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Pocket medecin2014 Document Transcript

  • 1. Pocket MEDICINE Fifth Edition Edited by MARC S. SABATINE, MD, MPH ASSOCIATE PROFESSOR OF MEDICINE HARVARD MEDICAL SCHOOL
  • 2. The Massachusetts General Hospital Handbook of Internal Medicine Health Philadelphia • Baltimore • New York • London Buenos Aires • Hong Kong • Sydney • Tokyo
  • 3. Executive Editor: Rebecca Gaertner Product Manager: Kristina Oberle Vendor Manager: Bridgett Dougherty Manufacturing Coordinator: Beth Welsh Marketing Manager: Kim Schonberger Creative Director: Doug Smock Production Service: Aptara, Inc. © 2014 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business Two Commerce Square 2001 Market Street Philadelphia, PA 19103 USA LWW.com
  • 4. All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form by any means, including photocopying, 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 o cial duties as U.S. government employees are not covered by the above-mentioned copyright.
  • 5. Printed in China Not authorised for sale in United States, Canada, Australia, New Zealand, Puerto Rico, and United States Virgin Islands. 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
  • 6. 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 616–dc23 2013019655 DISCLAIMER Care has been taken to con rm the accuracy of the information presented and to
  • 7. describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information in a particular situation remains the professional responsibility of the practitioner. The authors, editors, and publisher have exerted every e ort to ensure that drug selection and
  • 8. dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant ow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug.
  • 9. Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams &
  • 10. Wilkins on the Internet: at LWW.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6 pm, EST. 10 9 8 7 6 5 4 3 2 1
  • 11. 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
  • 12. 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
  • 13. 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
  • 14. 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
  • 15. 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
  • 16. 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
  • 17. 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
  • 18. 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
  • 19. 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
  • 20. 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
  • 21. 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
  • 22. Radiology Echocardiography & Coronary Angiography Peripheral Blood Smears & Leukemias Urinalysis ACLS
  • 23. 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
  • 24. 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,
  • 25. 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,
  • 26. 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
  • 27. 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
  • 28. 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,
  • 29. 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
  • 30. 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
  • 31. 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
  • 32. 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
  • 33. 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
  • 34. 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,
  • 35. 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
  • 36. 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
  • 37. 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
  • 38. 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
  • 39. 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.
  • 40. DENNIS A. AUSIELLO, MD Physician-in-Chief, Massachusetts General Hospital Jackson Professor of Clinical Medicine, Harvard Medical School
  • 41. 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
  • 42. previous editions suggests we were able to help ll an important need for clinicians. With this fifth 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
  • 43. 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
  • 44. 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.
  • 45. 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
  • 46. 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.
  • 47. I hope that you nd Pocket Medicine useful throughout the arduous but incredibly rewarding journey of practicing medicine. MARC S. SABATINE, MD, MPH
  • 48. 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
  • 49. 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,
  • 50. 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
  • 51. 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
  • 52. 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,
  • 53. 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
  • 54. 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,
  • 55. 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
  • 56. 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
  • 57. 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)
  • 58. 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)
  • 59. • 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)
  • 60. 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
  • 61. 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)
  • 62. • 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′,
  • 63. 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
  • 64. 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)
  • 65. 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
  • 66. 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
