Sách POCKET MEDICINE

Pocket
MEDICINE
Fifth Edition

Edited by

MARC S. SABATINE, MD, MPH

ASSOCIATE PROFESSOR OF MEDICINE
HARVARD MEDICAL SCHOOL

The Massachusetts General Hospital
Handbook of Internal Medicine

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Library of Congress Cataloging-in-Publication Data
Pocket medicine (Sabatine)
Pocket medicine / [edited by] Marc S. Sabatine. — Fifth edition.
p. ; cm.
Preceded by Pocket medicine / edited by Marc S. Sabatine. 4th ed.
c2011.
Includes bibliographical references and index.
ISBN-13: 978-1-4511-8237-8
ISBN-10: 1-4511-8237-6
ISBN-13: 978-1-4511-8887-5
ISBN-10: 1-4511-8887-0
I. Sabatine, Marc S., editor of compilation. II. Title.
[DNLM: 1. Internal Medicine–Handbooks. 2. Clinical Medicine–Handbooks. WB 39]
RC55
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CONTENTS

Contributing Authors
Foreword
Preface
CARDIOLOGY
Neal A. Chatterjee, Ada Stefanescu, William J. Hucker, David M. Dudzinski, Marc S.
Sabatine, Michelle O’Donoghue
Electrocardiography
Chest Pain
Noninvasive Evaluation of CAD
Coronary Angiography and Revascularization
Acute Coronary Syndromes
PA Catheter and Tailored Therapy
Heart Failure
Cardiomyopathies
Valvular Heart Disease
Pericardial Disease
Hypertension
Aortic Aneurysms
Acute Aortic Syndromes
Arrhythmias
Atrial Fibrillation
Syncope
Intracardiac Devices
Cardiac Risk Assessment for Noncardiac Surgery
Peripheral Artery Disease
PULMONARYQ
Ian J. Barbash, Kathryn A. Hibbert, Atul Malhotra
Dyspnea
Pulmonary Function Tests
Asthma

Anaphylaxis
Chronic Obstructive Pulmonary Disease
Hemoptysis
Bronchiectasis
Solitary Pulmonary Nodule
Obstructive Sleep Apnea
Interstitial Lung Disease


Pleural Effusion
Venous Thromboembolism
Pulmonary Hypertension
Respiratory Failure
Mechanical Ventilation
Acute Respiratory Distress Syndrome
Sepsis
GASTROENTEROLOGY
Zachary A. Zator, Andrew S. de Lemos, Lawrence S. Friedman
Esophageal and Gastric Disorders
Gastrointestinal Bleeding
Diarrhea, Constipation and Ileus
Diverticular Disease
Inflammatory Bowel Disease
Intestinal Ischemia
Pancreatitis
Abnormal Liver Tests
Hepatitis
Acute Liver Failure
Cirrhosis
Hepatic Vascular Disease

Ascites
Biliary Tract Disease
NEPHROLOGY
Andrew S. Allegretti, Andrew L. Lundquist, Hasan Bazari
Acid-Base Disturbances
Sodium and Water Homeostasis
Potassium Homeostasis
Renal Failure
Glomerular Disease
Urinalysis
Nephrolithiasis
HEMATOLOGY-ONCOLOGY
Andrew M. Brunner, Sheheryar K. Kabraji, Mark M. Awad, Andrew J. Aguirre, Daniel J.
DeAngelo, David P. Ryan
Anemia
Disorders of Hemostasis
Platelet Disorders
Coagulopathies


Hypercoagulable States
Disorders of Leukocytes
Transfusion Therapy
Myelodysplastic Syndromes
Myeloproliferative Neoplasms
Leukemia
Lymphoma
Plasma Cell Dyscrasias
Hematopoietic Stem Cell Transplantation
Lung Cancer

