A Visual Guide to ECG Interpretation

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A Visual Guide to ECG Interpretation Third Edition

Susan R. Wilcox, MD Medical Director, 5c Medical ICU Lahey Hospital and Medical Center Burlington, Massachusetts

David F. M. Brown, MD President, Massachusetts General Hospital MGH Trustees Professor of Emergency Medicine

Harvard Medical School Boston, Massachusetts

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Third Edition

Copyright © 2017 Wolters Kluwer. Copyright © 2012 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at permissions@lww.com, or via our website at shop.lww.com (products and services).

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Library of Congress Cataloging-in-Publication Data Names: Wilcox, Susan R. (Susan Renee), author. | Brown, David F. M., author. | Martindale, Jennifer L. Visual guide to ECG interpretation. Title: A visual guide to ECG interpretation / Susan R. Wilcox, David F.M. Brown. Description: Third edition. | Philadelphia, PA : Wolters Kluwer, [2025] | Preceded by A visual guide to ECG interpretation / Jennifer L. Martindale, David F.M. Brown. Second edition. [2017]. | Includes bibliographical references and index. Identifiers: LCCN 2023050687 | ISBN 9781975213589 (hardback) Subjects: MESH: Electrocardiography | Emergencies | Pictorial Work Classification: LCC RC683.5.E5 | NLM WG 17 | DDC 616.1/207547--dc23/eng/20231215 LC record available at https://lccn.loc.gov/2023050687

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This work is no substitute for individual patient assessment based upon healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data, and other factors unique to the patient. The publisher does not provide medical advice or guidance and this work is merely a reference tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources. When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings, and side effects and identify any changes in dosage schedule or contraindications, particularly if the medication to be administered is new, infrequently used, or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work. Copyright © 2021 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited.

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To all my residents, past, present, and future.

– SRW

To the amazing inspiring people who care for patients in the MGH Emergency Department.

– DFMB

Preface

Now in its third edition, the objective of this book remains unchanged—to provide a visual tool that will help physicians and other emergency clinicians quickly recognize important ECG patterns. By the end of the book, the reader will have developed a mental repertoire of ECGs that represent medically significant conditions, including some that are potentially fatal. We hope that our illustrations and easy-to-follow explanations help demystify ECG inter pretation. This book is intentionally graphic and nontechnical. It is designed to help clinicians make visual diagnoses by highlighting abnormalities in a colorful and pictorial fashion. The third edition maintains the same format as the previous one. An ECG is first shown in its native state to give the reader a chance to recognize and interpret salient features. Abnormal patterns are enlarged, highlighted

in color, and described in brief on the following page. In the third edition, we have provided more enlarged illustrations and callouts, highlighting the nuances of key ECG patterns. We have added new ECGs and included those that emphasized critical pathologies, including hyperkalemia, coronary occlusion, and right ventricular dysfunction. In the ischemia chapter 13, we included ECGs with more subtle signs of coronary occlusion. In keeping with the evolution of cardiology, we have added ECGs for patients with left ventricular assist devices. The third edition is accompanied by an accessible, online appendix that presents ECG abnormalities in random order. We hope this will allow our readers to practice and consolidate their learning. We would like to thank everyone who contributed electrocardiograms to this collection.

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Contents

Preface vii

1 Concept Review

2 Sinus Dysfunction

16 28 63 99

3 Bundle Branch and Fascicular Blocks

4 AV Conduction Blocks

5 Premature Beats

6 Abnormal QRS Morphology

122 165 207 258 292 348 399 492

7 Abnormal T Waves

8 QT Abnormalities and Electrolyte Disturbances

9 Voltage Abnormalities

10 Fast and Narrow

11 Fast and Wide

12 Ischemic Patterns 13 Cardiac Devices

Online Appendix Index I-1

Voltage Abnormalities CHAPTER 9

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Chapter 9 • Voltage Abnormalities

The Low-Voltage ECG

Criteria Voltage is considered low in the limb leads when the average QRS amplitude is less than 5 mm and low in the precordial leads when the average QRS amplitude is less than 10 mm.