  • 67. CHEST PAIN
  • 68. 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
  • 69. 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
  • 70. 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)
  • 71. 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
  • 72. 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.
  • 73. 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
  • 74. (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),
  • 75. 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
  • 76. 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
  • 77. • 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
  • 78. • 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
  • 79. 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
  • 80. 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
  • 81. 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
  • 82. 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)
  • 83. CORONARY ANGIOGRAPHY AND REVASCULARIZATION Indications for coronary angiography in stable CAD or asx Pts • CCS class III–IV angina despite medical Rx or angina + systolic dysfxn • High-risk stress test findings (see prior topic) • Uncertain dx after noninvasive testing (& compelling need to determine dx), occupational need for definitive dx (eg, pilot) or inability to undergo noninvasive testing
  • 84. • Systolic dysfxn with unexplained cause • Survivor of SCD, polymorphic VT, sustained monomorphic VT • Suspected spasm or nonatherosclerotic cause of ischemia (eg, anomalous coronary) Precath checklist • Document peripheral arterial exam (radial, femoral, DP, PT pulses; bruits); NPO >6 h • ✓ CBC, PT, & Cr; give IVF (± bicarb, ± acetylcysteine; see “CIAKI”); blood bank sample • ASA 325 mg × 1; consider clopi
  • 85. 600 mg ≥2–6 h before PCI or, if ACS, ticagrelor pre- or peri- PCI or prasugrel peri-PCI; cangrelor (IV P2Y12 inhib) ↓ peri-PCI ischemic events vs. clopi w/o preload (NEJM 2013;368:1303); consider statin preRx (Circ 2011;123:1622) Coronary revascularization in stable CAD (Circ 2011;124:e574) • Optimal med Rx (OMT) should be initial focus if stable, w/o critical anatomy, & w/o ↓ EF • PCI: ↓ angina more quickly c/w OMT; does not ↓ D/MI (NEJM
  • 86. 2007;356:1503); in Pts w/ ≥1 stenosis w/ FFR ≤0.8 (see below), ↓ urg revasc c/w OMT (NEJM 2012;367:991); may be noninferior to CABG in unprotected left main dis. (NEJM 2011;364:1718) • CABG: in older studies, ↓ mort. c/w OMT if 3VD, LM, 2VD w/ critical prox LAD, esp. if ↓ EF; more recently, if EF <35% ↓ CV death vs. OMT (NEJM 2011;364:1607) insufficient evidence to support routine viability assessment (NEJM 2011;364:1617) in diabetics w/ ≥2VD, ↓ D/MI, but ↑ stroke
  • 87. c/w PCI (NEJM 2012;367:2375) • If revasc deemed necessary, PCI if limited # of discrete lesions, nl EF, no DM, poor operative candidate; CABG if extensive or diffuse disease, ↓ EF, DM or valvular disease; if 3VD/LM: CABG ↓ D/MI & revasc but trend toward ↑ stroke c/w PCI (Lancet 2013;381:629); SYNTAX score II helps identify Pts who benefit most from CABG (Lancet 2013;381:639) PCI • Balloon angioplasty (POBA):
  • 88. effective, but c/b dissection & elastic recoil & neointimal hyperplasia → restenosis; now reserved for small lesions & ? some SVG lesions • Bare metal stents (BMS): ↓ elastic recoil → 33–50% ↓ restenosis & repeat revasc (to ~10% by 1 y) c/w POBA; requires ASA lifelong & P2Y12 inhib × ≥4 wk • Drug-eluting stents (DES): ↓ neointimal hyperplasia → ~75% ↓ restenosis, ~50% ↓ repeat revasc (to <5% by 1 y), no ↑ D/MI c/w BMS (NEJM 2013;368:254); next
  • 89. generation DES may ↓ repeat revasc & stent thrombosis; require P2Y12 inhib ≥1 y (Circ 2007;115:813) • Radial access ↓ vasc. complic. vs. femoral, but no ∆ D/MI/CVA (Lancet 2011;377:1409) • Fractional flow reserve [FFR; ratio of max flow (induced by IV or IC adenosine) distal vs. proximal to a stenosis] guided PCI (<0.8) → ↓ # stents & ↓ D/MI/revasc (NEJM 2009;360:213) Post-PCI complications • Postprocedure ✓ vascular access
  • 90. site, distal pulses, ECG, CBC, Cr • Bleeding hematoma/overt bleeding: manual compression, reverse/stop anticoag retroperitoneal bleed: may p/w ↓ Hct ± back pain; ↑ HR & ↓ BP late; Dx w/ abd/pelvic CT (I–); Rx: reverse/stop anticoag (d/w interventionalist), IVF/PRBC/plts as required if bleeding uncontrolled, consult performing interventionalist or surgery • Vascular damage (~1% of dx
  • 91. angio, ~5% of PCI; Circ 2007;115:2666) pseudoaneurysm: triad of pain, expansile mass, systolic bruit; Dx: U/S; Rx (if pain or >2 cm): manual or U/S- directed compression, thrombin injection or surgical repair AV fistula: continuous bruit; Dx: U/S; Rx: surgical repair LE ischemia (emboli, dissection, clot): cool, mottled extremity, ↓ distal pulses; Dx: pulse volume recording (PVR), angio; Rx: percutaneous or surgical
  • 92. repair • Peri-PCI MI: >5× ULN of Tn/CK-MB + either sx or ECG/angio Δs; Qw MI in <1% • Renal failure: contrast-induced manifests w/in 24 h, peaks 3– 5 d (see “CIAKI”) • Cholesterol emboli syndrome (typically in middle-aged & elderly and w/ Ao atheroma) renal failure (late and progressive, eos in urine); mesenteric ischemia (abd pain, LGIB, pancreatitis); intact distal pulses but livedo pattern and toe necrosis
  • 93. • Stent thrombosis: mins to yrs after PCI, typically p/w AMI. Due to mech prob. (stent underexpansion or unrecognized dissection, typically presents early) or d/c of antiplt Rx (esp. if d/c both ASA & P2Y12 inhib; JAMA 2005;293:2126). Risk of late stent thrombosis may be higher with DES than BMS ( JACC 2006;48:2584). • In-stent restenosis: mos after PCI, typically p/w gradual ↑ angina (10% p/w ACS). Due to combination of elastic recoil and neointimal hyperplasia; ↓
  • 94. w/ DES vs. BMS.
