You'll learn simple waveform analysis and beyond to present ECGs as they are used in hospital wards, outpatient clinics, emergency departments, and most especially intensive care units — where the recognition of normal and abnormal patterns is the starting point in patient care. Clinical Electrocardiography: A Simplified Approach, 7th Edition goes beyond the simple waveform analysis to present ECGs as they are used in hospital wards, outpatient clinics, emergency departments, and intensive care units—where the recognition of normal and abnormal patterns is only the starting point in patient care.
With Dr. Goldberger's renowned ability to make complex material easy to understand, you'll quickly grasp the fundamentals of ECG interpretation and analysis. Features indispensable self-tests on interpreting and using ECGs to formulate diagnoses.
Presents complex information in a manner that is easy to understand. Represents practical, comprehensive coverage ideal for the beginning student as much as for the practicing clinician. Employs a unique approach that centers on the critical thinking skills required in clinical practice. Provides new chapters on "problem" rhythms—those that are commonly seen in practice and difficult to recognize.
Mirrors the true-to-life clinical appearance of ECGs with new and updated images incorporated throughout. Reflects the latest knowledge in the field through clinical pearls and review points at the end of each chapter. Reviews the diagnostic tips on key rhythm disorders that are relevant to today's clinical practice. Includes new ECG differential diagnoses on laminated cards for easy reference.
Clinical Electrocardiography: A Simplified Approach, 7th Edition goes beyond the simple waveform analysis to present ECGs as they are used in hospital wards, outpatient clinics, emergency departments, and intensive care units-where the recognition of normal and abnormal patterns is only the starting point in patient care.
Presents co. Ideal for students and practicing clinicians alike, this accessible, concise cardiology reference offers relevant guidance on understanding rhythm disorders and their clinical outcomes.
Trust Goldberger's Clinical Electrocardiography for all the in-depth coverage you need! Diagnose the key rhythm disorders that are relevant to today's clinical practice through expert pearls and advice.
Easily navigate the full text online at www. View clinical findings clearly with new illustrations and updated images throughout. Expand your clinical insights via a wealth of clinical highlights and review questions online, including diagnosis and management tips, as well as extended coverage of difficult-to-classify rhythms. Goes beyond the simple waveform analysis to present ECGs as they are used in hospital wards, outpatient clinics, emergency departments, and intensive care units where the recognition of normal and abnormal patterns is only the starting point in patient care.
With the author's ability to make complex material easy to understand, readers should quickly grasp the fundamentals of ECG interpretation and analysis.
Since the publication of the 3rd Edition 17 years ago, progress has been truly remarkable in all areas of electrocardiography. Five of the seven chapters in this 4th Edition have been extensively revised. Out of the total of ECGs, 65 are new. Each ECG is crisp and clear and all the abnormalities are highlighted by arrows for easy recognition and understanding.
This book is the culmination of the author's 45 years of experience in the teaching of electrocardiography to coronary care unit nurses, medical undergraduates, postgraduates, interns, residents, senior residents and above. As the title of the book implies, the approach to the subject has been entirely from the viewpoint of a clinician.
Hence, clinical-electrocardiographic correlations have been emphasized simply and succinctly throughout the text. This helpful resource provides quick references for a range of core as well as more complex clinical skills, including neurological assessment, ECG recording, chest auscultation, resuscitation guidelines, recognition and management of sepsis, and pain relief.
It also considers fluid and electrolyte balance, wound care and key aspects of nutrition. Written by experienced nurse practitioner Rob Schwarz, the easy to navigate text closes the gap between theory and practice, supporting nurses to build understanding and acquire new skills. It will be a much-used resource by training and qualified nurses alike.
This book is designed to teach healthcare professionals how to interpret electrocardiograms, presenting this information with numerous illustrations, solid practical content, questions to prompt critical thinking, case presentations, and plentiful practice ECG tracings to promote the application of skills. The breadth of information ranges from simple to complex, but regardless of how advanced the material, the explanations and visuals make the concepts easy to understand, making this a critical resource for all cardiology professionals.
This find- ing is sometimes called the P pulmonale pattern. The initial positive deflection of the P wave in lead Figure illustrates the characteristic P wave V1 therefore indicates right atrial depolarization, changes seen in LAA. As shown, the P wave some- whereas the deep negative deflection is a result of times has a distinctive humped or notched appear- left atrial depolarization voltages directed posteri- ance Fig.
