, which are usually superimposed.

There is then a short, physiological delay as the atrioventricular AV node slows the electrical depolarisation before it proceeds to the ventricles. Depolarisation of the ventricles results in usually the largest part of the ECG signal because of the greater muscle mass in the ventricles and this is known as the QRS complex.A practical and highly informative guide to a difficult subject.

But do not forget two important things: The right ventricle occupies the front of the heart anatomically, and normally depolarization of the right ventricle moving towards the recording electrode V1 is overshadowed by depolarization of the left ventricle moving away from V1. Cardiac axis none exist: Then ask the following questions — always in the same sequence: