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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
The Electrocardiogram in Emergency and Acute Care Clear, practical guidance in mastering ECG interpretation in the critically ill patient The Electrocardiogram in Emergency and Acute Care contains clear, practical guidance on mastering both single-lead and 12 lead ECGs, covering the full range of complexities and including a section on differential diagnosis of more common ECGs, with over 200 tracings from which to learn and self-test. The editors place an emphasis on readability and accessibility, with clearly written chapters and excellent illustrations that serve as a primary source of information for students, trainees, and practicing emergency physicians in all areas. In The Electrocardiogram in Emergency and Acute Care, readers can expect to find detailed information on topics such as: * Clinical applications, impact, and interpretation of the electrocardiogram, plus variants of the normal, lead misplacement, and electrocardiographic artifact encountered in clinical practice * Cardiac rhythms and cardiac dysrhythmias, covering cardiac rhythms with normal rates, narrow QRS complex tachycardia, wide QRS complex tachycardia, and bradycardia * Anatomic and physiologic considerations of ischemic heart disease, historical development of the prehospital electrocardiogram, and electrocardiographic findings in acute coronary syndrome * Special populations, high-risk presentation scenarios, and advanced electrocardiographic techniques, covering electrocardiograms in pediatric and poisoned patients The Electrocardiogram in Emergency and Acute Care is ideally suited to medical students, residents, and physicians in training, but is also a useful reference for established physicians as a review and reference text, along with all other health professionals working in this field.
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Table of Contents
Cover
Title Page
Copyright Page
Dedication Page
Editors and Contributors
Editors
Contributors
Foreword
Preface
Section I: The ECG in Clinical Care
1 Clinical Applications of the Electrocardiogram
Standard ECG Formatting and the Normal Electrocardiogram
Systematic Interpretation of the ECG
Common Indications and Clinical Applications
Other Indications
Clinical Context
References
2 Clinical Impact of the Electrocardiogram (ECG)
Management of the Patient with Dysrhythmia
Management of the Patient with Acute Coronary Syndrome
Management of non‐ACS Presentations
Ambulatory Electrocardiogram Monitoring
Computer Interpretation of the Electrocardiogram
3 Interpretation of the Electrocardiogram – Single‐, Multi‐, and 12‐Lead Analysis
Introduction
Rate
Rhythm
Axis
Intervals
Morphology
4 Variants of the Normal, Lead Misplacement, and Electrocardiographic Artifact Encountered in Clinical Practice
Benign Early Repolarization
Sinus Arrhythmia
Conditions Encountered in Athletes
T Wave Inversion
Lead Misplacement
Artifact
Section II: Cardiac Rhythms and Cardiac Dysrhythmias
5 Cardiac Rhythms with Normal Rates
Further Reading
6 Narrow QRS Complex Tachycardia
Regular Narrow Complex Tachycardia
Irregular Narrow Complex Tachycardias
Further Reading
7 Wide QRS Complex Tachycardia
Ventricular Tachycardia – Monomorphic and Polymorphic
Ventricular Fibrillation
Supraventricular Tachycardia with Aberrant Conduction
Further Reading
Note
8 Bradycardia
Sinus Bradycardia
Junctional Rhythm
Idioventricular Rhythm
Sinoventricular Rhythm of Severe Hyperkalemia
Other Bradycardias
Further Reading
9 Atrioventricular Conduction Block
First‐Degree Atrioventricular Block
Second‐Degree Atrioventricular Block
Third‐Degree Atrioventricular Block
Atrioventricular Dissociation
10 Intraventricular Conduction Block
The Bundle Branch Blocks
The Hemiblocks (Left Anterior and Left Posterior Hemiblocks)
Bifascicular and Trifascicular Blocks
Non‐specific Intraventricular Conduction Abnormality
11 Atrial and Ventricular Ectopic Beats
Premature Atrial Contractions
Premature Junctional Contractions
Premature Ventricular Contractions
Section III: Acute Coronary Syndrome and the 12‐Lead ECG
12 Ischemic Heart Disease
Cardiac Anatomy and Basic Physiology of Depolarization
Coronary Anatomy and Electrocardiograhic Regional Anatomic Issues
Cardiac Pathophysiology
13 Electrocardiographic Findings in Acute Coronary Syndrome
Introduction
The 12‐Lead Electrocardiogram in ST Segment Elevation Myocardial Infarction Evolution of Electrocardiogram Abnormalities
The 12‐Lead Electrocardiogram in non‐ST Segment Elevation Myocardial Infarction Presentations
Electrocardiogram ST Segment Elevation Myocardial Infarction Mimickers and Confounders
Further Reading
References
Section IV: Special Populations, High‐Risk Presentation Scenarios, and Advanced Electrocardiographic Techniques
14 The Electrocardiogram in the Pediatric Patient