  • 95. ACUTE CORONARY SYNDROMES Ddx (causes of myocardial ischemia/infarction other than atherosclerotic plaque rupture) • Nonatherosclerotic coronary artery disease Spasm: Prinzmetal’s variant, cocaine-induced (6% of CP + cocaine use r/i for MI)
  • 96. Dissection: spontaneous (vasculitis, CTD, pregnancy), aortic dissection with retrograde extension (usually involving RCA → IMI) or mechanical (catheter, surgery, trauma) Embolism: endocarditis, prosthetic valve, mural thrombus, AF, myxoma; thrombosis Vasculitis: Kawasaki syndrome, Takayasu arteritis, PAN, Churg-Strauss, SLE, RA Congenital: anomalous origin from aorta or PA,
  • 97. myocardial bridge (intramural segment) • Fixed CAD but ↑ myocardial O2 demand (eg, ↑ HR, anemia, AS) → “demand” ischemia • Myocarditis; Takatsubo/stress CMP; toxic CMP; cardiac contusion Clinical manifestations ( JAMA 2005;294:2623) • Typical angina: retrosternal pressure/pain/tightness ± radiation to neck, jaw or arms precip. by exertion, relieved by rest or NTG; in ACS, new- onset, crescendo or at rest
  • 98. • Associated symptoms: dyspnea, diaphoresis, N/V, palpitations or lightheadedness • Many MIs (~20% in older series) are initially unrecognized b/c silent or atypical sx Physical exam • Signs of ischemia: S4, new MR murmur 2° pap. muscle dysfxn, paradoxical S2, diaphoresis • Signs of heart failure: ↑ JVP, crackles in lung fields, S3, HoTN, cool extremities • Signs of other areas of atherosclerotic disease: carotid
  • 99. or femoral bruits, ↓ distal pulses Diagnostic studies • ECG: ST ↓/↑, TWI, new LBBB, hyperacute Tw. Qw/PRWP may suggest prior MI, ∴ CAD ✓ ECG w/in 10 min of presentation, with any Δ in sx and at 6–12 h; compare w/ baseline dx of STEMI if old 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%)
  • 100. • Cardiac biomarkers (Tn preferred, or CK-MB): ✓ Tn at baseline & 3–6 h after sx onset; a rise to >99th %ile in approp. clinical setting dx of MI (see “Chest Pain”); nb, in Pts w/ ACS & ↓ CrCl, ↑ Tn still portends poor prognosis (NEJM 2002;346:2047)
  • 101. • If low prob, stress test, CT angio or rest perfusion imaging to r/o CAD (see “Chest Pain”) • TTE (new wall motion abnl) suggestive of ACS; coronary angio gold standard for CAD Prinzmetal’s (variant) angina • Coronary spasm → transient STE usually w/o MI (but MI, AVB, VT can occur) • Pts usually young, smokers, ± other vasospastic disorders (eg, migraines, Raynaud’s) • Angiography → nonobstructive CAD, focal spasm w/
  • 102. hyperventilation, acetylcholine • Treatment: high-dose CCB, nitrates (+SL NTG prn), ? a- blockers; d/c smoking • Cocaine-induced vasospasm: use CCB, nitrates, ASA; ? avoid bB, but data weak and labetalol appears safe (Archives 2010;170:874; Circ 2011;123:2022)
  • 103. Approach to triage • If hx and initial ECG & biomarkers non-dx, repeat ECG & biomarkers 3–6 h later • If remain nl and low likelihood of ACS, search for alternative causes of chest pain • If remain nl, have ruled out MI, but if suspicion for ACS based on hx, then still need to r/o UA w/ stress test to assess for inducible ischemia (or CTA to r/o CAD); if low risk (age ≤70; prior CAD, CVD, PAD; rest angina) can do as outPt
  • 104. w/in 72 h (0% mortality, <0.5% MI, Ann Emerg Med 2006;47:427) if not low risk, admit and initiate Rx for possible ACS and consider stress test or cath
  • 105. Coronary angiography (Circ 2007;116:e148 & 2012;126:875) • Conservative strategy = selective angiography. Medical Rx with pre-d/c stress test; angio only if recurrent ischemia or strongly ETT. Indicated for: low TIMI risk
  • 106. score, Pt or physician preference in absence of high- risk features, low-risk women (JAMA 2008;300:71). • Invasive strategy = routine angiography w/in 72 h Immediate (w/in 2 h) if: refractory/recurrent ischemia, hemodynamic or electrical instability Early (w/in 24 h) if: Tn, ST Δ, TRS ≥3, GRACE risk score >140 (NEJM 2009;360:2165) Delayed (ie, acceptable anytime w/in 72 h) if: diabetes, EF <40%, GFR <60, post-MI
