ae NOTEBOOK POCKET MEDICINE SIXTH EDITION Marc S. Sabatine | The Massachusetts General Hospital NOM etl lr ave ica Celeb SS Wel ttn Na(U-tgSs ss 1 1 ee | Contributing Authors vi Foreword ix Preface x CARDIOLOGY Nino Mihatov, John D. Serfas, |. Sawalla Guseh, William J. Hucker, Mare S. Sabatine, Michelle L O'Donoghue Electrocardiography 1-1 Chest Pain 1-3 Noninvasive Evaluation of CAD 1-4 Coronary Angiography and Revascularization 15 Acute Coronary Syndromes 1-6 PA Catheter and Tailored Therapy 1-12 Heart Failure 1-14 Cardiomyopathies 1-17 Valvular Heart Disease 1-20 Pericardial Disease 1-25 Hypertension 1-28 Aortic Aneurysms 1-30 Acute Aortic Syndromes. 1-31 Arrhythmias 1-32 Atrial Fibrillation 1.35 Syncope 1.37 Cardiac Rhychm Management Devices 1-39 Cardiac Risk Assessment for Noneardiac Surgery 1-40 Peripheral Artery Disease 1-41 PULMONARY Alyssa Sclafani, Elias N. Baedorf Kassis, Walter J. O’Donnelt Dyspnea 21 Pulmonary Function Tests 2-1 Asthma 22 Anaphylaxis 24 ‘Chronic Obstructive Pulmonary Disease 25 Hemoptysis 27 Bronchiectasis 27 Solitary Pulmonary Nodule 28 Sleep Apnea 28 Interstitial Lung Disease 29 Pleural Effusion 2-11 Venous Thromboembolism 2-13 Pulmonary Hypertension 2-16 Respiratory Failure 2-18 Mechanical Ventilation 2-19 Acute Respiratory Distress Syndrome 2-22 Sepsis and Shock 2-23 Toxicology 2-24 Lung Transplant 2-24 GASTROENTEROLOGY Vanessa Mitsialis, Nneka N. Ufere, Lawrence §. Friedman Esophageal and Gastric Disorders 3-1 Gastrointestinal Bleeding 33 Diarrhea 35 Dysmotility & Nutrition 38 Disorders of the Colon 49Tick-Borne Diseases Fever Syndromes ENDOCRINOLOGY Taher Modarressi, Kelly Lauter Raszko, Michael Mannstadt Pituitary Disorders Thyroid Disorders Adrenal Disarders Calcium Disorders Diabetes Mellitus Lipid Disorders RHEUMATOLOGY Sarah Keller, Zachary S. Wallace, Robert P. Friday Approach to Rheumatic Disease Rheumatoid Arthritis Adult-Onset Still's Disease & Relapsing Polychondritis Crystal Deposition Arthritides Seronegative Spondyloarthritis Infectious Arthritis & Bursitis ‘Connective Tissue Diseases Systemic Lupus Erythematosus Vasculitis \gG4-Related Disease Cryoglobulinemia Amyloidosis NEUROLOGY Jessica M. Baker, Michael G. Erkkinen, Mark R. Ethertan, Khaled Moussowi, Tracey A. Cho Change in Mental Status Seizures Alcohol Withdrawal Stroke Weakness & Neuromuscular Dysfunction Headache Back and Spinal Cord Disease CONSULTS Sarah J. Carlson, jennifer F. Tseng, Katherine T. Chen, Stella K. Kim Surgical Issues Ob/Gyn Issues Ophthalmic Issues APPENDIX ICU Medications & Treatment of Hypotension/Shock Antibioties Formulae and Quick Reference ABBREVIATIONS INDEX PHOTO INSERTS Radiology Echocardiography & Coronary Angiography Peripheral Blood Smears & Leukemias Urinalysis ACLS 6-20 6-22 7-1 73 TT 7-11 7-13 7-16 8-1 8-3 84 8-5 87 8-9 8-11 8-15 8-17 8-20 8-21 8-22 10-1 10-3 10-4 1-1 13 14 RA (4 P.1 P.9 P13 P15 ACLS-1Inflammatory Bowel Disease Intestinal Ischemia Pancreatitis Abnormal Liver Tests Cirrhosis Hepatic Vascular Disease Ascites Biliary Tract Disease NEPHROLOGY Jacob Stevens, Andrew 5. Allegretti, Hasan Bazari Acid-Base Disturbances Sodium and Water Homeostasis Potassium Homeostasis Renal Failure Glomerular Disease Urinalysis Nephrolithiasis HEMATOLOGY-ONCOLOGY Edmond M. Chan, Tanya E. Keenan, Andrew M, Brunner, Sheheryar k. Kabroji, Jean M. Connors, 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 Michael $, Abers, Ang A. Weil, Nesli Basgoz Pneumonia Fungal Infections Infxns in immunosuppressed Hosts Urinary Tract Infections Soft Tissue and Bone Infections Infections of the Nervous System Bacterial Endocarditis Tuberculosis HIVIAIDS 3-10 3-12 3-13 3-15 3-17 3-20 3-21 3-25 3-26 3-27 44 4-6 4-10 4-12 417 419 420 6-1 63 6-4 6-5 6-6 6-9 6-12 6-15 6-17eA To the Ist Edition It is with the greatest enthusiasm that | introduce Packet Medicine. In an era of information glut, it will logically be asked,"Why another manual for medical house officers?” Yet, despite enormous information readily available in any number of textbooks, or at the push of a key on a computer, it is cften that the harried house officer is fess helped by the description of differential diagnosis and therapies than one would wish, Packet Medicine is the joint venture between house staff 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 officers with great frequency. Questions that frequently come from faculty co the house staff 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 facilitace the evidence-based medicine discussion that will follow the workup of the patient. This well-conceived hand- book should enhance the ability of every medical house officer to properly evalu- ate 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 Physicianin-Chief, Massachusetts General Hospital Jackson Professor of Clinical Medicine, Harvard Medical SchoolTo my parents, Matthew and Lee Sabatine, to their namesake grandchildren Matteo and Natalie, and to my wife Jennifer ‘Written by residents, fellows, and attendings, the mandate for Packet 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 medicat problems. The tremendous response to the previous editions suggests we were able to help fill an important need for clinicians, With this sixth edition come several major improvements. We have updated every topic thoroughly. In particular, we have included the latest pharmacotherapy for acute coronary syndromes, heart failure, pulmonary hypertension, hepatitis C, HIV, and diabetes, as well as the latest device- based treatments for valvular heart disease, atrial fibrillation, and stroke. Recent paradigm shifts in the guidelines for hypertension and cholesterol have been distilled and incorporated. We have expanded coverage of the molecular classification of malignancies and the corresponding biologic therapies. We have added new sections ‘on mechanical circulatory support, angioedema, non-invasive ventilation, toxicology, Jung transplantation, GI motility disorders, and the cardiorenal syndrome, just to name a few. We have also updated the section on Consults in which non-internal medicine specialists provide expert guidance in terms of establishing a differential diagnosis for common presenting symptoms and initiating an evaluation in anticipa- tion 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 field to ever summarize in a textbook of any size. Long monographs have been devoted to many of the topics discussed herein. Packet 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 definitive resources. Although the recommendations herein are as evidence-based as possible, medicine is bath a science and an art. As always, sound clinical judgement must be applied to every scenario. lam grateful for the support of the house officers, fellows. and attendings at the Massachusetts General Hospital. It is a privilege to work with such a knowk edgeable, dedicated, and compassionate group of physicians. | always look back on my time there as Chief Resident as one of the best experiences | have ever had. | am grateful to several outstanding clinical mentors, including Hasan Bazarl, Larry Friedman, Nesli Basgoz, Eric Isselbacher, Bill Dec, Mike Fifer, and Roman DeSanctis, as well as the late Charlie McCabe, Mort Swartz, and Peter Yurchak. This edition would not have been possible without the help of Melinda Cuerda, my academic coordinator, She shepherded every aspect of the project from start to finish, with an incredible eye to detail to ensure that each page of this book was the very best it could be. 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. | hope that you find Pocket Medicine useful throughout the arduous but incredibly rewarding journey of practicing medicine. Mage S. SABATINE, MD, MPHELECTROCARDIOGRAPHY a ch (a systematic approach is vital) * Rate (? tachy or brady) and rhythm (? P waves, regularity, P & QRS relationship) + 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 Vi-V;, ST T/l or TEwave As) Figure 1-1 QRS axis Left axis deviation (LAD) * Definition: axis beyond —30° ($ > R in lead Il} + Etiologies: LVH, LBBB, inferior Ml, WPW + Left anterior fascicular block (LAFB): LAD (-45 ta 90°) and gR in aVL and QRS <120 msec and no other cause of LAD (eg, Ml) Right axis deviation (RAD) * Definition: axis beyond +90° (§ > R in lead I) * Etiologies: RVH, PE, COPD (usually not > +110"), septal defects, lateral MI, WPW. * Left posterior fascicular block (LPFB): RAD (90- 180°) and rS in 1 & aL and qR in Ill & aVF and ORS < 120 msec and no other cause of RAD Bundle Branch Blocks (circ 2009,1196235) vy Vel Initial depol. left-to-right across septum (r In¥y & q in¥einb, absent in LBBB) followed by LV & RW free wall, with LV dominating (nb. RV depol. later and visible in RBBB). 1. QRS 2120 msec (110-119 = NCD or “ineomplete”) 2. FSR’ in R precordial leads (V.¥3) RBBB ah A |. Wide 5 wave in [and We 4 STL or TWI in R precordial leads QRS 2120 msec (110-119 = INCD ar “incampleto”) Broad, slurred, monophasic R in 1, aVL.¥5-V¢ (+ RS in LBEB dh Vos if cardiomegaly} Normal vos Absence of Q in IVs and Ve (may have narrow q in aVL) Displacement of ST & Tw opposite major QRS deflection + PRWP, LAD, Qw’s in inferior leads Bifscicular block: RBBB + LAFBYLPFB,“‘Trifascicula block”: bfascicular block + 1° AVB, Prolonged QT interval (Ney 2008:358-165, wwrtnrsades ong) = QT measured from beginning of QRS complex to end of T wave (measure longest QT} + QT varies wi HR — corrected w! Bazeut formula QTe = QT/JRR (RR in sec), overcorrects at high HR, undercorrects at low HR (nl OTe <440 msec J, <480 msec #) * Fridericia’s formula preferred at very high or low HR: QTc = QTARR + QT prolongation alw T risk TdP (espec >500 msec); establish baseline QT and monitor if using OT prolonging meds, no estab guidelines for stopping Rx if QT prolongs + Etiologies: Antiarrhythmics: dass la (procainamide, disopyramide}, dass Ill (aio, sotalel, dofet) Psych drugs: antipsychotics (phenothiazines, haloperidel, atypicals), Li,? SSRI,TCA Antimicrobials: macrolides, quinolones, azoles, pentamidine, atovaquone, atazanavir Other: antiemetics (droperidal, S-HT antagonists), alfuzosin, methadone, ranolazine Electrolyte disturbances: hypoCa (nb, hyperCa afw | QT), + hypoK, ? hypoMg Autonomic dysfan: ICH (deep TWi), Takotsubo, stroke, CEA, neck dissection Congenital (long QT syndrome): K, Na, & Ca channelopathies (Civ 2013:127:126) Misc; CAD, CMP bradycardia, high-grade AVB, hypothyroidism, hypothermia, BBB Left Atrial Abnormality (LAA) Right Atrial Abnormality (RAA) | ECG 2120s 240 ms T P-wave Criteria TN Sar yais 4" {\se wh [e500 Left ventricular hypertrophy (LVH) (circ 200%:11%«251) + Etiologies: HTN, ASIAI, HCM, coarcration 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 = diagnostic): ‘volt: limb lead Ror $ 220 mm or $ in; or Vi >30 mm or R in Vs or Ys 230 mm (3 pts) wae‘ST displacement opposite to QRS deflection: wie dig (3 pts); wi dig (1 pt) LAA (3 pts); LAD (2 pts); QRS duration 290 msec (1 pt) Incrinsicoid deflection (QRS onset to peak of R) ins or Vs 250 msec (1 pe) Sokolow-Lyon: 5 in; +R ins or ¥, 235 mm or R in aVL 211 mm (i Se wi | BMI) Cornell: B in aVL.