Rate and Rhythm
QRS Axis
T Waves
Intervals
Common Dysrhythmias
15 The Electrocardiogram in the Poisoned Patient
Potassium Efflux Blocking Agents
Sodium Channel Blocking Agents
Cardiac Glycoside Toxicity
Calcium Channel Blocker Toxicity
β
‐Adrenergic Blocker Toxicity
16 The Electrocardiogram in Hyperkalemia
Electrocardiographic Manifestations
17 Life‐Threatening Electrocardiographic Patterns
Wellens' Syndrome
Brugada Syndrome
Hypertrophic Cardiomyopathy
Long QT Syndrome
18 The Electrocardiogram in Patients with Implanted Devices
The Paced Electrocardiogram
Pacemaker Malfunction
The Paced Rhythm and Acute Myocardial Infarction
References
19 Electrocardiographic Tools in Clinical Care
Additional Electrocardiographic Leads
Serial Electrocardiography
20 Wolff–Parkinson–White Syndrome
21 Cardiac Arrest Rhythms
Asystole
Pulseless Electrical Activity
Pulseless Ventricular Tachycardia
Ventricular Fibrillation
Section V: Electrocardiographic Differential Diagnosis of Common ECG Presentations
22 Electrocardiographic Differential Diagnosis of Narrow Complex Tachycardia
23 Electrocardiographic Differential Diagnosis of Wide Complex Tachycardia
Ventricular Tachycardia
Ventricular Tachycardia versus Supraventricular Tachycardia with Aberrant Conduction
24 Electrocardiographic Differential Diagnosis of Bradyarrhythmia
25 Electrocardiographic Differential Diagnosis of ST Segment Elevation
26 Electrocardiographic Differential Diagnosis of ST Segment Depression
Acute Coronary Syndromes
Left Bundle Branch Block
Left Ventricular Hypertrophy
Rate‐Related ST Depression
Other Causes
27 Electrocardiographic Differential Diagnosis of T Wave Abnormalities
Prominent T Waves
T Wave Inversion
Index
End User License Agreement
List of Tables
Chapter 1
Table 1.1 Normal ECG Intervals.
Table 1.2 Causes of axis deviation.
Table 1.3 Abnormal ECG findings not related to coronary pathology.
Chapter 4
Table 4.1 ECG findings associated with athletic heart.
Chapter 5
Table 5.1 Age‐related normal heart rate ranges for children.
Chapter 8
Table 8.1 Causes of bradycardia.
Chapter 12
Table 12.1 Cardiac and coronary anatomy with corresponding coronary artery,...
Chapter 13
Table 13.1 The association of cardiac chamber and anatomic segment with ECG...
Chapter 14
Table 14.1 Pediatric ECG normal values by age.
Chapter 15
Table 15.1 Potassium efflux channel blocking drugs.
Table 15.2 Sodium channel blocking drugs.
Table 15.3 Plants associated with cardiac glycoside toxicity.
Table 15.4 Subtype classification of calcium channel blockers, channel affi...
Table 15.5
β
‐Adrenergic blocking drugs.
Chapter 16
Table 16.1 Serum potassium concentration and ECG manifestations.
Chapter 17
Table 17.1 Etiology and clinical manifestations of life‐threatening ECG pat...
Chapter 18
Table 18.1 Pacemaker coding sequence and letter designations.
Chapter 19
Table 19.1 ECG leads, anatomic segment, and coronary anatomy.
Chapter 21
Table 21.1 Pulseless electrical activity cardiac arrest: causes and primary...
Chapter 22
Table 22.1 Differential diagnosis of narrow complex tachycardia (NCT).
Chapter 23
Table 23.1 Differential diagnosis of wide complex tachycardia (WCT).
Chapter 24
Table 24.1 The differential diagnosis of bradycardia.
Chapter 25
Table 25.1 Differential diagnosis of ST segment elevation.
Chapter 26
Table 26.1 The differential diagnosis of ST segment depression.
Chapter 27
Table 27.1 Differential diagnosis of T wave abnormalities.
List of Illustrations
Chapter 1
Figure 1.1 A normal 12‐lead electrocardiogram.
Figure 1.2 Normal cardiac cycle segments and intervals.
Figure 1.3 Rapid, narrow complex tachycardia. (a) Demonstrates an irregular ...
Figure 1.4 ECG axis determination.
Figure 1.5 Wide complex tachycardia. The presence of retrograde P‐waves (arr...
Chapter 2
Figure 2.1 Findings of right heart strain in pulmonary embolism. The “S1Q3T3...
Figure 2.2 Lead aVR with terminal rightward axis; R wave is
≥
3 mm abov...
Figure 2.3 Prominent T waves and widened QRS complex of hyperkalemia.
Figure 2.4 Sine wave pattern in untreated hyperkalemia – this rhythm is term...
Figure 2.5 ECG of a patient with an elevated potassium level of 7.5 mEq/dl; ...
Figure 2.6 Pacemaker responding to bradycardia in a patient with a 3‐s pause...
Figure 2.7 Patient with a dual‐chamber pacemaker/ICD who develops ventricula...
Chapter 3
Figure 3.1 A much different perspective about injury is evident depending on...
Figure 3.2 If only lead I was monitored, it would be quite possible to false...
Figure 3.3 Comparison of the “6‐s method” and “thick line counting” method f...
Figure 3.4 This ECG demonstrates that the thick line counting method is espe...
Figure 3.5 Second‐degree type I atrioventricular heart block (also called Mo...
Figure 3.6 Algorithm for interpretation of the ECG.
Chapter 4
Figure 4.1 BER – This ECG demonstrates benign early repolarization with appr...