The second hump corresponds to orly away from the positive pole of lead V1. The older the biphasic P wave in lead V1. In other cases, only term P mitrale is sometimes still used to describe broad, notched P waves are seen. This wave has a small, initial positive deflec- tion and a prominent, wide negative deflection.
Clinically, LAA may occur in a variety of The negative component is longer than 0. The promi- nent negative deflection corresponds to the delayed stenosis, aortic regurgitation, mitral regur- stimulation of the enlarged left atrium.
A major clue to mitral stenosis is LAA or atrial fibrillation with signs of right ventricular hypertrophy RVH , as depicted in Figure Broad, humped P waves from the ECG of a patient with left atrial enlargement abnormality. As a result, leads placed over the right side of enlargement or abnormality may show a combina- the chest e. This R finding is most likely with severe cardiomyopathy or valve disease.
The resultant ECG effects chest e. Nor- the predominant depolarization voltages that point mally the left and right ventricles depolarize to the left and are generated by the left ventricle. Overload of the right atrium RA may cause tall, peaked P waves in the extremity or chest leads.
An R wave exceeding the S wave in lead left ventricle can be overcome. In this situation, what V1 is suggestive but not diagnostic of RVH. Some- type of QRS complex might you expect to see in the times a small q wave precedes the tall R wave in right chest leads? Instead of the rS complex mid-precordial leads. For reasons not How tall does an R wave in lead V1 have to be to fully understood, hypertrophy of the heart muscle make a diagnosis of RVH?
In adults the normal R alters the normal sequence of repolarization. Notice that left ventricular hypertrophy exaggerates the normal pattern, causing deeper right precordial S waves and taller left precordial R waves. By contrast, right ventricular hypertrophy shifts the QRS vector to the right, causing increased right precordial R waves.
So, not uncommonly, signs of RVH are appearance of inverted T waves in the right and accompanied by tall P waves. The major exception middle chest leads see Figs. Sometimes the middle and left chest leads be taller than the S wave in lead V1. In other often present. Some cases of RVH are more subtle, cases, normal R wave progression is preserved and and the ECG may show only one of these the left chest leads also show R waves see Fig.
With right ventricular hypertrophy, lead V1 sometimes shows a tall R wave as part of the qR complex. The T wave inversion in lead V1 and the ST segment depressions in leads V2 and V3 are due to right ventricular overload. The PR interval is also prolonged 0. Key Point disease may have pulmonary artery hypertension and RVH.
T wave inversions to marked RVH due to a pressure load pulmo- in leads V1 to V3 due to right ventricular overload nary hypertension or pulmonic stenosis : may also occur without other ECG signs of RVH, 1. Tall right precordial R waves as in acute pulmonary embolism see Chapter Right axis deviation RAD In patients who have right ventricular overload 3.
Right precordial T wave inversions in adults associated with emphysema, the ECG may not show any of the patterns just described.
Nor- rightward QRS axis. Pattern of left ventricular hypertrophy in a patient with severe hypertension. In addition, enlargement of the left atrium is indicated by a biphasic P wave in lead V1. In fact, many different cri- right ventricle. As a result, prominent negative S teria have been proposed, reflecting the imperfection waves are produced in the right chest leads, and of ECG in providing a test with both high sensitivity tall positive R waves are seen in the left chest and specificity.
When LVH is present, the balance of electri- The following ECG criteria and guidelines have cal forces is tipped even further to the left. If the sum of the depth of the S wave in lead V1 usually seen in the left chest leads, and abnormally SV1 and the height of the R wave in either lead deep negative S waves are present in the right V5 or V6 RV5 or RV6 exceeds 35 mm 3.
LVH should be considered Fig. Consequently, high voltage in the chest mal R wave seen in lead aVL. This LV overload- Fig. In other cases the with tall R waves see Fig. The two most common and important pres- sure overload states are systemic hyper- tension and aortic stenosis.
The three major clinical conditions associated with left ventricular volume overload are aor- tic regurgitation, mitral regurgitation, and dilated cardiomyopathy. LVH pat- terns may also occur with hypertrophic cardiomyopathies.
Repolarization abnormalities associated with left ventricular hypertrophy were formerly referred to as the 2. With LVH the electrical axis is usually horizon- arrest. As noted, the myocardial fibrosis tal. Actual left axis deviation i. In addition, the accompanying hypertrophy may potenti- QRS complex may become wider. Not uncom- ate both the mechanical decompensation monly, patients with LVH eventually develop an and electrical instability.