Breast Cancer
Prostate Cancer
Colorectal Cancer
Chemotherapy Side Effects
Pancreatic Tumors
Oncologic Emergencies
Cancer of Unknown Primary Site
INFECTIOUS DISEASES
Ana A. Weil, Emily P. Hyle, Nesli Basgoz
Pneumonia
Fungal Infections
Infections in Immunosuppressed Hosts
Urinary Tract Infections
Soft Tissue and Bone Infections
Infections of the Nervous System
Bacterial Endocarditis
Tuberculosis
HIV/AIDS
Tick-Borne Diseases
Fever Syndromes
ENDOCRINOLOGY
Kelly B. Lauter, Marc N. Wein, Michael Mannstadt
Pituitary Disorders
Thyroid Disorders
Adrenal Disorders
Calcium Disorders
Diabetes Mellitus
Lipid Disorders
RHEUMATOLOGY

Zachary S. Wallace, Eli Miloslavsky, Robert P. Friday
Arthritis—Overview
Rheumatoid Arthritis
Adult Onset Still’s Disease & Relapsing Polychondritis
Crystal Deposition Arthritides
Seronegative Spondyloarthritis
Infectious Arthritis & Bursitis
Connective Tissue Diseases
Systemic Lupus Erythematosus
Vasculitis
IgG4-Related Disease
Cryoglobulinemia
Amyloidosis
NEUROLOGY
Michael P. Bowley, Todd M. Herrington, Eyal Y. Kimchi, Sarah Wahlster, Tracey A. Cho
Change in Mental Status
Seizures
Alcohol Withdrawal
Stroke
Weakness & Neuromuscular Dysfunction
Headache
Back and Spinal Cord Disease
CONSULTS
Kiran H. Lagisetty, Jennifer F. Tseng, Katherine T. Chen, Stella K. Kim
Surgical Issues
Ob/Gyn Issues
Ophthalmic Issues
APPENDIX
ICU Medications & Treatment of Hypotension/Shock

Antibiotics
Formulae and Quick Reference
ABBREVIATIONS
INDEX
PHOTO INSERTS
Radiology
Echocardiography & Coronary Angiography


Peripheral Blood Smears & Leukemias
Urinalysis
ACLS


CONTRIBUTING AUTHORS

Andrew J. Aguirre, MD, PhD
Hematology-Oncology Fellow, Dana-Farber/Partners CancerCare Hematology/Oncology
Program
Andrew S. Allegretti, MD
Internal Medicine Resident, Massachusetts General Hospital
Mark M. Awad, MD, PhD
Hematology-Oncology Fellow, Dana-Farber/Partners CancerCare Hematology/Oncology
Program
Ian J. Barbash, MD
Internal Medicine Resident, Massachusetts General Hospital
Nesli Basgoz, MD
Associate Chief and Clinical Director, Infectious Disease Division, Massachusetts General
Hospital
Associate Professor of Medicine, Harvard Medical School

Hasan Bazari, MD
Clinical Director, Nephrology Unit, Massachusetts General Hospital
Program Director, Internal Medicine Residency, Massachusetts General Hospital
Associate Professor of Medicine, Harvard Medical School
Michael P. Bowley, MD, PhD
Neurology Resident, Partners Neurology Residency
Andrew M. Brunner, MD
Internal Medicine Resident, Massachusetts General Hospital
Neal A. Chatterjee, MD
Internal Medicine Resident, Massachusetts General Hospital
Katherine T. Chen, MD, MPH
Associate Professor of Obstetrics, Gynecology, and Reproductive Science
Associate Professor of Medical Education
Vice-Chair of Ob/Gyn Education, Career Development, and Mentorship
Icahn School of Medicine at Mount Sinai, New York


Tracey A. Cho, MD
Associate Program Director, Partners-Harvard Neurology Residency
Assistant Professor of Neurology, Harvard Medical School
Assistant Neurologist, Massachusetts General Hospital
Andrew S. de Lemos, MD
Transplant Hepatology Fellow, Massachusetts General Hospital
Daniel J. DeAngelo, MD, PhD
Adult Leukemia Program, Dana-Farber Cancer Institute & Brigham and Women’s
Hospital
Associate Professor of Medicine, Harvard Medical School
David M. Dudzinski, MD, JD
Cardiology Fellow, Massachusetts General Hospital
Robert P. Friday, MD, PhD