Figure 4.2 Sinus arrhythmia – note the beat to beat variation in the R–R int...
Figure 4.3 ECG findings associated with athletic heart – in this ECG, note b...
Figure 4.4 Persistent T wave inversions in the precordial leads in an older ...
Figure 4.5 “Toothbrush tachycardia” is a common source of telemetry alarms (...
Chapter 5
Figure 5.1 Normal sinus rhythm.
Figure 5.2 Sinus arrhythmia. Note the normal morphology of P wave, QRS compl...
Figure 5.3 Atrial fibrillation. Note the absence of P waves and irregular R–...
Figure 5.4 Atrial flutter with 4 : 1 conduction. Note the regularly occurrin...
Figure 5.5 Atrial flutter with variable conduction. Note the varying ratio o...
Figure 5.6 Atrial fibrillation/atrial flutter. Note the irregularly irregula...
Chapter 6
Figure 6.1 Using R–R interval to determine rhythm regularity. Sinus tachycar...
Figure 6.2 Decision pathway for narrow complex tachycardia. RVR, rapid ventr...
Figure 6.3 Sinus tachycardia.
Figure 6.4 Atrial tachycardia. Note the P waves (arrows) denoting a fast und...
Figure 6.5 Atrial tachycardia with variable AV conduction. Identical, regula...
Figure 6.6 Two examples of AVNRT‐type supraventricular tachycardia (also kno...
Figure 6.7 Mechanisms for (a) orthodromic and (b) antidromic atrioventricula...
Figure 6.8 WPW re‐entrant tachycardia. (a) Orthodromic AVRT with clearly vis...
Figure 6.9 Atrial flutter. While distinct P waves can be seen in lead I, lea...
Figure 6.10 Atrial fibrillation with rapid ventricular response.
Figure 6.11 Common causes of atrial fibrillation and atrial flutter. CABG, c...
Figure 6.12 Multifocal atrial tachycardia. Note the multiple P wave morpholo...
Chapter 7
Figure 7.1 Monomorphic ventricular tachycardia. Note the consistent morpholo...
Figure 7.2 Polymorphic ventricular tachycardia. Note the varying QRS complex...
Figure 7.3 Polymorphic ventricular tachycardia, torsade de pointes. Note the...
Figure 7.4 Monomorphic ventricular tachycardia with AV dissociation. Note di...
Figure 7.5 Ventricular tachycardia with capture beat. Note that the second b...
Figure 7.6 Ventricular tachycardia with fusion beats. Note the intermediate ...
Figure 7.7 Ventricular fibrillation. (a) Coarse ventricular fibrillation. Th...
Figure 7.8 Supraventricular tachycardia with aberrant ventricular conduction...
Figure 7.9 Supraventricular tachycardia with aberrant ventricular conduction...
Figure 7.10 Supraventricular tachycardia with aberrant ventricular conductio...
Chapter 8
Figure 8.1 Sinus bradycardia. In essence, sinus rhythm with a rate less than...
Figure 8.2 Sinus bradycardia with sinus arrhythmia. Note the varying R–R int...
Figure 8.3 Sinus pause/sinus arrest. Note the long pause between conducted b...
Figure 8.4 Junctional rhythm. (a) Junctional rhythm with no evident P wave; ...
Figure 8.5 Idioventricular rhythm. The rhythm is regular without evidence of...
Figure 8.6 Wide QRS complex rhythm in the setting of hyperkalemia. The QRS c...
Figure 8.7 Atrial fibrillation with slow ventricular response.
Chapter 9
Figure 9.1 First‐degree AV block with coexisting sinus bradycardia. Note the...
Figure 9.2 Second‐degree type I AV block (Mobitz I or Wenckebach). Note prog...
Figure 9.3 Second‐degree type II AV block type (Mobitz II). Note the consist...
Figure 9.4 Second‐degree heart block type II (Mobitz II). Note the prolonged...
Figure 9.5 Second‐degree AV block (Mobitz II) with high‐grade block. Note th...
Figure 9.6 Third‐degree AV block, or complete heart block. Note the regular ...
Chapter 10
Figure 10.1 The cardiac conduction system. SA, sinoatrial.
Figure 10.2 Identifying characteristics of right bundle branch block involvi...
Figure 10.3 Right bundle branch.
Figure 10.4 Identifying characteristics of left bundle branch block involvin...
Figure 10.5 Left bundle branch block.
Figure 10.6 Identifying characteristics of left anterior fascicular block in...
Figure 10.7 Left anterior fascicular block.
Figure 10.8 Identifying characteristics of left posterior fascicular block i...
Figure 10.9 Left posterior fascicular block in a patient with anterior wall ...
Figure 10.10 Identifying characteristics of bifascicular block involving a R...
Figure 10.11 Bifascicular block demonstrating characteristics of RBBB (bipha...
Figure 10.12 Non‐specific intraventricular conduction delay. The QRS complex...
Chapter 11
Figure 11.1 Premature atrial contraction. Normal sinus rhythm with premature...
Figure 11.2 Premature junctional contraction. Sinus bradycardia with prematu...
Figure 11.3 Unifocal premature ventricular contraction (indicated by the arr...
Figure 11.4 The wide complex ectopic beat (arrow) may at first glance appear...