Most conditions that lead to LVH ulti- clue to biventricular hypertrophy is LVH with right- mately produce left atrial overload as well. Biventricular hypertrophy In summary, the diagnosis of LVH can be made may be present, for example, in some cases of severe with a high degree of certainty from the ECG if you dilated cardiomyopathy or rheumatic valvular find high QRS voltages and associated ST-T disease.
Because high voltage in Always remember that in the assessment of the chest or extremity leads can sometimes be seen cardiac size, the ECG is only an indirect labora- in normal people, especially athletes and young tory test and not an absolute measurement. A adults, the diagnosis of LVH should not be made person may have underlying cardiac enlarge- on this finding alone.
Con- left ventricular overload can also occur without versely, the ECG may show high voltage in a voltage criteria for LVH. For some suspected condi- Key Point tions, such as arrhythmogenic right ventricular cardiomyopathy or apical hypertrophic cardio- The recognition of LVH is clinically important myopathy, a cardiac magnetic resonance imaging for two major reasons: MRI study may be indicated. The first part of the ventricles to be stimu- this structure.
Obviously, right ventricular stimu- lated depolarized is the left side of the ventricular lation will be delayed and the QRS complex will be septum. Soon after, the depolarization spreads to widened. The shape of the QRS with a right bundle the main mass of the left and right ventricles by branch block RBBB can be predicted on the basis way of the left and right bundle branches.
Nor- of some familiar principles. This is the reason the normal width of A. The left side of the septum is stimulated the QRS complex measured by computer from first by a branch of the left bundle. On the nor- all 12 leads is less than or equal to msec about mal ECG, this septal depolarization produces a 2. Clearly, RBBB should near simultaneous stimulation of the ventricles not affect the septal phase of ventricular stimula- may prolong the QRS width or change the QRS tion because the septum is stimulated by a part of axis.
This chapter primarily focuses on a major the left bundle. The change A unifying principle in predicting what the ECG in the QRS complex produced by RBBB is a result will show with a bundle branch or fascicular block of the delay in the total time needed for stimula- is the following: The last and usually dominant tion of the right ventricle.
This means that after component of the QRS vector will be shifted in the the left ventricle has completely depolarized, the direction of the last part of the ventricles to be right ventricle continues to depolarize.
In other words, the major QRS vector This delayed right ventricular depolarization pro- shifts toward the regions of the heart that are most duces a third phase of ventricular stimulation.
The delayed in being stimulated Box The rightward spread of To make the initial diagnosis of RBBB, look at the delayed and slow right ventricular depolarization leads V1 and V6 in particular. The characteristic voltages produces a wide negative S wave deflection appearance of QRS complexes in these leads makes in the left chest leads e. RBBB can be derived. Lead cess in RBBB can be divided into three phases.
The V6 shows a qRS-type complex with a broad S wave. The third phase is delayed the deep terminal S wave in the left chest leads rep- stimulation of the right ventricle. Occa- V1 and negative in V6. Consequently, the complex point toward the left ventricle negative in V1 and in lead V1 has the appearance of a large notched R positive in V6. If you look forces point in an inferior and rightward direction carefully, you can see that the T waves in the right negative in I and positive in II and III.
Step-by-step sequence of ventricular depolarization in right bundle branch block see text. Inverted T waves in the right precordial leads in this case V1 to V3 are common with right bundle branch block and are called secondary T wave inversions.
Note also the left atrial abnormality pattern biphasic P in V1 with prominent negative component and prominent R waves in V5, consistent with underlying left ventricular hypertrophy. Notice the secondary T wave inversions in leads V1 to V2. V1 and a qRS in lead V6. These inversions are referred to as secondary changes because they reflect just the delay in ven- Clinical Significance tricular stimulation. First, abnormalities reflect an actual change in repolariza- some people have this finding without any identi- tion, independent of any QRS change.
Examples of fiable underlying heart disorder. Therefore RBBB, primary T wave abnormalities include T wave itself, is an isolated ECG abnormality in many peo- inversions resulting from ischemia see Chapters 8 ple; however, RBBB may be associated with organic and 9 , hypokalemia and certain other electrolyte heart disease.