Low voltage can result from cardiac causes in which the myocardium fails to generate significant voltage. Low voltage can also result when sufficient voltage signal is attenuated by extracardiac factors. Some of these decrease the signal by increasing the distance from the heart to the chest wall.

The Differential Diagnosis

Cardiac Causes

Extracardiac Causes

Ischemic Myocardium

Air

Fluid

Adipose

Other

Severe cardiomyopathy

Hypothyroidism

Pneumothorax

Pericardial Effusion Large Pleural Effusion

Morbid Obesity

Possibly from a combination of pericardial effusion and low thyroid hormone.

Especially left-sided pneumothorax

Cardiac amyloidosis Infiltrated Myocardium

Hypothermia

Especially left-sided pleural effusion

COPD

Subcutaneous emphysema

Anasarca

Constrictive pericarditis

Electrical Alternans

QRS Wave Alternans

Pericardial Effusion

Alternating voltage of the QRS complex results from the pendular motion of the heart within a fluid-filled pericardial space.

Supraventricular Tachycardias

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Left Ventricular Hypertrophy (Fig. 9.1) Left ventricular hypertrophy (LVH) is independently associated with increased morbidity in patients with hypertension. 1 The diagnosis of LVH requires advanced imaging. Increased Voltage The most commonly used diagnostic criteria for LVH are based on measurements of QRS voltages. In LVH, leftward ventricular forces largely outweigh rightward forces and become unopposed briefly after right ventricular activation is completed. The resultant QRS complexes are exaggerated forms of those in a normal ECG with deeper S waves in right-sided leads (V1 and V2) and taller R waves in left-sided leaves (aVL, V5, and V6). Two of the most commonly used criteria are listed in Table 9.1.

TABLE 9.1 Two Most Commonly Used Diagnostic Criteria for LVH Sokolow-Lyon Index 2 Cornell Voltage Criteria 3 S in V1 + R in V5 or V6 ≥ 35 mm or

Men: S in V3 + R in aVL > 28 mm Women: S in V3 + R in aVL > 20 mm

R in aVL > 11 mm

The sensitivities associated with these criteria are very low. 4 Although QRS voltage increases with left ventricular mass, there are a number of other factors including age, gender, lung disease, and body habitus that affect voltage. The ECG cannot be used as a screening tool for LVH. Fulfillment of voltage criteria alone does not make an ECG diagnostic for LVH. Increased voltage can be seen in young, thin adults. The following non–voltage-based abnormalities support the diagnosis of LVH.

QRS Widening It takes longer for activation to spread from endocardium to epicardium in the thicker left ventricular myocar dium. The QRS complex becomes slightly widened, and the time to the peak of the R wave is increased (>50 ms in lead V5 or V6). ST Depression and TW Inversion Repolarization can occur before the entire left ventricular myocardium has depolarized. This can result in a downward shift of the ST segment in leads with tall R waves. Earlier repolarization of the endocardium allows repolarization to proceed from endocardium to epicardium, resulting in asymmetric TW inversion. TW inver sion may also result from subendocardial ischemia. In leads with tall R waves, downsloping ST depression next to inverted T waves is a secondary repolarization abnormality commonly referred to as the “LV strain pattern.” Left Atrial Abnormality Changes in left ventricular pressure and volume commonly result in left atrial enlargement. Left Axis Deviation A more horizontal axis of the QRS complex may result in increased left ventricular mass. ST Elevation in Leads V1 to V3 Some ST elevations in leads with deep S waves represent appropriate proportional discordance.

Left atrial enlargement

ST elevation

Deep S wave

Tall R wave

ST depression

Asymmetric TW inversion

Left atrial enlargement

QRS widening

FIGURE 9.1 Morphologic features of LVH.

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Chapter 9 • Voltage Abnormalities

Right Ventricular Hypertrophy Due to the opposing forces of the thicker left ventricle, the sensitivity of electrocardiographic criteria for right ventricular hypertrophy (RVH) is generally low. The mass of the left ventricle is still greater than that of the right ventricle in patients with RVH. The presence of several ECG features, however, can be helpful in cases of significant RVH.

