‘Section 00. Table of CONTENTS - (00.4 HOW 70 USE the ACLS.2013-0.04 sec. name Lead? 0625 — WCT Disa le tere AV Dissociation! (0824— WCT Diagnosis Lge M Waveia Lead VR? (0§25~ WCT Diagnosis: Does Lead V1 sageet Aberaes? (06.26— WCT Diagnosis Ite i of WCT greceded bv PAC? (0827 WCT Summary with Review of Simple Rules (sure 08 27-1) oo. PRACTICE TRACINGS 08.0 WCT Practice Fane: (O91 WOT. Vie sr? (08,.2— KEY Potts What To Do Fit? (09.3 — Fig 091-1 i 3 Sino Raler (00.14 Figue 091-1: Bevood the-Coxe (092.0-WCT Practice Fxample2 (082.1 — Heat “Awareness” and Tachvarn: Whats the Rien? (082.2 KBY Posts What To Do Fit (082.3=DoesFinwe 092 te WCT Section? (092.4 Whats the Riv Fine U9 2.2? (092.5 Finue 09 2-2 the 3 Sule Rules (08.2.6~ Fine 092-2 Beyond the-Core 993.0-WCT Practice Fxample3 (09.1 — Hea Fae and Tacha: What ete Rich? (0935.2 KEY Poss: What the Rn n Figs 093-17 (083.3 When You Don't Know For Sore What he Rint Is (9053.8 Figure 09 3-1: Bevood the-Cove 093.5 PEARL: Use Calpers 094.0 WCT Practice Fsample-4 (0941 —Paptaion ad Tachicar: What ithe Rh? (004.2 KEY Posts: What the Ran n Figs 09 4-17 (0943 Figwe 094-1 10 Managenent (094.5 — Figwe 09 4-1: Bovood-ti-Core 095.0—WCT Practice Example (0051 Pakatios and Tachscar: Whats the Rint? (085.2— KEY Posts: What is th Rv in Fe 09 5-17 (985.3 Figwe 095-1 Wea Uncrate (09.4 Figue 09 1. Beyood the-Core Use ofa Lewis Lead 101 = Use of Spec Lead Sretems 10.2 Aopbcsin of Levis Leed ise 101-1 110 Polemorphic VI/Torsades de Pointer TLL = We See Tacveara 11.2 Figye 11-1: What isthe Rt? 113 = Saagesed Approach oP vivTorsades ILA Besondte-Cores the Bascne QT Prolonged?” us ‘he Olle the Or ip Fig 11 £1 es 116 Answer to Figue 11 -1-ls the QT Proloaged” 11.7 Common Castes of QI Pislorsmion 1s) 'VT-Kthe QT is Not rolnged 11 = Besond.te-Core: About Iberted LOTS. 110 SUMMARY: Os. wr 12.0 = Fast Iregular WCT (VT vs AFibvs WPW) T21 = We See Tachycardia 12.2=Figme 12 1: Whats the Rtn? 12:3 ~Figwe 12-1; Wh isis AFD with WPW ond Noe VT 124 Brsond te Tebook ECG Featees of WPW. 125 Figure 12 5-1: WPW dine See 12.6=SVI Pathwavs with WPW 12.7 = DSVT with WPW: When the QRS During Tachycardia s Narowe 12S Very Rapid AFB wih WPW 129= Ail Fer wih WPW 12.10 PSUT wis WPW: When the ORS ie Wise 1211 =Sogested Ag ‘AED vith WDW 12.12 = Bevond he. Core: Dries for AF» Fer seth WPW 12.13 = WPW wah Rapid AFB Dr of Choise? ‘21> PRACTICE: Whats the Ris in ame 12 14.17 130 SVTs of Vacertia Etiology TEL WeSee Taeinenra 15.2 Assan Figue 131-1 the Rint an SVT? 133 = Daeretal Dnoss of SUT 184 KEY Poin: bore SV] Riots 15.5 Step 1A Is the SVT anes 2 155 Step 1 ehe SVT Ist=) 18.7 Step 2: Which Repu SVT? 13.8 Vagal Maneaers To Diagnose Treat SVT Rime 155 Chaise Valse: Damoste Use of Adesosae 12.10 = Ua Response fo Vara! Manewers 15.11 Soneeted Aporoach to SV Rinse 13.12 = Consider