It may occur with virtually any con- abnormalities see Chapter 10 , and drugs such as dition that affects the right side of the heart, digitalis see Chapter Note: Some authors also require that for classical LBBB, present here, the time V1 V1 from QRS onset to R wave peak, the so-called intrinsicoid deflection or R wave peak time, in leads V5 and V6 be greater than 60 msec; normally this subinterval is 40 msec or less. A B shunting of blood, chronic pulmonary disease variant and should not be over-read as an incom- with pulmonary artery hypertension, and valvular plete right ventricular branch block.
However, system. It may occur after cardiac surgery. The major reason for this differ- right-sided heart overload, may cause a right ven- ence is that RBBB affects mainly the terminal tricular conduction delay, usually associated with phase of ventricular activation, whereas LBBB also sinus tachycardia. By itself, RBBB does not require any specific Recall that, normally, the first phase of ven- treatment.
RBBB may be permanent or transient. However, as pattern. When LBBB is present, the septum depo- noted later in patients with acute anterior wall larizes from right to left and not from left to right. The right chest leads e. Notice the characteristic wide QS complex in lead V1 and the wide R wave in lead V6 with slight notching at the peak. The inverted T waves in leads V5 and V6 secondary T wave inversions are also characteristic of left bundle branch block.
An example of an in LBBB. As Figure a characteristic W shape. Similarly, the broad R shows, the T waves in the leads with tall R waves wave in lead V6 may show a notching at its peak, e. This superfi- solely on the basis of LBBB. If present, these T wave cially suggests that the septum is being stimulated normally from left to right.
However, lead V6 shows an abnormally wide and inversions reflect some primary abnormality such notched R wave without an initial q wave. LBBB may develop in patients with long-standing hypertensive heart disease, a valvular lesion e. It is also seen in patients with coro- nary artery disease and often correlates with impaired left ventricular function. Often, more than one contributing factor may be identified e.
Echocardiograms usually show septal dyssynchrony due to abnormal ventricular activa- tion patterns; other findings e. It also may appear only when the heart rate bundle branch block LBBB. Normally lead V1 shows an rS com- exceeds a certain critical value rate- or accelera- plex and lead V6 shows a qR complex.
In such cases the n Cardiomyopathy general term intraventricular delay is used Fig. With complete LBBB the QRS complex has underlying cardiac disease, but the loss of ventricu- the characteristic appearance described previously lar synchrony dyssynchrony syndrome induced by and is 0. However, such a pattern is not typical of left or right bundle branch block.
In this patient the pattern was caused by an anterolateral wall Q wave myocardial infarction see Chapter 8. With RBBB the last 2. Ventricular preexcitation Wolff-Parkinson-White tricles are activated from the electrode posi- [WPW] syndrome can create ECG patterns sim- tioned in the right ventricular apex close to the ilar to bundle branch blocks.
Notice branch that the left bundle branch subdivides into left anterior fascicle and left posterior fascicle. This highly schema- tized diagram is a revision of the original drawing of the Left posterior conduction system see Fig. In actuality, the fascicles fascicle are complex, tree-like branching structures.
AV, atrioven- tricular; SA, sinoatrial. The clue to the pres- by blocks in both subdivisions anterior and poste- ence of preexcitation is a short PR interval and a rior fascicles. Ventricular arrhythmias especially at slower A block in either fascicle of the left bundle branch rates can look very similar to bundle branch system is called a hemiblock or fascicular block. Rec- blocks.
Experiments and clinical observa- Fascicular blocks, or hemiblocks, are a slightly more tions have shown that the main effect of cutting complex but important topic. To this point the these fascicles is a change in the QRS axis, with left bundle branch system has been described as if only minor increases in QRS duration. Specifically, it were a single pathway. This revised concept of in the left bundle branch system, involving either the bundle branch system as a trifascicular high- the anterior or posterior subdivisions.
The diagno- way one right lane and two left lanes is illus- sis of a fascicular block is made primarily from the trated in Figure We believe, however, that fascicular system. This is in contrast to the diagnosis of com- disease, coronary disease, and aging and some- plete or incomplete RBBB or LBBB, which is times without identifiable cause Fig.
In contrast, LAFB width of less than 0. However, the diagnosis of LPFB can the left ventricle. LPFB shifts it inferiorly and to be considered only after other, more common causes of the right by delaying activation of the more infe- RAD have been excluded see Chapter These fac- rior and rightward portions of the left ventricle.