Figure 11.5 Several examples of unifocal premature ventricular contractions ...
Figure 11.6 Multifocal PVCs. Note the multiple PVCs in this rhythm strip wit...
Figure 11.7 PVCs in a couplet: two consecutive PVCs (arrows), in this case, ...
Figure 11.8 Ventricular bigeminy: every other beat is a PVC (arrows) with an...
Figure 11.9 Ventricular trigeminy. In this multilead rhythm strip, the arrow...
Figure 11.10 R‐on‐T phenomenon with PVC leading to polymorphic VT. Note how ...
Chapter 12
Figure 12.1 The cardiac conduction system (LA, left atrium; RA, right atrium...
Figure 12.2 (a) The cardiac conduction system with superimposed cardiac elec...
Figure 12.3 Cardiac and coronary anatomy with corresponding coronary artery,...
Figure 12.4 The development of atherosclerotic lesions in the coronary arter...
Chapter 13
Figure 13.1 (a) Hyperacute, or prominent, T waves of early STEMI. (b) Hypera...
Figure 13.2 ST segment elevation subtypes in STEMI and non‐STEMI presentatio...
Figure 13.3 Evolution of ECG abnormalities in STEMI. The ECG structures in (...
Figure 13.4 Subtle STEMI. (a) Subtle ST segment elevation in an inferior STE...
Figure 13.5 (a) Q wave likely manifesting a completed myocardial infarction....
Figure 13.6 (a) Reciprocal ST segment depression, also known as reciprocal c...
Figure 13.7 LBBB with normal, or anticipated, ST segment and T wave configur...
Figure 13.8 The anticipated, or “normal,” ECG findings in the LBBB pattern. ...
Figure 13.9 (a) The modified Sgarbossa criteria in LBBB. These three finding...
Figure 13.10 Anterior wall STEMI with ST segment elevation in leads V1–V4. A...
Figure 13.11 Inferior STEMI with reciprocal change in the anterior and later...
Figure 13.12 Inferior STEMI. RV infarction is also suspected for the followi...
Figure 13.13 Additional ECG lead imagining the right ventricle, lead RV4. Th...
Figure 13.14 Lateral STEMI with ST segment elevation in leads V5 and V6.
Figure 13.15 “Isolated” posterior wall acute myocardial infarction. Note the...
Figure 13.16 Additional posterior leads, V8 and V9. Lead V8 is placed on the...
Figure 13.17 ST segment depression.
Figure 13.18 T wave inversions associated with ACS.
Figure 13.19 Wellens' syndrome with deeply inverted T waves in the anterolat...
Figure 13.20 (a) de Winter Syndrome: note the prominent T wave, J point depr...
Figure 13.21 Benign early repolarization with concave ST segment elevation i...
Figure 13.22 Acute myopericarditis, also commonly referred to as acute peric...
Figure 13.23 Left ventricular hypertrophy by voltage pattern with strain. No...
Chapter 14
Figure 14.1 (a) Normal sinus rhythm in two pediatric patients. The upper pan...
Figure 14.2 Normal sinus rhythm in an infant with the T wave inversions in t...
Figure 14.3 Paroxysmal supraventricular tachycardia. (a) Rapid, narrow compl...
Figure 14.4 Bradycardia. (a) Sinus bradycardia. (b) Junctional bradycardia. ...
Chapter 15
Figure 15.1 Impact of sodium channel and potassium efflux blocking drugs on ...
Figure 15.2 (a) Sinus tachycardia at 104 with prolonged QT interval. (b) Pol...
Figure 15.3 (a) Minimally widened QRS complex in the setting of a cardiotoxi...
Figure 15.4 (a) ECG with characteristic changes of “digitalis effect,” a non...
Figure 15.5 (a) Bradydysrhythmia (idioventricular rhythm) with heart rate of...
Figure 15.6 Junctional bradydysrhythmia with heart rate of 30 in the setting...
Chapter 16
Figure 16.1 Peaked, or prominent, T waves. Note the tall, narrow, symmetric ...
Figure 16.2 QRS complex widening in hyperkalemia: The 12‐lead ECG with promi...
Figure 16.3 Severe hyperkalemia with widened QRS complex and symmetric peake...
Figure 16.4 Widened QRS complex in severe hyperkalemia.
Figure 16.5 Significantly widened QRS complexes in three separate patients w...
Figure 16.6 ECG‐directed guideline for the treatment of hyperkalemia. Of cou...
Chapter 17
Figure 17.1 T wave morphologies in Wellens' syndrome. (a) Deeply inverted T ...
Figure 17.2 Polymorphic ventricular tachycardia, seen in patients with the B...
Figure 17.3 Brugada syndrome. (a) The convex/upward “coved” type precordial ...
Figure 17.4 The 12‐lead with findings suggestive of hypertrophic cardiomyopa...
Figure 17.5 Normal sinus rhythm with prolonged QT syndrome with QTc interval...
Chapter 18
Figure 18.1 (a) Atrial paced rhythm. Note the pacer spike (small arrow) imme...
Figure 18.2 Failure to pace. The pacemaker is not functioning properly – in ...
Figure 18.3 Failure to capture. The pacemaker is firing (i.e. a pacer spike ...