  • 107. angina, PCI w/in 6 mo, prior CABG or high-risk stress results 32% ↓ rehosp for ACS, nonsignif 16% ↓ MI, no Δ in mortality c/w cons. (JAMA 2008;300:71) ↑ peri-PCI MI counterbalanced by ↓↓ in spont. MI Mortality benefit seen in some studies, likely only if cons. strategy w/ low rate of angio
  • 108. Figure 1-2 Approach to UA/NSTEMI
  • 109. STEMI Requisite STE (at J point) • ≥2 contiguous leads w/ ≥1 mm (except for V2–V3: ≥2 mm in and ≥1.5 mm in ) • New or presumed new LBBB Reperfusion (“time is muscle”) • Immediate reperfusion (ie, opening occluded culprit coronary artery) is critical • In PCI-capable hospital, goal should be primary PCI w/in 90 min of 1st medical contact • In non-PCI-capable hospital, consider transfer to PCI-
  • 110. capable hospital (see below), o/w fibrinolytic therapy w/in 30 min of hospital presentation • Do not let decision regarding method of reperfusion delay time to reperfusion Primary PCI (NEJM 2007;356:47) • Indic: STE + sx <12 h; ongoing ischemia 12–24 h after sx onset; shock regardless of time • Superior to lysis: 27% ↓ death, 65% ↓ reMI, 54% ↓ stroke, 95% ↓ ICH (Lancet 2003;361:13) • Thrombus aspiration during
  • 111. angio prior to stenting ↓ mortality (Lancet 2008;371:1915) • Do not intervene on nonculprit lesions; risk stratify w/ imaging stress (Circ 2011;124:e574) • Transfer to center for 1° PCI may also be superior to lysis (NEJM 2003;349:733), see below Fibrinolysis
  • 112. • Indic: STE/LBBB + sx <12 h; benefit if sx >12 h less clear; reasonable if persist. sx & STE • Mortality ↓ ~20% in anterior MI or LBBB and ~10% in IMI c/w reperfusion Rx • Prehospital lysis (ie, ambulance): further 17% ↓ in mortality ( JAMA 2000;283:2686) • ~1% risk of ICH; high-risk groups include elderly (~2% if >75 y), women, low wt • Although age not contraindic., ↑ risk of ICH in elderly (>75 y) makes PCI more attractive
  • 113. Nonprimary PCI • Facilitated PCI: upstream lytic, GPI or GPI + ½ dose lytic before PCI offers no benefit • Rescue PCI if shock, unstable, failed reperfusion or persistent sx (NEJM 2005;353:2758) • Routine angio ± PCI w/in 24 h of successful lysis: ↓ D/MI/revasc (Lancet
  • 114. 2004;364:1045) and w/in 6 h ↓ reMI, recurrent ischemia, & HF compared to w/in 2 wk (NEJM 2009;360:2705); ∴ if lysed at non-PCI capable hospital, consider transfer to PCI-capable hospital ASAP esp. if high-risk presentation (eg, anterior MI, inferior MI w/ low EF or RV infarct, extensive STE or LBBB, HF, ↓ BP or ↑ HR) • Late PCI (median day 8) of occluded infarct-related artery: no benefit (NEJM 2006;355:2395)
  • 115. LV failure (~25%) • Diurese to achieve PCWP 15–20 → ↓ pulmonary edema, ↓ myocardial O2 demand • ↓ Afterload → ↑ stroke volume & CO, ↓ myocardial O2 demand
  • 116. can use IV NTG or nitroprusside (risk of coronary steal) → short- acting ACEI • Inotropes if HF despite diuresis & ↓ afterload; use dopamine, dobutamine or milrinone • Cardiogenic shock (~7%) = MAP <60 mmHg, CI <2 L/min/m2, PCWP >18 mmHg; inotropes, mech support [eg, VAD, IABP (trial w/o benefit NEJM 2012;367:1287)] to keep CI >2; pressors to keep MAP >60; if not done already, coronary revasc (NEJM 1999;341:625)
  • 117. IMI complications (Circ 1990;81:401; NEJM 1994;330:1211; JACC 2003;41:1273) • Heart block (~20%, occurs because RCA typically supplies AV node) 40% on present., 20% w/in 24 h, rest by 72 h; high-grade AVB can develop abruptly Rx: atropine, epi, aminophylline (100 mg/min × 2.5 min), temp wire • RV infarct (30–50%, but only ½ of those clinically signif). HoTN; ↑ JVP, Kussmaul’s; 1 mm STE in V4R; RA/PCWP
  • 118. ≥0.8; RV dysfxn on TTE; prox RCA occl. Rx: optimize preload (RA goal 10–14, BHJ 1990;63:98); ↑ contractility (dobutamine); maintain AV synchrony (pacing as necessary); reperfusion (NEJM 1998;338:933); mechanical support (IABP or RVAD); pulmonary vasodilators (eg, inhaled NO) Mechanical complications (incid. <1% for each; typically occur a few days post-MI) • Free wall rupture: ↑ risk w/
