MGH Housestaff Manual 2023-2024 PDF

Housestaff Manual July 2023 - June 2024 Department of Medicine Massachusetts General Hospital Harvard Medical School Boston, MA Editors Hannah Abrams, MD Alexandra Doms, MD MGH Housestaff Manual Preface It is an honor to present the 29th Edition of the MGH Department of Medicine Housestaff Manu...

Housestaff Manual July 2023 - June 2024 Department of Medicine Massachusetts General Hospital Harvard Medical School Boston, MA Editors Hannah Abrams, MD Alexandra Doms, MD MGH Housestaff Manual Preface It is an honor to present the 29th Edition of the MGH Department of Medicine Housestaff Manual. We submit this manual, which we view as a great tradition of the Internal Medicine Residency Program, to function as a resource for medical residents and other clinicians at MGH. We hope that it exemplifies the energy, compassion, and spirit of growth with which MGH medical residents approach their training and their profession. The Housestaff Manual includes lessons from our clinical experiences on the medical services, updated society guidelines, and review of the most recent literature. Each year, this book reflects the diligent work of the residents whose contributions join them with past generations of house officers. We extend our gratitude to those residents who contributed their time and expertise to edit entire sections of this manual: Cardiology: Aditya Achanta, Dolphurs Hayes & Will Pohlman Pulmonology & Critical Care: Danielle Crabtree & Kyle Saysana Gastroenterology: Kelly Buchanan, Gregory Fricker, & Rachael Mahle Nephrology: Audrey Carr & Giovana Jaen Infectious Disease: Matthew A. Adan & Christopher Radcliffe Hematology: Justin Cheung & Andrew Song Oncology: Paige Herman & Kevin Miller Geriatrics & Palliative Care: Allison Zhong Rheumatology: Jennie Hanberg Endocrinology: Devanshi Dove & Lauren Maldonado Allergy & Immunology: Marissa Savoie Neurology: Abigail Healy & Rachel Muster Psychiatry: Daniel Harris Primary Care: Rachael Carricaburu & Esdras Rodriguez Consultants: Hannah Abrams & Alexandra Doms Radiology: Rachel Grenier & Eric Tung Procedures: Max Quinn & Rupali Sood Logistics: Hannah Abrams & Alexandra Doms We would like to thank the many faculty, fellows, and administrators who assisted with production of this book. In addition, we are grateful to the residents in the ENT, General Surgery, Neurology, Ophthalmology, OBGYN, Radiology, and Urology programs who lent their expertise to the relevant sections. Our work would not be possible without the countless hours of work by the previous editors of the MGH Department of Medicine Housestaff Manual. We hope we have lived up to their example. 1994 1995 1996 1998 2000 2001 2003 2004 2005 2006 2007 2008 2009 2010 Albert Shaw & Ravi Thadhani Barry Kitch Sam Hahn Marc Sabatine Sherri-Ann Burnett & Bill Lester Jose Florez Andrew Yee Ishir Bhan Aaron Baggish & Yi-Bin Chen Bobby Yeh & Eugene Rhee Rajeev Malhotra Maha Farhat & W. Steve Sigler David Dudzinski & Elizabeth Guancial Roby Bhattacharya & Paul Cremer 2011 2012 2013 2014 2015 2016 2017 2018 2019 2020 2021 2022 2023 Kerry Massman & Vilas Patwardhan Michelle Long & Mihir Parikh Molly Paras & David Sallman Zaven Sargsyan & George Anesi Ang Li & Jehan Alladina Nino Mihatov & Tessa Steel Michael Abers & C. Charles Jain Kelsey Lau-Min & Jonathan Salik Melissa Lumish & Shilpa Sharma Jacqueline Henson & Alexandra Wick Leslie Chang & Daniel Gromer Mitu Bhattatiry & Sirus Jesudasen Hannah Abrams & Alexandra Doms None of this would be possible without the support of the Department of Medicine. We extend special thanks to Gabby Mills, Libby Cunningham, Rachel Peabody, and Paula Prout. We also thank our Chief Residents – Bobby Arao, Radhika Jain, Jessie Logeman, and Sarah Street – as well as Jay Vyas and Joshua Metlay for their devotion to the housestaff and our education. It has been an incredible honor to edit the Housestaff Manual. We look forward to the contributions of future generations of authors and editors in the years to come. Hannah Abrams, MD & Alexandra Doms, MD Department of Medicine, Massachusetts General Hospital June 2023 As with any other medical reference, this manual is not intended to provide specific clinical care decisions in any individual case and should not substitute for clinical judgment. Please continue to consult your colleagues and supervisors, as well as the primary literature, whenever possible. We hope to provide guidance in the form of peer education and a forum for future experts to share their knowledge and hone their teaching craft for the benefit of their colleagues. We encourage you to use the manual, not only as a quick reference, but also as a teaching tool, a source of relevant publications, and a jumping-off point for personal exploration. Although we have reviewed every page, errors may exist. Please inform next year’s editors here to ensure these errors are corrected. MGH Housestaff Manual CARDIOLOGY ACLS: Cardiac Arrest & TTM ACLS: Bradycardia ACLS: Tachycardia ACLS: Defibrillation/Cardioversion/Pacing EKG Interpretation Narrow Complex Tachycardia Wide Complex Tachycardia Atrial Fibrillation & Flutter QTc Prolongation Chest Pain Acute Coronary Syndrome MI Complications Cardiac Catheterization Non-Invasive Cardiac Testing Echocardiography Heart Failure Right Ventricular Failure Mechanical Circulatory Support Pulmonary Artery Catheterization Cardiac Devices: PPM, ICD, & CRT Valvular Heart Disease Pericardial Disease Aortic Disease Syncope Severe Asymptomatic HTN & Emergency Peripheral Artery Disease Cardio-Oncology Outpatient CV Health Anti-Arrhythmic Medications Telemetry & Physical Exam PULMONOLOGY & CRITICAL CARE Respiratory Distress Hypoxemia & Hypercapnia Noninvasive Oxygenation/Ventilation Interpretation of Chest Imaging PFTs & Asthma COPD Bronchiectasis & Hemoptysis Interstitial Lung Disease VTE Diagnostics VTE Management Pulmonary Hypertension Mechanical Ventilation ARDS ECMO Sedation Shock Sepsis Vasopressors Toxicology Lung Transplant GASTROENTEROLOGY Upper GI Bleeding Lower GI Bleeding Abdominal Pain GERD & Peptic Ulcer Disease Nausea & Vomiting Diarrhea Constipation, IBS, & Colonic Disorders Esophageal & Upper GI Disorders Inflammatory Bowel Disease Intestinal Disorders Nutrition & Feeding Weight & Weight Loss Pancreatitis & Pancreatic Masses Liver Chemistry Tests Biliary Disease Acute Liver Injury & Failure Viral Hepatitis Alcohol-Related Liver Disease NAFLD End Stage Liver Disease Hepatorenal Syndrome Liver Transplant NEPHROLOGY Acute Kidney Injury 1 3 4 5 6 8 9 10 12 13 14 16 18 19 21 22 25 26 27 28 29 31 32 34 35 36 37 38 41 42 43 44 45 46 47 48 49 50 51 52 53 54 56 58 59 60 61 63 64 65 66 67 68 69 70 71 72 74 75 77 78 79 80 81 82 83 84 85 86 87 91 92 93 Glomerular Disease Chronic Kidney Disease Dialysis & Transplant Advanced Diuresis Acid-Base Disorders Sodium Disorders Potassium Disorders Magnesium & Phosphorus Disorders IV Fluids & Electrolyte Repletion Urinalysis & Nephrolithiasis INFECTIOUS DISEASE Empiric Antibiotics Multidrug Resistant Organisms Community Acquired Pneumonia HAP/VAP & Aspiration Pneumonia Viral Respiratory & Head & Neck Infections Urinary Tract Infections Skin & Soft Tissue Infections Osteomyelitis Bloodstream Infections & Endocarditis Meningitis & Encephalitis C. Difficile Infection Invasive Fungal Infections Tuberculosis HIV/AIDS & Opportunistic Infections Transplant