Figure 18.4 Undersensing. The pacemaker does not detect normal cardiac activ...
Figure 18.5 The concept of appropriate discordance in ventricular paced rhyt...
Figure 18.6 The modified Sgarbossa criteria in the right ventricular paced p...
Chapter 19
Figure 19.1 Placement of the ECG posterior leads V7–V9.
Figure 19.2 The posterior wall of the left ventricle is imaged with leads V7...
Figure 19.3 ECG leads V1–V3 in a patient with posterior wall acute myocardia...
Figure 19.4 Placement of lead RV4, the lead that will directly image the rig...
Figure 19.5 Right‐sided ECG leads. (a) Lead RV4 with ST segment elevation co...
Figure 19.6 (a) Inferior STEMI with RV and posterior wall infraction. This p...
Figure 19.7 Serial ECGs. (a) 12‐lead ECG with concerning findings for early ...
Figure 19.8 Serial ECGs. (a) Borderline, or subtle, ST segment elevation in ...
Chapter 20
Figure 20.1 The ECG in the patient with WPW syndrome while in normal sinus r...
Figure 20.2 (a) Narrow QRS complex tachycardia (rapid and regular). The impu...
Figure 20.3 Algorithm for the differentiation of the three dysrhythmias seen...
Chapter 21
Figure 21.1 Asystole noted in the three limb leads, as seen in (a–c).
Figure 21.2 Pulseless electrical activity potential rhythm presentations. (a...
Figure 21.3 Ventricular tachycardia. (a) Monomorphic VT. (b) Monomorphic VT....
Figure 21.4 Ventricular fibrillation (VF). (a) Coarse VF. “Coarse” indicates...
Chapter 22
Figure 22.1 Sinus tachycardia, three examples in lead II. Note the P wave pr...
Figure 22.2 Atrial fibrillation with rapid ventricular response.
Figure 22.3 Atrial flutter with rapid ventricular rates.
Figure 22.4 Paroxysmal supraventricular tachycardia (PSVT). (a) PSVT with a ...
Figure 22.5 Multifocal atrial tachycardia (MAT). Note the presence of at lea...
Chapter 23
Figure 23.1 Ventricular tachycardia – monomorphic. (a) Monomorphic VT with a...
Figure 23.2 Polymorphic VT. (a) polymorphic VT, (b) polymorphic VT, (c) poly...
Figure 23.3 Supraventricular tachycardia (SVT) with aberrant ventricular con...
Figure 23.4 Supraventricular tachycardia (SVT) with aberrant ventricular con...
Figure 23.5 Supraventricular tachycardia (SVT) with aberrant ventricular con...
Figure 23.6 Atrioventricular (AV) dissociation. The presence of AV dissociat...
Figure 23.7 Capture beat – the arrows indicate a narrow QRS complex, which r...
Figure 23.8 Fusion beats – the arrows indicate QRS complexes, which are inte...
Figure 23.9 Positive concordance. The QRS complexes in leads V1–V6 are all p...
Figure 23.10 Supraventricular tachycardia (SVT) with aberrant ventricular co...
Figure 23.11 Supraventricular tachycardia (SVT) with aberrant ventricular co...
Figure 23.12 Miscellaneous causes of supraventricular tachycardia (SVT) with...
Figure 23.13 Artifact mimicking wide complex tachycardia (WCT). (a) Rhythm s...
Chapter 24
Figure 24.1 Bradycardias. (a) Sinus bradycardia – criteria for sinus rhythm ...
Figure 24.2 (a) Atrial fibrillation with slow ventricular response. (b) Atri...
Figure 24.3 Atrioventricular blocks. (a) First‐degree AV block. Note the pro...
Figure 24.4 The sinoventricular rhythm of severe hyperkalemia. Note the very...
Chapter 25
Figure 25.1 Various causes of ST segment elevation in adults with chest pain...
Figure 25.2 ST segment elevation subtypes in STEMI and non‐STEMI presentatio...
Figure 25.3 Determination of the morphology of the elevated ST segment. (a) ...
Figure 25.4 Inferolateral STEMI with obvious ST segment elevation in leads I...
Figure 25.5 Anterior STEMI with ST segment elevation in leads V1–V4.
Figure 25.6 STEMI presentations with less obvious ST segment elevation.
Figure 25.7 Appropriate Discordant Relationship of ST Segment to QRS Complex...
Figure 25.8 ST segment elevation in leads V1–V4, resulting from left bundle ...
Figure 25.9 ST segment elevation in leads II, III, aVF, and V1–V6, resulting...
Figure 25.10 Left ventricular hypertrophy by voltage pattern with strain. No...
Figure 25.11 Acute myopericarditis, also commonly referred to as
acute peric
...
Figure 25.12 Benign early repolarization (BER) with concave ST segment eleva...
Figure 25.13 Left ventricular aneurysm with ST segment elevation in leads V1...
Chapter 26
Figure 26.1 ST segment depression (arrows) resulting from ACS. In this situa...
Figure 26.2 Acute inferoposterior STEMI with two forms of ST segment depress...
Figure 26.3 ST segment depression in leads V1–V3. This pattern of ST segment...
Figure 26.4 ST segment depression (arrows) in leads II, III, and aVF – recip...