Attending Physician, Rheumatology Unit, Massachusetts General Hospital
Associate Director, Rheumatology Fellowship Program, Massachusetts General Hospital
Instructor in Medicine, Harvard Medical School
Lawrence S. Friedman, MD
Anton R. Fried, MD, Chair, Department of Medicine, Newton-Wellesley Hospital
Assistant Chief of Medicine, Massachusetts General Hospital
Professor of Medicine, Harvard Medical School
Professor of Medicine, Tufts University School of Medicine
Todd M. Herrington, MD, PhD
Neurology Resident, Partners Neurology Residency
Kathryn A. Hibbert, MD
Pulmonary and Critical Care Fellow, Harvard Medical School
William J. Hucker, MD, PhD
Cardiology Fellow, Massachusetts General Hospital
Emily P. Hyle, MD
Assistant in Medicine, Infectious Disease Division, Massachusetts General Hospital
Instructor in Medicine, Harvard Medical School
Sheheryar K. Kabraji, BM, BCh
Internal Medicine Resident, Massachusetts General Hospital


Stella K. Kim, MD
Director, Clinical Research in Opthalmology
Director, Opthalmology Residency Rotation Program
Associate Professor of Opthalmology
UT MD Anderson Cancer Center
Eyal Y. Kimchi, MD, PhD
Neurology Resident, Partners Neurology Residency
Kiran H. Lagisetty, MD
Surgical Resident, Beth Israel Deaconess Medical Center

Kelly B. Lauter, MD, PhD
Internal Medicine Resident, Massachusetts General Hospital
Andrew L. Lundquist, MD
Nephrology Fellow, BWH/MGH Joint Nephrology Fellowship Program
Atul Malhotra, MD
Associate Physician, Divisions of Pulmonary & Critical Care and Sleep Medicine,
Brigham and Women’s Hospital
Associate Professor of Medicine, Harvard Medical School
Michael Mannstadt, MD
Attending Physician, Endocrine Unit, Massachusetts General Hospital
Assistant Professor of Medicine, Harvard Medical School
Eli Miloslavsky, MD
Rheumatology Fellow, Massachusetts General Hospital
Michelle O’Donoghue, MD, MPH
Investigator, TIMI Study Group and Associate Physician, Cardiovascular Division,
Brigham and Women’s Hospital
Affiliate Physician, Cardiology Division, Massachusetts General Hospital
Assistant Professor of Medicine, Harvard Medical School
David P. Ryan, MD
Clinical Director, Massachusetts General Hospital Cancer Center
Chief of Hematology/Oncology, Massachusetts General Hospital
Associate Professor of Medicine, Harvard Medical School
Marc S. Sabatine, MD, MPH


Chairman, TIMI Study Group and Physician, Cardiovascular Division, Brigham and
Women’s Hospital
Affiliate Physician, Cardiology Division, Massachusetts General Hospital
Associate Professor of Medicine, Harvard Medical School
Ada Stefanescu, MD, CM

Internal Medicine Resident, Massachusetts General Hospital
Jennifer F. Tseng, MD, MPH
Chief, Division of Surgical Oncology, Beth Israel Deaconess Medical Center
Associate Professor of Surgery, Harvard Medical School
Sarah Wahlster, MD
Neurology Resident, Partners Neurology Residency
Zachary S. Wallace, MD
Internal Medicine Resident, Massachusetts General Hospital
Ana A. Weil, MD, MPH
Internal Medicine Resident, Massachusetts General Hospital
Marc N. Wein, MD, PhD
Endocrinology Fellow, Massachusetts General Hospital
Zachary A. Zator, MD
Internal Medicine Resident, Massachusetts General Hospital