ID STIs & Travel Medicine Tick-Borne Diseases Mpox & Ectoparasites Fever of Unknown Origin Rare Diseases at MGH Infection Control Antimicrobial Dosing HEMATOLOGY Pancytopenia & Anemia Sickle Cell Disease Thrombocytopenia Eosinophilia Coagulation Disorders Anticoagulation Agents Anticoagulation Management Transfusion Medicine Transfusion Reactions Peripheral Smear Interpretation ONCOLOGY Acute Leukemia Lymphadenopathy & Lymphoma Plasma Cell Disorders MDS & MPN Hematopoietic Stem Cell Transplantation CAR T cell Therapy Solid Organ Malignancies Immune Checkpoint Inhibitors Oncologic Emergencies Febrile Neutropenia Inpatient Leukemia & Lymphoma Regimens GERIATRICS & PALLIATIVE CARE Pain Management Adv Care Planning & Code Status Death & Pronouncement End of Life Care & Hospice Frailty & Polypharmacy Geriatric Assessment & Elder Abuse RHEUMATOLOGY Approach to Rheumatologic Disease Arthritis Connective Tissue Diseases Vasculitis Miscellaneous Rheumatologic Diseases Autoantibodies Rheumatologic Medications ENDOCRINOLOGY Outpatient Type 2 Diabetes Mellitus Inpatient Diabetes Mellitus Management DKA/HHS Adrenal Insufficiency Pituitary Disorders 95 96 97 98 99 101 102 103 104 105 106 108 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125 126 127 128 129 131 132 133 134 135 136 137 139 140 141 143 144 145 146 149 150 152 153 154 155 157 159 161 162 163 164 165 166 168 169 171 172 173 174 176 177 178 179 Table of Contents Calcium Disorders Osteoporosis & Vitamin D Thyroid Disorders Male Hypogonadism ALLERGY & IMMUNOLOGY Drug & Contrast Allergy Angioedema & Anaphylaxis Mast Cell Disorders Primary Immunodeficiency NEUROLOGY Altered Mental Status Delirium Dementia Headache & Vertigo Stroke & TIA CNS Emergencies Seizures Weakness & Neuromuscular Disease Neuroprognostication PSYCHIATRY Consent & Capacity Agitation Psychosis Catatonia, NMS, & Serotonin Syndrome Depression Anxiety Disorders Alcohol Use Disorder & Withdrawal Opioid Use Disorder & Withdrawal Other Substance Use Drug Testing PRIMARY CARE Health Screening & Maintenance Transgender Health Women’s Health Men’s Health Sleep Medicine HEENT Concerns Nodules Musculoskeletal Pain Immigrant & Refugee Health Climate Change & Health Health Equity & Insurance CONSULTANTS Calling Consults Perioperative Medicine Dermatology Surgery Urology ENT Ophthalmology OB/GYN RADIOLOGY Radiology Basics Contrast Protocols Interpretation of Common Studies PROCEDURES Ultrasound Basics Ultrasound-Guided Peripheral IV Central Line Arterial Line Intraosseous Line Paracentesis Lumbar Puncture Thoracentesis Pericardial Drain Fluid Analysis Tube Management Exposures & Needle Sticks LOGISTICS Monitoring & Prophylaxis Peri-Procedural Anticoagulation Senior On Encounters Post-Acute Care Microaggressions/Bias, Patient-Directed Discharge, ICE MGH Directory 180 181 182 183 184 186 187 188 189 190 191 192 193 195 196 197 198 199 200 201 202 203 204 205 207 208 209 210 212 213 216 217 218 220 221 223 224 225 226 227 229 232 233 234 235 236 237 238 239 241 243 245 246 248 249 250 251 252 253 254 255 258 259 260 261 262 263 264 TOC ACLS: Cardiac Arrest & TTM Cardiology UNRESPONSIVE PATIENT Check circulation (pulse), airway and breathing (C-A-B) No definite pulse within 10 sec. MGH CODE ROLES - Code leader: Senior On - Code Whisperer: AM = Consult SAR PM = Units NT - Pulse: SDU JAR - Compressions: Interns - Bring Lucas: MICU intern - Bring IO: nursing sups QUICK GUIDE: DOSING - DEFIB: Biphasic (MGH) vs. Mono (360J), if unknown, use max setting. repeat shocks @ same or ↑dose - AMIODARONE: 1st dose = 300 mg, 2nd dose = 150 mg - LIDOCAINE: 1st dose: 1-1.5 mg/kg, 2nd dose: 0.5-0.75mg/kg - MGSO4: if TdP 1-2g over 15m - HYPERKALEMIA: Ca gluc 12g IV (or CaCl2), bicarb 1-2 amp IV, D50W 1-2 amp, insulin 10u IV - NALOXONE: minimum 2 mg IV if pulseless, if apneic but has pulse, 0.2-1 mg IV START CARDIOPULMONARY RESUSCITATION start compressions CODE TASKS Access (IV>>IO), Airway Backboard Code status Defibrillator, Drips ECMO/Embolus Early: o page <10min of coding o Consider tPA (takes 30 min to prepare) - Family (call HCP) - Run tele + meds - PEA / Asystole Maternal Code Blue Algorithm: AHA 2020 ACLS 2022 Guidelines: Circ 2022 Evidence Evaluation: ILCOR 2020, COsTR 2020 (comprehensive literature reviews) Call CODE BLUE (x6-3333, blue button on wall) Call for defibrillator, backboard, ambu bag Monitoring: tele, defib pads, cont O2, BP cuff Compress 2-2.4” deep, 100-120BPM, minimize interruptions & allow full recoil Without ETT: 30:2 compressions to mask vent With ETT:  compressors q2min, breaths q6-8s Rhythm check as soon as pads are on for both witnessed and unwitnessed arrest REVERSIBLE CAUSES (H&Ts) VT / VF SHOCK! Biphasic 120-200J (MGH) EPI 1mg q3-5m NO pulse continue CPR PULSE / RHYTHM CHECK q2 minutes Return of spontaneous circulation (ROSC) criteria: (1) Pulse + BP (2) Sustained ETCO2 > 40 (3) Spontaneous waves on a-line EPI 1mg q3-5m +/- AMIO, LIDO MgSO4 - Go to post-arrest care/TTM evaluation - Hypovolemia Hemorrhage Hypoxia H+ ion (acidosis) Hypokalemia, hyperkalemia Hypothermia Thrombosis, coronary (ACS) & pulmonary (PE) Tension pneumothorax Tamponade (cardiac) Toxins (drugs, accidents) MATERNAL CODE: ABCDEFGH ACLS LOGISTICS & UPDATES - ACCESS: try IV first, IO if necessary or IV not feasible; c/f reduced drug delivery esp with pre-tibial placement (AHA 2020 ACLS) - STAT LABS: ABG with K & Hgb, CBC, BMP, LFTs, lactate, T&S, coags, fibrinogen, cardiac enzyme - MONITORING: recommend wave capnography during CPR, keep ETCO2 at least >10mm H20, ideally >20 - PROGNOSTICATION: ETCO2 <10 mmHg in intubated pts after 20min CPR ~90% sensitive for no ROSC - PREGNANT WOMEN: Apply left lateral uterine displacement, IVs above diaphragm, if recieving IV Mg, stop and give CaCl or Ca gluc, prep for perimortem delivery early, suggest delivery if no ROSC within 5min, TTM should still be considered with ROSC - VSE PROTOCOL: vasopressin 20U with first 5 doses of epi + hydrocortisone 200mg x1; not currently used at MGH Thrombolysis for Known or Suspected PE During Code • Alteplase (tPA) - Pulseless: 50mg IV/IO bolus over 2min, may repeat 50mg IV/IO in 15min - Pulse present: 100mg infusion over 2h • Reteplase: 10U IV, may repeat 10U in 30min • Contraindications (absolute): prior ICH at any time, ischemic CVA or head trauma within 3mo, known intracranial neoplasm or AVM, suspected aortic dissection or active bleeding • Will need anticoagulation after lysis for compensatory up-regulation of pro-coagulant factors. ASA 325mg + UFH or LMWH. If already on UFH gtt, d/c infusion and restart without bolus after lysis (if PTT<100). If not on UFH, start with bolus • Must continue cardiac arrest protocol for at least 15 min after tPA infusion to give time to work Smrithi Sukumar ECMO for Cardiac Arrest • At MGH, recommended to contact ECMO team <10 minutes from code initiation. • STAT page “ECMO Consult MGH” or use “MGH STAT” app to call consult and for MGH ECMO guidelines • No RCTs, all data observational Circ 2019;S881-894; Intensive Care Med 2016;42:1922 • See ECMO 1 TOC ACLS: Cardiac Arrest & TTM Cardiology Initial Post-ROSC Stabilization Oxygenation: maintain SpO2 92-98% Ventilation: maintain ETC02 35-40 - ETT: start with set RR 10 Avoid hypotension: MAP >65 - IV fluid boluses - Start vasopressor infusion: code meds will wear off! o Epi 0.1-0.5 mcg/kg/min o Norepi 0.1-0.5 mcg/kg/min o Dopamine 2-10 mcg/kg/min