Figure 26.5 Normal appearing left bundle branch block pattern with anticipat...
Figure 26.6 ST segment depression (with T wave inversion) indicated by the a...
Figure 26.7 ST segment depression (with T wave inversion) as indicated by th...
Figure 26.8 Rate‐related ST segment depression in a patient with PSVT. This ...
Figure 26.9 ST segment depression (arrows) resulting from the “digoxin effec...
Chapter 27
Figure 27.1 Hyperacute T waves of early STEMI. Note the tall appearance with...
Figure 27.2 Prominent T waves of hyperkalemia. Note the tall appearance with...
Figure 27.3 Prominent T waves of benign early repolarization.
Figure 27.4 Prominent T waves of acute pericarditis.
Figure 27.5 Prominent T waves of left bundle branch block.
Figure 27.6 Prominent T waves of ventricular paced rhythm in leads V1–V4.
Figure 27.7 Inverted T waves of acute coronary syndrome. Note the symmetric ...
Figure 27.8 Inverted T waves of acute coronary syndrome.
Figure 27.9 Inverted T waves of Wellen's syndrome. (a) Biphasic T wave (upri...
Figure 27.10 Inverted T waves of left bundle branch block pattern. Note the ...
Figure 27.11 Inverted T waves of ventricular paced pattern. A small pacer sp...
Figure 27.12 Inverted T waves of left ventricular hypertrophy with strain pa...
Figure 27.13 Deeply inverted T waves of CNS hemorrhage.
Guide
Cover Page
Title Page
Copyright Page
Dedication Page
Editors and Contributors
Foreword
Preface
Table of Contents
Begin Reading
Index
WILEY END USER LICENSE AGREEMENT
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The Electrocardiogram in Emergency and Acute Care
Edited by
Korin B. Hudson, | MD, FAAEM, FACEP, CAQ‐SMAmita Sudhir, | MD, FACEPGeorge Glass, | MD, FACEPWilliam J. Brady, | MD, EMT‐B, FACEP, FAAEM
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Library of Congress Cataloging‐in‐Publication DataNames: Hudson, Korin B., editor. | Sudhir, Amita, editor. | Glass, George (George F.), editor. | Brady, William, 1960– editor.Title: The electrocardiogram in emergency and acute care / edited by Korin B. Hudson, Amita Sudhir, George Glass, William J. Brady.Description: Hoboken, NJ : Wiley‐Blackwell, 2023. | Includes index.Identifiers: LCCN 2022037475 (print) | LCCN 2022037476 (ebook) | ISBN9781119266891 (paperback) | ISBN 9781119266860 (Adobe PDF) | ISBN9781119266792 (epub) | ISBN 9781119266938 (obook)Subjects: MESH: Electrocardiography–methods | Emergencies | Critical Care| Heart Diseases–diagnosisClassification: LCC RC683.5.E5 (print) | LCC RC683.5.E5 (ebook) | NLM WG140 | DDC 616.1/207547–dc23/eng/20221110LC record available at https://lccn.loc.gov/2022037475LC ebook record available at https://lccn.loc.gov/2022037476
Cover Design: WileyCover Image: © JY FotoStock/Shutterstock
Korin B. Hudson – I would like to thank my husband, Christopher for his unwavering support and patience; our children, Andrew and Alexander, for encouraging me and making me laugh; my parents, Kathy and David, for supporting and inspiring a career in academics; and to all my mentors and colleagues who demonstrate excellence in clinical medicine, education, and patient care every day. A special thanks to Bill Brady who has been a friend and mentor for 25 years and to our co‐editors and authors who have helped to bring this project to life.
Amita Sudhir – Thank you to my husband, Aaron, my children, Anisha and Anand, and my parents, Romila and Sudhir for their support. Thank you also to Bill Brady for his educating me about ECGs during residency, and for his continued mentorship ever since.
George Glass – I'd like to thank my wife, Heather, for her constant support and my six kids who inspire me every day to be a little bit better. To my parents, for teaching the meaning of love and service. Finally, to my patients: thank you for teaching me every shift and trusting me to care for you. It's truly an honor.
William J. Brady – To my wife, King Brady, my partner and a truly amazing person, thank you for everything; to my children, Lauren (and husband Robert), Anne, Chip, and Katherine, and to my new grandson Eli, all my inspiration; to Amal Mattu, MD, my friend, fellow ECG nerd, and mentor in many ways, thank you for years of collaboration (past, present, and future); and finally to emergency healthcare providers across the globe, both prehospital‐ and hospital‐based, for the your dedication to patient care and your expertise in emergency medicine … and for always “being there” when needed. And, of course, I want to thank my co‐editors and authors for their hard work and expertise in the creation of this work.