In tors include right ventricular hypertrophy RVH , both cases the QRS axis therefore is shifted toward normal variant, emphysema, lateral wall infarc- the direction of delayed activation. Most often it occurs with RBBB, of less than 0. As rough but useful rule of as shown in Figure Lead aVL usually shows a qR complex, Fig. This finding of both the anterior and posterior fascicles.
Additional damage to this third remaining fascicle may com- I aVR V1 V4 pletely block AV conduction, producing complete heart block trifascicular block.
However, chronic bifascicular blocks with normal sinus rhythm have a low rate of pro- gression to complete heart block and are not indica- tions by themselves for permanent pacemakers. Many asymptomatic people have ECGs resem- Figure Left anterior hemiblock fascicular block. Patients with the QRS duration. Left atrial abnormality is also present.
Compare this most common type of fascicular block with left chronic bifascicular block of this kind do not gen- posterior fascicular block Fig. By contrast, patients with acute ante- Caution: A very common misconception is that rior MI in whom bifascicular block suddenly occurs bifascicular block especially RBBB and LAFB have a poor prognosis because of underlying exten- with a prolonged PR interval is diagnostic of trifas- sive myocardial necrosis, and they are also at higher cicular disease.
This assumption is not correct. How can one infer trifascicular disease in concert with bifascicular block. How- block from a lead ECG without sustained or ever, trifascicular disease cannot be inferred on the intermittent complete or advanced AV block? The basis of this combination. Right bundle branch block with left anterior fascicular block. Thus, a bifascicular block involving the right bundle branch RBB and the anterior fascicle of the left bundle branch LBB system is present as shown in the diagram.
AV, atrioventricular. Bifascicular block right bundle branch block [RBBB] with left posterior fascicular block. The combination of these two findings in the absence of other more common causes of RAD such as right ventricular hypertrophy or lateral myocardial infarction [MI] is consis- tent with chronic bifascicular block due to left posterior fascicular block in concert with the RBBB. This elderly patient had severe coronary artery disease.
A few general guidelines are evidence of left atrial abnormality virtually ensures helpful. Unfortunately, RBBB often masks these typical voltage increases. CHAPTER 8 Myocardial Infarction and Ischemia, I: ST Segment Elevation and Q Wave Syndromes This chapter and the next forming one unit left ventricle consists of an outer layer epicardium examine one of the most important topics in clini- or subepicardium and an inner layer subendocar- cal electrocardiography and clinical medicine—the dium.
Basic of the ventricular wall transmural ischemia. Oxygenated blood is supplied by The right coronary artery supplies both the the coronary arteries. If severe narrowing or com- inferior diaphragmatic portion of the heart and plete blockage of a coronary artery causes the the right ventricle.
The left main coronary artery is blood flow to become inadequate, ischemia of the heart muscle develops. For example, patients who experience angina pectoris infarction with exercise are having transient myocardial isch- emia.
If the ischemia is more severe, necrosis of a portion of heart muscle may occur. This discussion focuses primarily on ischemia and infarction of the left ventricle, the predomi- nant pumping chamber of the heart. The impor- tant clinical topic of right ventricular infarction is also discussed briefly. Cross section of the left ventricle showing the dif- ference between a subendocardial infarct, which involves the A simplified cross-sectional diagram of the left inner half of the ventricular wall, and a transmural infarct, which ventricle is presented in Figure Notice that the involves the full thickness or almost the full thickness of the wall.
As discussed in the text, pathologic Q waves may be a marker of transmural infarction. Most patients who present with acute tricular septum and a large part of the left ventric- MI have underlying atherosclerotic coronary ular free wall, and the left circumflex coronary artery disease. This circulation pattern may be variable. MIs tend to be localized to the region e. STEMI, including cocaine, coronary artery dissec- Chapter 9 discusses the diversity of ECG patterns tions spontaneous or induced during interventional associated with non—ST segment elevation isch- procedures , coronary emboli, and other factors.
The three major coronary coronary artery arteries that supply blood to the heart. The acute phase is marked by the appearance of acute anterior wall MI, the ST segment elevations ST segment elevations and sometimes tall posi- and tall hyperacute T waves appear in one or more tive hyperacute T waves in multiple usually two of the anterior leads chest leads V1 to V6 and or more leads.