+5 ins >28 mm in men or >20 mm in women HLAFB present: $ in ll: max (R+S) in any lead >30 mm in men or 228 mn in women Right ventricular hypertrophy (RWH) (cin 2009119257 jac 201463672) * Etiologies: cor pulmonale, congenital (tetralogy, TGA, PS, ASD, VSD), MS,TR. + Criteria [all insensitive, but specific (except in COPD): all wi poor PPM in general population] Re>S inVi.Rin¥; 26 mm,$ inVs 210 mm, in ¥4 23 mm, R in a¥R =4 mm RAD 210° (IVH + RAD or prominent § inVs or Vs ~» consider biventricular hypertrophy) Ddx of dominant R wave inV, or Vy * Ventricular enlargement: RVH (RAD, RAA, deep S waves in I, s,s); HCM + Myocardial injury: posterior MI (anterior R wave = posterior Q wave: often with IMl) + Abnormal depolarization: RBBB (QRS >120 msec, rSR’); WPW (! PR, 3 wave, T QRS) * Other: dextroversion; counterclockwise ratation, Duchenne's; lead misplacement, nl variant Poor R wave progression (PRWP) (Ae Heo | 2004:140:80) * Definition: loss of anterior forces w/o frank Q waves (V;-¥3);R wave in V3 <3 mm + Possible etiologies (nonspecific): old anteroseptal MI (usually wi R wave; 51S mm, + persistent ST T or TWIY & V3) LVH (delayed RWP w/ T left precordial voltage}, RVH, COPD {may also have RAA, RAD. limb lead ORS amplitude <5, SiSoSu w/ RUS ratio <1 in those leads) LBBB; WPW; clockwise rotation of the heart; lead misplacement, CMP; PTX Pathologic Q waves * Definition: 230 msec (220 msec ¥2-V;) or >25% height of R wave in that QRS complex * Small (septal) q waves in |, aVL.Vs & Vs are nl, as can be isolated Qw in Ill, aVR.V) * “Pseudoinfarct” pattern may be seen in LBBB, infiltrative dis., HCM, COPD, PTX, WPW ST elevation (STE) (nije 20033472128; Gr 2009.119:0241 & 262) Acute MI: upward convexity STE (ie, a"frown") TWI (or prior Ml vw! persistent STE) Coronary spasm: Prinzmetal’s angina; transient STE in a coronary distribution Pericarditis: diffuse, upward concavity STE (ie, a''smilo"):a/w PR 1; Tw usually upright HCM, Takotsubo CMP, ventricular aneurysm, cardiac contusion Pulmonary embolism: occ. STEV)—s elassically alw TWIV;-V), RAD, RBBB, SiQsTs Repolarization abnormalities: LBBB (tT QRS duration, STE discordant (rom QRS complex; see “ACS” for dx Ml in LBBB) LVH (7 QRS amplitude): Brugada syndrome (rSR’, downsloping STE V;—¥); pacing Hyperkalemia (7 QRS duration, tall Ts,no Ps) a¥R: STE >1 mm alw ? mortality in STEMI; STE aVR >V; afw left main disease Early repolarization: most often seen in V2-Vs in young adults (Acc 2015-66470) 1-4 mm elev of peak of notch or start of slurred downstroke of R wave (ie,] point); + up concavity of ST & large Fw (.. ratio of STEMT wave <25%:may disappear w/ exercise) 2 early repol in inf leads may be alw t risk of VF (NEJM 2009;361:2529: Cre 2011:124-2208) ST depression (STD) + Myocardial ischemia (+ Tw abni) + Acute true posterior Ml: posterior STE appearing as anterior STD (7 R wave) inVi-V3 posterior ECG leads; manage as a STEMI with rapid reperfusion (see"ACS") + Digitalis effect (downsloping ST + Tw abnl, does aot correlate w/ dig levels) + Hypokalemia (i U wave) * Repolarization abn a/w LBBB or LVH (usually in leads Vs.Vu, |, a¥VL) T wave inversion (TW; generally 21 mm; deep if 25 ram) (cr 2009.1 176241 Ischemia or infarc: Wellns' sign (deep, symm precordial TWI) ~ critical prox LAD lesion Myopericarditis; CMP (Takotsubo,ARVC, apical HCP); MVP; PE (espec if TWIV-V)) Repolarization abnl in afw LVH/RWH (’‘strain pattern”), BBB Posttachycardia or postpacing ("memory” T waves) Electrolyte, digoxin, PaQ:, PaCO;. pH or core temperature disturbances Intracranial bleed (“cerebral T waves." usually w! T QT) Normal variant in children (Vi-Vs) and leads in which QRS complex predominantly © Low voltage + QRS amplitude (R + S) <5 mm inall limb leads & <10 mm in all precordial leads + Etiol: COPD, pericard./pleural effusion, myxedema, 1 BMI, amyloid, diffuse CAD Electrolyte abnormalities + 1 Ks tented Tw, | QT, ? PRAVE, wide QRS, STE; 4 Ks flattoned Tw, U waves, ? QT + 1 €az L QT, flattened Tw & Pw,| point elevation; | Caz 7 QT: Tw AsCHEST PAIN Disorder ‘Typical Characteristics & Diagnostic Studies | 2 Cardiac Causes 5 acs Substernal pressure” (/ LR 1.3) — neck, jawrarm (© LR 1.3-2.6) 2 (15-25% of Sharp. pleuritie, positional, or reprod. wi palp all w/ ® LR 50.35 = chest pain in Diaphoresis (® LR 1.4), dyspnea (# LR 1.2), alw exertion (® LR 15-18) ED) = prior MI (® LR 2.2): w! NTGlrest (but not reliable; Aancs £m 2005:45:531) | 4 ECG as: STE, STD, TWI, Qw: + T Troponin. | Pericarditis Sharp pain + trapezius, T w/ respiration, |. w! sitting forward, + Pericardial | & myo. friction rub. ECG As (diffuse STE & PR 4, opposite in aVR) + pericardial pericarditis effusion. f myocarditis, same as above + Tn and + s/s HF and | EF. Aortic Sudden severe tearing pain (absence © LR 0.3). + Asymm (520 mmHg) dissection BP or pulse (2 LR 5.7), focal neuro deficic (}® LR >6),Al, widened mediast. on CXR {absence © LR 0.3):false lumen on imaging, (aa 2000.287-2262) Pulmonary Causes Pneumonia Pleuritic; dyspnea, fever, cough, sputum. 1 RR, crackles. CXR infiltrate. Pleuritis Sharp, pleuritie pain. + Pleuritic frietion rub. PTX Sudden onset, sharp pleuritic pain. Hyperresonance, | BS. PTX on CXR. PE Sudden onset pleuritic pain. T RR & HR, | $,02,ECG As (sinus tach, | RAD, RBBB, SQuTis, TWIVi-Ys occ STE Y:-¥5}, CTA or VQ. tTn | | Pulm HTN Exertional pressure, DOE. | 9,0z, loud Ps, RV heave, right S: and/or Se. | GI Causes | Esophageal Substernal burning, acid taste in mouth, water brash. T by meals, | reflux recumbency; | by antacids. EGD, manometry, pH monitoring. | [Esoph spasm Intense substernal pain. T by swallowing, | by NTG/CCB.Manometry. | Mallory-Welss _ Esoph tear precipated by vomicng. Hemnatemesis. Dx vi! EGD. | Boerhaave Esoph rupture. Severe pain, 7 wi swallow, Mediastinal air palpable & on CT. PUD Epigastric pain, relieved by antacids. + GIB. EGD, + H. pylon’ test. Biliary dis, RUQ pain, NIV. 7 by fatty foods. RUQ US; 1 LFTs. Pancreatitis Epigastric/back discomfort. 1 amylase & lipase; abd CT. ‘Musculoskeletal and Miscellaneous Causes Costochond Localized sharp pain, 1 w/ movement. Repraduced by palpation. Zoster Incense unilateral pain, Pain may precede dermatoral rash. “Anxiety “Tightness.” dyspnea, palpitations, other somatic symptams (Brounwald’s Heart Disease, 10 ed, 2094; JAMA 2015;314:1955) Initial approach + Focused history: quality, severity, location, radiation; pravoking'palliating factors: intensity at onset: duration, freq & pattern; setting; assoc sx; cardiac hx & risk factors + Targeted exam: V5 (incl. BF in both arms); gellops, murmurs, rubs; signs of vascular dis. {carotidifemoral bruits, | pulses) or CHF; lung & abd. exam; chest wall for reproducibility * 124ead ECG: obtain win 10 min; dw priors & obain serial ECGs; consider posterior leads {V>-Vs) to. for posterior STEM! if hx cw ACS but stnd ECG unrevealing or ST LVs-V3 fant ischemia vs. post STEMI) and angina that is hard to relieve or R/S >1 in Vy-V2 + CXR; other imaging (echo, PE CTA, etc.) as indicated based on H&P and al testing * Troponin: / at baseline & 3-6 h after sx onset; repeat 6h tater if clinical or ECG As; level >99th %ile w/ rise & fall in appropriate setting is dx of Ml;>95% Se, 90% Sp detectable 1-6 h after inj ry, peaks 24 h, may be elevated for 7-14 d in STEMI high-sens, assays (not yet available in U.S.) offer NPV =99% at 1h (Loocer 20153862481) Causes for Th other than plaque rupture (= “type 1 MI"): (1) Supply-demand mismatch nat due to «in CAD (= “type 2 MI": eg, 11 HR, shack. HTN crisis spasm, severe AS). (2) non-ischemic injury (myocarditis/toxic CMP. cardiac contusion) or (3) ruiltifactorial (PE. sepsis, severe HF renal failure, Takotsubo, infil: dis) (cic 2012.1262020) + CK-MB: less Se & Sp than Tn (other sources: skel. muscle, intestine, etc); CK-MB/CK ratio >2.5 — cardiac source, Useful for dx of past-PCICABG MI or (re)Ml if Tn already high. Early noninvasive imaging + If low prob of ACS (eg, ECG & Tn) & stable + outPt or inPt noninvasive fxnal or imaging test (qv). CCTA wi high NPV but low PPW; | LOS clw fxnal testing (NEJM 2012.366 1393), + “Triple rio” CT angiogram sometimes performed to rlo CAD, PE, AoD if dic unclearGBS eae ae ate) ie) Stress testing (circ 2007;115:1464 JAC 201260;1808) + Indications: dx CAD, evaluate A in clinical status in Pt w/ known CAD, risk stratify after ACS, evaluate exercise tolerance, localize ischemia (imaging required) * Contraindications (crc 2002-106: 1883; & 2012-126:2465) Absolute: AMI wiin 48 h, high-risk UA, acute PE, severe sx AS, uncontrolled HF, uncontrolled arrhythmias, myopericarditis, acute aortic dissection Relative (discuss with stress lab): left main CAD, mod valvular stenosis, severe HTN, HCMP high-degree AVE, severe electrolyte abn Exercise tolerance test (w/ ECG alone) + Generally preferred if Pt can meaningfully exercise; ECG As wi Se ~65%, Sp ~80% + Typically via treadmill w/ Bruce protacol (modified Bruce or submax if decond. or recent Ml) + Hold anv-isch. meds (eg, nitrates, BB) if dx’ing CAD but give to assess adequacy of meds Pharmacologic stress test (nb, requires imaging as ECG nat interpretable) + Use if unable to exercise, low exercise tolerance, or recent MI. Se & Sp + Preferred if LBBB or V-paced, as higher prob of false © imaging with exercise + Coronary vasodilator: diffuse vasodilation — relative “coronary steal” from vessels. w/ fixed epicardial disease. Reveals CAD, but not if Pt ischemic wi exercise. Regadenoson, dipyridamole, adenosine, Side effects: flushing, |. HR & AWB, dyspnea & bronchospasm. * Chronotrepestinotropes (dobuta}: more physiologic, but longer test: may precip arrhythmia Imaging for stress test + Use if uninterpretable ECG (V-paced, LBBB, resting ST 1 >1 mm, digoxin, LVH, WPW), after indeterminate ECG test, or if pharmacologic test + Use when need to localize ischemia (often used if prior coronary revasc) * Radionuclide myocardial perfusion imaging w/ images obtained at rest & w/ stress SPECT (og, ""Tc-sestamibi): Se -85%, Sp -80% PET (rubidium-82): Se -90%, Sp -B5%: requires pharmacologic stress not exercise ECG-gated imaging allows assessment of regional LV fan (sign of ischemialinfarction) + Echo (exercise ar dobuta): Se ~85%, Sp -85% no radiation; operator-dependent + Cardiac MRI (w/ pharmacologic stress) another option with excellent Se & Sp Test results + HR (must achieve 285% of max pred HR [220-age] for exer. test to be dx), BP response, peak double product (HR * BP; nl >20k), HR recovery (HRpaak— HR¢ min eri nl >12) + Max exercise capacity achieved (METS or min); occurrence of symptoms + ECG As: downsloping or horizontal ST J (21 mm) 60-80 ms after QRS predictive of CAD (but does not localize ischernic 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 25 > <1% 1-7 mort;-10 ta +44 2-3% <-11 + 25% + Imaging: radionuclide defects or echocardiographic regional wall motion abnormalities reversible defect = ischemia: fixed defect = infarct;transient isch dilation — ? severe IVD. false ©: breast —» ant defect; diaphragm ~ inf defect. False ©; balanced (3VD) ischemia. -risk test results (PPV 50% for LM or 3VD, -, consider coronary angio) * ECG:ST 1 22 mm or 21 mm in stage 1 or in 25 leads or 25 min in recovery; ST 1;VT + Physiologic J or fail to T BP, <4 METS, angina during exercise, Duke score <-11; 4 EF + Radionudide:>1 lg or >2 mod. reversible defects, transient LY cavity dilation, T lung uptake whadbility (Gre 2008:117 103; Kur Meare 2271:31-2984 8 20112210) * Goal: identify hibernating myocardium that could regain fxn after revascularization * Options: MRI (Se ~85%, Sp ~75%), PET (Se —90%, Sp ~65%), dobutamine stress ‘echo (Se -80%, Sp -80%); SPECTirest-redistribution (Se ~85%. 