FOREWORD

To the 1st Edition
It is with the greatest enthusiasm that I introduce Pocket Medicine. In an era of
information glut, it will logically be asked, “Why another manual for medical house
o cers?” Yet, despite enormous information readily available in any number of
textbooks, or at the push of a key on a computer, it is often that the harried house
o cer is less helped by the description of di erential diagnosis and therapies than one
would wish.
Pocket Medicine is the joint venture between house sta and faculty expert in a
number of medical specialties. This collaboration is designed to provide a rapid but
thoughtful initial approach to medical problems seen by house o cers with great
frequency. Questions that frequently come from faculty to the house sta on rounds,
many hours after the initial interaction between patient and doctor, have been

anticipated and important pathways for arriving at diagnoses and initiating therapies
are presented. This approach will facilitate the evidence-based medicine discussion that
will follow the workup of the patient. This well-conceived handbook should enhance the
ability of every medical house o cer to properly evaluate a patient in a timely fashion
and to be stimulated to think of the evidence supporting the diagnosis and the likely
outcome of therapeutic intervention. Pocket Medicine will prove to be a worthy addition
to medical education and to the care of our patients.
DENNIS A. AUSIELLO, MD
Physician-in-Chief, Massachusetts General Hospital
Jackson Professor of Clinical Medicine, Harvard Medical School


PREFACE

To my parents, Matt and Lee Sabatine, to their namesake
grandchildren Matteo and Natalie, and to my wife Jennifer
Written by residents, fellows and attendings, the mandate for Pocket Medicine was to
provide, in a concise a manner as possible, the key information a clinician needs for the
initial approach to and management of the most common inpatient medical problems.
The tremendous response to the previous editions suggests we were able to help ll an
important need for clinicians. With this fth edition come several major improvements
including a thorough updating of every topic, the addition of several new topics
(including treatment of anaphylaxis, approach to inpatient nutritional issues,
chemotherapy side e ects, and workup of a fever in a recent traveler), and inclusion of
additional photomicrographs. We have also added a new section on Consults in which
non-internal medicine specialists provide expert guidance in terms of establishing a
di erential diagnosis for common presenting symptoms and initiating an evaluation in
anticipation of calling a consult. As always, we have incorporated key references to the
most recent high-tier reviews and important studies published right up to the time Pocket
Medicine went to press. We welcome any suggestions for further improvement.

Of course medicine is far too vast a eld to ever summarize in a textbook of any size.
Long monographs have been devoted to many of the topics discussed herein. Pocket
Medicine is meant only as a starting point to guide one during the initial phases of
diagnosis and management until one has time to consult more de nitive resources.
Although the recommendations herein are as evidence-based as possible, medicine is
both a science and an art. As always, sound clinical judgement must be applied to every
scenario.
I am grateful for the support of the house o cers, fellows, and attendings at the
Massachusetts General Hospital. It is a privilege to work with such a knowledgeable,
dedicated, and compassionate group of physicians. I always look back on my time there
as Chief Resident as one of the best experiences I have ever had. I am grateful to several
outstanding clinical mentors, including Hasan Bazari, Larry Friedman, Nesli Basgoz,
Mort Swartz, Eric Isselbacher, Bill Dec, Mike Fifer, and Roman DeSanctis, as well as the
late Charlie McCabe and Peter Yurchak.
This edition would not have been possible without the help of two individuals in the
TIMI Study Group Chairman’s O ce. Melinda Cuerda, my academic coordinator, was an
invaluable resource for this edition. She shepherded every aspect of the project from
start to nish, with an incredible eye to detail to ensure that each page of this book was
the very best it could be. Pamela Melhorn, my executive assistant, expertly manages the
Chairman’s O ce, miraculously coordinating the complex clinical, research, and
educational missions.
Lastly, special thanks to my parents for their perpetual encouragement and love and,


of course, to my wife, Jennifer Tseng, who, despite being a surgeon, is my closest
advisor, my best friend and the love of my life.
I hope that you nd Pocket Medicine useful throughout the arduous but incredibly
rewarding journey of practicing medicine.
MARC S. SABATINE, MD, MPH