Evaluate for Reversible Causes - Obtain 12-lead EKG - Consider other reversible H&Ts Consider Targeted Temp Mgmt (TTM) Neuroprognostication Is patient able to follow commands? Multimodal eval at minimum of 72h, off of sedating meds No Consider emergent coronary angiography (Hypothermia not a contraindication for PCI (Resusc 2010;81:398) - Page Stroke/ICU Neuro (p20202) - See TTM below - Preparation: NCHCT, CVC, arterial line After 24h: can consider MRI, N20 SSEP 24-48h  ?status myoclonus (+EEG), serum NSE eval >72h: can evaluate pupillary light reflex, quant pupillometry, corneal reflex T A R G E T E D T E M P E R A T U R E M A N A G E M E N T A F T E R C A R D I A C A R R E S T (Circ 2020;S266-468) Rationale: Hyperthermia/fever is associated with worse neurological outcomes and neuronal damage due to inflammatory changes and biochemical cascades that develop following ischemia and reperfusion injury associated with cardiac arrest (Arch Intern Med 2001). Goal is to avoid fevers and to be aggressive about diagnosing/treating infections. Causes of fever: Infection (high risk of aspiration/pneumonia, global ischemia -> gut ischemia -> bacterial translocation). Pan-culture and consider aggressive antibiotic treatment. Drug fever *Importantly*: Previously low-quality data; many new trials and evolving MGH guidelines. After ROSC discuss with ICU attending and consult neuro to discuss TTM plan (hypothermia at 33°C vs normothermia at 36°C) TTM options if patient is not following commands (patient needs to be stable enough to wean sedation and paralysis for this exam): • Hypothermia (33°C) o European and American society guidelines recommend (Circ 2020:142:S366) (Int Care Med 2015:41:2039) o Improves neurologic outcomes (NNT 6) & survival to discharge (OR 5.25) following out-of-hospital cardiac arrest from VF, pulseless VT, or PEA/asystole of presumed cardiac cause (NEJM 2002;346:549; NEJM 2002;346:557; NEJM 2013;369:2197; Circ 2015;132;2146; NEJM 2019;381:2327) o Unclear if benefit is from hypothermia or avoidance of hyperthermia • Normothermia (36°C) o TTM2 Trial: no difference in mortality or functional outcome at 6 months for out of hospital cardiac arrest w/ hypothermia vs normothermia, more hemodynamically significant arrythmias in hypothermia arm (NEJM 2021;284:2283) o Since TTM2, MGH protocol has changed so patients admitted after out of hospital cardiac arrest will be started on the normothermia protocol in the Emergency Room (see Ellucid) o Normothermia helps avoid use of paralytics and lower required sedation, but some patients may still require medication to avoid shivering Methods of temperature control: Foley catheter temperature monitoring, cold saline injection, external cooling device (Arctic Sun), shivering management (Mg, acetaminophen, meperidine, buspirone, dexmedetomidine, dantrolene, paralysis) Duration of TTM: Multiple considerations including age of patient, existing neurologic damage, risk of infection, etc. Discuss with ICU attending and neuro about duration of TTM and rate of temperature change (NEJM 2022) • Normothermia: per Ellucid, 36°C for 24 hours then 37°C for at least 48 hours • Hypothermia: per Ellucid, 33°C for 24 hours, then rewarm at rate of 0.25°C per hour and maintain at 36°C for 48 hours Neuro-prognostication see Neurology - Neuroprognostication section Smrithi Sukumar 2 TOC Cardiology ACLS: Bradycardia Bradycardia with Pulse Bradycardia Diagnostic Algorithm HR<60 bpm and symptomatic Circ 2020 Evidence Review | ACC/AHA Brady 2018 ASSESS PATIENT • Focused exam  vitals, mental status, pupils, pulmonary edema, murmurs, warm/cold, other sx • Review recent ECG, tele & labs, current meds, recent dose changes • Obtain 12-Lead ECG, have pacing pads available • IV Access: BMP, Mg, lactate ± trop • Monitor BP freq., keep O2 > 94%, maintain airway IF PATIENT IS UNSTABLE: Any of the following present? o Hypotension/shock o Altered mental status o Ischemic chest discomfort o Acute heart failure/pulmonary edema Trial medications, low threshold to pace If pulseless arrest develops → ACLS PEA/Asystole ATROPINE* 1mg bolus | q3-5mins (max 3g); 2hr half-life * less effective s/p heart transplant, avoid with AV block Mobitz II or CHB DOPAMINE IV infusion 5-20mcg/kg/min OR EPINEPHRINE IV infusion 2-10mcg/min & ANTIDOTES BY CAUSE Are P waves present? Yes Regular P-P interval? Yes TRANSVENOUS PACING WIRE - Wire placed by cardiology - Indications: 1) need for transcutaneous pacing despite meds, 2) unstable rhythm with no quickly reversible cause *Wide QRS 1. Sinus arrest w/ junctional escape 2. Sinus arrest w/ ventricular escape [idioventricular]* 3. A fib/flutter w/ slow/variable conduction No Regular P-R interval? Yes 1. Sinus pause/sinus arrhythmia 2. Wandering pacemaker 2. Non-conducting PACs No 1. Sinus bradycardia (# of P = # of QRS) 2. Mobitz II (# of P > # of QRS) TRANSCUTANEOUS PACING - See pacing page for details - Basics: Emergent 2mg lorazepam + 2mg dilaudid OR RICU for fentanyl/midazolam +/intubate  turn to PACER  SET RATE: 100 BPM + SET OUTPUT: 100 mA  turn output down to minimum needed to capture  adjust rate down No 1. Mobitz I (# of P > # of QRS) 2. CHB w/ junctional escape OR ventricular escape* (P unrelated to QRS) RHYTHM PEARLS - If grouped beats  look for Mobitz I & II - In 2nd degree AV block with 2:1 conduction, it is not possible to differentiate Mobitz I vs. Mobitz II - Always remember to consider hyperkalemia! ETIOLOGIES OF SINUS BRADYCARDIA Bold also considered in CHB - Meds, esp. in liver, renal dz - SSS, degenerative, calcific conduction system dz - Elderly - Hypoxia - Inc. vagal tone - Elevated ICP - Hypothermia - Carotid dz + recent stent - Infiltrative dz - Hypothyroidism - Nocturnal - Athlete - Ischemia/ACS (inferior MI, esp. 2/2 AV nodal artery lesion) - Endocarditis, - Lyme carditis, myocarditis - Pericarditis - Hyperkalemia IF PATIENT IS STABLE: Monitor + Assess for reversible causes - Mobitz II & CHB with wide QRS  always gets pacing wire even if stable, call cards + ensure prepared to pace - HOLD nodal blockers/anti-HTN if applicable ATROPINE & AV BLOCKS Take-home message: Atropine will not help in the setting of CHB and Mobitz II o Ineffective for blocks below AV node (response to atropine in pt with AVB; Resuscitation 1999;41:47) o Potential worsening of Mobitz II 2/2 HR (Am J Card 1974;33:333) Tom Sommers Specific Antidotes by Cause - Beta blocker: glucagon 3-10mg IV (if no response, repeat bolus, if response, infusion at 3-5mg/h) - Calcium channel blocker: glucagon as above, calcium gluconate 3-6g q10-20min or gtt, insulin 1U/kg bolus with 0.5U/kg gtt - Digoxin: dig immune FAB vial, 1 vial binds ~ 0.5mg digoxin, administer over 30min - Opioids: naloxone 0.4-0.8mg IV, consider gtt - Organophosphate: atropine 2-5mg IV (double dose q5min until effect), pralidoxime 1-2g IV over 15-30min 3 TOC Cardiology ACLS: Tachycardia Tachycardia with Pulse HR>100 bpm and symptomatic ACLS Guidelines 2021 ASSESS PATIENT • Focused exam  vitals, MS, pulmonary edema, murmurs, warm/cold, pupils, other sx • Review: most recent ECG, tele, labs, meds, events • Obtain: 12-Lead ECG, Defib + pads • IV Access: BMP, Mg, lactate ± trop if c/f ischemia • Monitor BP frequently • O2: supplement to >94%, maintain airway IS THE PATIENT UNSTABLE? Any of the following present? o Hypotension / shock o Altered mental status o Ischemic chest discomfort o Acute heart