With an infe- phase. Anterior means that procity. The anterior and inferior leads tend to show the infarct involves the anterior or lateral wall of inverse patterns. Thus in an anterior infarction the left ventricle, whereas inferior indicates involve- with ST segment elevations in two or more of leads ment of the inferior diaphragmatic wall of the V1 to V6, I, and aVL, ST segment depression is often left ventricle Fig. Reciprocal changes are illustrated in Figures and The ST segment elevation seen with acute MI is called a current of injury and indicates that damage has occurred to the epicardial outer layer of the heart as a result of severe ischemia.
Normally the ST segment is isoelectric neither positive nor negative because no net current flow is occurring A B at this time. MI alters the electrical charge on the myocardial cell membranes in a number of ways. Myocardial infarctions are most generally local- As a result, current flow becomes abnormal ized to either the anterior portion of the left ventricle A or the current of injury and produces ST segment inferior diaphragmatic portion of the walls of this chamber B.
A, Acute phase of an anterior wall infarction: ST segment elevations and new Q waves. B, Evolving phase: deep T wave inversions. A, Acute phase of an inferior wall myocardial infarction: ST segment elevations and new Q waves.
These T waves have the same significance as the ST elevations. In some cases, hyperacute T waves actu- ally precede the ST elevations. Guidelines for assessing whether ST segment and usually J point elevations are due to acute ischemia have been suggested.
However, strict criteria are limited because of false-positives due to normal variants, left ventricular hyper- trophy, etc.
Clinicians should be aware that ST changes in acute ischemia may evolve with the patient under observation. Variable shapes of ST segment elevations seen with acute myocardial infarctions. After a variable time lag usually hours to a few days the elevated ST segments start to return to The ST segment elevation seen with acute the baseline. At the same time the T waves become MI may have different shapes and appearances inverted in leads that previously showed ST seg- Fig.
Notice that the ST segment may be pla- ment elevations. This phase of T wave inversions is teau-shaped or dome-shaped. Sometimes it is called the evolving phase of the infarction. Thus with obliquely elevated. With an inferior wall infarction the T and are generally seen within minutes of blood waves become inverted in one or more of the infe- flow occlusion.
These T wave inversions are may also be seen at this time Figs. A, In the earliest phase of the infarction, tall, positive hyperacute T waves are seen in leads V2 to V5. B, Several hours later, marked ST segment elevation is present in the same leads current of injury pattern , and abnormal Q waves are seen in leads in V1 and V2.
This patient was complaining of severe chest pain. Notice the very tall hyperacute T waves in the chest leads. Notice the atrial premature beat APB in lead V4.
Recall that normally the height of the R wave increases progressively as you move from lead V1 to lead V6. An anterior infarct interrupts QRS Changes: Q Waves of Infarction this progression, and the result may be pathologic MI, particularly when large and transmural, Q waves in one or more of the chest leads.
In clini- often produces distinctive changes in the QRS cal practice cardiologists often subdivide anterior depolarization complex. The characteristic depo- MIs into a number of subsets depending on the larization sign is the appearance of new Q waves. Clinicians should be aware Why do certain MIs lead to Q waves? Recall that that these ECG localizations may not correspond a Q wave is simply an initial negative deflection of exactly with imaging or postmortem findings and the QRS complex.
If the entire QRS complex is that different authors may not use exactly the same negative, it is called a QS complex: definitions. With a waves. Now consider the effect of damaging the sep- transmural infarction, necrosis of heart muscle tum.
Obviously, septal depolarization voltages are occurs in a localized area of the ventricle. As a lost. Thus the r waves in leads V1 and V2 may disap- result the electrical voltages produced by this por- pear and an entirely negative QS complex appears.
Instead of posi- The septum is supplied with blood by the left tive R waves over the infarcted area, Q waves are anterior descending coronary artery. Septal infarc- often recorded either a QR or QS complex. If an infarction occurs in the anterior In summary, abnormal Q waves are characteris- wall of the left ventricle, the positive R waves that tic markers of infarction.
They signify the loss of reflect the voltages produced by this muscle area positive electrical voltages caused by the death of are lost. A strictly The new Q waves of an MI generally appear anterior infarct generally results from occlusion of within the first day or so of the infarct. With an the left anterior descending coronary artery. Anterior wall infarction. The QS complexes in leads V1 and V2 indicate anteroseptal infarction. A characteristic notch- ing of the QS complex, often seen with infarcts, is present in lead V2 arrow.