ELECTROCARDIOGRAPHY
Approach (a systematic approach is vital)
• Rate (? tachy, brady) and rhythm (? relationship between P and QRS)
• Intervals (PR, QRS, QT) and axis (? LAD or RAD)
• Chamber abnormality (? LAA and/or RAA, ? LVH and/or RVH)
• QRST changes (? Q waves, poor R-wave progression V1–V6, ST ↑/↓ or T-wave Δs)
Figure 1-1 QRS axis

Left axis deviation (LAD)
• Definition: axis beyond –30° (S > R in lead II)
• Etiologies: LVH, LBBB, inferior MI, WPW
• Left anterior fascicular block: LAD (–45 to –90°) and qR in aVL and QRS <120 msec
and no other cause of LAD (eg, IMI)
Right axis deviation (RAD)
• Definition: axis beyond +90° (S > R in lead I)
• Etiologies: RVH, PE, COPD (usually not > +110°), septal defects, lateral MI, WPW
• Left posterior fascicular block: RAD (90–180°) and rS in I & aVL and qR in III & aVF
and QRS <120 msec and no other cause of RAD

Prolonged QT interval (NEJM 2008;358:169; www.torsades.org)


• QT measured from beginning of QRS complex to end of T wave (measure longest QT)
• QT varies w/ HR → correct w/ Bazett formula: QTc = QT/√RR (in sec), formula
inaccurate at very high and low HR (nl QTc <440 msec and <460 msec )
• QT prolongation a/w ↑ risk TdP (esp. >500 msec); perform baseline/serial ECGs if
using QT prolonging meds, no estab guidelines for stopping Rx if QT prolongs
• Etiologies:
Antiarrhythmics: class Ia (procainamide, disopyramide), class III (amiodarone,

sotalol)
Psych drugs: antipsychotics (phenothiazines, haloperidol, atypicals), Li, ? SSRI,
TCA
Antimicrobials: macrolides, quinolones, azoles, pentamidine, atovaquone,
atazanavir
Other: antiemetics (droperidol, 5-HT3 antagonists), alfuzosin, methadone,
ranolazine
Electrolyte disturbances: hypoCa (nb, hyperCa a/w ↓ QT), ? hypoK, ? hypoMg
Autonomic dysfxn: ICH (deep TWI), stroke, carotid endarterectomy, neck
dissection
Congenital (long QT syndrome): K, Na, Ca channelopathies (Circ 2013;127:126)
Misc: CAD, CMP, bradycardia, high-grade AVB, hypothyroidism, hypothermia, BBB

Left ventricular hypertrophy (LVH) (Circ 2009;119:e251)
• Etiologies: HTN, AS/AI, HCMP, coarctation of aorta
• Criteria (all w/ Se <50%, Sp >85%; accuracy affected by age, sex, race, BMI)
Romhilt-Estes point-score system: 4 points = probable, 5 points = definite ↑
Amplitude (any of the following): largest R or S in limb leads ≥20 mm or S in V1
or V2 ≥30 mm or R in V5 or V6 ≥30 mm (3 points)

ST displacement opposite to QRS deflection: w/o dig (3 points); w/ dig (1 point)
LAA (3 points); LAD (2 points); QRS duration ≥90 msec (1 point)
Intrinsicoid deflection (QRS onset to peak of R) in V5 or V6 ≥50 msec (1 point)

Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm or R in aVL ≥11 mm
Cornell: R in aVL + S in V3 >28 mm in men or >20 mm in women
If LAD/LAFB, S in III + max (R+S) in precordium ≥30 mm

Right ventricular hypertrophy (RVH) (Circ 2009;119:e251)
• Etiologies: cor pulmonale, congenital (tetralogy, TGA, PS,  ASD,  VSD), MS, TR

• Criteria (all tend to be insensitive, but highly specific, except in COPD)
R > S in V1 or R in V1 ≥7 mm, S in V5 or V6 ≥7 mm, drop in R/S ratio across

precordium
RAD ≥ +110° (LVH + RAD or prominent S in V5 or V6 → biventricular hypertrophy)