5p ~60%) In Pts wi LV dysten, viabil. doesn't predict ? CABG benefit vs. med Rx (NEJM 2011;364:1617} Coronary CTIMR angio (Nj 2008-1992526 Cre 2010:121-2508, Lancet 2012:379453) * In Pes wi CR CCTA 100% Se, 54% Sp for ACS, .. NPV 100%, PPV 17% yacc 208,53: 1642). | LOS, but 7 cath/PC, radiation vs. final study (NEjé 2012:367:299; JACE 201 461:800). * Insx ourPt, CCTA vs. fxnal testing -+ T radiation, eath/PC, = outcomes (Ney 2015372:1291) * Unlike CCTA,MR does not require iodinated contrast, HR control or radiation. Can assess LY fan, enhancement (early = microvasc abstr; late = Ml), Grossly = SelSp to CCTA. Coronary artery calcium score (CACS; Mijn 202368294; /4M4 2012.308-788) * Quantifies extent of calcium; thus estimates plaque burden (but not % coronary stenosis) + CAC sensitive (91%) but nat specific (49%) for presence of CAD; high NPV to r/o CAD + May provide incremental value to clinical scores for risk stratification (AMA 2004291210). ACCIAHA guidelines note CAC assessment is reasonable in asx Pts w/ intermed risk (10-20% 10-y Framingham risk; ? value if 610% 10-y risk) (Cec 2010:172:c584),DRONARY ANGIOGRAPHY AND REVASCULARIZA Indications for coronary angiography in stable CAD or asx Pts * CCS class II-IY angina despite med Rx, angina + systolic dystxn, or unexplained low EF + High-risk stress test findings (qv) or uncertain dx after noniny testing (& info will A mgmt) * Occupational need for definitive dx (eg. pilot) or inability to undergo noninvasive testing * Survivor af SCD, polymorphic VT, sustained monomorphic VT + Suspected spasm or nonatherosclerotic cause of ischemia (eg, anomalous coronary) Precath checklist & periprocedural pharmacot! + Decument peripheral arterial exam (radial, femoral, DP PT pulses; bruits). For radial access, / palmar arch intact (eg, w/ pulse oximetry & plethysmmography). Ensure can lie flat for several hrs. NPO >6 h. Ensure blood bank sample. + # CBC, PT, & Cr; IVF (? NaHCO;), + acetylcysteine (see “CIA! hold ACEVARB * ASA 325 mgs 1.Timing of P21 inhib debated.ASAP for STEMI.? preRx NSTEACS if ‘lopi (MA 2012:308:2507) or ticag (PLATO).not prasugrel. Cangrelor (IV P2Y 12 inhib) |. peri- PCI events vs. clopi w/o preload (NEM 2013.3681303).? statin preRx (Circ 2011:123: 1622). Coronary revascularization in stable CAD (crx 201 1)1240574 Nijm 2163741167 * Optimal med Rx (OMT) should be initial focus if stable, w/o critical anatomy, & wio | EF * PCI: L angina more quickly ciw OMT: does not J. D/MI (NEjM 2007:356:1503 & 2015:373-1204); iF 21 stenosis w! FFR (qv) <0.8, 1 urg revasc & ? DIM! chy OMT (ejm 2014371:1208); 2 noninf to CABG in unpros LM da, (veya 2017:364-17 18) © CABG (ne 2018;374.1954) in older studies, | mort. cw OMT if 3VD,LM, 2VD wi crit. prox LAD, esp. if | EF; recendy confirmed if multivessel dis, & EF <35% qvejvt 20163741511); in diabetics w/ 22VD, 1 D/MI, bur 7 stroke chw PCI (ey 2012:3672375) * Frevasc deemed necessar'y, 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 1 DIMI & revase but trend toward T stroke c/w PCI (Lancet 20133816: SYNTAX score Il helps identify Pts who benefit most from CABG (lancer 2013:381639) PCI and peri-PCI interventions Access: radial vs femoral, w! former + 4 bleeding and MACE acc inve 20149-1419) * Fractional flow reserve (FFR): ratio af max flow (induced by IV or IC adenosine) distal vs. prox to stenosis; help ID lesions that are truly hemodyn, significant * Balloon angioplasty by itself rare b/c elastic recoil, reserved for lesians too narraw to stent + Bare metal stents (BMS): | restenosis & repeat revase e/w angioplasty alone + Drug-eluting stents (DES): | neointimal hyperplasia + ~75% | restenosis, -50% | repeat revasc (<5% by 1y),? 1 late stent thrombosis, no A DIMI c/w BMS (vein 2013:368254): latest gen. DES wi very low rates of restenosis, repeat revasc & stent thrombosis * Bioresorbable stent: resorbe over yrs, but ? T MACE & stent throm, (Mei 2015.373:1905) * Duration of DAPT: ASA (81 mg) lifelong. If SIHD, P2Y,, inhib x 4 wk (BMS) or 26 ma (DES). IFACS, P2V 12 12 mo -+ ~20% | MACE, t bleeding and -15% 4 CV death (nejm 2V4371.2185 & 2015,372:7791). If need oral anticoag, consider clopi + NOAC +ASA. Post-PCI complications * Postprocedure “ vascular access site, distal pulses, ECG, CBC, Cr + Bleeding hematomalavert bleeding: manual compression, reverse!stop anticoag ‘retroperitoneal bleed: may pfw 4 Het + back pain; T HR & + BP late: Dx w/ abdipelvic CT (1); Roc reverse/stap anticoag (diw interventionalist), IVF/PRBCiples as required if bleeding uncontrolled, consult performing interventionalist or surgery + Vascular damage (-1% of dx angio, 5% of transfemoral PCI; Gre 2007,115.2666) pseudoaneurysm: triad of pain, expansile mass, systolic bruit; Dx: WS; Rx (if pain or >2 em): manual or U/S-directed compression, thrombin injection or surgical repair AY fistula: continuous bruit; Dx: U'S: Rx: surgical repair if large or sx LE ischemia (emboli, dissection, clot): cool, mottled extremity, | distal pulses; Dac pulse volume recording (P¥R), angio: Rx: percutaneous or surgical repair * Peri-PCI MI: >Sx ULN of To/CK-MB + either sx or ECG/angio As; Qw MI in <1% + Contrast-induced acute kidney injury: manifests win 48 h,peaks 3-5 d (see “CIAKI") + Cholesterol emboli syndrome (yppically in middle-aged & elderly and w/ Ao atheroma) renal failure (lave and progressive, + eos in urine); mesenteric ischemia (abd pain, LGIB, Pancreatitis); ntact distal pulses but livedo pattern and toe necrosis + Stent thrombosis: mins to yrs after PCI, typically piw AMI. Due to mech prob. (stent ion or unrecognized dissection, typicaly presents early) or dic of antiplt Roc (espec if dic both ASA & P24» inhib; JAMA 2005:203:2126), + In-stent restenosis: mos after PCI, typically pw gradual ? angina (10% piw ACS). Due to combination of elastic recoil and neointimal hyperplasia; { w/ DES vs. BMS.a CAS Se ea ae a ee Spectrum of Acute Coronary Syndromes Fy | Dx uA NSTEMI STEMI i | Coronary thrombosis Subtotal ceclusion Total ccelusion Ee) | History angina that is new-onset, crescendo angina at rest 4 ‘or at rest; usually <30 min ECG £ ST depression and/or TI ST elevations ‘TroponiniCK-MB a 6 CE Dax (causes of myocardial ischemia/infarction other than atherosclerotic plaque rupture) + Nonatherosclerotic coronary artery disease Spasm: Prinzmetal’s variant, cocaine-induced (6% of chest pain + cocaine use r/i for Ml) Dissection: spontaneous (vasculitis, CTD, pregnancy), aortic dissection with retrograde extension (usually involving RCA — IMI) or mechanical (PCI, surgery, trauma) Embolism (Gre 2015:132241):AF. thrambus/myxoma. endocard., prosth valve thrombosis Vasculitis: Kawasaki syndrome. Takayasu arteritis, PAN, Churg-Strauss, SLE. RA ‘Congenital anomalous origin from aorta or PA myocardial bridge (intramural segment) + Ischemia wio plaque rupture {‘“type 2" MI): 1 demand (eg, 1 HR), | supply (eg, HoTN) + Direct myocardial injury: myocarditis; Takotsubo/stress CMP, toxic CMP; cardiac contusion Clinical manifestations (jams 2015314:1955) + Typical angina: retrosternal pressure/pain/tightness + radiation to neck, jaw, arms; precip. by exertion, relieved by rest! NTG. In ACS: new-onset, crescendo or at rest. + Associated symptoms: dyspnea, diaphoresis, NIV, palpitations or light-headedness + Many Mls (20% in older series) are initially unrecognized b/c silent or atypical sx * Atypical sxs (incl NIV & epig pain) ? more common in &, elderly, diabetes, inferior ischemia Physical exam * Signs of ischemia: Ss, new MR murmur 2° pap. muscle dysfxn, paradoxical 8;, diaphoresis + Signs of heart failure: T JVP, crackles in lung fields, © S;, HoTN, cool extremities + Signs of other vascular disease: asymmetric BP, carotid or femoral bruits, | distal pulses Diagnostic studies + ECG: ST 4/1, TWI, new LBBB, hyperacute Tw; Qw/PRWP miy suggest prior MI & -. CAD 7 ECG wlin 10 min of presentation, with any «in sx & at 612 h; compare w/ baseline STEMI dk if old LBBB: >1 mm STE concordant w/ QRS (Se 73% Sp 92%),$TD 21 mm Vi-¥s (Se 25%, Sp 96%), STE 25 mm discordant wi QRS (Se 31%, Sp 92%) Localization of Mi ] Anatomic area ECG leads w/ STE Coronary artery Septal ViVi aVR, Proximal LAD Anterior Vs-Va, LAD Apical VoVa Distal LAD, LCx, or RCA Lateral aVb Les Inferior Ht aVF RCA (-B5%), LCx (-15%) RV Vi-¥; &VAR (most Se) Proximal RCA Posterior ST depression W)-V3 (= STEV,—Vs RCA or LCx posterior leads, if clinical suspicion) WECG nonde & suspicion high, leads Vy to assess distal LCWRCA territory.’ Resided precordial beads in IM to help desact RY invabremenc (STE in WR most Se). STE in Il > STE in land fack of STE inf or aL suggest RCA rather than LCx culprit in IMLSTE a¥R suggests LM or prox LAD occlusion ec difuse ischemia. + Cardiac biomarkers: / Tn (preferred over CK-MB) at presentation & 3-6 h after sx onset, repeat & h later i clinical or ECG As; rise to >99th Shile in appropriate clinical setting dx of MI (sce “Chest Pain’); rise in Tn in CKD still partends poor prognosis (Neji 2002:46:2047) + Iflow prob, stress test, CT angio to rlo CAD; new wall motian abnl on TTE suggests ACS + Coronary angio gold standard for CAD Prinzmetal's (variant) angina + Coronary spasm — transient STE usually w/o MI (but Ml, AVB,VT can occur) + Pts usually young, smokers, + ocher vasospastic disorders (eg, migraines, Raynaud's) . Anglegrapy: nonobstructive CAD (spasm can be provoked during cath but rarely done) + Treatment high-dose CCB & standing nitrates (SL prn),! a-blockers/statins; d/c smoking. avoid high-dose ASA (can inhibit prostacyclin and worsen spasm), nonselect AB, triptans + Cocaine-induced vasospasm: CCB, nitrates, ASA; ? avoid BB, but labetalol appears safeLikelihood of ACS (cr: 2007116148) Feature High (any of below) Intermediate (no high Low (no high/inter features. any of below) features, may have below) History ‘Chest or Larm pain Chest or arm pain, Atypical sx (eg, pleuritic. | like prior angina, age >70 y, male, sharp or positional pain) | [isd io CAD {incl Ml) diabetes i Exam HoTN,daphoresis, HF PAD or cerebrovas- Pain reproduced on palp. transient. MR ‘cular disease p ECG New STD (21mm) Old Qu, STD (05-09 TWETW! (<1 mm) in TWI1 in mult leads mm), TWI (>1 mm) Jeads wl dominant R wave Biomarkers ©Tn or CK-MB Normal Normal ‘h to triage * ffx and initial ECG & Tr non-thx, repeat ECG q15-30min x 1h &Tn 3-6 h after sx onset * Hfremain nl and low likelihood of ACS, search for alternative causes of chest pain + fremain nl, have ruled out MI, but if suspicion for ACS based on hx, then still need to ro UA w/ stress test to assess for inducible ischemia (ar CTA to ro CAD): if low risk (eg, age <70; 2 prior CAD, CVD, PAD: @ rest angina) can do before dle from ED or as ourPt wlin 72 h (0% mortality, <0.5% MI; Ann Ene Med 2008-47.427) if not low risk, admit and initiate Rx for possible ACS and consider stress test or cath Acute Anti-Ischemic and Analgesic Treatment Nitrates (SL or IV) Use for relief of sx. Rx for HTN or HFNo clear + in mortality, 03-04 mg SL qSmin x3, Caution if preload-sensitive (eg, HoTN, AS, sx RV infarct): then consider IV if still sx contraindicated if recent PDES inhibitor use. B-blockers + ischemia & progression of UA to MI (AMA 1988;260:2259) eg,metop 25-50 mg PO qéh STEMI: | arrhythmic death & reMl, but ? cardiogenic shock titrate