ECG Features

Right Axis Deviation QRSVoltage Criteria

This is a consistent sign in RVH. The most common cause of right axis deviation in an adult is RVH (Fig. 9.2).

COPD

ECG Features

Right-Sided Leads (V1) R>7mm R:S > 1

Left-Sided Leads (V5 or V6)

DeepS

R:S ratio ≥ 1

Lung Hyperinflation

S > 7 mm

Air can dampen the ECG signal.

Low Voltage

FIGURE 9.2 ECG appearance of RVH in precordial leads.

Lowered diaphragms cause the heart to be positioned more vertically.

Vertical Heart Position

S1 S2 S3 Pattern Peaked P Waves: Amplitude ≥ 2.5mm in lead II S waves in leads I, II, and III ST/TWave Changes ST Depression and TWI in V1 to V2 are secondary repolarization abnormalities that may accompany tall R waves P Pulmonale

Results from clockwise rotation of the vertical heart. The P-, QRS-, and T-wave vectors are all almost perpendicular to lead I. These waves in lead I have low amplitudes. Due to right ventricular hypertrophy or dilation

Right Axis Deviation

Poor R-Wave Progression

The Lead I Sign (Figure 9.3)

Causes to Consider

Right Atrial Abnormality

Peaked P waves in leads II, III, and aVF often accompany the above ECG changes.

Pressure Overload

Volume Overload

Deep S waves in V5 and V6.

RVH

Primary Pulmonary Hypertension COPD Mitral Stenosis Pulmonary Embolism Pulmonic Stenosis Ventricular Septal Defect

Tricuspid Regurgitation Atrial Septal Defect

FIGURE 9.3 Example of the lead I sign in a patient with severe COPD. P and T waves are unidentifiable. QRS complexes are 1 mm in amplitude.

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Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder most often caused by mutations in genes that encode proteins in the cardiac sarcomere. In some cases, this cardiomyopathy is caused by other genetic disorders such as Friedrich ataxia (Fig. 9.4).

Hypertrophic Patterns Hypertrophy is frequently diffuse but can be limited to segmental areas of the left ventricle. There is no classic hypertrophic pattern.

Dominant and partially unopposed LV activation

ECG Findings

Thickened septum

Deep Q waves in II, III, aVF, V5, and V6, especially in patients who are in teenage years, may be the most specific finding in HCM. LVH and its associated repolarization abnor malities are the two most common abnor malities. 5 The magnitude of voltage does not predict the extent of hypertrophy. 6 Giant negative T waves in the precordial leads occur when hypertrophy is localized in the apex.

LV free wall

Q Waves

Left Ventricular Hypertrophy

Left-to-right septal depolarization

RV free wall B FIGURE 9.4 ( A ) Vector forces in hypertrophic cardiomyopathy. ( B ) Resultant QRS morphology. A

Giant TWI

Patients may be asymptomatic or may complain of dyspnea on exertion, angina, presyncope, or syncope. Syncope may result from outflow tract obstruction or dysrhythmias.

Clinical Presentations

Clinical Complications

Occur in up to 38% of patients. 7

Supraventricular Dysrhythmias

Ventricular Dysrhythmias

Asymptomatic nonsustained ventricular tachycardia occurs in 25% of adult with HCM. 7,8

Structural abnormalities of the mitral valve apparatus are common in HCM. Abnormal papillary muscle and mitral valve leaflets contribute to left ventricular outflow tract obstruction. Obstruction can also occur in the left ventricular midcavity. Diastolic dysfunction is common in patients with HCM, and Doppler imaging is recommended as a routine diagnostic study in patients with HCM. 9 Some patient with apical or distal LVH may develop apical scarring or aneurysm. This may cause coved ST segment elevation in the lateral precordial leads. Copyright © 2021 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited.

Outflow Tract Obstruction

Diastolic Dysfunction

Apical Aneurysm

Infective Endocarditis

Occurs in patients with outflow tract obstruction. Antibiotic prophylaxis is recommended for invasive procedures.