Ddx of dominant R wave in V1 or V2
• Ventricular enlargement: RVH (RAD, RAA, deep S waves in I, V5, V6); HCMP

• Myocardial injury: posterior MI (anterior Rw = posterior Qw; often with IMI)
• Abnormal depolarization: RBBB (QRS >120 msec, rSR′); WPW (↓ PR, Δ wave, ↑ QRS)
• Other: dextroversion; Duchenne muscular dystrophy; lead misplacement; nl variant
Poor R wave progression (PRWP) (Am Heart J 2004;148:80)
• Definition: loss of anterior forces w/o frank Q waves (V1–V3); R wave in V3 ≤3 mm

• Possible etiologies (nonspecific):
old anteroseptal MI (usually w/ R wave V3 ≤1.5 mm, ± persistent ST ↑ or TWI V2
& V3) cardiomyopathy

LVH (delayed RWP with prominent left precordial voltage), RVH, COPD (which
may also have RAA, RAD, limb lead QRS amplitude ≤5, SISIISIII w/ R/S ratio <1
in those leads)
LBBB; WPW; clockwise rotation of the heart; lead misplacement; PTX

Pathologic Q waves
• Definition: ≥30 msec (≥20 msec V2–V3) or >25% height of R wave in that QRS

complex

• Small (septal) q waves in I, aVL, V5 & V6 are nl, as can be isolated Qw in III, aVR, V1
• “Pseudoinfarct” pattern may be seen in LBBB, infiltrative dis., HCMP, COPD, PTX,
WPW

ST elevation (STE) (NEJM 2003;349:2128; Circ 2009;119:e241 & e262)
• Acute MI (upward convexity ± TWI) or prior MI with persistent STE
• Coronary spasm (Prinzmetal’s angina; transient STE in a coronary distribution)
• Myopericarditis (diffuse, upward concavity STE; a/w PR ↓; Tw usually upright)
• HCMP, Takotsubo CMP, ventricular aneurysm, cardiac contusion
• Pulmonary embolism (occ. STE V1–V3; typically associated TWI V1–V4, RAD, RBBB)

• Repolarization abnormalities
LBBB (↑ QRS duration, STE discordant from QRS complex)
dx of STEMI in setting of LBBB: ≥1 mm STE concordant w/ QRS (Se 73%, Sp
92%), STD ≥1 mm V1–V3 (Se 25%, Sp 96%) or STE ≥5 mm discordant w/ QRS
(Se 31%, Sp 92%) (“Sgarbossa criteria,” NEJM 1996;334:481)
LVH (↑ QRS amplitude); Brugada syndrome (rSR′, downsloping STE V1–V2)


Hyperkalemia (↑ QRS duration, tall Ts, no Ps)
• aVR: STE >1 mm a/w ↑ mort in STEMI; STE aVR > V1 a/w left main disease

• Early repolarization: most often seen in V2–V5 & in young adults (Ann Emerg Med

2012;60:45)
J point ↑ 1–4 mm; notch in downstroke of R wave; upward concavity of ST; large
Tw;
ratio of STE / T wave amplitude <25%; pattern may disappear with exercise
? early repol in inf leads may be a/w ↑ risk of  VF (NEJM 2009;361:2529; Circ
2011;124:2208)

ST depression (STD)
• Myocardial ischemia (± Tw abnl) or acute true posterior MI (V1–V3)

• Digitalis effect (downsloping ST ± Tw abnl, does not correlate w/ dig levels)
• Hypokalemia (± U wave)
• Repolarization abnl in a/w LBBB or LVH (usually in leads V5, V6, I, aVL)
T wave inversion (TWI; generally ≥1 mm; deep if ≥5 mm) (Circ 2009;119:e241)
• Ischemia or infarct; Wellens’ sign (deep early precordial TWI) → proximal LCA lesion
• Myopericarditis; CMP (Takotsubo, ARVC, apical HCM); MVP; PE (esp. if TWI V1–V4)
• Repolarization abnl in a/w LVH/RVH (“strain pattern”), BBB
• Posttachycardia or postpacing
• Electrolyte, digoxin, PaO2, PaCO2, pH or core temperature disturbances