slowly to HR 50-60 early (espec if signs of HF) (Loncec 2005:366:1622). IV BB IV only if HTN and no HF price to 1° PCI infarce size and 1 EF (Cre 2013;126-1435). Contraindic. PR >0.24 see, HR <60, 2°/3° AVB, severe bron: chospasm, s/s HF or low output, risk factors for shock (€g,>70 y, HR >110, SBP <120, late presentation STEMI) (CCB (nandihydropyridines} If cannot tolerate (IB b/c bronchospasm Morphine Relieves pain/anxiety; venodilation | preload. De not mask refractory sx. May delay antipit effects of P2Y 12 inhib. Oxygen Use pin for resp distress or to keep 8,0 590% 27 infarct size in STEMI wio hypoxia (Gic 2015:131:2143) Other early therapy + High-intensity statin therapy (eg, avorva 80 mg qd; PROVE-T THM 22 NEM 2004:350:1485) Lischemic events w/ benefit emerging wiin wks YAMA 001,285,171 8 JACC 2005 46:1405) J peri-PCI MI gacc 2010561099); |. contrast-induced nephropathy acc 20148371) + ACEIJARB: start once hemodynamics and renal function stable Strong indication for ACEI if heart failure, EF <40%, HTN, DM, CKD; ~10% J mortality, greatest benefit in ant. STEMI or prior MI (lence 1994;343-1115 & 1995;345:469) ARB appear = ACEI (NéjM 200334929); give if contraindic to ACEI + Ezetimibe, aldosterone blockade, and ranolazine discussed later (long-term Rx) + IABP: can be used for refractory angina when PCI not available NSTE-ACS 44202344) Key sues are antithrombotic regimen and irrasive vs. conservative strategy Antiplatelet Therapy Aspirin 50-70% | D/MI que 1998:79:1105) 162-325 mg x 1, then 81 mg qd Low dose (-81 mg) pref long term ye 2010.33.00) {non-enteric-coated, chewable) Kf allergy, use clopi and/or desensitize to ASA P2Y;; (ADP receptor) inhibitor (choose one of the following in addition to ASA), Timing remains controversial, European guidelines recommend P2 inhibitor as soon as possible (except prasugrel =H) 201132299), See below for specific recommendations. + Tieagrelor (preferred over clopl) More rapid and potent pe inhib c/w clopi 180 mg x 1-90 mg bie 16% | CYDIMi/stroke & 21% + CV death ciw ck Reversible, uc wait 3-5 d prior T non-CABG bleeding él 200836 1.1045) to surg Given upstream or at time of PCI Use only with ASA <100mg gd Dyspnea (but §,0) & PFTs nl) & ventricular pauses* Prasugrel (preferred over clopi) More rapid and potent pit inhib clw clopi Omg x Tat PCl +10 mgqd 19% 4 CVDiMUistroke in ACS w! planned PCI ys. eopi, (consider 5 mgid if <80 kg} but T bleeding (wep 20073582001), incl fatal bleeds Wait 7 d prior to surgery Not sup to clopi if med mgnnt wfo PCI (Nj 2012:3571297) In NSTE-ACS, should be given at time of PCI and not upstream due to T bleeding (vEjs 201;360999) Contraindic. if hlo TIVICVA: ? avoid # >75 y + Clopidogrel? ASAtclopi + 20% 4. CVD/Mi/stroke vs.ASA alone 300-600 mg x 1 + 75 mg qd T benefit if given hrs prior to PCI (JAMA 1012;308:2507),, Requires ~6 h to steady stave butif require CABG, need to wait>5 ¢ after dic clopi + Cangrelor 22% 4 CV events (mostly peri-PCI MI and stent Only IY P22: inhibitor thrombosis) vs. clopi 300 mg at time of PCI; no Rapid onsevofiset ti 3-3 min _ significant T bleeding (wé}m 2013:68:1303) Unclear benefit # upstream clopi administered (Ne 7009;341:2318) and no data vs. prasugrel or ticagrelor GP Iibillla inhibitors (GPI) No clear benefit for routinely starting prior to PCI abciximab; epufibatide; tirofiban and T bleeding (Nem 2009:360.2176) Infusions given <24 h peri & post. Consider if refractory ischemia despite optimal Rx while PCI; shorter (-2 h) as effective awaiting ang or in high-risk Prs (eg, large lot burden) at wi 1 bleeding yice 200053097, time of PCI espec if using clopi and no preRex. *-30% pop has 4 fxn CYPZCI9 > T CV events if PCI on clopi (NEJM 2009;360:354) Anticoagulant Therapy (choose one) 1 UFH: 60 U/kg IVB (max 4000 U) then 24% | DMI yauea 1996276811) 12 Ufleg/h (max 1000 Urh initially) 5° 48h — Titrate to aPTT 1.5-2« control (-50-70 sec} or until end of PCI Hold uncil INR <2 if already on warfarin Enoxaparin (low-molec-wt heparin) —10% 4 DIMI vs, UFH (ama 2004.292-45 89). Can ‘1_mgileg SC bid (£ 30 mg IVB) (qd if CrCl) perform PCI on enox (Cire 2001;10%658), but 7 <30) x 2-8 d or until PCL bleeding if switch b/w enox and UFH Bivalirudin (direct thrombin inhibitor) _—_ bleeding (espec vs. UFH + GP!), 4 early MI 0.75 mgikg IVB at PCI — 1.75 mgfkgih (lone 2014:384599), Use instead of UFH if HIT. Fondaparinux (Xa inhibitor) Chw enox, 17% 1 death & 38% 4. bleeding U5 mg SC qd x 2-8d {NEjea 2006.354:1484), However, 1 risk of catheter thrombosis; «. must supplement wl UFH if PCI. Coronary angiography (Coc 20141 M2144 + Immediate/urgent coronary angiography (win 2 h) if refractory/recurrent angina or hemodynamic or electrical instability + Invasive (INV) strategy = routine angiography win 72 h Early (wlin 24h) if © Tn, ST A, GRACE risk score: (www.outcomes- umassmed.org/grace) >140 (nem 2009:360:2165) Delayed (ie, wlin 72 h) acceptable if wio above fectures but wi: diabetes, EF <40%, GFR <60, post.Ml angina, TRS 23, GRACE score 109-140, PC! wiin 6 mo,prior CABG 32% | rehosp for ACS, nonsignif 16% 4 MI, no 4 in mortality cw cons, AMA 2096;300:71) ‘T peri-PCI MI counterbalanced by . in spont. MI mortality benefit seen in some studies, likely only if cons. strategy wi low rate of angio + Conservative (CONS) strategy = selective angio. Med Rx w! pre-dic stress test;angio only if recurrent ischemia or strangly ® ETT. Indicated for: low TIMI Risk Score, Pt or physician pref in absence of high-risk features, or low-risk women (AMA 2008;300:77), TIMI Risk Score (TRS) for UA/NSTEMI (java 2ocnani215, Calculation of Risk Score Application of Risk Score Characteristic Point ‘Score D/MUUR by 14d Historical ot 5% Age 265 y 1 2 8% 33 Risk factors for CAD 1 3 13% | Known CAD (stenosis 250%) 1 4 20% | ASA use in past 7d 1 5 26%. | Presentation 67 41% | Severe angina (22 episodes wiin 24 h) 1 Higher risk Pts (TRS >3) derive | ST deviation 20.5 mm 1 + benefit from LMWH, GP Hlb/llla | @ cardiac marker (troponin, CK-MB) 1 oe _ RISK SCORE = Total points (0-7)Figure 1-2 Approach to UANSTEM! LOW RISK HIGH RISK ASA ASA P2Y 2 inhib: clopi or tea. P2Y yo Init ticag (or elopi) Janiicoag: ENOX, fonda, or UH Aniicoag: UFH, ENO, o: bival jaepersng en cari pth + GP! (uniess bivaly CONS strategy INV strategy > eecuront win 72 [eae [sce ‘Stress test conse stabilized and before dic Anaioarachy / \ ¥ few risk highinisk Berar eat gi frost acon 11 seater ager tae ge perfuzton cote (exp. ant) (or lap: # GPL untass bival rote ies ee Mex! x Med Rx —> Long-term madical Px += CABG STEMI Requisite STE (st | point) * 22 contiguous leads w/ 21 mm (except for VV: 22 mm in d and 21.5 mm in @),or * New or presumed new LBBB w/ compelling H&P, or * True posterior Mi: ST depression ¥;—V3 + tall Rw w/ STE on posterior leads (¥;—V») Reperfusion (“time is muscle") + Immediate reperfusion (ie, opening occluded culprit coronary artery) is critical + In PCl-capable hospital, goal should be primary PCI win 90 min of 1* medical contact * Innon-PCl-capable hospital, consider transfer to PCl-capable hospital (see below), olw fibrinolytic therapy w/in 30 min of hospital presentation + Do not let decision regarding method of reperfusion delay time to reperfusion Primary PCI (vein 200725647 jACC 20161978 & 2016671238) + Definition: immediate PC! upon arrival to hospital or transfer for immediate PCI + Indic: STE + sx onset wlin <12 h; ongoing ischemia 12-24 h after sx onset; shock + Superior to lysis: 27% | death, 65% 4 reMl, 54% 4 stroke, 95% | ICH (lancet 2003:361:13) + Transfer to center for 1° PCI superior to lysis (vejm 2003349733), see below Routine thrombus aspiration: no benefit, T stroke (Loncet 2015;287:127; 2015;372:1389) Complete revasc: | MACE vs. culprit artery alone ivejvt 2013; 36%1115:JACC 2015;65:963); alternatively, assess ischemia due to residual lesions wi imaging stress (Circ 2011;124:574) Fibrinolysis vs, Hospital Transfer for Primary PCI: Assess Time and Risk 1. Time required for transport to skilled PC! lab: door-to-balloon <120 min & [doorsts- balloon]-[door-to-needle] <1 h favors transfer for PCI 2. Risk from STEMI: high-risk Pts (eg, shock) fare better with mechanical reperfusion 3. Time to presentation: efficacy of lytics | wi T time from sx onset, espec >3 h 4, Risk of fibrinolysis: if high risk of |CH or bleeding, PCI safer option Adapted from ACC/AHA 2013 STEMI Guidelines (Circ 2013;127529) Fibrinolysis: * Indic: STE/LBBB + sx <12 h (& >120 min before PCI be done); benefit if'sx >12 h less clear; reasonable if persist. sx & STE or hemodynamic instability or large territory at risk * Mortality | ~20% in anterior MI or LBBB and ~10% in IMI ciw @ reperfusion Rx + Prehospital lysis (ie, ambulance): further 17% 1 in mortality YAMA 2000.2832686) + 1% risk of ICH; high risk incl elderly (2% if >75 y), @, low we, . PCI more attractive ‘Contraindications to Fibrinolysis ] Absolute contraindications Relative contraindications * Any prior ICH + Hlo severe HTN, SBP >180 or DBP >110 + Intracranial neoplasm, aneurysm, AVM on presentation (? absolute if low-risk Ml) Ischemic stroke or clased head trauma wlin 3 mo; headispinal surg. wiin 2 mo» CPR >10 min, traumaimajor surg. wiin 3 wk Active internal bleeding or known Interral bleed wiin 24 wk: active PUD + Ischemic stroke >3 mo prior bleeding diathesis + Noncompressible vascular punctures Suspected aortic dissection Pregnancy Severe uncontrollable HTN Current use of anticoagulants For SK, SK Rx wiin 6 mo For SK, prior SK exposure‘Nonprimary PCI + Reseue PCI if shock, unstable, failed reperfusion o persistent sx (NEW 2005 353.2758) + Routine angio & PCI w/in 24 h of successful lysis: 1 D/Mlirevase (Lonces 2008;36¢:1045) and wiin 6h + reMl, recurrent ischemia, & HF compared to w/in 2 wk (NEW 2009;360:2705); if lysed at non-PC-capable hosp, consider transfer ta PCl-copable hosp. ASAP espec if hivtisk (eg, ant. Ml, (MI wi | EF or RV infarct, extensive STE/LBBB, HE | BP or 1 HR) + Lote PCI (median day 8) of occluded infaret-related artery: no benefit (Ney 2006,355:2395) Antiplatelet Therapy | Aspirin 162-325 mg x 1 23% 1 in death tact 1986349) | (crushed/chewed) then 81 mg qd Should not be stopped if CABG required P2¥ 12 inhibitor Lysis: clopidogrel 41% T in patency, 7% 4 mort, no Give ASAP (do not wait for angio) ble A major bleed or ICH (nejte 20053521179, lancet ‘onset inhib delayed in STEM pis 2008;366-1607); no data for pras or ticag wl lytic Ticagrelor or prasugrel {if PCI) as PCL: prasugrel and ticagrelor CV events c/w clapi detailed above (Loncet 2009,373:723 & Circ 20105122:2131) Clopidogrel: 600 mg pre-PCi 300 mg if Prehospital ticagrelor may be safe & 7 1 rate of lysis (no LD i =75 y) 78 mg qd stent thrombosis {NEJM 20143711016) | GP Iib/iila inhibitors Lysis: no indication (lancet 2007;397:1905) “abciximab, eptifibatide, tirafitan ———__Per-PCI: 60% 1 DIMI/UR (Nejat 2001;144-1895) Adgpted from ACC/AHA 2013 STEMI Guidelines Update (Cire 2013:127:528); Loncet 2017;302:623 Anticoagulant Therapy (choose one) | UFH No demonstrated mortality benefit 0 Urkg 1VB (max 4000 Uj 7 patency with fibrin-specific lyties 12. Uregh (max 1000 Uih intially) Titrate to aPTT 1.5-2x control (-50-70 sec) | Enoxaparin Lysis: 17% | DIMI wi ENOX x 7 dvs, UFH x 2d | Lysis: 30 mg IVB—+ 1 mg/kg SC bid vege 20n6.354:1477) |" (adjust for age 275 & CrCl) PCI: J DIMVrevasc and = bleeding vs. UFH tance | PCOS mgikg NB 2011378893) Bivalirudin PCI: 4 bleeding (espee vs. UFH + GP Iib/illa inhib), | 075 VB 1.75 hr IW 7 MI, T stent thromb,? | mortality (lancer 1014;384.599; ty Aus avis 1336.g 2015373897) Fondaparinax cin be used (f CrCl >30 ml/min) in seeting of lysis where superior ta UFH wl less blending JAMA 2006:295:1519}. Adapted from ACCIAHA 2013 STEMI Guidelines (Cre 20131127529 Lancet 20133822633) Intraaortic Balloon Pump (IABP) Counterpulsation + Routine use in high-risk STEMI 7 strokerbleeds w/o A in survival (AMA 2011:306.1329) + In-cardiogenic shock, no survival benefit w/ IABP if early revase (NEJM 2072:367-1287% 18% L death in Pts w/ cardiogenic shock treated with lytic (E4) 200930459) LY failure (-25%) * Diurese to achieve PCWP -14 — | pulmonary edema, | myocardial Q; demand + LAfterload — t stroke volume & CO, J myocardial OQ; demand can use I¥ NTG or nitroprusside (risk of coronary steal) -» shareacting ACEI + Inatropes if HF despite diuresis & 1 afterload; use dopamine, dobutamine, or milrinone + Cardiogenic shock (7%) = MAP <80 mmHg, Cl. <2 Umin/m®, PCWP >18 mmHg: inotropes, mech circulatory support to keep C! >2; pressors to keep MAP >60; if noc done already. coronary revase (NEJM 1999:341:625) IME complications (cre 199081401: MEpin 1743307211: jACC 2003:4 11273) + Heart block: ~20%, occurs in part because RCA typically supplies AV node 40% on present,, 20% wiin 24 h, rest by 72 h; high-grade AVB can develop abruptly Rx: atrepine, epi, aminophylline (100 mgimin x 2.5 min), temp pacing wire + RV infarct (proximal RCA occlusion + compromised flow to RV marginal branch) Angiographically present in 30-50%, but only ¥: of those clinically signif. HoT; t J¥P.