failure / pulmonary edema NO ACUTE DRUG DOSING • Adenosine: 6mg rapid IV push (followed by NS flush) + arm raise, can repeat x1  12mg if required, central line = ½ peripheral dose, relative contraindication in pts s/p heart transplant • Amiodarone: 150mg IV over 10min (may repeat x1); then infusion at 1mg/min x6h followed by 0.5mg/min x18h (max 2.2g/24h) • Diltiazem: 0.25mg/kg IV bolus over 2min  gtt @ 5-10mg/h • Lidocaine: 1.0-1.5mg/kg IV bolus (usually 100mg), refractory  repeat 0.5-0.75mg/kg IV push q5-10min PRN, max 3mg/kg  maintenance infusion at 1-4mg/min; preferred agent if QTc • Metoprolol: 2.5-5 mg over 2 min; repeat q5 min; max dose 15 mg • Procainamide: 20-50mg/min or 100mg q5min until any of the following: arrythmia terminates, BP, QRS prolongs by 50% from baseline, or total 17mg/kg given  maintenance infusion at 1-4mg/min (adjusted for CrCl), avoid with QTc • Sotalol: 1-1.5mg/kg IV over 5 min; then maintenance infusion at 10mg/min, contraindicated with QTc & caution in pts w/ ↓EF YES Analgesia (1-2mg dilaudid)+ sedation (2 mg lorazepam) If narrow & regular, can trial adenosine SYNCHRONIZED CARDIOVERSION VS. DEFIBRILLATION Rhythm Narrow & Regular Narrow & Irregular Wide & Regular Wide & Irregular Mode Sync Sync Sync Defib Dose (J) * 50-100 120-200 100 120-200 *Biphasic (MGH) MEDICATIONS DETERMINE QRS WIDTH (> or <120 ms) & REGULARITY NARROW & REGULAR NARROW & IRREGULAR WIDE & REGULAR WIDE & IRREGULAR Vagal Maneuvers IV BB or Dilt** Amiodarone (OK for VT or SVT) Lido + 2g Mg (over 15min) & treat myocardial ischemia Adenosine* IV BB or Dilt** Amio/Procainamide *avoid post OHT **avoid if HFrEF DDx: ST, AT, orthodromic AVRT, AVNRT, Aflutter If difficult to discern P waves, adenosine can slow rate to differentiate If persists Amiodarone (rhythm)* Digoxin (rate) *possible cardioversion, consider AC status **avoid if HFrEF DDx: AF + RVR, MAT, Aflutter/AT + variable block, ST + freq PACs Consider chronicity/AC status prior to giving rhythm control to Afib/Aflutter EF >40%: Lidocaine, Sotalol, Procainamide, Metoprolol EF <40%: Lidocaine -----------Suspect SVT+ conduction abnl  can trial vagal + adenosine (will not worsen VT) DDx: monomorphic VT, SVT with aberrant conduction, antidromic AVRT, preexcitation, meds & electrolyte abnormality  b/l QTc nml b/l QTc Torsades (TdP) Non-TdP Mg gtt & HR 2nd line = (dopa, overdrive Amio, pacing, procainamide isoproterenol) -----------Pre-Excited SVT  Procainamide (nodal agents contraindicated) DDx: PMVT (TdP & non-TdP), AFib/Aflutter/AT + pre-excitation vs aberrancy Lido generally safe  effective for all PMVT and will not worsen pre-excited rhythms VAGAL MANEUVERS: - Unilateral Carotid Massage: supine with neck extended  steady pressure to carotid sinus (inferior to angle of the mandible at level of thyroid cartilage near carotid pulse), avoid if prior TIA/CVA in past 3mo, and those with carotid bruits; 5%-33% success - Modified Valsalva Maneuver: semi-recumbent  blow forcefully into a 10cc syringe x10-15 seconds  reposition to supine and passively raise legs at 45° for 15 seconds; 43% effective in breaking SVTs vs 17% with standard Valsalva (Lancet 2015;386:1747) - Also consider: cold ice face immersion or ice-water bag to face (diving reflex, more effective in children); 17% success. Will Pohlman 4 TOC Cardiology ACLS: Defibrillation/Cardioversion/Pacing EXTERNAL DEFIBRILLATION/CARDIOVERSION/TRANSCUTANEOUS PACING • • • About the device: the Zoll R Series is on all code carts & ICUs at MGH. This device allows for external defibrillation, cardioversion, and pacing with additional benefits (e.g. display ET-CO2, CPR quality feedback, & upload rhythm strips into Epic) Additional supplies/resources: Ambu bag, intubation equipment, RICU staff, backboard, suction Medications: use procedural sedation (typically 50mcg fentanyl  2mg midazolam) when possible, requires Cardiac Anesthesia/RICU. In emergent situations, Dilaudid 1-2mg  lorazepam 2mg are reasonable alternatives (often readily available). DISPLAY/OPERATION OF ZOLL R SERIES • Remove all clothing covering the patient’s chest. Dry chest if necessary. If the patient has excessive chest hair, shave it to ensure proper adhesion of the electrodes. Can rip off hair with extra set of pads if razor not readily available in acute situations. • Attach hands-free therapy electrodes in anteroapical position (pictured) or anteroposterior position Pearls: • CPR ok to perform while pacing, take R-sided pulses (L not reliable) • Failure to capture? Increase output, ensure pads are in correct location, consider ddx (barrel chest, COPD, tamponade/pericardial effusion, acidosis, hyperK, obesity, MI, cardiac drug tox [dig, anti-arrhythmic]) • Failure to sense? Only happens with synchronous pacing – can switch to asynchronous pacing, reposition pads Manual Defibrillation Indications: pulseless VT or VF Synchronized Cardioversion Indications: Unstable SVT or VT Transcutaneous Pacing Indications: Unstable bradycardia FIRST turn the Selector Switch to ON. Then press Manual (bottom left soft key) to change to ALS 1. Default energy selection is 120 J. Initial dose 120-200 J. Use Energy Select (UP) & (DOWN) arrow keys to change the energy. 2. If there is a shockable rhythm on the pulse/rhythm check, press Charge. Continue CPR while charging. 3. Once charged, the red shock button illuminates. Shout “Clear!” then press and hold the illuminated Shock button at the top right of the console. 4. Resume CPR for 2 minutes before the next pulse/rhythm check 1. Select the desired energy using the up and down arrow keys on the front panel • Narrow, regular: 50-100 J (atrial flutter often converts with 50 J) • Narrow, irregular: 120-200 J (atrial fibrillation typically requires 150 J) • Wide, regular: 100 J • Wide, irregular: 150-200 J (defib dose) 2. Press the Sync On/Off button • Confirm that a Sync marker () appears on the monitor above each detected Rwave to indicate where discharge will occur • If necessary, use the LEAD and SIZE buttons to establish settings that yield the best display 3. Press the CHARGE button on the front panel. Ensure patient is “clear” 4. Press and hold the illuminated SHOCK button on the front panel. The defibrillator will discharge with the next detected R wave 5. If additional shocks are necessary, increase the energy level as needed • Confirm that a Sync marker () appears above each R-wave; you may need to press Sync between shocks 1. PACER appears as an option on the Selector Switch. Turn to PACER 2. Set the PACER RATE (BPM) to a value 20 bpm higher than the patient’s intrinsic heart rate. If unknown or absent intrinsic rate, use 100 bpm • Observe the pacing stimulus marker on the display and verify that it is well-positioned in diastole 3. Increase PACER OUTPUT (mA) until the paced beats demonstrate capture (“threshold”); the output value is displayed on the screen. • Capture = widened QRS complex + loss of underlying intrinsic rhythm 4. Set the PACER OUTPUT to the lowest setting that maintains consistent capture • Usually ~10% above threshold (typical threshold: ~40-80 mA) • Pressing and holding the 4:1 button temporarily withholds pacing stimuli, thereby allowing you to observe pt’s underlying EKG rhythm & morphology • Treat underlying cause and/or pursue transvenous/permanent pacing Will Pohlman 5 TOC Cardiology EKG Interpretation Approach all EKGs systematically. Note rate, rhythm, QRS