• Intracranial bleed (“cerebral T waves,” usually w/ ↑ QT)
• Normal variant in children (V1–V4) and leads in which QRS complex predominantly
Low voltage
• QRS amplitude (R + S) <5 mm in all limb leads & <10 mm in all precordial leads
• Etiologies: COPD (precordial leads only), pericardial effusion, myxedema, obesity,
pleural effusion, restrictive or infiltrative CMP, diffuse CAD


CHEST PAIN

Initial approach
• Focused history: quality & severity of pain; location & radiation; provoking &
palliating factors; intensity at onset; duration, frequency & pattern; setting in which
it occurred; associated sx; cardiac hx and risk factors
• Targeted exam: VS (including BP in both arms), cardiac gallops, murmurs or rubs;
signs of vascular disease (carotid or femoral bruits, ↓ pulses), signs of heart failure;

lung & abdominal exam; chest wall exam for reproducibility of pain
• 12-lead ECG: obtain w/in 10 min; c/w priors & obtain serial ECGs; consider posterior
leads (V7–V9) to reveal posterior MI if hx c/w ACS but ECG unrevealing or ST ↓ V1–
V4

• Cardiac biomarkers (Tn ± CK-MB): ✓ Tn at baseline & 3–6 h after sx onset
troponin: >95% Se, 90% Sp; level >99th %ile w/ rise & fall in approp. setting is
dx of MI detectable 1–6 h after injury, peaks 24 h, may remain elevated for 7–10 d
in STEMI high-sens. Tn: 98% Se, 90% Sp w/in 3 h of admit, 90% Se w/in 1 h ( JAMA


2011;306:2684)
Causes for ↑ Tn other than ACS (= “type 1 MI”): (1) Supply-demand mismatch not
due to Δ in CAD (= “type 2 MI”; eg, ↑↑ HR, shock, HTN crisis, spasm, HCM,
severe AS), (2) non-ischemic injury (myocarditis/toxic CMP, cardiac contusion) or
(3) multifactorial (PE, sepsis, severe HF, renal failure, Takotsubo, infilt dis.) (Circ
2012;126:2020)
CK-MB: less Se & Sp (skel. muscle, tongue, diaphragm, intestine, uterus, prostate),
useful for dx of post-PCI/CABG MI or MI if Tn already elevated
• CXR; other imaging (echo, PE CTA, etc.) as indicated based on H&P and initial testing
• If low prob of ACS (eg, ECG & Tn) & stable → noninvasive fxnal or imaging test
• Coronary CT angio (CCTA): NPV 98% for signif CAD, but PPV 35% for ACS; helpful to
r/o CAD if low-intermed prob of ACS. CCTA vs. noninv. fxnal test for ischemia → ↓
time to dx & LOS, but ↑ prob of cath/PCI, contrast exposure & ↑ radiation (NEJM
2012;366:1393 & 367:299; JACC 2013;61:880). “Triple r/o” CT angiogram for CAD,
PE, AoD.