ICDs are recommended for secondary prophylaxis in patients who survive VF or sustained VT. Primary prevention of sudden cardiac death with an ICD is reserved for patients who are considered high risk based on 48-hour ambulatory ECG monitoring, 2D Doppler echocardiogram, and history. 9

Sudden Cardiac Death

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Chapter 9 • Voltage Abnormalities

ECG 9.1A A 69-year-old male presents with shortness of breath.

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ECG 9.1B A 69-year-old male presents with shortness of breath.

COPD

There is minimal voltage in lead I. P waves are barely visible, and QRS complexes are 1.5 mm in amplitude. The P waves are peaked and tall (2.5 mm), suggesting right atrial enlargement caused by this patient’s pulmonary disease.

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Chapter 9 • Voltage Abnormalities

ECG 9.2A A 54-year-old woman presents with dyspnea.

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ECG 9.2B A 54-year-old woman presents with dyspnea.

Electrical Alternans

The low voltage is most profound in the limb leads and right precordial leads. Subtle changes in QRS amplitude suggestive of pericardial effusion can be appreciated even in these low-voltage leads.

ECG 9.2C Detail for variation in QRS amplitude.

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Chapter 9 • Voltage Abnormalities

ECG 9.3A An asymptomatic 9-year-old boy with Friedreich’s ataxia.

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A VISUAL GUIDE TO ECG INTERPRETATION

ECG 9.3B An asymptomatic 9-year-old boy with Friedreich’s ataxia.

Hypertrophic Cardiomyopathy

HCM is associated with a number of syndromes (Friedreich’s ataxia, Noonan syndrome, and Lentiginosis), metabolic disorders (Hunter syndrome, Hurler syndrome, and Fabry disease), and mitochondrial diseases.

ECG 9.3C Detail for deep, narrow Q waves, R-wave enlargement.

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Chapter 9 • Voltage Abnormalities

ECG 9.4A A 48-year-old woman complains of dyspnea on exertion.

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ECG 9.4B A 48-year-old woman complains of dyspnea on exertion.

Electrical Alternans

The voltage in the precordial leads is low (<10 mm). As the heart swings to and fro within the pericardial fluid, its electrical axis changes. This is inscribed on the ECG as alternating levels of QRS amplitude. The transthoracic echocardiogram of this patient is shown to the right. Almost 3 cm of pericardial fluid was measured anterior to the right ventricle. This image demonstrates scalloping of the right ventricle (indentation of the right ventricular wall) in diastole as the hydrostatic pressure of the pericardial fluid exceeds the end-diastolic pressure of the right ventricle. This patient had 610 mL of fluid drained from the pericardial space (Fig. 9.5).

FIGURE 9.5 Image from this patient’s echocardiogram.

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Chapter 9 • Voltage Abnormalities

ECG 9.5A A 59-year-old presents with dyspnea and hypoxia (oxygen saturation 72% on room air).

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ECG 9.5B A 59-year-old presents with dyspnea and hypoxia (oxygen saturation 72% on room air).

Right Ventricular Hypertrophy

A chest CT revealed centrilobular emphysema and dilated pulmonary arteries. There was no evidence of pulmonary embolism. RVH in this patient is secondary to COPD and pulmonary hypertension.

ECG 9.5C Detail for enlarged P waves, deep S waves.

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Chapter 9 • Voltage Abnormalities

ECG 9.6A A 63-year-old male presents with lethargy and confusion.

Reprinted from, with permission from Elsevier. 10

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A VISUAL GUIDE TO ECG INTERPRETATION

ECG 9.6B A 63-year-old male presents with lethargy and confusion.

Hypothermia and Myxedema Coma

This patient’s rectal temperature was 31°C (87.8°F). His serum TSH was 216.9 mIU/mL. Atrial fibrillation with slow ventricular response is a common arrhythmia in hypothermic patients.

ECG 9.6C Detail for low voltage.

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Chapter 9 • Voltage Abnormalities

ECG 9.7A A 67-year-old male presents with shortness of breath.

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ECG 9.7B A 67-year-old male presents with shortness of breath.