axis, intervals, complexes, chambers, ischemia/infarction. Compare with prior EKG. R A T E (atrial, ventricular) • • • If rhythm regular, use the counting method (300 / #large boxes) If rhythm irregular, count R waves on rhythm strip, multiply x 6 (printout = 10 sec) Normal 60-100bpm; <60 = bradycardia, >100 = tachycardia 1 small box = 40 ms R H Y T H M (regular or irregular; sinus vs non-sinus) • • • • Sinus rhythm = P before every QRS and QRS following every P, regular w/ rate 60-100, P wave upright in I, II, aVF, V5-V6 P waves/morphology: determine 1) if P wave is present (best leads to visualize P wave are II and V1), 2) atrial rate (100-180: sinus tachycardia; 140-220: atrial tachycardia, AVNRT, AVRT; 260-320: atrial flutter), and 3) axis (e.g., P wave upright in II, biphasic in V1) QRS morphology: narrow (<120 ms) = supraventricular origin; wide (>120 ms) = aberrant supraventricular conduction or ventricular origin P wave/QRS complex association: if not 1:1, determine if number of P>QRS (AV block) or P<QRS (AV node, His-Purkinje, or ventricular rhythm). If P precedes QRS, evaluate PR interval. If P after QRS, evaluate RP interval. Determine if PR or RP interval is fixed or variable o AVB: first degree (PR >200ms); second degree Mobitz I/Wenckebach (PR progressively longer until dropped QRS); second degree Mobitz type II (sudden dropped QRS without PR lengthening); third degree (dissociation of P and QRS) Q R S A X I S (use direction of QRS complex) Axis Deviation Normal (-30 to +90º) Lead I ⊕ Lead II ⊕ Lead aVF ⊕/- Leftward (-30 to -90º) ⊕ - - Differential Diagnosis Normal variant, mechanical shifts, LVH, LBBB, LAFB, congenital heart disease, emphysema, hyperK, ventricular ectopic rhythms, WPW, inferior MI Normal variant, mechanical shifts, RVH, LPFB, Rightward dextrocardia, ventricular ectopic rhythms, WPW, ⊕ ⊕ (+90 to +180º) lateral MI (RBBB rarely causes RAD) Extreme/Northwest Lead transposition, ventricular ectopic rhythms, (180 to -90º) hyperK, artificial pacing, severe RVH • Clockwise/counterclockwise rotation (“R wave progression”): R wave amplitude typically increases from V1 to V5, amplitude of R becomes greater than S at V3 or V4. Early or late R wave progression is nonspecific and can be normal (Am Heart J 2004;148:80) o CCW (“early R wave progression”): R>S prior to V3. Causes: RVH, WPW, LAFB, posterior MI. o CW (“late R wave progression”): R>S after V4. Causes: cardiomyopathy, LVH, LBBB, anterior MI. • Low voltage: average QRS amplitude <5 mm in I, II, III and <10 mm in precordial leads o DDx: obesity, pericardial effusion, PTX, COPD, PE, restrictive or infiltrative CM (particularly amyloidosis), severe hypothyroidism, or anasarca C O M P L E X E S A N D I N T E R V A L S (Circ 2009;119:e241) • • • P wave: right and left atrial depolarization. Normal duration <120ms PR interval: atrial depolarization, AV node and His-Purkinje conduction. Normally 140-200ms, changes with rate (shortened at faster rates, longer at lower rates) d/t autonomic effects on AV nodal conduction QRS: ventricular depolarization. Normal duration 60-110ms, not influenced by HR. QRS 100-120ms = incomplete BBB or intraventricular conduction delay (IVCD). QRS >120ms = BBB, ventricular activation (PVC, VT, fusion beats, WPW, paced beats), hyperK, Na channel poisoning, aberrancy, hypothermia LBBB: QRS >120, wide negative QS RBBB: QRS >120, rSR’ in V1, wide LAFB: left axis deviation, QRS <120, qR in I, aVL and rS in II, in V1, wide tall R in I, aVL, V5, V6. qRS in V6, shallow broad S in I. III, aVF. Common, nonspecific Causes: primarily dilated Causes: infection (myocarditis), cardiomyopathy (ischemia, infection, infarction, increased RV pressure LPFB: right axis deviation, QRS <120, rS in I, aVL and qR in valvular, infiltrative). (PE, Cor Pulmonale), RHC. II, III, aVF. Rare to see in isolation, usually occurs with RBBB Bifascicular block: RBBB with either LAFB or LPFB • • • • ST segment: represents a time of electrical silence. See below T wave: ventricular repolarization, with a slow upstroke and a rapid return to the isoelectric line after peaking. Usually asymmetric and in the same direction as the QRS. Should have smooth contours (bumps in T are usually buried P waves) U wave: occurs in the same direction as the T wave, rate-dependent (shorter at faster rates); DDx: bradycardia, hypoK/Mg/Ca, hypothermia QT interval: ventricular depolarization and repolarization. Excludes U wave unless fused with T wave. Rate-dependent (shortened at faster rates). Normal <440ms (M) and <460ms (F). Reassuring if QT is less than half R-R interval with normal HR C H A M B E R E N L A R G E M E N T (Circ 2009;119:e251) all have low Sn and Sp • • • • LVH: Sokolow-Lyon criteria: S in V1 + R in V5 or V6 LAE ≥35mm OR R in aVL ≥11mm. Cornell criteria: S in V3 + R in aVL >28mm (M) or >20mm (F). For non-voltage based criteria consider Romhilt-Estes score RVH: R>S or R ≥7mm in V1, S ≥7mm in V5 or V6 LAE: P wave duration ≥120ms (>2.5mm), widely notched P (≥40ms), negative component of P in V1 >1mm wide and deep RAE: P wave height >2.5mm in II (“P-pulmonae”), initial positive P wave in V1/V2 ≥1.5mm David Iskhakov RAE 6 TOC Cardiology EKG Interpretation I S C H E M I A / I N F A R C T I O N (JACC 2009;53:1003) • • • • Analyze abnormalities along the vectors of ventricular depolarization and repolarization (QRS-ST-T) T wave abnormalities: hyperacute, symmetric T waves can be found within minutes, followed by T wave inversions (≥1mm in 2 contiguous leads). TWI normal if only in aVR, V1 or III. Isolated TWI in aVL may indicate mid-LAD lesion vs inferior MI (J Emerg Med 2014;46:165) o TWI DDx: myocardial ischemia (symmetric), prior MI, acute PE (RV strain pattern: TWI V1-V4, II, III, aVF, RBBB, S1Q3T3), intracranial pathology (“cerebral T waves”, asymmetric), myocarditis, pericarditis, BBB pattern, V-paced, LVH with “strain”, normal variant, digoxin effect o De Winter’s T waves: 2% of STEMIs present with tall, symmetric T waves + >1mm STD at J point in precordial leads + 0.5-1mm STE in aVR c/w acute LAD occlusion (NEJM 2008;359:2071) ST depression: suggests subendocardial injury, ≥0.5mm below the baseline (PR segment), measured 80ms after the J point in 2 contiguous leads o Downsloping or horizontal = more ominous. STD do not localize to territories (Circ Res 1998;82;957) o Always look for STE to rule out reciprocal STD. STD in V1-V3 can be posterior MI (check posterior leads) ST elevation: suggests transmural ischemia, ≥1mm in leads except for leads V2-V3 (≥2mm in M ≥40y and ≥1.5mm in F), use PR segment (isoelectric interval), measured at the J point. Differential diagnosis (NEJM 2003;349:2128; Annals 2004;141:858; NEJM 2004;351:2195): Diagnosis w/ STE Acute STEMI LVH LBBB Acute pericarditis Printzmetal’s angina/vasospasm Acute PE Stress-induced cardiomyopathy (Takotsubo’s) Ventricular aneurysm Early repolarization Brugada syndrome Male pattern Normal variant Cardioversion EKG Lead V1-V2 V5-V6 I, aVL II, III, aVF V7-V9 V4R aVR • • Characteristic ECG Findings STE in ≥2 contiguous leads in coronary distribution (see table), reciprocal STD Concave STE in V1-V3 with STD and TWI in I, aVL, V5-V6, voltage criteria as above Concave STE in V1-V3, discordant with negative QRS Diffuse STE (usually <5mm), PR depression, amplitude of STE:T wave (in mm) >0.26 is specific Transient STE in coronary distribution as in STEMI STE in inferior and anteroseptal