Editors and Contributors
Editors
Korin B. Hudson, MD, FACEP, FAAEM, CAQ‐SMProfessor of Clinical Emergency MedicineDepartment of Emergency MedicineGeorgetown University School of MedicineMedStar HealthTeam Physician: Georgetown Athletics, Washington Wizards, Washington MysticsConsulting Physician: Washington Capitals, Maryland Jockey Club EMSWashington, D.C. USA
Amita Sudhir, MD, FACEPAssociate Professor and Program Director of Emergency MedicineUniversity of Virginia Health SystemCharlottesville, USA
George Glass, MDAssistant Professor of Emergency MedicineUniversity of Virginia Health SystemCharlottesville, USA
William J. Brady, MD, FACEP, FAAEMProfessor of Emergency Medicine, Medicine (Cardiovascular), and NursingVice Chair for Faculty AffairsThe David A. Harrison Distinguished EducatorUniversity of Virginia Health SystemCharlottesville, USAEMS Physician and Operational Medical DirectorAlbemarle County Fire RescueCharlottesville, USA
The editors would like to acknowledge and thank the following physician colleagues who served as editors on a prior text which served as the foundation for this volume. Their support is greatly appreciated and highly valued.
Dr. Robin NaplesDr. Steven MitchellDr. Jeffrey FergusonDr. Robert Reiser
Contributors
J. Aidan Boswick, BA, EMT‐BSenior Director, Crossix Analytics Services, Veeva Systems Inc, New York, NY, USA
David Carlberg, MDAssociate Program Director, Georgetown Emergency Medicine Residency, Assistant Professor of Emergency Medicine, Georgetown University School of Medicine, Washington, DC, USA
Jeffrey D. Ferguson, MD, FACEP, FAEMS, NRPAssociate Professor, Department of Emergency Medicine, Virginia Commonwealth University, Richmond, VA, USA
Christopher P. Holstege, MDProfessor of Emergency Medicine and Paediatrics, Director, Division of Medical Toxicology, University of Virginia School of Medicine, Charlottesville, VA, USA
Erik Iszkula, MDClinical Assistant Professor of Emergency Medicine, University of Pittsburgh, Pittsburgh, PA, USA
Michael Levy, MD, FAEMS, FACEP, FACPChief Medical Director Anchorage Areawide EMS, Medical Director State of Alaska Emergency Programs, Anchorage, AK, USA
Steven H. Mitchell, MD, FACEPAssociate Professor, Department of Emergency Medicine, Medical Director, Harborview Medical Center, University of Washington, Seattle, WA, USA
Peter Monteleone, MDAssistant Professor, Department of Internal Medicine, University of Texas at Austin Dell School of Medicine, Austin, TX, USA
Robin Naples, MDClinical Professor of Emergency Medicine, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA
Francis X. Nolan Jr, BS, MICP†Chief Medical Officer (Ret.), Anchorage Fire Department, Anchorage, AK, USA
Peter Pollak, MDConsultant and Chair, Division of Interventional Coma Ischemia & Structural Heart Disease, Interventional Cardiology Specialist, Mayo Clinic Specialist, Jacksonville, FL, USA
Robert C. Reiser, MDAssociate Professor, Department of Emergency Medicine, University of Virginia, Charlottesville, VA, USA
Robert Rutherford, MDAttending Physician, Swedish Medical Centre‐Edmonds Campus, Edmonds, WA, USA
Courtney B. Saunders, MDDepartment of Cardiology, Vidant Health, Greenville, NC, USA
Robert C. Schutt, MDDepartment of Cardiology, Ascension Medical Group, Austin, TX, USA
Megan Starling, MDAssistant Professor of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA; Attending Physician, Culpeper Memorial Hospital, Culpeper, USA
Richard B. Utarnachitt, MD, MSClinical Associate Professor, Medical Director, Airlift Northwest, Department of Emergency Medicine, University of Washington, Seattle, WA, USA
Alvin Wang, DO, NREMT‐PEmergency Medicine Specialist, Jefferson Health System, Philadelphia, PA; Chief, Emergency Medical Services, Jefferson Health System Northeast
Kelly Williamson, MDAssociate Professor and Assistant Program Director, Residency Program of Emergency Medicine, Northwestern University, Chicago, IL, USA
Note
†
Deceased.
Foreword
The electrocardiogram (ECG) is an essential instrument in the evaluation of a broad array of clinical conditions related to cardiac and non‐cardiac disorders. The ECG is commonly used to evaluate the electrical and mechanical function of the heart, but the tracing can also be used to detect systemic disorders such as electrolyte disarray or toxic and metabolic abnormalities. The indications for an ECG encompass all aspects of medical care. In fact, the only contraindication to obtaining an ECG tracing is patient refusal. Acquisition of an ECG tracing is an easily learned skill, but the interpretation can be difficult and nuanced, thus requiring significant effort on the part of the learner to develop competence and confidence in the skill. Reading an ECG can be a high‐stakes endeavor as incorrect interpretation can have profound consequences. Because the stakes are so high, it is incumbent on any health care providers responsible for ECG interpretation to study the full spectrum of clinical conditions that may be evident on the tracing.
The history of the ECG is a relatively recent one. An understanding that electrical impulses were produced by the heart was not known until the 1850s, but it took four more decades to develop instruments to measure the myocardial action potential. Willem Einthoven, a Dutch physiologist devoted the 1890s to gain an understanding the heart's electrical activity and how to best measure it. By 1902, he had devised the first ECG machine consisting of a fine (less than 3 μm in diameter) filament made of silver and quartz suspended in a powerful magnetic field. The electrical activity of the heart caused the string to resonate within the field and these vibrations were recorded photographically. The photographic plate was set to move at 25 mm per second, a convention that is used on paper tracings to this day. An obscure 1902 paper by Einthoven was the first known writing to describe the device. Einthoven was awarded the 1924 Nobel Prize for his invention.