@ Kussmaul’s; 21 mm STE in ¥ apical VSD. IMI = basal septum: 90% w/ harsh murmur chill yea 2002.247-1424); Roc diuretics, vasodil,inotropes, ABE surgery, perc. closure + Papillary muscle rupture: more common after IMI (PM pap m. supplied by PDA a lone) than AMI (AL supplied by OMs & diags);50% wi new murmur; * v wave in PCWP tracing;asymmetric pulmonary edema on CXR.Rx: diuretes, vasodilators, ABR surgery. Arrhythmias post-M1 (treat all per ACLS protocols if unstable or symptomatic) + AF (10-16% incidence): BB or amio, + digoxin (particularly if HF}, heparin + VTIVEF: lido or amio x 6-24 h, then reassess; 7 BB as tol, replete K & Mg, r/o ischemia; monomorphic VT <48 h post-MI does not worsen prognosis; >48 h, consider ICD ( wearable; see below) * Accelerated idioventricular rhythm (AIVR): slow VT (<100 bprn), often seen after successful reperfusion; typically asx, self-terminates,and does not require treatment * May consider backup transcutaneous pacing (TP) if 2° AVB type |. BBB + Backup TP or initiate transvenous pacing if, 2° AVB type II: BBB + AVB: * Transvenous pacing (TV) if: 3° AVB; new BEB + 2° AVB type Il; alternating LBBB RBBB (can bridge wi TP uncil TV, which is best accomplished with fluoroscopic guidance) Other Post-MI Complications Complication Clinical features Treatment LV thrombus -30% incid, (espee Ig antero-apieal MI) Anticoagulate x 3-6 mo. Ventricular Noncontractile outpouching of LV; Surgery or pere repair if HE aneurysm 8-15% incid, (espec ant); persist STE thromboemboli, arrhythmia Ventricular Rupture (narrow neck) -+ sealed by Urgent surgery (or pseudoanaurysm thrombus and pericardium (esp in inf). pereutaneous repair} Pericarditis 10-20% incid; 1-4 d post-Ml & High-dose ASA, colchicine, pericardial rub; ECG As rare narcotics; minimize anticoag Dressler’s 4% incid.;2-10 wk post-MI fever, High-dose aspirin, NSAIDs syndrome pericarditis, pleuritis Prognosis + In registries, in-hospital mortality is 6% w/ reperfusion Rx {lytic or PCI) and ~20% wio + TIMI Risk Score for STEMI (includes age, time to Rx, anterior MI or LBBB, Killip class, tachycardia, HOTN) defines 30-d mortality after STEMI (jaima 2001286 1356) 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 dlc; EF 16% in STEMI over & mo (JACC 2007:50-749) Medications (barring contraindications)} i 1 mg daily (no clear benefit ta higher doses) inhib (ticagrelor or prasugrel preferred over clopi): treat for at least 12 mo Prolonged Rx >12 mo — |. MACE & CV death, ? in bleeding but no t ICH. Beyond 1* 12 mo, ticag 60 bid preferred to 90, as better tolerability (NEM 2015372179 1, EH] 207637:390), Pls | Gl complic; some PPls 4 antiplt effect, but no clear T in CV risk «neji 20103831907) B-blocker: 23% | mortality after Mi ‘Statin: high-intensity lipid-lowering (eg. atorva 80 mg, PRONE-(T TIMI 2t, MEM 2004:350:1495) Ezetimibe: | CV events when added to statin (IMPROVELT, NEIM 2015.372: 1500} ACEI: lifelong if HE | ER HTN, DM; 4-6 wk or at least until hosp, d/c in all STEMI 7 long-term benefit in CAD wa HF (Neyat 2000:342+745 & 2004:351:2058: (oncet 2003:367782) Aldosterone antag: 15% | mort if EF <40% & either s/s of HF or DM (nen 20033487309) Nitrates: standing if symptomatic; SL NTG prn for all Ranolazine: | recurrent ischemia, no impact on C¥D/MI ama 2007:297:1775) ‘Oral anticoag:if needed (eg,AF or LY thrombus), warfarin w/ target INR 2-2.5 or NOAC. Clopi (not ticag or pras) and ? stop ASA if at high bleeding risk (lorcet 20133811107). Not FDA approved: low-dose rivaroxaban (2.5 mg bid) in addition to ASA & clopi in Patients without an indication for anticoag > 16% 4 D/Ml/stroke and 32%. 4 all-cause death, but f major bleeding and ICH (ej 2012:3669, HCD (wey 2008:3592245: cre 2074130094) + Ifsust.VTIVF >2 d past-MI not due to reversible ischemia; consider wearable defib * Indicated in 1° prevention of SCD if post-MI w/ EF =30—40% (NYHA IHIl} or £30-35% (NYHA |); need to wait 240 d after MI vey 20083512481 & 2000:361:1427) Risk factors and lifestyle modifications (cre 2014129Suppt 2:51 8 * Low chol. (<200 mg/d) & fat (<7% saturated) diet; ? 0-3 FA + Traditional LDL-C goal <70 mg/dL; current recs wio target; given IMPROVE-IT, 2 mid 505 + BP <140/90 & 7 120-130/80 mmm (9M 2015:48:1372: Neat 2015:3732102); quit smoking + If diabetic, tallor HbATe goal based on Pt (avoid TZDs if HF}; in Pts we! CAD. empagiflozin (NEM 2015, 373.2117) and liraglutide (wey 2016375311) 4 cardiovascular events + Exercise (30-60 min 5-7dwk); cardiac rehab; BMI goal 18.5~24,9 kg/m? + Influenza & S.pneumo vaccines (circ 2006;114: 1549; JAMA 2013.3 10:1711); ¢ for depression| ea i ed Rationale * Cardiac output (CO) = SV x HR; optimize SV (and thereby CO) by manipulating preload! LVEDV (w/ IVE diuretics), contractilicy (w! inatropes), & afterload (w/ vasodilators) * Balloon at catheter tip inflated — floats into “Wedge” positon. Column of blood extends fram tip of catheter, through pulm vencus circulation to a point just prox to LA. Under conditions of no fiow, PCWP = LA pressure = LIVED. which is proportional to LVEDY. + 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) (4) ALVEDP-LVEDV relationship (ie,abni compliance, «. “nl LVEDP may not be optimal) Indications (Grc 2005, 112391; NEjM 2015,16%035) * Diagnosis and evaluation Dek of shock (cardiogenic vs. distributive: espec if trial of IVF failed or is high risk) and of pulmonary edema (cardiogenic vs. not: espec if trial of diuretic failed or is high risk) Evaluation of CO, intracardiac shunt. pulm HTN, MR, tamponade, cardiorenal syndrome Evaluation of unexplained dyspnea (PAC during provocation wi exercise, vasodilator) + Therapeutics (crc 2006;113:1020) Tailored therapy to optimize PCWP. SY, SwvO2, RAP. PVR in heart failure or shock Guide to vasodilator therapy (eg, inhaled NO, nifedipine) in PHT, RY infarction Guide periop mgmt in some high-risk Pts, candidacy for mech circ support & transplant + Contraindications Absolute: right-sided endocarditis, thrombusimass or mechanical valve; proximal PE Relative: coagulopathy (reverse), recent PPM or CD (place under fluoroscopy), LBBB. (-5% risk of RBBB — CHB, place under fluoro), bioprosthetic R-sided valve Efficacy concerns (NE/M 2006;354:2213, JAMA 2006-254:1644) + No benefit to routine PAC use in high-risk surgery. sepsis, ARDS + No benefit in decompensated HF yam 2005294 1425); untested in cardiogenic shock + But—/ of cinical CO & PCWP estimates incorrect: CVP & PCWP not well correl; -. use PAC to (a) answer hemodynamic ? and then remove. or (bh) manage cardiogenic shock Placement vey 2013367935 + Insertion site: R internal jugular or L subclavian veins for “anatomic” flotation into PA + Inflate balloon (max 1.5 mL) 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 + Hfcatheter cannot be floated (ic.,severe TR, RV dilatation), consider fluoroscopic guidance Complications + Central venous access: pneumo/hemothorax (~1%), arterial puncture (if inadvertent cannulation ¥/ 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/amponade, PA rupture * Maintenance: infection (espec if catheter >3 d old), thrombus, pulm infarction (<1%), valvelchordae damage, PA rupture/pseudoaneurysm (espec 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, when intrathoracic pressure ‘dosest to 0 (“high point” in spont. breathing Pts. "low point” in Pts.on © pressure vent) + If T intrathoracic pressure (eg, PEEP), measured PCWP overestimates true transmural pressures. Can approx by subtracting —Y1 PEEP (x 44 to convert cm HO to mmHg). + PCWP: LY preload best estimated at a wave; risk of pulmonary edema from avg PCWP Cardiac output + Thermodilution: saline injected in RA or prox thermal filament. A in temp over time measured at thermistor (in PA) used to calc CO. Inaccurate if | CO,sev TR, or shunt. + Fick method: ©: consumption (¥O2)(Limin) = CO (Limin) x A arteriovenous O2 content » CO = VOr/ C(av)Oz VO) ideally measured (esp. if t metab demands), but freq estimated (125 mLimin/m?) ‘ClaeyJOh = [10 x 1.36 mL Onlg of Hb x Hb gidL x (8,03 ~ SevO,)]. SverOh i hey varigble that As. If SOx >80%, consider if the PAC is “wedged (ie, pulm vein sat), LR shunt, impaired O, utilization (severe sepsis, cyanide, carbon monoxide), tT FiO,PA Catheter Waveforms Location RA RV PCWP Distance -20 cm -30 cm ~40 cm ~50cm Normal mean <6 syst 15-30 syst 15-30 mean <12 Pressure: diast 1-8 mean 9-18 (mmHg) diast 6-12 Scie y a=aral comraction, occurs | RVEDP occurs Waveform should ‘Similar to RA except in PR nvarval right before conmin noch (closure dmpened and c= bulking of TV backinco upstroke and of pulmonic valve}. delayed. a wave after RAacsar ofspstole = = mean RA Peak during T wave. QRS, ¢ distinee ¢ x= tral relaczton and sure unless | PAsystolc = RV wave, wave afer Comment “creas ote of heat. | Saree TS orTR fee unless theres (helps dstingulsh v= blood anaering Ra, a pradenc (og,PS. PCWP wf large v coeurs mid T ne 7A dase «PCWP waves 2 MR from 1 = blood axing RA ater TY unless ttrans-puim PAY opens at tare of ace sradient (eg, TPYR), PCWP waveform abnarmalities: bluneed y descent >? amponsi rge a wave —+ } mitral stenosis large ¥ wave —> ? mitral regurgitation: steep x & y descents -» ! constriction Hemodynamic Profiles of Various Forms of Shack (weit 2013369 1726) Type of shock RA PCWP co ‘SYR Hypovolemic 1 4 4 t Cardiogenic lor? 1 4 t RV infarct/massive PE T nlor + t Tamponade T 1 1 + Distributive variable variable _usvally t (can be + in sepsis £ Surrogates: RA = JVP (11 mmHg = 1.36 cm HQ}; pulmonary edema on CXR implies T PCWP, UOP = CO (barring AKI}; delayed capillary refi ie, 52-3 sec) implies T S¥R Tailored therapy in cardiogenic shock (cic 10041194341) + Goals: optimize both MAP and CO while | risk of pulmonary edema MAP = CO x SYR: CO= HR x SV (which depends on preload, afterload and contractility) pulmonary edema when PCWP >20-25 (7 levels may be toleraved in chronic HF) hepatic and renal congestion when CVP/RAP >15 mmbg * Optimize preload = LVEDV ~ LVEDP = LAP = PCWP (NEJM 1973.299:1263) 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 T by giving NS (albumin wo clinical benefit over NS; PREC if significant anernia) J by diuresis (qv), ultrafiltration or dialysis if refractory to diuretics * Optimize afterload = wall stress during LV ejection = [(-SBP x radius) / (2x wall thicke)] ind. e« MAP and e« SWR = (MAP — CVP/ CO); goals: MAP >60, SVR 800-1200 MAP >60 & SVR T:vasadifators (og, nitroprusside, NTG,ACEI, hydral) or wean pressors MAP <60.