NONINVASIVE EVALUATION OF CAD

Stress testing (Circ 2007;115:1464; JACC 2012;60:1828)
• Indications: dx CAD, evaluate Δ in clinical status in Pt w/ known CAD, risk stratify
s/p ACS, evaluate exercise tolerance, localize ischemia (imaging required)
• Contraindications (Circ 2002;106:1883; & 2012;126:2465)
Absolute: AMI w/in 48 h, high-risk UA, acute PE, severe sx AS, uncontrolled HF,
uncontrolled arrhythmias, myopericarditis, acute aortic dissection
Relative: left main CAD, mod valvular stenosis, severe HTN, HCMP, high-degree
AVB, severe electrolyte abnl
• Exercise: standard Bruce (↑ speed & incline q3min), modified Bruce (begins w/o
treadmill incline), submax (if <3 wk post-MI) or sx-limited; hold
nitrates/βB/CCB/ranolazine if trying to dx CAD, but give when assessing if Pt
ischemic on meds
• Pharmacologic: if unable to exer., low exer. tol, or recent MI. Se & Sp exercise.
Preferred if LBBB (requires imaging since ECG not interpretable). Coronary
vasodilators (will reveal CAD, but not tell you if Pt ischemic): regadenoson,
dipyridamole or adenosine (may precipitate bradycardia and bronchospasm).
Chronotropes/inotropes (more physiologic): dobutamine (may precipitate
tachyarrhythmias).
• Imaging: used if uninterpretable ECG (paced, LBBB, resting ST ↓ >1 mm, dig., LVH,
WPW), after indeterminate ECG test, pharmacologic tests, or localization of
ischemia
SPECT (eg, 99mTc-sestamibi), PET (rubidium-82; usually w/ pharm test), echo, MRI
Test results
• HR (must achieve ≥85% of max pred HR [220-age] for exer. test to be dx), BP
response, peak double product (HR × BP; nl >20k), HR recovery (HRpeak – HR1
min later;

nl >12)

• Max exercise capacity achieved (METS or min)

• Occurrence of symptoms (at what level of exertion and similarity to presenting sx)
• ECG Δs: downsloping or horizontal ST ↓ (≥1 mm) 60–80 ms after QRS predictive of CAD
(but does not localize ischemic territory); however, STE highly predictive & localizes


• Duke treadmill score = exercise min – (5 × max ST dev) – (4 × angina index) [0
none, 1 nonlimiting, 2 limiting]; score ≥5 → <1% 1-y mort; –10 to + 4 → 2–3%;
≤ –11 → ≥5%
• Imaging: radionuclide defects or echocardiographic regional wall motion
abnormalities
reversible defect = ischemia; fixed defect = infarct; transient isch dilation = severe
CAD
false : breast → ant “defect” and diaphragm → inf “defect”
false may be seen if balanced (eg, 3VD) ischemia (global ↓ perfusion w/o
regional Δs)
High-risk test results (PPV ~50% for LM or 3VD, ∴ consider coronary angio)
• ECG: ST ↓ ≥2 mm or ≥1 mm in stage 1 or in ≥5 leads or ≥5 min in recovery; ST ↑;  
VT
• Physiologic: ↓ or fail to ↑ BP, <4 METS, angina during exercise, Duke score ≤ –11; ↓
EF
• Radionuclide: ≥1 lg or ≥2 mod. reversible defects, transient LV cavity dilation, ↑ lung
uptake
Myocardial viability (Circ 2008;117:103; Eur Heart J 2011;31:2984 & 2011;32:810)
• Goal: identify hibernating myocardium that could regain fxn after revascularization
• Options: MRI (Se ~95%, Sp ~85%), PET (Se ~90%, Sp ~65%), dobutamine stress
echo (Se ~80%, Sp ~80%); SPECT/rest-redistribution (Se ~85%, Sp ~70%)
In Pts w/ LV dysfxn, viabil. doesn’t predict ↑ CABG benefit vs. med Rx (NEJM
2011;364:1617)
CT & MR coronary angio (NEJM 2008;369:2324; Circ 2010;121:2509; Lancet
2012;379:453)

• Image quality best at slower & regular HR (? give bB if possible, goal HR 55–60)
• Calcium generates artifact for CT angiography
• MRI: angiography, perfusion, LV fxn, enhancement (early = microvasc obstr; late =
MI)
Coronary artery calcium score (CACS; Circ 2010;122:e584; NEJM 2012;366:294; JAMA
2012;308:788)
• Quantifies extent of calcium; thus estimates plaque burden (but not % coronary
stenosis)
• ? Risk strat. (<100 = low; >300 = high) in asx Pts w/ intermed risk (10–20% 10-y
risk)
• ? Value as screening test to r/o CAD in sx Pt (CACS <100 → 3% probability of signif
CAD; but interpretation affected by age, gender)