  • 119. lysis, large MI, ↑ age, , HTN; p/w PEA or hypoTN, pericardial sx, tamponade; Rx: volume resusc., ? pericardiocentesis, inotropes, surgery • VSD: large MI in elderly; AMI → apical VSD, IMI → basal septum; 90% w/ harsh murmur ± thrill (NEJM 2002;347:1426); Rx: diuretics, vasodil., inotropes, IABP, surgery, perc. closure • Papillary muscle rupture: more common after inf MI (PM pap. muscle supplied by PDA alone)
  • 120. than ant MI (AL pap. muscle supplied by diags & OMs); 50% w/ new murmur, rarely a thrill, ↑ v wave in PCWP tracing; asymmetric pulmonary edema. Rx: diuretics, vasodilators, IABP, surgery. Arrhythmias post-MI • Treat as per ACLS for unstable or symptomatic bradycardias & tachycardias • AF (10–16% incidence): β- blocker or amio, ± digoxin (particularly if HF), heparin • VT/VF: lido or amio × 6–24 h,
  • 121. then reassess; ↑ βB as tol., replete K & Mg, r/o ischemia; early monomorphic (<48 h post-MI) does not carry bad prognosis • Accelerated idioventricular rhythm (AIVR): slow VT (<100 bpm), often seen after successful reperfusion; typically self-terminates and does not require treatment • May consider backup transcutaneous pacing (TP) if: 2° AVB type I, BBB • Backup TP or initiate transvenous pacing if: 2° AVB type II; BBB + AVB
  • 122. • Transvenous pacing (TV) if: 3° AVB; new BBB + 2° AVB type II; alternating LBBB/RBBB (can bridge w/ TP until TV, which is best accomplished under fluoroscopic guidance) Prognosis • In registries, in-hospital mortality is 6% w/ reperfusion Rx (lytic
  • 123. or PCI) and ~20% w/o • Predictors of mortality: age, time to Rx, anterior MI or LBBB, heart failure (Circ 2000;102:2031)
  • 124. PREDISCHARGE CHECKLIST AND LONG-TERM POST-ACS MANAGEMENT Risk stratification • Stress test if anatomy undefined; consider stress if signif residual CAD post-PCI of culprit • Assess LVEF prior to d/c; EF ↑ ~6% in STEMI over 6 mo ( JACC 2007;50:149) Medications (barring contraindications) • Aspirin: 81 mg daily • P2Y12 inhib (eg, clopi, prasugrel or ticagrelor): ≥12 mo if stent (min 1 mo after BMS); some
  • 125. PPIs interfere w/ biotransformation of clopi and ∴ plt inhibition, but no convincing impact on clinical outcomes (Lancet 2009;374:989; NEJM 2010;363:1909); use w/PPIs if h/o GIB or multiple GIB risk factors ( JACC 2010;56:2051) • β-blocker: 23% ↓ mortality after MI • Statin: high-intensity lipid- lowering (eg, atorvastatin 80 mg, NEJM 2004;350:1495) • ACEI: lifelong if HF, ↓ EF, HTN, DM; 4–6 wk or at least until hosp. d/c in all STEMI
  • 126. ? long-term benefit in CAD w/o HF (NEJM 2000;342:145 & 2004;351:2058; Lancet 2003;362:782) • Aldosterone antag: 15% ↓ death if EF <40% & either DM or s/s of HF (NEJM 2003;348:1309) • Nitrates: standing if symptomatic; SL NTG prn for all • Oral anticoagulants: if warfarin needed in addition to ASA/clopi (eg,  AF or LV thrombus), target INR 2–2.5. ? stop ASA if at high bleeding risk on triple Rx (Lancet
  • 127. 2013;381:1107). Low-dose rivaroxaban (2.5 mg bid) in addition to ASA & clopi → 16% ↓ D/MI/stroke and 32% ↓ all- cause death, but ↑ major bleeding and ICH (NEJM 2012;366:9). ICD (NEJM 2008;359:2245) • If sust. VT/VF >2 d post-MI not due to reversible ischemia • Indicated in 1° prevention of SCD if post-MI w/ EF ≤30–40% (NYHA II–III) or ≤30–35% (NYHA I); need to wait ≥40 d after MI (NEJM 2004;351:2481 & 2009;361:1427)
  • 128. Risk factors and lifestyle modifications (Circ 2011;124:2458) • Low chol. (<200 mg/d) & fat (<7% saturated) diet; LDL goal <70 mg/dL; ? Ω;-3 FA • BP <140/90 mmHg; smoking cessation • If diabetic, tailor HbA1c goal based on Pt (avoid TZDs if HF) • Exercise (30–60 min 5–7 ×/wk); cardiac rehab; BMI goal 18.5– 24.9 kg/m2 • Influenza vaccination (Circ 2006;114:1549); screen for depression
  • 129. PA CATHETER AND TAILORED THERAPY Rationale • Cardiac output (CO) = SV × HR; SV depends on LV end-diastolic volume (LVEDV) ∴ manipulate LVEDV to optimize CO while minimizing pulmonary edema • Balloon at tip of catheter inflated → floats into “wedge” position. Column of blood extends from tip of catheter, through pulmonary circulation, to a point just proximal to LA. Under conditions of no flow,