In addition, the diffuse ischemic T wave inversions in leads I, aVL, and V2 to V5 indicate generalized anterior wall ischemia or non—Q wave myocardial infarction. Evolving anterior wall infarction. The patient sustained the infarct 1 week earlier. Marked left axis deviation resulting from left anterior fascicular block is also present see Chapter 7.
An infarction of the anterolateral or apical wall of The infarcts are often caused by occlusion of the left ventricle produces changes in the more the left circumflex coronary artery, but they may laterally situated chest leads V5 and V6.
Evolving extensive anterolateral wall infarction. The infarct occurred 1 week earlier. The T waves are slightly inverted in these leads. These three overlap. To avoid ambiguity, you can simply leads, as shown in the diagram of the frontal plane describe Q wave MIs by simply referring to any axis, are oriented downward or inferiorly see Fig. The latter finding may be reciprocal to lateral or posterior ischemia. An inferior wall infarction producing characteristic changes in lead V6, or to may produce abnormal Q waves in leads II, III, and the inferior wall of that ventricle, producing char- aVF.
Less com- Because of the overlap between inferior, lat- monly it occurs because of a left circumflex coro- eral, and posterior infarctions, the more general nary obstruction. Posterior Infarctions Infarctions can occur in the posterior back sur- Right Ventricular Infarctions face of the left ventricle. These infarctions may be A related topic is right ventricular infarction. Clin- difficult to diagnose because characteristic abnor- ical and autopsy studies have shown that patients mal ST elevations may not appear in any of the 12 with an inferoposterior infarct not uncommonly conventional leads.
Instead, tall R waves and ST have associated right ventricular involvement. In depressions may occur in leads V1 and V2 recipro- one postmortem study, right ventricular infarc- cal to the Q waves and ST segment elevations that tion was found in about one of four cases of infero- would be recorded at the back of the heart. Dur- posterior MI but not in cases of anterior MI. Inferior wall infarction. This patient sustained a myocardial infarction 1 month previously. In addition, T wave flattening is seen in lead V6.
After infarction, Q waves and ST-T changes may persist indefinitely or may resolve partially or completely. Many of these patients also have ST changes produced by an acute MI have been dis- segment elevations in leads reflecting the right cussed separately.
As shown in Figures and , ventricle, such as V1 and V3R to V5R, as shown in these changes often occur sequentially. Figure see also Chapter 3. Ordinarily, the earliest sign of transmural ischemia Recognition of right ventricular infarction is of is ST segment elevations with reciprocal ST depres- major clinical importance. Careful volume expan- sions. The ST elevations current of injury pat- sion may be critical in improving cardiac output in tern usually persist for hours to days.
During this patients who are hypotensive and have a low or same period, Q waves often begin to appear in the normal pulmonary capillary wedge pressure leads that show ST elevations. Once these changes despite elevated central venous pressure.
Prior inferior wall infarction. The ST-T changes have essentially reverted to normal. Notice the tall R waves in leads V1 and V2. Notice also the reciprocally tall, positive T waves in anterior precordial leads V1 and V2.
Louis, Mosby, The answer is Normal and Abnormal Q Waves: that you cannot make any certain predictions. In A Brief Overview most cases the abnormal Q waves persist for A frequently encountered diagnostic problem is months and even years after the acute infarction. For example, a Q wave diminish in size and even disappear entirely.
In is normally seen in lead aVR. Acute right ventricular ischemia with inferior wall infarction. The ST-T changes in lead V6 are consistent with lateral wall ischemia.
B, Follow-up tracing obtained the next day, showing diminution of the ST changes. Recall from Chapter 4 the signifi- are less than 0. A Q wave is gen- cance of these septal q waves. The ventricular sep- erally abnormal if its duration is 0. A large QS com- spread of left ventricular voltages toward the lead. When the may be the only evidence of an anterior septal MI. Further criteria for differen- Normal septal q waves are characteristically nar- tiating normal from abnormal Q waves in these row and of low amplitude.
As a rule, septal q waves leads lie beyond the scope of this book. Hypertrophic obstructive cardiomyopathy HOCM. Notice the prominent pseudoinfarction Q waves, which are the result of septal hypertrophy. These wave- leads V1 and V2.