leads, mimics acute MI, complete or incomplete RBBB Diffuse STE in precordial leads w/o reciprocal inferior STD, STE followed by deep TWI Persistent STE after MI, often with abnormal Q waves J point elevation ≥1mm in 2 contiguous leads (esp V4), amplitude of STE:T wave (in mm) <0.25 rSR’ and downsloping STE in V1-V2 (see below) 1-3mm concave STE, often highest in V2 STE in V3-V5, TWI, short QT, high QRS voltage Marked (often >10mm) and transient following DCCV Coronary Distribution Territory Coronary Vessel Anteroseptal Proximal-mid LAD Apical Distal LAD, Distal LCx, RCA Lateral LCx (proximal) Inferior RCA (85%), LCx Posterior LCx > RCA RV RCA, LCx L main or 3vD Modified Sgarbossa Criteria: To diagnose acute MI w/ LBBB (does not apply to pacers). Below = traditional version (need 3pts) • Concordant STE >1mm in any lead = 5 points • Discordant STE >5mm in any lead = 2 points • STD >1mm in V1-V3 = 3 points Q wave: usually a marker of scar, pathologic Q waves must be deep (>1mm), 25% height of QRS, and 40ms long. More likely 2/2 prior MI if inverted T wave in same lead. Small “septal” Q physiologic in V5, V6, I, aVL Wellens Type A Wellens Type B Wellens Syndrome: sign of critical proximal LM or LAD lesion, 75% MI in <2w. Often pain free with h/o angina. Normal/slightly elevated troponin. Type A: 25% biphasic (up then downsloping morphology) T waves in V2 and V3. Type B: 75% symmetric, deeply inverted precordial T waves. Isoelectric or minimally elevated (<1mm) ST segment. No precordial Q waves (Am J Emerg Med 2002;20:7; Am Heart J 1982;103:730) OTHER • • • Acute PE: 10-25% nml EKG, nonspecific: sinus tach (↑Sn), RBBB, RAD/LAD, TWI V1-V4, inferior STE; ↑Sp/↓Sn: S1Q3T3. High PPV when dx PE vs ACS: TWI in III+V1 (Am J Card 2007;99:817;Am J Emerg Med 2001;19:514) J-Point Elevation Syndromes: J point is when QRS transitions to ST segment o Early repolarization pattern: benign STE in absence of chest pain, terminal QRS slur, or terminal QRS notch  Suspicious features: FH of sudden cardiac arrest or early unexplained death, eval and workup suggestive of channelopathy, h/o unheralded syncope suggestive of arrhythmogenic pathogenesis (Circ 2016;133:1520) o Brugada Syndrome: autosomal dominant SCN5A loss Epsilon wave of function mutation in 10-30%, M>F, more common to have nocturnal cardiac arrest, p/w VT/VF or sudden cardiac death (Circ Arrhythm Electrophys 2012;5:606) o Osborn wave: hypothermia T<93ºF, elevation of J Brugada Syndrome: Type 1 point height ~ proportional to degree of hypothermia. More dome-shaped compared to Epsilon wave. o Epsilon wave: found in arrhythmogenic right ventricular cardiomyopathy (ARVC; inherited, age 10-50, fibro-fatty replacement of RV myocardium → ventricular arrhythmias [Circ 2005;112:3823]), most Sp in V1 (30% with ARVC), low frequency, positive terminal deflection in V1-V3 Electrolyte Abnormalities Abnormality Characteristic ECG Findings Hypokalemia Prolonged QT, ST depression, flattened T wave, prominent U wave Hyperkalemia Peaked, symmetric T wave → flat P → prolonged PR ± AVB → widened QRS ± BBB (severe) → sinusoidal Hypocalcemia Prolonged QT, unchanged T wave Hypercalcemia Shortened QT David Iskhakov 7 TOC Cardiology NARROW COMPLEX TACHYCARDIA (QRS <120MS) Narrow Complex Tachycardia (NEJM 2012;367:1438; Mayo Clin Proc 1995;70:371) Diagnostic approach & general principles: 1. Determine the width of the QRS complex 2. Determine if the rhythm is regular or irregular 3. Assess for the presence of p-waves (noting location, axis and morphology) 4. Compare to baseline ECG 5. Treatment (See ACLS: Tachycardia and Atrial Fibrillation/Flutter) • If unstable  synchronized cardioversion • If stable  vagal maneuvers (carotid massage/valsalva/ice water on face). Adenosine can resolve diagnostic dilemmas and treat AVNRT and AVRT (adenosine is blocked by theophylline/caffeine & potentiated by dipyridamole) • Acute treatment for all others is BB, CCB or amiodarone (use caution with pharmacologic cardioversion and consider ruling out intra-atrial clot if pt has been in Afib/flutter for > 48 hours and has not been anticoagulated for 3 weeks prior to cardioversion) Irregular, narrow complex tachycardias Regular, narrow complex tachycardias Sinus Tachycardia (rate >100, maximum HR = 220-age) Gradual onset Most important to determine underlying cause: hypovolemia, hemorrhage, withdrawal (EtOH, BZD, opiate, BB), intoxication, fever/infection, pain, hypoxemia, PE, anemia, tamponade, dissection, endo (hyperthyroidism, adrenal insufficiency, pheo) Ectopic Atrial Tachycardia (AT) (atrial rate 100-200) Due to abnormal automaticity at a singe atrial focus, other than the SA node or due to a reentrant circuit within the atria Discrete P waves present, but of abnormal morphology +/- axis (i.e. p wave inverted in Classic digoxin toxicity is AT w/ variable AVB Usually seen in otherwise normal hearts Junctional Tachycardia Due to increased automaticity within the AV node (or due to reentrant rhythms, e.g., AVNRT) P waves may be absent (e.g. buried within the QRS complex), inverted and or retrograde Atrioventricular Nodal Re-entrant Tachycardia (AVNRT) (rates 150–250) Arises from functional re-entry within AV node P wave, if visible, is retrograde (may be seen as a pseudo R-wave in lead V1, or pseudo S wave in lead II) – note that retrograde P waves appear earlier in AVNRT than in AVRT Short RP (when conducting fast-slow), however more commonly no RP (when conducting slow-fast) Trigger PAC (slow-fast) > PVC (fast-slow) Young adults, F>M, usually arises within structurally normal hearts Multifocal Atrial Tachycardia (MAT) (rate ~100-150) Discrete P waves present, of ≥3 morphologies Irregular due to varying PP, PR, and RR intervals Seen in COPD, pHTN, CAD, electrolyte disarray, aminophylline/ theophylline use Atrial Fibrillation (AF) No coordinated atrial activity (P wave absent), irregular, fibrillatory waves present Arises from numerous re-entrant tracts in atria or pulmonary veins If associated with pre-excitation, the result is an irregular, WCT Atrial Flutter (AFL) (P waves present at rate of 250-300) Arises from true (isthmus-dependent, typical) or functional (isthmus-independent, atypical) re-entry in R atrium May be regular (e.g. 2:1, 3:1, 4.1, etc.) or irregular (if variable AV block) Counterclockwise: negative flutter waves in II, III, aVF Clockwise: positive flutter waves in II, III, aVF No isoelectric baseline, atrial rate ~300, always >250, usually with 2:1 conduction but can have variable conduction AVRT Note: blue arrows = retrograde P waves Orthodromic Atrioventricular Re-entrant Tachycardia (AVRT) (rates usually 140-250) Ventricular depolarization occurs via the AV node, however an accessory tract allows for retrograde conduction to the atria (if ventricular depolarization occurs via the accessory tract, the resultant QRS is wide and is termed “anti-dromic, see WCT) Retrograde P waves may be present (if so, they appear later than those seen in AVNRT) Junctional Tachycardia Elliott Winford 8 TOC Cardiology WIDE COMPLEX TACHYCARDIA (QRS ≥120MS) Wide Complex Tachycardia Etiology • Ddx: VT (80%), SVT with aberrant conduction, and pacemaker-mediated tachycardia ECG Factors that Favor VT Very wide QRS (>160 msec) Superior axis (II, III, aVF neg) or northwest axis (I, aVF neg) AV dissociation (often V rate > A rate)  diagnostic of VT Concordance: all QRS across precordium