& SVR T (& -. CO J): temporize w/ pressors until can t CO (see below) MAP <60 & SWR low/nl (& -. inappropriate vasoplegia): vasopressors (eg, norepineph- rine [o,f]. dopamine [D,c.,B], phenylephrine [cr] or vasopressin [V;] if refractory}; better outcomes w/ norepi than dopa even in cardiogenic shock (NEJM 2070362:779) * Optimize contractility = CO for given preload & afterload: goal Cl= (CO | BSA) >2.2 if too low despite optimal preload & vasodilators (as MAP permits): 2 inotropes: eg, dobutamine (mod inotrope & mild vasodilator) or milrinone (strong, inotrope & vasodilator, inc! pulm), beth proarrhythmie,or epi (strong inotrope & pressor) mech circulatory support (Limin): IABP (0.5), Impella (2-5), TandemHeart (5), VAD (L-sided, R-sided or both: temp or perm: 10) or ECMO (6) uace 2015:65:07 4 2542)a HEART FAILURE Definitions {ermoirs Heort Deore, 100s ec 2014) Failure of heart to pump blood forward at rate sufficient to meet metabolic demands of peripheral tissues, or ability to do so only at abnormally high cardiac filling pressures Low output (L cardiac output) vs. high output (T stroke volume + T cardiac output) Left-sided (pulmonary edema) vs. right-sided (T JV. hepatomegaly, peripheral edema) Backward (7 filling pressures, congestion) vs. forward (impaired systemic perfusion) Systolic (inability to expel sufficient blood) vs. diastolic (failure to relax and fill normally) Reduced (HFrEF, EF <40%), mid-range (HFmrEF, EF 40-49%), & preserved (HFpEF EF >50%); combination of systolic and diastolic dysfxn may occur regardless of EF Figure 1-3 Approach to left-sided heart fire Lett-sided Heart Failure Flo mitral vaive disease consider puim ven stenosis (eg, after PV!) myxoma, pulmonary VOD TLvEDP fie — normal LVEDV 4K tesy Tsv x “ Systolic High S¥ Dysfunction Failure “o™ {Contractility tT Afterload WH (usually lschemiaM! AS, HCMP. 7° HEMP snght-sided DCMP ——HINorsis 2°10 HTN, AS faire) ‘Choni¢ AUMR Coaretation or Tamponade taco Constriction Thyrotaxicosis or or RCMP |. Forwatd Flom Myocardial VSD, PDA —_Endomyocardial History + Low output: fatigue, weakness, exercise intolerance, A MS. anorexia + Congestive: left-sided — dyspnea, orthopnea, paroxysmal nocturnal dyspnea right-sided —+ peripheral edema, RUQ discomfort, bloating, satiety Functional classification (New York Heart Association ol * Class k:no sx w/ ordinary activity; class Il: sx wi ordinary activity: class Ill: sx wi minimal activity; class IV: sx at rest Physical exam (''2-minute” hemodynamic profile: AMA 1994275630 A 200%787-628) = Congestion (‘“dry” vs.““wet”)}: 1 JVP (-80% of the time JYP >10 + PCWP >22) ci hepatojugular reflux: 24 em Tin J¥P for 215 sec w/ abdominal pressure Se/Sp 73/87% for RA >8 and Se/Sp 55/83% for PCWP >15 (ajc 1990;46;1002) ‘Abn Valsalva response: square wave (1 SBP w/ strain),na overshoot (no 1 BP after strain) 5; (in Pts wl HF ~40% 1 risk of HF hosp. or pump failure death; NEJM 2601:345:574) rales, dullness at base 2° pleural effus. (often absenc in chronic HF due ta lymphatic compensation) + hepatomegaly, ascites and jaundice, peripheral edema + Perfusion (‘warm ys. “‘cold’) narrow pulse pressure (<25% of SBP) — Cl <2.2 (91% Se, 83% Sp: yarns 19a9:261-884); soft Sy (1. dP/dt), pulsus alternans, cool & pale extremities, 1 UOP muscle atrophy + £ Other: Cheyne-Stokes resp..abn! PMI (diffuse, sustained or lifting depending on cause of HP), $4 (diase. 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; lung UIS better than CXR (PPV & NPV 92% vs. 77%; Chest 2015:146:202) + BNP/NT-proBNP can help exclude HF; levels T wi age, renal dysfxn,AF; + w/ obesity Se 295%, Sp: ~50%, PPV ~65%, NPV > 94% for HF in Pes phv SOB (am) 2015:350:n910) + Evidence of | organ perfusion: ? Cr, | Na, abnl LFTs + Echo (see inserts): | EF & 7 chamber size + systolic dyshxn: hypertrophy. abn! MY inflow. abpl tissue Doppler — ? diastolic dysfxn; abnl valves or pericardium; f estimated RVSP + PA catheterization; T PCWP. CO, and 7 SYR (in low-output failure)Evaluation for the potential causes of heart failure + ECG: evidence for CAD,LVH, LAE, heart block or low voltage (? inftrative CMP/DCMP) + THE: LY & RY size & fin, valve abnl (cause or consequence!), infiltrative or pericardial dis. + Cardiac MRI: distinguishes ischemic vs. nonischemic and can help determine etiol.of latter + Coronary angio (or noninvasive imaging, eg, CT angio); if no CAD, wiu for NICM 4 Precipitants of acute heart failure Sie * Dietary indiscretion or medical nonadherence (-40% of cases) oa Myocardial ischemia or infarction (~10-15% of cases); myocarditis = Renal failure (acute, progression of CKD, or insufficient dialysis) = 7 preload Hypertensive crisis (incl. from RAS), worsening AS | left-sided afterload Drugs (3B, CCB, NSAIDs TZDs), chemo (anthracyclines, trastuzumab), or toxins (ECOH) mias; acute valvular dystxn (eg, endocarditis), expec mitral or aortic regurgitati COPDIPE — 1 right-sided afterload; extreme stress, anemia, systemic infxn, thyraid dis, ‘Treatment of acute decompensated heart failure Congestion? + Assess degree of congestion & adequacy ol perfusion N + For congestion: “LMNOP” =o, Warm & Dry Lasix IV; total daily dose 2.5x usual daily 5 =) ourtrr Diuresis PO dose + 1 UOP, but transient 1 in Cr 3 | Cold&Dry Cold & Wet vs. Tx usual dase: 2 clear diff berween 5 @| fnoopes §=———iluresis, contin, get vs.q12h (NEJM 2011364797) gS) iccuy ee Morphine (1 sx, venadilator, | afterload) 8 me Nitrates (venodilacor) ai ‘Oxygen + noninvasive vent (| sx 1 P,Ox:no A mortality, see "Mechanical Ventilation”) Position (sitting up & legs dangling over side of bed ~ J preload) * For low perfusion, see below. + Adjustment of oral meds ‘ACEWARB: hold if HTN, consider 4 to hydralazine & nitrates if renal decompensation (B:reduce dose by at least 2 if mod HF. dic if severe HF and/or need inotropes Treatment of acute advanced heart failure (ci-- 2009;11%391) + Consider PAC if not resp to Rx, unsure re: vol status, HoTN, | Cr. need inotropes * Tailored Roc wil PAC (av): goals of MAP 260, Cl =2.2 (MVQz >60%), SVR <800, PCWP <18 * IV vasodilators: NTG, nitroprusside (risk of coronary steal if CAD; prolanged use —» cyanideithioeyanate toxicity}; nesiritide (rBNP) net rec for routine use (MEM 207 1;365:32) + Inotropes (properties in addition to 7 inotropy listed below) dobutamine: vasodilation at doses <5 ag/kg/min: mild 4 PVR; desensitization over time dopamine: splanchnic vasodil. +? GFR & natriuresis; vasoconstrictor at 25 jigfleg/min milrinone: preminent systemic & pulmonary vasodilation; | dose by S0% in renal failure + Ultrafiltration: similar wt loss to aggressive diuresis, but T renal failure (vem 2012:367:2296) * Mechanical circulatory support (also see “Tailored Therapy,” JACC 201545287 & 1542) Temporary: bridge to recovery, transplant, ar durable MCS; periprocedural support Intra-aortic balloon pump (IABP): inflates in diastole & deffates in systole to J impedance +o LV ejection, |. myocardial C2 demand & 1 coronary perfusion. +05 Limin CO Axial flow puraps (eg, Impella): Archimedes screw principle in LV; +2.5-§ Limin Extracorporeal centrifugal pumps: TandemHeart (+5 Limin, percutaneous) & CentriMag (10 Limin, surgical), Extracorporeal membrane oxygenation (ECMO): 6 Limin (cre 2015.137676) Durable: surgically placed LVAD £ RVAD as bridge to recovery (NEJM 2006:355:1873) or transplant (HeartMate Il or Heart Ware LVAD or Total Artificial Heart if BIV failure}, or as destination Rx (250% | Tey mort. vs. ved Rx NEIM 2007 345:1435 & 2009:36172241), + Cardiac transplantation:~2500/yr in US. 10% mort. in 1 y, median survival -10 y “Recommended Chronic Therapy by HF Stage (circ 200%,11%4341) Stage (not NYHA Class) Therapy At risk for HF (eg HTN, Rx HTN, lipids, DM. A FHxCMP):bur asx & Stop smoking. ECOH. T exercise | wig struct. heart dis. ACEVARB if HTN/DM/CAD/PAD |g © Struct heart dis, As per stage A +ACEVARB & fi8 if MIICAD or | EF (eg CMP.LVH), butase NICD. c Struct heart dis. As per stage A + diuretics, | Na. if | BF:ACEI.ARB or © Any hio Sx of HF ARNI; BB; aldo antag; ICD; ? CRT; nitrate/hydral: dig, 1p Refractory HF requiring All measures for stages A~C. Consider IV inotropes. specialized interventions VAD; transplant. end-ofelife care (4-y mortality »50%)+ Utility of BNP-guided Rx remains debated (Eur Heort | 201435-16) + Implantable PA pressure sensor in NYHA Ill + ~33% 4 risk of hosp (Loncet 2016:387:453) ‘Treatment of Chronic Heart Failure with Reduced Ejection Fraction Diet, exercise Na <2 g/d. fluid restriction, exercise training in ambulatory Pts ACEI L mortality: 40% in NYHA IV; 16% in NYHA I/II 20-308 in asx bur EF (Ne}M 1992:327-685 & Loncee 2000255:1575) High-dose more effic. than low. Watch for 1 Cr, 1 K (ameliorate by low-K diet, diuretics, K binders), cough, angioedema. ATI receptor Consider as alternative if cannot tolerate ACEI (eg, b/c cough) blockers (ARBs) = Naninferior to ACEI (Lencet 2000.355:1582 & 200336272) ‘As with ACEI, higher doses more efficacious (lancet 2009:374'1840) Adding co ACEI > T risk of TK and T Cr any 2013.346./360) ARNi (ARB + Alternative to ACEVARB, espec if sx despite ACEWARB. Neutral eprilysin inhib) endopeptidase (NEP aka nepritysin) degrades natriuretic peptides, (do not use w!ACE!, bradykinin & angiatensins. Valsartan + sacubitril (NEPi) 1 CV mort & | allow 264) washout) HF hosp c/w ACE: t HoTN.AKI,? angioedema (nejm201437199). | Hydralazine + Consider if cannot tolerate ACEIJARB ar in blacks wi class III/IV nitrates 25% 1 mort, (NEM 19969141547); infer. to ACEI (Neva 1997325 303) 40% | mort. in blacks on standard Rx (A-HBFT, NEJM 2004;351:2049) f-blocker EF will transiently |, then 1, Contraindic, in decompensated HF (data for carvediol, 35% | mort. & 405% | rehosp. in NYHA IHIV yaa 2002:287 82) ‘metoprolol, bisoprolol) Carvedilol superior to low-dose metop in 1 trial (Lint 20033027, but meta-analysis suggests no diff between BB (ai 2012348455). Aldosterone Consider if adeq, renai fart and wlo hyperkclemie; watch for t K antagonists 25-30% | mort. in NYHA I-IV & EF $35% (NEJM 2011;364-11) 13% | mort. in HF post-Ml, EF <40% (EPHESUS, NEJM 2003:348:1309) Cardiac Consider if EF <35%, LBBB (QRS >! 