  • 130. PCWP LA pressure LVEDP, which is proportional to LVEDV. • Situations in which these basic assumptions fail: (1) Catheter tip not in West lung zone 3 (and ∴ PCWP = alveolar pressure ≠ LA pressure); clues include lack of a & v waves and if PA diastolic pressure < PCWP (2) PCWP > LA pressure (eg, mediastinal fibrosis, pulmonary VOD, PV stenosis) (3) Mean LA pressure > LVEDP (eg, MR, MS)
  • 131. (4) Δ LVEDP-LVEDV relationship (ie, abnl compliance, ∴ “nl” LVEDP may not be optimal) Indications ( JACC 1998;32:840 & Circ 2009;119:e391) • Diagnosis and evaluation Ddx of shock (cardiogenic vs. distributive; esp. if trial of IVF failed or is high risk) and of pulmonary edema (cardiogenic vs. not; esp. if trial of diuretic failed or is high risk) Evaluation of CO, intracardiac shunt, pulmonary HTN, MR,
  • 132. tamponade Evaluation of unexplained dyspnea (PAC during provocation w/ exercise, vasodilator) • Therapeutics (Circ 2006;113:1020) Tailored therapy to optimize PCWP, SV, SvO2 in heart failure (incl end-stage) or shock Guide to vasodilator therapy (eg, inhaled NO, nifedipine) in pulm HTN, RV infarction Guide to perioperative management in some high-
  • 133. risk Pts, pretransplantation • Contraindications Absolute: right-sided endocarditis, thrombus/mass or mechanical valve; PE Relative: coagulopathy (reverse), recent PPM or ICD (place under fluoroscopy), LBBB (~5% risk of RBBB → CHB, place under fluoro), bioprosthetic R-sided valve Efficacy concerns (NEJM 2006;354:2213; JAMA 2005;294:1664) • No benefit to routine PAC use in high-risk surgery, sepsis, ARDS
  • 134. • No benefit in decompensated HF ( JAMA 2005;294:1625); untested in cardiogenic shock • But: ~½ of CO & PCWP clinical estimates incorrect; CVP & PCWP not well correl.; ∴ use PAC to (a) answer hemodynamic ? and then remove, or (b) manage cardiogenic shock Placement • Insertion site: R internal jugular or L subclavian veins for “anatomic” flotation into PA • Inflate balloon (max 1.5 mL)
  • 135. when advancing and to measure PCWP • Use resistance to inflation and pressure tracing to avoid overinflation & risk of PA rupture • Deflate the balloon when withdrawing and at all other times • CXR should be obtained after placement to assess for catheter position and PTX • If catheter cannot be successfully floated (typically if severe TR or RV dilatation) or if another relative contraindication exists, consider fluoroscopic
  • 136. guidance Complications • Central venous access: pneumo/hemothorax (~1%), arterial puncture (if inadvertent cannulation w/ dilation → surgical/endovasc eval), air embolism, thoracic duct injury • Advancement: atrial or ventricular arrhythmias (3% VT; 20% NSVT and >50% PVC), RBBB (5%), catheter knotting, cardiac perforation/tamponade, PA rupture
  • 137. • Maintenance: infection (esp. if catheter >3 d old), thrombus, pulm infarction (≤1%), valve/chordae damage, PA rupture/pseudoaneurysm (esp. w/ PHT), balloon rupture Intracardiac pressures • Transmural pressure ( preload) = measured intracardiac pressure – intrathoracic pressure • Intrathoracic pressure (usually slightly ) is transmitted to vessels and heart • Always measure intracardiac pressure at end-expiration,
  • 138. when intrathoracic pressure closest to 0 (“high point” in spont. breathing Pts; “low point” in Pts on pressure vent.) • If ↑ intrathoracic pressure (eg, PEEP), measured PCWP overestimates true transmural pressures. Can approx by subtracting ~½ PEEP (× ¾ to convert cm H2O to mmHg). • PCWP: LV preload best estimated at a wave; risk of pulmonary edema from avg PCWP Cardiac output • Thermodilution: saline injected
  • 139. in RA. Δ in temp over time measured at thermistor (in PA) is integrated and is 1/CO. Inaccurate if ↓ CO, sev TR or shunt. • Fick method: O2 consumption ( O2) (L/min) = CO (L/min) × ∆ arteriovenous O2 content ∴ CO = O2 / C(a-v)O2 O2 ideally measured (esp. if ↑ metab demands), but freq estimated (125 mL/min/m2) C(a-v)O2 = [10×1.36 mL O2/g of Hb × Hb g/dL × (SaO2–SvO2)]. SvO2 is key
  • 140. variable that Δs. If SVO2 >80%, consider if the PAC is “wedged” (ie, pulm vein sat), L→R shunt, impaired O2 utilization (severe sepsis, cyanide, carbon monoxide), ↑↑ FiO2.