Prominent Q waves in the absence forms can also occur normally. Although a discus- of MI are sometimes referred to as a pseudoinfarct sion of the precise criteria for differentiating pattern see Chapter If prominent Q waves does not contract normally. Instead, during ven- appear just in leads III and aVF, the likelihood of tricular systole the aneurysmic portion bulges out- MI is increased by the presence of abnormal ward while the rest of the ventricle is contracting.
ST-T changes in all three inferior extremity leads. Look for abnormal Q waves inferior surface of the heart. Patients with ventricular aneurysm frequently Furthermore, just as not all Q waves are abnormal, have persistent ST segment elevations after an all abnormal Q waves are not the result of MI.
For infarct. As mentioned earlier, the ST segment ele- example, slow R wave progression in the chest vations seen with acute infarction generally resolve leads, sometimes with actual QS complexes in the within several days. The persistence of ST segment right to middle chest leads e. However, the ventricular hypertrophy, amyloidosis, and chronic absence of persisting ST segment elevations does lung disease in the absence of MI, in addition to not rule out the possibility of an aneurysm.
Prominent noninfarction Ventricular aneurysms are of clinical impor- Q waves are often a characteristic feature in the tance for several major reasons.
They may lead to ECGs of patients with hypertrophic cardiomyopa- congestive heart failure. They may be associated thy Fig. Noninfarction Q waves also occur with serious ventricular arrhythmias.
A thrombus with dilated cardiomyopathy see Fig. As may form in an aneurysm and break off, resulting mentioned previously, the ECGs of normal people in a stroke or some other embolic complication. Anterior wall aneurysm. The patient had a myocardial infarction several months before this ECG was taken.
The persistence of ST elevations more than 2 to 3 weeks after an infarction suggests the presence of a ventricular aneurysm. Sometimes, how- MIs at different times. Therefore, it is not unusual for an previous inferior wall infarction. During the anterior infarct, history of definite MI. Then the ECG picture crushing substernal chest pain, or they may have becomes more complex. Multiple myocardial infarctions.
This ECG shows evidence of previous anterior wall and inferior wall infarcts. Remember that RBBB affects primarily mary ST-T changes indicative of ischemia or actual the terminal phase of ventricular depolarization, infarction.
MI affects prominent R waves. The appearance of T wave the initial phase of ventricular depolarization, pro- inversions in leads V1 to V3 with prominent S waves ducing abnormal Q waves. When RBBB and an is a primary abnormality that cannot be ascribed to infarct occur together, a combination of these pat- the bundle branch block itself Fig.
If the infarction those seen with infarction. Highlights the latest information on intraventricular and atrioventricular AV conduction disturbances; sudden cardiac arrest; myocardial ischemia and infarction; drug toxicities; and electronic pacemakers and ICDs.
Ary Goldberger's award-winning teaching style to clarify complex concepts in an easy-to-read manner. You'll learn simple waveform analysis and beyond to present ECGs as they are used in hospital wards, outpatient clinics, emergency departments, and most especially intensive care units - where the recognition of normal and abnormal patterns is the starting point in patient care.
This enhanced eBook experience allows you to search all of the text, figures, images, and references from the book on a variety of devices.
Enhances your understanding of difficult concepts through several new illustrations and animations. Electrocardiography is an essential tool in diagnosing cardiacdisorders. This second edition of the ABC of ClinicalElectrocardiography allows readers to become familiar with the widerange of patterns seen in the electrocardiogram in clinicalpractice and covers the fundamentals of ECG interpretation andanalysis.
Fully revised and updated, this edition includes a self-assessmentsection to aid revision and check comprehension, clear anatomicaldiagrams to illustrate key points and a larger format to showlead ECGs clearly and without truncation. Edited and written by leading experts, the ABC of ClinicalElectrocardiography is a valuable text for anyone managing patientswith heart disorders, both in general practice and in hospitals.
Junior doctors and nurses, especially those working in cardiologyand emergency departments, as well as medical students, will findthis a vaulable introduction to the understanding of this keyclinical tool.
Clinical Electrocardiography: A Simplified Approach, 7th Edition goes beyond the simple waveform analysis to present ECGs as they are used in hospital wards, outpatient clinics, emergency departments, and intensive care units—where the recognition of normal and abnormal patterns is only the starting point in patient care.
With Dr. Goldberger's renowned ability to make complex material easy to understand, you'll quickly grasp the fundamentals of ECG interpretation and analysis. Features indispensable self-tests on interpreting and using ECGs to formulate diagnoses.
Presents complex information in a manner that is easy to understand.
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