30 ms) and symptomatic HF resynch therapy 36% | mort. & 7 EF in NYHA III-IV (CARE-HF.NEWM 200535211539) (CRT, qv) 41% 1 mort. if EF <30%, LBBB and NYHA ill pep 2014:370.1694) ICD (see “Cardiac For 1° prevention if EF <30-35% or 2° prevention; not if NYHA IV Rhythm Mgmt | mort. in ischemic & non-isch CMP, no A mort. early post-Ml (NEM Devices”) ‘2004.35 1:2481 A 2009:361:1427), .. wait 240 d Diuretics Loop 4 thiazides diuretics (3x relief, no mortality benefit) Digoxin 23% | HF hosp.,no A mort (NEM 1997:336525);? T mort w/ T levels (EMM 2002:247:1403); optimal 0.5-0.8 ng/ml (AMA 2003:289:871) Wvabradine (|p ‘Consider if EF <35%, NYHE Il or Ill, HR 270, NSR on max B. blocker w/o © ina) 18% 4 CV mart or HF hosp (lancet 2010:37675) | Iron 2 if NYHA Ill, EF <40%, Fe-defc ferritin <100 or ferritin 100-200 & supplementation SAT <20%). | Sx, T 6MWD, independent of Het (véjst 2009:361:2436) Anticoagulation IFAEVTE, LV thrombus, + if large akinetic LY segments In SR wi EF <35%, 1 isch stroke, but 1 bleed (NEIM 2012;366:1859) Heart rhychm Catheter ablation of AF — 7 im EF. sx (ve 200835122373) No mortality benefit to AF rhythm vs. rate cnt! (NEJM 20083582667) Pulm vein isolation | sx c/w AVN ablation & CRT (NEM 20081551778) Meds to avoid NSAIDs, nondihydrapyridine CCB,TZDs Experimental Serelaxin = ! dyspnea & ? | mortality (lance: 29123612) Empagiiflazin (SGLT2i) death/HF hosp in DM neji 20183722117) Ineeratrial shunting L PCWP & sx (lances 2076:387:1250) (Cre 2013; 16240 & 2076 ACCIAMAIHFSA Update: i] 201637-2129) Heart failure with preserved EF (MFpEF; “Diastolic HF") (Cer 201).1242540) *+ Epidemiology:~¥ of Pts w/ HF have normal or only min. impaired systolic fin (EF 240%); risk factors for HFEF incl ? age, 2, DM,AF Mortality = to those w/ systolic dysfkn. + Etiologies (impaired relaxation andlor 1 passive stiffness): ischemia, prior Ml, LVH, HCMP infiltrative CMP RCMP aging, hypothyroidism * Precipitants of pulmonary edema: volume overload (poor compliance of LV -s sensitive to even modest 7 in volume); ischemia (|. relaxation); tachycardia (| filling time in diastole). AF (loss of atrial boost to LV filling); HTN (7 afterload -- | stroke volume) + Dix wl clinical s/s of HF w! preserved systolic fen. Dx supported by evidence of diast dysfxr: (1) echo: abn! MV inflow (E/A reversal and As in E wave deceleration cime) & ‘L myocardial relax, (I isovol relax. time & 4 early diastole tissue Doppler vel) (2) exercise-induced | PCWP (+ 1 response chronotropic & vasodilator reserve) + Treatment: diuresis for vol overload, BP control, prevention of tachycardia and ischemia: no benefit to: ACEVARE (NEjs 20083582458) or PDES inhib MA 20133081268) spironolactone ? | CV death & HF hosp (at least in Americas) (NEJM 2014,370.1383) ARNi (Loncet 20123001367) and serelaxcin (Lance: 2012361:29) under studyCARDIOMYOPATHIES &B Diseases with mechanical andlor electrical dysfimetion of the myocardium Ditateo CaapiomyopatHy (DCM) Definition and epiderniology (circ 2913,128--240 ace 2013622088) * Ventricular dilatation and | contractility + | wall thickness in the absence of myocardial disease caused by ischemialinfarct, valvular disease or hypertension * Incidence: 5-8/100,000/y; prevalence: 1/2500, Most common reason for heart transplant. Etiologies Acc 2011-57:1641; Circ Res 20121112131) + Familial (-35%): Pt & >2 closely related family members w/ otherwise unexplained DCM; -30 genes identified to date, encoding structural & nuclear proteins + Idiopathic (<20%); ? undiagnosed infectious, alcoholic or genetic cause * Infectious myocarditis (10-15%; Lancet 2012:379-738;jACC 2012;59:779) Viruses (parvoB19 & HH'V6 > Coxsackie, adeno, echo, CMV, HCV): from subacute (dilated LV. mild-mod dysfxn) co fulminant (nondil, thick, edematous LM sev dysixn) Bacterial, fungal, ricketesial, TB, Lyme (mild myocarditis, often with AWB) HIV; -8% of asx HIV ©; due to HIV, other virus or antiretroviral; also premature CAD Chagas: apical aneurysm + thrombus, RBBB, megaesophagus/colon (NEM 2015:373-456) * Toxic: alcohol (-20%) typ. 7-8 drinks/d >5 y, but variable; cocaine; XRT (usu RCMP); anthracyclines (risk? >550 mg/m? may manifest late), cyclophosphamide, trastuzumab + Infiltrative (5%): often mix of DCMP + RCMP (qv) with thickened wall artyloidosis, sarcoidasi, hemochromatosis, tumor + Autoimmune: collagen vasc. dis, (3%): PM, SLE, scleroderma, PAN, RA, Wegener's; peripertum (last month + 5 mo postpartum; Hf 2015:36:1030): ~1:3000 preg. 1 risk w! multiparity, age, Afr Am; stnd HF Rx (if preg.no ACEI or spironolact,);? bromacriptine to | prolactin; 72% normalize EF yacc 201566905); -30% recur wi next prez idiopathic giant cell myocarditis (GCM): avg age 42, fulminant, AVBIT te Cine HF 20134: 15) Eosinophilic (variable peripheral eas); hypersensitivity (mild HF but at risk for SCD) or acute necrotizing eosinophilic myocarditis (ANEM; STE, effusion, severe HF) + Stress-induced (Takotsubo = apical ballooning} Typically postmenopausal $; mimics MI (chest pain,+ STE & Tn; deep TWI & T QT):midlapex dyskinesis; ? Rx w/ BB, ACEI: usu. improves over wks: (JAMA 2071;306277), In-hosp morbimere similar to ACS (NEM 2015373929). + Arrhythmogenic right ventricular cardiomyopathy (ACM/ARVC}fibrafatry replacement of RV — dilation (ee wi MRI}; ECG: + RBBB, TVVIV.—¥3,¢ waves risk WT (loncet 20093731289) + Tachycardia: likelincod « rate/duration; often resolves w/ rate cnt! (Circ 2005;112-1092) + LY noncompaction yace 2015.6:578); prominent trabeculae, arrhythmias, eardiaembolt * Metab/other: hypothyroid, acromegaly, pheo, OSA, Vit Bi, selenium or carnitine defic, Clinical manifestations * Heart failure: both congestive & poor forward flaw sx; signs of L- & R-sided HF diffuse, laterally displaced PMI, S3, + MR or TR (annular dilat, displaced pap, muscle} * Embolic events (~ 10%), supraventricular/ventricular arrhthnias, & palpitations * Chest pain can be seen wi! same etiologies (eg, myocarditis) Diagnostic studies and workup (JAcc 2016.47:29%6) + CXR: moderate to marked cardiomegaly, + pulmonary edema & pleural effusions + ECG: may see PRP. Q waves or BBB; low-voltage; AF (20%): may be normal Echocardiogram: LV dilatation, | EF, regional or global LW HK + RV HK, + mural thrombi Cardiac MRI: up to 76% Se, 96% Sp for myocarditis or infiltrative dis. YACC name 2914:7254); extent of midwall fibrosis correlated w/ mortality in NICMP yaa 2013:30%696) Labs: TFTs, Fe panel, HIV, SPER. ANA; viral sero not recommended; others per suspicion Family hx (20-35% w! familial dis.), genetic counseling = genetic testing (AMA 2009:30220471) Stress test: useful to r/o ischemia (low false © rate), high false © rate, even wi imaging Coronary angiography to rfo CAD if risk factors, h/o angina, Qw Ml-on ECG, equivocal ETT;consider CT angiography yacc 2007-49200) * 2 Endomyocardial biopsy acc 2007,50.1914) yield 10%; of these, 75% myocarditis (for which no proven Rx) & 25% systemic disease; 40% false © rate (patchy dis.) & false {necrosis > inflammation); .. biopsy acute & hemodyn compromise (rio GCM, NEM) arrhythmia or RCMP features (r/o infiltrative); or suspect toxic, allergic, tumor ‘Treatment (see “Heart Failure” for standard HF Rix) + Possibility of reversibility of CMP may temper implantation of devices » Immunosuppression: for giant cell myocarditis (prednisone + AZA), collagen vascular disease, peripartum (? Vlg}, & eosinophilic; no proven benefit for viral myocarditis + Prognosis differs by etiology (NEj# 2000:342:1077); postparcum (best), ischemicIGCM (worst)HyPeRTROPHIC CARDIOMYOPATHY (HEM) Definition and epidemiology + LY (usually 215 mm) and/or RV hypertrophy disproportionate to hemodynamic [oad + Prevalence: 1/500; 50% sporadic, 50% familial, most asymptomatic. + Dd: LVH 2° to HTNAAS, elite athletes (wall usually <13 mm & symmetric and nit rates of tissue Doppler diastolic relaxation; Gre 30111232725), Fabry dis. (1 Cr, skin findings) P + Autosomal dominant mutations in cardiac sarcomere genes (eg, myosin heavy chain) + Myocardial fiber disarray with hypertrophy, which creates arrhythmogenic substrate + Morphologic hypertrophy variants: asymmetric septal; concentric; midcavity; apical Pathophysiology + Subaortic outflow obstruction: narrowed tract 2° hypertrophied septum + systolic anterior motion (SAM) of ant. MY leaflet (imay be fied, variable or nonexistent) and papillary muscle displacement. Gradient (V) worse w T contractility (digoxin, Be agonists, exercise, PYCs), | preload (eg, Valsalva maneuver) or | afterload. + Mitral regurgitation: due to SAM (mid-to-late, post.-directed regurg. jet) and/or abnl mitral leaflets and papillary muscles (pansystolic, ant.-directed regurg. jet) + Diastolic dysfunction: 1 chamber stiffness + impaired relaxation * Ischemia:small vessel dis., perforating artery compression (bridging), | coronary perfusion + Syncope: As in load-dependent CO, arrhythmias Clinical manifestations (70% are asympcormatic at dx) + Dyspnea (90%): due to 1 LVEDP, MR, and diastolic dysfunction + Angina (25%) even w/o epicardial CAD; microvase. dysfxn (Ne}M 2003;249:1027) + Arrhythmias (AF in 20-25%: VT/VF); palpitations, syncope, sudden cardiac death ical exam * Sustained PMI, Sp paradoxically split if severe outflow obstruction, S4 (ccc, palpable) + Systolic murmur: crescendo-decrescendo; LLSB; ? w/ Valsalva & standing (1 preload) * + mid-to-late or holasystolic murmur af MR at apex * Bifid carotid pulse (brisk rise, decline, then 2™ rise); JVP w! prominent a wave + Contrast to AS, which has murmur that J w! Valsalva and J carotid pulses Diagnostic studies (ej 201435735) + CXR: cardiomegaly (LV and LA) + ECG: LVH, anterolateral TWI and inferior pseudo-Qu, + apical giant TWI (apical variant) + Echo: any LY wall segment 215 mm (or ? even 213 if ® HFx).cften but not necessarily involving septum; other findings include dynamic outflow obstruction, SAM, MR + MRI: hypertrophy + patchy delayed enhancement (useful for dx & prog) (Cir 2015,132.292) + Cardiac cath: subaortic pressure V; Brockenbrough sign = | pulse pressure post-P¥C (in contrast to AS, in which pulse pressure T post-PVC) + 2 Genotyping for family screening, but pathogenic mutation ID'd in <}2 (Gre 2011;124:276) Treatment (Circ 2011;124:0783 & 2012,125:1432; Loncee 2013:381:242) + Heart failure © inotrapes/chronatropes: f-blockers, CCB (verapamil), disopyramide Careful use of diuretics, as may further J. preload. Vasodilators only if systolic dysfen. Avoid digoxin. If sx refractory to drug Rx + abstructive physiology (V >50 mmHg): (a) Surgical myectomy: long-term | symptoms in 90% (Ci 2074;130-1617) (b) Alcohol septal ablation ucHF 201538961: gradient J by -B0%, only 520% remain w/ NYHA ILIV sxc 1486 require repeat ablation or myectomy. Good alternative for older Pis, multiple comorbidities, Complic: transient (& occ. delayed) 3° AVB wi 10-20% req. PPM;VT due to scar formation. No clear benefit of dual-chamber pacing (JACt 1997:29-435; Cie 159599:2927) If refractory to drug therapy and there is nonobstructive pathophysiology: transplant + Acute HF: can be precip. by dehydration or tachycardia; Rx w! fluids, RB, phenylephrine + AF rate control w/ 8B, maintain SR w/ disopyramide or amig; low threshold to anticoag + SCD: ICD yacc 2003:42:1687). Risk factors: hie VT/VE, & FHx SCD, unexplained syncope, SVT, | SBP or rel HoTIN (7 SBP <20 mmHg) wi exercise, LV wall 230 mm, ? extensive MRI delayed enhancement EPS not useful. Risk 4%b/y if high-risk gama 2007238405). * Counsel to avoid dehydration, extreme exertion * Endocarditis prophylaxis not recommended (Che 2007:16:1736) + T*-degree relatives: periodic screening w! echo, ECG (as timing of HCMP onset variable}. Genetic testing if known mutation.Restrictive CarpiomrorarHy (RCM) Definition (cic 2004112:1007) + Impaired ventricular filing with |. compliance