  • 141. Tailored therapy in cardiogenic shock (Circ 2009;119:e391) • Goals: optimize both MAP and CO while ↓ risk of pulmonary edema MAP = CO × SVR; CO = HR × SV (which depends on preload, afterload and contractility) pulmonary edema when PCWP
  • 142. >20–25 (↑ levels may be tolerated in chronic HF) • Optimize preload = LVEDV LVEDP LAP PCWP (NEJM 1973;289:1263) goal PCWP ~14–18 in acute MI, ≤14 in acute decompensated HF optimize in individual Pt by measuring SV w/ different PCWP to create Starling curve ↑ by giving NS (albumin w/o clinical benefit over NS; PRBC if significant anemia) ↓ by diuresis (qv), ultrafiltration or dialysis if
  • 143. refractory to diuretics • Optimize afterload wall stress during LV ejection = [(~SBP × radius) / (2 × wall thick.)] and ∴ ∝ MAP and ∝ SVR = (MAP – CVP / CO); goals: MAP >60, SVR 800–1200 MAP >60 & SVR ↑: vasodilators (eg, nitroprusside, NTG,  ACEI, hydral.) or wean pressors MAP <60 & SVR ↑ (& ∴ CO ↓): temporize w/ pressors until can ↑ CO (see below) MAP <60 & SVR low/nl (& ∴ inappropriate vasoplegia): vasopressors (eg,
  • 144. norepineph-rine [a, b], dopamine [D, a, b], phenylephrine [a] or vasopressin [V1] if refractory) • Optimize contractility ∝ CO for given preload & afterload; goal CI = (CO / BSA) >2.2 if too low despite optimal preload & vasodilators (as MAP permits): inotropes: eg, dobutamine (mod inotrope & mild vasodilator) or milrinone (strong inotrope & vasodilator, incl pulm), both
  • 145. proarrhythmic, or epi (strong inotrope & pressor) mechanical support devices: eg, IABP, percutaneous or surgical VAD (left-sided, right-sided or both) or ECMO (Circ 2011;123:533)
  • 146. HEART FAILURE Definitions (Braunwald’s Heart Disease, 9th ed., 2012) • Failure of heart to pump blood forward at sufficient rate to meet metabolic demands of peripheral tissues, or ability to do so only at abnormally high cardiac filling pressures • Low output (↓ cardiac output) vs. high output (↑ stroke volume ± ↑ cardiac output) • Left-sided (pulmonary edema) vs. right-sided (↑ JVP, hepatomegaly, peripheral edema)
  • 147. • Backward (↑ filling pressures, congestion) vs. forward (impaired systemic perfusion) • Systolic (inability to expel sufficient blood) vs. diastolic (failure to relax and fill normally) • Reduced (HFrEF) vs. preserved (HFpEF) left ventricular ejection fraction • Some degree of systolic and diastolic dysfxn, may occur regardless of ejection fraction Figure 1-3 Approach to left- sided heart failure
  • 148. History • Low output: fatigue, weakness, exercise intolerance, Δ MS, anorexia • Congestive:  left-sided → dyspnea, orthopnea,
  • 149. paroxysmal nocturnal dyspnea right-sided → peripheral edema, RUQ discomfort, bloating, satiety Functional classification (New York Heart Association class) • Class I: no sx w/ ordinary activity; class II: sx w/ ordinary activity; class III: sx w/ minimal activity; class IV: sx at rest Physical exam (“2-minute” hemodynamic profile; JAMA 1996;275:630 & 2002;287:628) • Congestion (“dry” vs. “wet”) ↑ JVP (~80% of the time JVP
  • 150. >10 → PCWP >22;  J Heart Lung Trans 1999;18:1126) hepatojugular reflux: >4 cm ↑ in JVP for ≥15 sec w/ abdominal pressure Se/Sp 73/87% for RA >8 and Se/Sp 55/83% for PCWP >15 (AJC 1990;66:1002) Abnl Valsalva response: square wave (↑ SBP w/ strain), no overshoot (no ↑ BP after strain) S3 (in Pts w/ HF → ~40% ↑ risk of HF hosp. or pump failure death; NEJM 2001;345:574)
  • 151. rales, dullness at base 2° pleural effus. (often absent in chronic HF due to lymphatic compensation) ± hepatomegaly, ascites and jaundice, peripheral edema • Perfusion (“warm” vs. “cold”) narrow pulse pressure (<25% of SBP) → CI <2.2 (91% Se, 83% Sp; JAMA 1989;261:884) soft S1 (↓ dP/dt), pulsus alternans, cool & pale extremities, ↓ UOP, muscle atrophy • ± Other: Cheyne-Stokes resp.,
  • 152. abnl PMI (diffuse, sustained or lifting depending on cause of HF), S4 (diast. dysfxn), murmur (valvular dis., ↑ MV annulus, displaced papillary muscles) Evaluation for the presence of heart failure • CXR (see Radiology insert): pulm edema, pleural effusions ± cardiomegaly, cephalization, Kerley B-lines • BNP/NT-proBNP can help exclude HF; levels ↑ w/ age, ↓ w/ obesity, ↓ renal fxn, AF • Evidence of ↓ organ perfusion: ↑