The first machines commercially available were built between 1905 and 1907, were expensive, weighed 300 kg, and required a team of highly trained personnel to operate. Refinements of the machines brought down the size and weight, but doctors needed to transmit electrical impulses from the patient at the hospital to the machine in the laboratory off‐site. Early clinical applications refined the understanding of, what was termed at the time as delirium cordis; which became known as atrial fibrillation. These early machines grew in popularity to aid clinicians in diagnosing cardiac arrhythmias, but information was limited owing to the fact that the machine had only the three leads.
By the 1920s, hypertrophy and infarction had been identified and described as the ECG became an essential medical device. In the 1930, angina pectoris was being identified by ECG, which led to an understanding of the ailment's vascular etiology. Precordial leads were developed, initially as a single lead, but later as multiple leads. In the 1940s, our contemporary precordial leads, V1 through V6 were standardized, and a refinement of the limb leads led to use of leads AVR, AVL, and AVF. During the 1950s and 1960s, acquisition of the ECG became widespread, and training in tracing interpretation became standard for medical students. The 1970s saw the introduction of computer interpretation to assist clinicians in identifying rate, rhythm, axis, hypertrophy, intervals, ischemia and infarction, but reading by a trained eye was (and is) still required.
By 1990, 50 million ECGs were performed annually in the United States, and time from first medical contact to ECG image acquisition became a measured performance standard for emergency medicine and EMS. By 2010, ECG acquisition an essential skill for EMS Basic Life Support personnel and ECG interpretation of STEMI was an essential skill for Paramedics. By 2020, the 300 kg behemoth from 1902 had been miniaturized to something that can be worn on a wrist.
The Electrocardiogram in Emergency and Acute Care is a text where readers are guided through a systematic approach to understanding the physics behind the ECG and are given clinical examples where the tracing can be interpreted to make a diagnosis. This approach places ECG interpretation within the reach of learners at every level making the text valuable to students learning about the ECG for the first time to experienced clinicians. Enjoy!
Robert E. O'Connor, M.D., MPH
Marcus L. Martin Distinguished Professor and Chair of Emergency MedicineUniversity of VirginiaDaniel A. Griffith, DHA, MBAAssistant Administrator for OperationsDepartment of Emergency MedicineUniversity of Virginia
Preface
Electrocardiographic monitoring is one of the most widely applied diagnostic tests in clinical medicine today; its first application to the patient occurs in the prehospital setting, in the clinician's office or by emergency medical services (EMS) … its use continues on into the hospital. The electrocardiogram, whether in monitor mode using single or multichannel rhythm monitoring or in diagnostic mode using the 12‐lead ECG, is an amazing tool; it assists in establishing a diagnosis, ruling‐out various ailments, guiding the diagnostic and management strategies in the evaluation, providing indication for certain therapies, offering risk assessment, and assessing end‐organ impact of a syndrome. As noted in this impressive list of applications, the ECG provides significant insight regarding the patient's condition in a range of presentations, whether it be the chest pain patient with ST segment elevation myocardial infarction (STEMI), the patient in cardiac arrest with ventricular tachycardia, the poisoned patient with bradycardia, or the renal failure patient with rhythm and morphologic findings consistent with hyperkalemia, among many, many other presentations. This extremely useful tool is non‐invasive, portable, inexpensive, quickly obtained, and easily performed. Yet, ECG interpretation is not easily performed and, in fact, requires considerable skill and experience as well as an awareness of the limitation surrounding its use.
This textbook has been prepared to assist clinicians who wish to learn, review, and refine the skills required to interpret the electrocardiogram and develop a deeper understanding of its use across the range of presentations and applications. This textbook is arranged into five sections. Section 1 is a brief introduction and review of the ECG in the clinical setting. Section 2 focuses on the electrocardiographic rhythm diagnosis, considering the electrocardiographic findings from an in‐depth differential diagnostic perspective – in other words, rhythms with normal rates as well as bradycardia and tachycardia, allowing for the QRS complex width and regularity. Section 3 reviews the 12‐lead ECG in patients suspected of acute coronary syndrome, including ST segment elevation myocardial infarction. Section 4 discusses the range of special presentations, patient populations, and uses of the electrocardiogram. Section 5 is a listing of various electrocardiographic findings, again from the differential diagnostic perspective; in this section, various rhythm and morphologic presentations are discussed, such as the narrow and wide complex tachycardias and ST segment elevation syndromes.
This textbook addresses the use of the ECG in its many forms by clinicians in a wide range of clinical settings. The novice electrocardiographer can use this text as his or her primary ECG reference; additionally, the experienced interpreter can use this textbook to expand his or her knowledge base. This work stresses the value of the ECG in the range of clinical situations encountered daily by health care providers – it illustrates the appropriate applications of the electrocardiogram in emergency and acute care scenarios.
Most importantly, this textbook is written by clinicians for clinicians, with an emphasis on the reality of the patient care. I and my co‐editors and authors have enjoyed its creation – we hope that you, the clinician, will not only enjoy its content but also find it of value in the care of your patients. We thank you for what you do every day.
William J. Brady, MD
Charlottesville, USA