in nonhypercrophied, nondilated ventricles; normal or 4 diastolic volumes, normal or near-normal EF; must r/o pericardial disease Etiology yAcc 2010:55:1769) + Myocardial processes Autoimmune (scleroderma, polymyositis-dermatomyositis) Infitrative diseases (see primary entries for extracardiac manifestations, Dx, Rx) Amyloidosis (Cic 2011:174 1079); age at presentation ~60 y; d:? = 3:2 AL (eg, MM, etc); familial (transthyretin, ATTR); AA/senile (dep. of TTR. ANP) ECG: 1 QRS amplitude (50%), pseudoinfarction pattern (Qw),AVB (10-208), hemiblock (20%), BBE (S-20%) Echo: biventricular wall thickening (yet w/ fow voltage on ECG), granular sparkling texture (30%), biatrial enlargement (40%), thickened atrial septum, valve thickening (65%), diastolic dysfan, small effusions NI voltage/septal thickness has NPV ~90% Labs: 7 SPEP/UPEP. serum free light chain ratio (<0.25 or >1.65 r-to-A ratio) MRI: distinct lace gadolinium enhancement pattern (jacc 2008511072) Sarcoidosis (can also be DCM): presents at age ~30 y; 1’d in blacks, N. Europe, @ ‘5% w/ systemic sarcoid have overt cardiac involvements cardiac w/o systemic in 10% ECG:AVB (75%), RBBB (20-60%).VT; PET: 1 FOG uptake in affected area Echo: regional WMA (particularly basal septum) w/ thinning or mild hypertrophy Gallium or FOG uptake at areas of inflam,;sestaMIBI w/ nen-cor. perfusion defects Cardiac MRI:T2 early gad (edema); fibrosis/scar in basal septum; LGE prognostic Cardiac bx low yield b/c patchy Hemochromatosis: in middle-aged men (espec N. European); 15% p/w cardiac sx Diabetes; storage diseases: Gaucher's, Fabry, Hurler’s, glycogen storage diseases + Endomyocardial processes Chronic eosinophilic: Léfiler’s endocarditis (temperate climates: 1 cos: mural thrombi that embolize); endomyocardial fibrosis (tropical climates; var. eos; mural thrombi) ‘Toxins: radiation (also pi constrictive pericarditis, valvular di, osital CAD),andhracycines. Serotonin: carcinoid, serotonin agonists, ergot alkaloids, Metastatic cancer. & pathophysiology + Path:normal or T wall thickness + infiltration or abnormal deposition ‘+ 4 myocardial compliance —+ nl EDV but 7 EDP — T systemic & puim. venous pressures + 4 ventricular cavity size + | SV and | CO Clinical manifestations (cre 2000:101:2490) + Right-sided > left-sided heart failure with peripheral edema > pulmonary edema + Diuretic “refractoriness”; thromboembolic events * Poorly tolerated tachyarrhythmias: VT — syncape/sudden cardiac death Physical exam * TJVP. Kussmaul's sign (VP not 4 wi inspir.. classically seen in constrict. pericarditis) * Cardiac: + 5; and S.,+ murmurs of MR and TR + Congestive hepatomegaly, + ascites and jaundice, peripheral edema Diagnostic studies * CXR: normal ventricular chamber size, enlarged atria, + pulmonary congestion ECG: low voltage, pseudoinfarction pattern (Qw), + arrhythmias Echo: symmetric wall thickening, biatrial entarge.,:t mural thrombi, * cavity oblit. wi diast dysfen: T early diast (E) and 4 late atrial (A) filling, T E/A ratio, | decel, time Cardiac MRI/PET: may reveal inflammation or evidence of infiltration (but nonspecific) Cardiac catheterization ‘Atria: M’s or Ws (prominent x and y descents) Ventricles: dip & plateau (rapid | pressure at onset of diastole, rapid T to early plateau) Concordance of LV & RV pressure peaks during respiraory cycle (ys. discordance in constrictive pericarditis; Ge 1995:93:2007) + Endomyocardial biopsy if suspect infiltrative process; fat pad bx for amyloid + Restrictive cardiomyopathy vs. constrictive pericarditis: see “Pericardial Disease” Treatment ( Gentle diu addition to Rx’ing underlying disease) . May not tolerate CCB or other vasodilators. + Control HR (but can | CO); maintain SR (helps filing). Digaxcin 1 arrhythmias in amyloid + Anticoagulation (particularly with AF or low CO) + ‘Transplantation for refractory cases dWAZ) a Aortic STENosIs (AS) Calcific: predominant cause in Pts 70 y; risk factors include HTN, 1 cho, ESRD Congenital (ie, bicuspid Ao w/ premature calcification): cause in 50% of Pts <70 y Rheumatic heart disease (AS usually accompanied by AR and MY disease) AAS mimickers: subvalvular (HCMP, subAo membrane) or supravalvular stenosis Clinical manifestations (usually indicates AVA <1 cm’ or concomitant CAD) + Angina: 1 OQ; demand (hypertrophy) + | 2 supply (| cor perfusion pressure) + CAD + Syncope (exertional): peripheral vasodil, w/ fixed CO > | MAP 4 cerebral perfusion + Heart failure: outflow obstruct + diastolic dysfxn — pulm. edema, esp. if * Acquired VWF disease (-20% of sev. AS): destruction of vWF: Gl angiodysplasia * Natural hx: usually slowly progressive (AVA | 0.1 cm’/y, but varies; Cr: 1997952262), until sx develop; mean survival based on sx:angina = 5 yssyncope = 3 y: CHF = 2 y Physical exam + Midsystolic crescendo-decrescendo murmur at RUSB, harsh, high-pitched, radiates to. carotids, apex (holosystolic ~ Valsalva. Dynamic outflow obstruction (HCM) is the reverse. + Ejection click after 5; sometimes heard with bicuspid AoV + Signs of severity: jate-peaking murmur, paradoxically split Ss or inaudible A;, small and delayed carotid pulse (“‘pulsus parvus et tardus”), LV heave, Sy (occasionally palpable) Gallavardin effect}, 1 w/ passive leg raise, 4 wi standing & 2 E Diagnostic studies + ECG: may see LVH, LAE, LBBB, AF (in late disease) + CXR: cardiomegaly, AoW caleifieation, poststenotic dilation of ascending Ao, pulmonary congestion T HIRYAF (1 LY fill), eh Pitot Hert Os. 6" TOTS for thi ot ab * Echo: valve morphology, jet velocity, estim pressure gradient (V) & calculate AVA, LVEF * Cardiac cath: usually t0 rio CAD (in ~"/) of calcific AS): for hemodyn if disparity between exam & echo: / pressure gradient (V) across AV, calc AVA (underestim. if mod/sev AR) + Dobutamine challenge (echo or cath): if low EF and mean V <30, use to differentiate: afterload mismatch: 20% T SV & ¥.no A AVA (implies contractile reserve, 7 EF post-AWR) pseudostenosis: 20% T SV.no A in 7.1 AVA (implies low AVA artifact of LV dystxn) limited contractile reserve: no & SV, or AVA (implies EF prob. will not improve w/ AVR) Classification of Aortic Stenosis (Circ 10141290521) Stage Sx Severity [nla N Normal AN Atrisk & Mild | _ Moderate Severe cl No Very severe a “Sevres LER 1 Severe D2 Y Severe + low flow/V +1 EP 3 Severe + low flow/V + nl EF Max Jet Mean Grad Nal i) | frnenbig) 1 0 a 10 229 <20 339 20-39 “AWA. indexed to BSA <0.6 emir also severe; "DSE — max jet vel 24 & AVA $1.0;‘small LV wi J stroke vol. Treatment (Cec 204:124 0521: MEM 2014.37 1:744: Concer 2016:387:13 12) * Based on symptoms: once they develop, AVR needed. If asx, HTN can be cautiously Rx’d. + AVR: C1) and undergoing other cardiac surgery Reasonable if indicated in sx (stage D1); asx severe + EF <50% (stage C2}ior asx severe (stage Asx severe (stage C1) but either sx or | BP wi exercise (can carefilly exercise asx 'AS co uncover sx.ddo not exercise sx AS) or very severe. Sx severe w! low flow/V w/ low EF & response to dobuma (stage D2) or normal EF but AS felt to be cause of sx (stage D3) ‘Asx moderate AS (stage B) and undergoing cardiac surgery + Transcatheter AoV replacement (TAVR.see below) indicated if surgical risk prohibitive or as reasonable alternative to surgery if medium (STS predicted 30-d mortality ~4-8%) or high (mortality 815%) operative risk+ Medical (if not AVR candidate or to temporize): careful diuresis prn, control HTN. maintain SRs digoxin if | EF & HF or if AF; avoid venodilators (nitrates) & &' inotropes (BBICCB) if severe AS; avoid vigorous physical exertion once AS mad-severe: 2 nitroprusside in HF wi sev.AS, EF <35%, Cl <2.2, & MAP >60 (nejit 2003:348-1758) or if low flow w/ 1 EF and HTIN (cre 2073s128:1349) + IABP: stabilization, bridge to surgery * Balloon AoV valyotomy (BAV): 50% 1 AVA & | peak V, but 50% restenosis by 6-12 mo & 1 risk of peri-PAV strokelAR (Weim 1988319:125), «. bridge to AVR. or palliation TAVR (transcatheter AoW replacement) + Valves: balloon-expandable (Edwards SAPIEN) or self-expanding (Medtronic CoreValve) + Approaches: most commonly retrograde via perc. transfemoral access;also retrograde via axillary art or ascend. Ao [via small sternotomy & aortotomy), Alternatively antegrade ‘ransepical via small thoracotomy & LV puncture: (if narrow ilofem art. or calcified Ao). + Peri- & pastprocedural complic.:low CO; annular rupture or coronary occlusion {both rare}; local vascular; paravalvular leaks; CHB, + Lifelong ASA +? clopidogrel (or GAC) x 6 mor? subclinical valve thrombus in -20%, | wi anticoag (NEJM 20153722015) + Qurcames w/ TAVR. In nonoperative Pts (je, vs. med Rx}; 44% |. mortality but still -20% annual mortality in TAVR group (NEJM 2012:3661836.JACC 20443-1872). In high-risk Prs vs. surg AVR. (NGM 2012:366:7696 8 2074:370-1790): moreality = (balloon- expand) or 28% | (self-expand); T vase complic; | early risk of stroke/TIA w! balloon expands PPM required for CHB in -20% w/ set-expand; paravalvular leaks in ~7%4, In mediurr-risk Pts (NE 2016:374:1608); death/stroke =, T vasc complic but | bleeding, AKI, AF. If transfemoral 21%, 1 deathistrake, whereas tended to be 21% 7 if transapical. Aortic REGURGITATION (AR) Etiology cx 2005:174922) * Valve disease (43%): rheumatic heart disease (usually mixed AS/AR + MY disease); bicuspid AoV (natural fac s+ normal, "fs > AS, Ve AR, Ve endocarditis > AR), infective endocarditis; valvulitis (RA, SLE, certain anorectics & serotonergics, XRT) + Root disease (57%): HTN, aortic aneurysmidissection, annuleaortic ectasia (ie, Marfan), aortic inflammation (GCA, Takayasu's, ankylosing spond, reactive arthritis, syphilis) Clinical manifestations + Acute: sudden | forward SV and 7 LVEDP (noncompliant ventricle) - pulmonary edema + hypotension and cardiogenic shock + Chronic: clinically silent while LV dilates (to T compliance to keep LVEDP low} more than it hypertrophies -> chronic volume overload —» LV decompensation —> CHF + Natural hve variable progression (unlike AS, can be fast or slow); once decompensation begins, prognosis poor w/o AVR (mortality ~10%/y) Physical exam + Early diastolic decrescende murmur at LUSB (RUSB if dilated Aa root); t wi sitting forward, expir, handgrip; ” severity of AR = duration of murmur (except in acute and severe late); Austin Flat murmur: mid-to-late diastolic “ sk rumble at apex (AR jet interfering w! mitral inflow) ie, + Wide pulse pressure due to 7 stroke volume, hyper- £ Cy dynamic pulse; pulse pressure narrows in late AR we with U LV fin; bisferiens (twice-beating) arterial pulse Te + PMI diffuse and laterally displaced; soft 8; (early closure of =o | |i, MV); Ss (2.1 EF but rather just volume overload in AR) ho Classic Eponymous Signs in Chronic AR (Suuth ed 1931;74459) Sign Description Corrigan’s pulse “water hammer” pulse (ie, rapid riseifall or discentionécollapse) Hill's sign (popliteal SBP — brachial SBP) >60 mmHg Duroziez’s sign to-and-fro. murmur heard over femoral artery wi light compression Pistol shot sounds pistol shot sound heard over femoral artery Traube'’s sound double sound heard ever femoral artery whan compressed distally de Musser’ sign _head-babbing with each heartbeat (law Se) Muller's sign systolic pulsations of the uvula Quincke’s pulses subungual capillary pulsations (low Sp) Diagnostic studies + ECG: can see LVH, LAD, abni repol; CXR: cardiomegaly + ascending Ao dilatation