  • 153. Cr, ↓ Na, abnl LFTs • Echo (see inserts): ↓ EF & ↑ chamber size → systolic dysfxn; hypertrophy, abnl MV inflow, abnl tissue Doppler → ? diastolic dysfxn; abnl valves or pericardium; estimate RVSP • PA catheterization: ↑ PCWP, ↓ CO and ↑ SVR (in low-output failure) Evaluation of the causes of heart failure • ECG: evidence for CAD, LVH, LAE, heart block or low voltage (? infiltrative CMP/DCMP)
  • 154. • Coronary angio (or noninvasive imaging, eg, CT angio); if no CAD, w/u for CMP Precipitants of acute heart failure • Dietary indiscretion or medical nonadherence (~40% of cases) • Myocardial ischemia or infarction (~10–15% of cases); myocarditis • Renal failure (acute, progression of CKD, or insufficient dialysis) → ↑ preload • Hypertensive crisis (incl. from
  • 155. RAS), worsening AS → ↑ left- sided afterload • Drugs (bB, CCB, NSAIDs, TZDs), chemo (anthracyclines, trastuzumab), or toxins (EtOH) • Arrhythmias; acute valvular dysfxn (eg, endocarditis), esp. mitral or aortic regurgitation • COPD or PE → ↑ right-sided afterload; anemia, systemic infection, thyroid disease Treatment of acute decompensated heart failure • Assess degree of congestion & adequacy of perfusion
  • 156. • For congestion: “LMNOP” Lasix IV w/ monitoring of UOP; total daily dose 2.5× usual daily PO dose → ↑ UOP, but transient ↑ in renal dysfxn vs. 1× usual dose; clear diff between cont gtt vs. q12h dosing (NEJM 2011;364:797) Morphine (↓ sx, venodilator, ↓ afterload) Nitrates (venodilator) Oxygen ± noninvasive vent (↓ sx, ↑ PaO2; no ∆ mortality; see “Mechanical Ventilation”)
  • 157. Position (sitting up & legs dangling over side of bed → ↓ preload) • For low perfusion, see below • Adjustment of oral meds ACEI/ARB: hold if HoTN, consider Δ to hydralazine & nitrates if renal
  • 158. decompensation βB: reduce dose by at least ½ if mod HF, d/c if severe HF and/or need inotropes Treatment of advanced heart failure (Circ 2009;119:e391) • Consider PAC if not resp to Rx, unsure re: vol status, HoTN, ↑ Cr, need inotropes • Tailored Rx w/ PAC (qv); goals of MAP >60, CI >2.2 (MVO2 >60%), SVR <800, PCWP <18 • IV vasodilators: NTG, nitroprusside (risk of coronary steal if CAD; prolonged use →
  • 159. cyanide/thiocyanate toxicity); nesiritide (rBNP) not rec for routine use (NEJM 2011;365:32) • Inotropes (properties in addition to ↑ inotropy listed below) dobutamine: vasodilation at doses ≤5 µg/kg/min; mild ↓ PVR; desensitization over time dopamine: splanchnic vasodil. → ↑ GFR & natriuresis; vasoconstrictor at ≥5 µg/kg/min milrinone: prominent systemic & pulmonary vasodilation; ↓ dose by 50% in renal failure
  • 160. • Ultrafiltration: similar wt loss to aggressive diuresis, but ↑ renal failure (NEJM 2012:367:2296) • Mechanical circulatory support (Circ 2011;123:533) Intra-aortic balloon pump (IABP): inflates in diastole & deflates in systole to ↓ impedance to LV ejection of blood, ↓ myocardial O2 demand & ↑ coronary perfusion ventricular assist device (LVAD ± RVAD): as bridge to recovery (NEJM 2006;355:1873) or
  • 161. transplant (some temporary types can be placed percutaneously = PVAD), or as destination therapy (45– 50% ↓ mort. vs. med Rx; NEJM 2009;361:2241) • Cardiac transplantation: 15–20% mort. in 1st y, median survival 10 y
  • 162. • Utility of BNP-guided Rx remains debated (Circ 2013;301:500 & 509) • Implantable PA pressure sensor in NYHA III → ~30% ↓ risk of hosp (Lancet 2011;377:658)
  • 163. Heart failure with preserved EF (HFpEF; “Diastolic HF”) (Circ 2011;124:e540) • Epidemiology: ~½ of Pts w/ HF have normal or only min. impaired systolic fxn (EF ≥40%); risk factors for HFpEF incl ↑ age, , DM, AF. Mortality to those w/ systolic dysfxn. • Etiologies (impaired relaxation and/or ↑ passive stiffness): ischemia, prior MI, LVH, HCMP, infiltrative CMP, RCMP, aging, hypothyroidism
  • 164. • Precipitants of pulmonary edema: volume overload (poor compliance of LV → sensitive to even modest ↑ in volume); ischemia (↓ relaxation); tachycardia (↓ filling time in diastole), AF (loss of atrial boost to LV filling); HTN (↓ afterload → ↓ stroke volume) • Dx w/ clinical s/s of HF w/ preserved systolic fxn. Dx supported by evidence of diast dysfxn: (1) echo: abnl MV inflow (E/A reversal and Δs in E wave deceleration time) & ↓ myocardial relax. (↑ isovol