completely positive or completely negative Partial (fusion beat) or complete (capture beat) depolarization of ventricle by underlying supraventricular rhythm R wave peak time ≥50msec (measured in lead II) Brugada criteria (Circ 1991;83:1649) (only applicable if rhythm is regular); Rwave peak time criteria (Heart Rhythm 2010;7:922); VT score (Europace 2016;18:578) • • • • • • • • • • • ECG Factors that Favor SVT with Aberrancy Pre-existing BBB  functional/ratedependent BBB d/t encroachment on bundle refractory period; RBBB > LBBB QRS with sharp initial deflection followed by broad terminal deflection Pre-excitation on baseline ECG  antidromic AVRT or pre-excited atrial fibrillation R wave peak time < 50msec (measured in lead II) Other important considerations: • Hyperkalemia, antiarrhythmic drugs (digoxin, class IA or IC, amiodarone), TCA overdose • Pacemaker-mediated/endless loop tachycardia: retrograde VA conduction of V-paced beat misidentified as native A-beat  Vpacing. ECG shows V pacing at upper rate limit • Sensor induced tachycardia: inappropriate sensing of nonphysiologic stimuli (vibrations, electrocautery, etc.) and pacing. MANAGEMENT • • • OF V T (also see ACLS: Tachycardia) Often no way to confidently distinguish VT or SVT with aberrancy. If there is any doubt, treat like VT Underlying processes: active ischemia, CAD with scar, electrolyte derangement (low K, low Mg), indwelling lines Check and replete lytes (K>4, Mg>2), think about ischemia Monomorphic VT DDx: ischemia, structural heart disease, idiopathic 1. Non-sustained VT (>3 complexes, <30 secs) Asymptomatic  monitor, treat underlying cardiac comorbidities (e.g., CAD, HF) Symptomatic  nodal blockade (BB>CCB), then AADs 2. Stable and sustained (>30 seconds)  antiarrhythmic agent (e.g. amiodarone) 3. Unstable  synchronized cardioversion (100J) if pulse; defibrillation if pulseless Polymorphic VT DDx: ischemia (acute, CAD, ICM) vs. prolonged QTc 1. Evaluate for ischemia & need for revascularization 2. Stable  magnesium 2-4g over 10-15min, HR above intrinsic rate (dopa, epi, iso, burst overdrive pacing), QTc (lido), avoid bradycardia (amio, CCB/BB) 3. Unstable  defibrillation Torsades de Pointes Polymorphic VT that occurs with underlying prolonged QTc (congenital or acquired). Can be prompted by PVC falling on T wave of previous beat (R on T phenomenon) VT Storm: multiple sustained episodes of unstable VT within 24 hours • Reduction of autonomic tone: intubation and sedation, stellate ganglion block/cardiac sympathetic denervation • Treatment of underlying ischemia: revascularization, IABP to improve coronary perfusion, reduce cardiac afterload • Anti-tachycardia pacing (ATP): overdrive pacing at a faster rate than VT • Amiodarone 150mg IV + gtt, co-administer propranolol 60mg q6h (superior to metoprolol [JACC 2018;71:1897]) • Catheter ablation (VANISH trial, NEJM 2016;375:111): in patients with ischemic CM and ICD w/ persistent VT, ablation superior to escalation of antiarrhythmic drugs (lower rate of death, VT storm and ICD shocks) 9 Elliot Winford TOC Cardiology Atrial Fibrillation & Flutter ATRIAL FIBRILLATION Epidemiology (Heart Rhythm 2012;9:632) • RF: age, obesity, HTN, smoking, EtOH, DM, previous MI, HF, OSA • Recurs in majority of cases due to secondary precipitant (surgery, infection, MI, thyrotoxicosis, acute alcohol, PE) • Often co-exists with atrial flutter (Circ Arrythmia EP 2009;2:393) Classification of Atrial Fibrillation AF detected w/ monitoring w/o sx or Subclinical prior diagnosis of AF Self-termination within 7 days (includes Paroxysmal if cardioverted within 7 days) Persistent Continuous AF lasting >7 days Long-standing Continuous AF lasting >12 mos persistent Persistent AF for which decision is Permanent made to no longer pursue rhythm control Clinical Evaluation of New-Onset AF • H&P: presence & timing of sx, HTN, DM, valve dz, HF, angina, congenital heart disease, OSA, FH of AF, acute precipitants (e.g. EtOH, thyrotoxicosis, sympathomimetic drugs, surgery, MI, myocarditis, PE, acute pulmonary disease, infection) • ECG: absence of discernible p waves, irregularly irregular R-R intervals (if regularized, may represent escape rhythm and CHB) • TTE: LV function, LA/RA size, valve function, pulmonary HTN, LA thrombus (better visualized with TEE) • CXR: evaluate for pulmonary parenchymal processes, pulmonary vasculature/edema • Labs: TFTs, LFTs, BUN/Cr, CBC, NT-proBNP • May also need longer term rhythm monitoring (Holter, Zio patch). Consider stress test if signs/sx of ischemic heart disease. • Smartwatch notification has PPV 0.84 for AF on subsequent simultaneous EKG in patients > 65 (NEJM 2019; 381:1909-1917) Acute Management of AF with Rapid Ventricular Response Hemodynamically stable? Stable (SBP >90) 1. Address underlying etiology of RVR (sepsis, hypovolemia, hypervolemia, etc.) 2. Rate control (IV if HR >130 or sx, follow with PO agent once rates controlled) - Beta blocker: metoprolol preferred in most cases - IV: bolus 2.5-5mg over 2min, repeat as required q5min for max 15mg total - PO: fractionated, up to 400mg total daily dose - Caution if severe bronchospasm and w/ rapid escalation in pts w/ ADHF - Calcium channel blocker: diltiazem - IV: bolus 0.25mg/kg (average adult dose 10-25 mg) over 2min, repeat as needed q10-15min - PO: fractionated, up to 360 mg total daily dose - Reduce dose with hepatic or renal impairment - Avoid in pts with LVEF<40% and in ADHF Peri-stable (SBP 80-90) Unstable (SBP<80) If borderline BP, carefully attempt low dose BB or CCB (can try concomitant IVF if pulm edema not a concern) Usually HR >150, signs of shock (AMS, cool ext.), refractory pulmonary edema or angina Consider BP-sparing agents: (weigh risk of pharmacologic cardioversion if not on AC) - Amiodarone: 150mg IV over 10 min, can repeat x1 if needed and start gtt at 1mg/min - Digoxin: 0.5mg IV followed by 0.25mg IV q6h x2, total load 1mg. Can lead to toxicity with renal impairment, contraindicated if accessory pathways Synchronized cardioversion: start with 150J If pressors needed: phenylephrine is first-line given reflex bradycardia Higher HRs (>140) more likely to cause HoTN alone; lower HRs may cause HoTN if systolic or diastolic dysfxn, or decreased preload (“loss of atrial kick”) Correct underlying causes or precipitants whenever possible once stable (e.g. infection, PE, EtOH, PTX, PNA, MI, pericarditis) Cardioversion (ALWAYS consider high risk of embolic stroke if any breaks in AC for 3 weeks prior) • Indications: Urgent: ischemia, end-organ hypoperfusion, symptomatic hypotension, severe pulmonary edema; Elective: new-onset AF or unacceptable symptoms from persistent AF • Synchronized Electrical Cardioversion (DCCV): start with 150J (biphasic), increase energy stepwise if sinus rhythm not achieved. See ACLS: Cardioversion. • Chemical Cardioversion: success rate significantly higher for acute (<7d) compared with longer duration AF o Pill-in-pocket (flecainide, propafenone, dofetilide, ibulitide) o Amiodarone (IV infusion weakly effective for cardioversion, PO load over 3-4w, 27% rate of cardioversion) • Anticoagulation (applies to BOTH chemical and electrical) o Pre-cardioversion: if definitive new onset <48h: may proceed without anticoagulation. If Afib onset >48h or unclear: anticoagulate for 3w prior to cardioversion or obtain TEE immediately prior to cardioversion (NEJM 2001;344:1411) o Post-cardioversion: anticoagulate for at least 4 weeks after cardioversion (risk of myocardial stunning and AF recurrence, but unproven efficacy). Anticoagulation 4 weeks after reversion to sinus rhythm is based on CHA2DS2-VASc and HAS-BLED scores Risk Assessment • CHA2DS2-VASc: 1pt for CHF, HTN, Age 65-74, DM, female Sex, Vascular disease; 2pt for Age≥75, Stroke/TIA. CHA2DS2-VASc > CHADS2 in “truly low risk” subjects (Thromb Haemostasis 2012;107:1172) Tristan Alfie 10 TOC Cardiology Score 0 = no AC or ASA; Score 1 (2 in women)= no AC vs oral AC based on clinical judgment  how high is risk from specified risk factor? (e.g. HTN, DM, age bring greater risk compared to female sex, vascular dz); Score ≥2 (≥3 in women) = oral AC o NOT used to guide decision making for HOCM or mitral stenosis (MS) with moderate severity or greater. HAS-BLED: risk stratification of bleeding risk w/ oral AC. HTN (SBP>160); abnl renal function (CrCl<50); liver disease (cirrhosis or Bili 2x ULN or AST/ALT/AlkPhos 3x ULN); stroke; bleeding history; labile INR (<60% in Rx range); elderly (>65y); antiplatelet meds (ASA, NSAID); alcohol (>8 drinks/w) or other drug use. Score ≥3 suggests caution and regular follow-up SPARCtool can aid in risk/benefit assessment and choice of anticoagulation o • • Atrial Fibrillation & Flutter Anticoagulation (AHA/ACC/HRS: Circ 2019;140:e125, Stroke 2010;41:2731) • Tx recommended for all pts except CHA2DS2-VASc 0 or contraindications to anti-coagulation • Subclinical AF is also associated w/ increased stroke/systemic embolism (NEJM 2012;366:120) • DOACs vs warfarin: DOACs (dabigatran, rivaroxaban, apixaban, edoxaban) recommended > warfarin in all except w/ mod-severe mitral stenosis, HOCM, or mechanical valve. Warfarin may be > rivaroxaban in rheumatic heart dz (NEJM 2022;387:978-988). DOACs: risk of stroke, mortality, & ICH, risk of GIB (Lancet 2014;383:955), apixaban lowest GIB risk (Annals 2022:175:1515-1524) • Dosing: see Anticoagulation Agents for dosing. Dose-reduce apixaban to 2.5mg BID if 2/3: Cr ≥1.5, Wt ≤60kg, age ≥80 • Renal impairment: for pts w/ CrCl<15 or on dialysis, can use either warfarin or apixaban • Bridging AC: see Anticoagulation Management • Pts at low risk for thromboembolism may be maintained on ASA alone (see above), no reliable data to guide between 81 vs 325mg Left Atrial Appendage (LAA) closure • LAA is the source of at least 90% of thrombi in pts with CVA and AF • Watchman device: in non-valvular AF, device placement  comparable stroke prevention to warfarin with bleeding risk & improved mortality (JACC 2017;70:2964). AC can be discontinued 6w after LAA closure per MGH protocol • Surgical occlusion: decreases risk of stroke and systemic embolism. Grade 1B recommendation for surgical occlusion only for patients undergoing cardiac surgery for another indication w/ CHA2DS2-VASc ≥ 2 (NEJM 2021;38422:2081) Long-Term Rate vs Rhythm Control • Rate control noninferior to rhythm control for AF sx, CV mortality, & stroke risk (AFFIRM, RACE, PIAF, STAF, HOT CAFÉ, AF-CHF) • Rhythm control (antiarrhythmics and AF ablation) superior to usual care (rate control) for patients with recently diagnosed AF (within 1 year) and concomitant CV conditions in decreasing CV mortality, stroke, and hospitalization for HF or ACS (EAST-AFNET 4) o Consider rhythm control if persistent AF sx impairing quality of life, age <65, or comorbid HF (esp if systolic dysfxn) o Restoration of NSR may lead to increased quality of life & exercise performance (NEJM 2005;352:1861; JACC 2004;43:241) • Rate Control o BB > CCB in achieving rate control (70% vs 54%), either alone or in combination with digoxin o Digoxin alone is moderately effective in controlling V-rate at rest (time to onset 3-6 hrs), ineffective w/ high adrenergic tone  Long-term digoxin a/w increased mortality in AF patients (JACC 2018;71:1063) o Targets: lenient rate control (resting HR <110) non-inferior to strict (HR <80) w/ similar outcomes in CV death, stroke, bleeding, arrhythmia, & hospitalization for HF (RACE II). Strict HR (or rhythm) control may be beneficial in younger pts or pts w/ HF o Contraindications/Warnings: evidence of pre-excitation on ECG (in these patients, IV procainamide is 1st line), cautious use in high-degree AVB. CCB should not be used in pts with LVEF <40% given negative inotropy • Rhythm Control (Circ 2012;125:381) o Choice of Agents:  No structural heart disease: “pill-in-pocket” (flecainide/propafenone), dofetilide, dronedarone, sotalol, amiodarone  Structural heart disease: CAD: dofetilide, dronedarone, sotalol, amiodarone; HF or LVH: amio, dofetilide o “Pill-in-Pocket”: for pts with recent pAF and infrequent and well-tolerated episodes, ppx may have risk>benefit. PRN flecainide or propafenone at sx onset is safe and effective (NEJM 2004;351:2384) o Catheter ablation (pulmonary vein isolation [PVI]): long-term AF recurrence rate vs AADs in both pAF (MANTRA-PAF, RAAFT-2) & persistent AF (EHJ 2014;35:501). Ablation in pts w/ HF morbidity/mortality (CASTLE-AF). Ablation more effective than antiarrhythmic for maintaining sinus rhythm for pts w/ pAF. Cryoablation not yet established 1st line (STOP-AF, EARLY-AF) o AV nodal ablation with PPM: indicated when pharmacologic rate/rhythm control not achievable (JACC 2014;64:2246) A T R I A L F L U T T E R (less prevalent but often coexists with or precedes AF) • • • • ECG: “sawtooth” P waves (F waves), atrial rate typically 250-300bpm w/ 2:1 conduction (~V-rate 150), though can be variable block, 3:1, or 4:1. 1:1 conduction can briefly precede VT/VF o Type 1 (typical): reentrant loop in RA via cavo-tricuspid isthmus  Counterclockwise: more common, inverted flutter waves II, III, aVF + upright flutter waves V1  Clockwise: less common, upright flutter waves in II, III, aVF + inverted flutter waves in V1 o Type 2 (atypical): does not meet criteria for Type 1; is typically faster and often refractory to ablation Anticoagulation: risk of thromboembolism lower than AF (J Stroke Cerebrovasc 2018;27:839) but anticoagulation management is similar to AF (Chest 2012;141:e531S) Rate control: similar strategies (BB, CCB) to AF, but more difficult to successfully rate-control Rhythm control: cavo-tricuspid isthmus (CTI) ablation for typical flutter >90% effective at 1y (Circ Arrhythmia EP 2009;2:393) Tristan Alfie 11 TOC QTc Prolongation Cardiology D E F I N I T I O N (Circ 2009; 119: e241) • • • • • QT interval correlates with repolarization time of ventricles Normal: ≤460ms; Borderline (adult): 460-479ms (female), 450-459ms (male) Measure from beginning of QRS to end of T wave in a lead with T wave > 2mm (best in II, V5), define end point using tangent from peak of steepest slope to isoelectric line; can use ECG or caliper function on telemetry QTc is QT corrected for HR; linear (i.e., Hodges/Framingham) formulas are recommended by AHA (J Electrocardiology 2004;37:81) Can be calculated using MDCalc or with formulas below: Framingham = QT + 0.154 * (1-RR) | Fridericia = QT/3√RR | Hodges = QT + 1.75 * (60/RR-60) | Bazett = QT/√RR | Rautaharju = QT * (120+HR)/180 o Framingham and Fridericia provide best rate correction and mortality prediction (JAHA 2016;5:e003264) A S S E S S M E N T O F Q T W I T H U N D E R L Y I N G B B B (Heart Rhythm 2014;11:2273) • Bundle branch blocks lengthen QT interval; can calculate using Mayo calculator, or obtain rough estimate using QT - (QRS-120) o JT prolo