Chronic Obstructive Pulmonary Disease

The voltage is low in both limb and precordial leads. The voltage is particularly low in lead I (lead I sign) and lead V6 because the vertically oriented heart in COPD results in a vertical axis perpendicular to these leads. This patient has been on home oxygen (2L) for the past five years. Copyright © 2021 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited.

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Chapter 9 • Voltage Abnormalities

ECG 9.8A A 52-year-old woman presents with shortness of breath.

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ECG 9.8B A 52-year-old woman presents with shortness of breath.

Cardiac Tamponade

The ECG diagnosis of cardiac tamponade was overlooked by the first clinician who saw ECG 9.8. Hours later, the ECG was reviewed by another clinician who immediately performed a bedside ECG to find RV collapse during diastole and a large pericardial effusion. The patient’s condition deteriorated over the next several hours, and emergent pericardiocentesis was performed.

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Chapter 9 • Voltage Abnormalities

ECG 9.9A A 46-year-old male is sent from his doctor’s office for having a blood pressure of 230/110.

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ECG 9.9B A 46-year-old male is sent from his doctor’s office for having a blood pressure of 230/110.

Left atrial abnormality

R > 20 mm in a

ST depression and TWI in LV strain pattern

limb lead

Minimal discordant ST elevations

R > 30 mm in V6

ST depression and TWI in LV strain pattern

ECG 9.9C Detail for ST depressions and TWI.

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Chapter 9 • Voltage Abnormalities

ECG 9.10A An 83-year-old male on amiodarone presents with bradycardia, hypotension, and altered mental status.

Image courtesy of Sarah Frasure, MD.

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ECG 9.10B An 83-year-old male on amiodarone presents with bradycardia, hypotension, and altered mental status.

<10 mm precordial leads

<5 mm limb leads

Low voltage

Junctional bradycardia, HR = 49 bpm

Mild Hypothermia and Myxedema Coma

This patient’s rectal temperature was 92.9°F.

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Chapter 9 • Voltage Abnormalities

ECG 9.11A A 61-year-old male presents with chest tightness.

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ECG 9.11B A 61-year-old male presents with chest tightness.

COPD

Voltage is minimal in lead I because the ventricular axis in this patient’s heart is perpendicular to this limb lead. Hyperinflated lungs cause the heart to hang more vertically within the thoracic cavity. This patient’s chest radiograph (Fig. 9.6) shows hyperinflated lungs and a vertically elongated heart.

FIGURE 9.6 Chest radiograph.

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Chapter 9 • Voltage Abnormalities

ECG 9.12A A 58-year-old man complains of dyspnea.

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ECG 9.12B A 58-year-old man complains of dyspnea.

Low voltage

<10 mm precordial leads

<5 mm limb leads

Low voltage + Tachycardia = Cardiac tamponade until proven otherwise

Cardiac Tamponade

This patient was taken urgently to the cath lab, where 1,250 mL of sanguineous pericardial fluid was drained. Cytology demonstrated high-grade large B-cell lymphoma. Copyright © 2021 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited.

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Chapter 9 • Voltage Abnormalities

ECG 9.13A

Image courtesy of Henry Cheng, MD .

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ECG 9.13B

R > 20 mm in a limb lead

Deep and narrow Q waves

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Chapter 9 • Voltage Abnormalities

ECG 9.14A A 60-year-old male complains of having to stop every 30 feet to catch his breath.

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ECG 9.14B A 60-year-old male complains of having to stop every 30 feet to catch his breath; his ECG 1 year prior.

Pericardial fluid

ECG 9.14C

Cardiac Tamponade

The voltage of this patient’s more recent ECG is notably less than the one obtained 1 year prior. Even if an ECG does not satisfy low-voltage criteria, a significant decrease in voltage from a prior study can be clinically significant. This patient’s transthoracic echocardiogram is shown to the right (Fig. 9.7). A total of 1,200 mL of fluid was drained during this patient’s pericardiocentesis. The cytology obtained from this pericardial fluid demonstrated non-small cell lung cancer.

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Chapter 9 • Voltage Abnormalities

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