Use of Vagal Manaver 13.13 — Use of ADENOSINE for SVT Rite 1d Asverse iBous of Aceoonae TLIS= DILTIAZEM fx SVT Rina 15.16 BETA-BLOCKERS for SV7 Riss 140 -SVF: PRACTICE TRACINGS 141.0 SVT Practice Frample-1 LiLJ- SVL Wose the Bintan? TLD = Whats the Riv Fine 1411.17 13 KEY Poste BOG Diagnose of Ab 1.14 = AF Doing the Vericuls Resoonse [ILS Rapid AF: Dstncton fom PSVT. L116 KEY Cina Posts: Resarig Ai iz 142.0 _SVT Practice Frample-2 14.2.1 SVT What ie Rt? 142.2 = Whats the Rint ms Finze 1421.17 11.23 KEY Poute: 1CG Diamosis of MAT 1424 MAT vs Sine Tacineardia wth Maile PACS 11125 — Wanders Pacec Diferent fom MAT 14.2.5 MAT: Trealuew Pros 430 SVT Practice Pxample3 13 1= SVT. What the Rist? 11.3.2 — Whats the Rint in Fine 143.11? 14.33 KEY Pests EOG Diagnosis of PSVT 113.4 KEY Cincal Pots: Reeardng SVT L135 PSVE: The Clnsal mporaace of Reso 143.6—PSVT- Use ofa Vaal Manewvex [1137 — Beyond she. Core: Recopisine Revograde P Waves nth PSVT [138 — Was Bevond the. Core Disistion Betveen AVNRT vs AVET [139 PSVT- Acie Treatment Portier 144.0 SVT Practice Framed LA 1 SVT. What the Rist? [42 — Whats the Rit in Fine 1.41.1? 4S KEY Poute BCG Diagnosis of ater HAs Aes: i Use ofa Vaal Manerer 14S KBY Clinical Pout: Resor AFhnee T44.6— AFkaer Appeatnes on a 12-Lead Traciog [147 — AF ater Varinle Condon 4S ashner Uniaa 31 AV Contacto TLL 9=AFhaer Ie AF: or Atal Tach vith Blok? 144.10 aFomer ei AF) — APhuner~ orfib-Pher? TALL Akitas Real r Ane? 114.12 Bevond.the Core Topical and Atypical AFhite 144.13 — Auer: Ticats Price 144.14 Summary. Treatment of New. Onset AFaer 145.0- SVT Practice Examples 151 = SVT. What the Rint? TAS) — Whet is the Riv Fie 145.117 1.83 KEY Cinicl Ponts: Rerareig Snas Tachvcareis LSS Sh Taciveards A Tins of Tine 1.5 $= Sous Tashcards: Ciscal PEARLS 11156 Siar Tachcards: Ciel Covet in ECG Diagnose 14.57 = Sous Tachieards: Tester! Priors 150 BradveatdiaPacisg Ts =Biadyearda Descipioe 15.2 Braden Kev Cine! Pons 15.3 = Bradyeard: Suagesed lal APPROACH 1541 Speci Treatment of Brashcarda IS Incicated 15.5 Brews devond the Textbook 156 Bradycardis What Ar te Usa Slow Rinne? 15.7 Brsdveucda Kev Cine! Poss 1S © Use of ATROPINE fer Bradhcercia 159 —Vee of PRESSOR Ara for Bradvearia 15.10 Use f PACING for asvewais 15.11 = Pacing CAVEATS. Te thre Captre? Asvstole 16.1 ~ Asvsole: Deeipton 16.2 Acistle: Kev Cical Posts ‘163 = Asso: Susesed Intnl APPROACH 16:4 ~ Asvsle: Pots Fable Cause 16.5 = Chiical Perapecive reves of AsytolePEAVED 16.6 ~ Acyl: Bevood.the-Tetbook 16.7 = Actos: A Praca! Clisal Approach \sistole: Uae of BICARB. scsle: Us of AMNOPHYLLINE 16.10 Asysole Botom Lie 17.0 PEA @Patecless Electrica Activity TTL =PEA- Description 112 KEY Pein’ Potente Paable Cones cf PEA 1T3=DEA. Sugsested nial APPROACH 174 DEA: Revond-the-Textoole 17S=DEA. Use of EPINEPHRINE andoe VASOPRESSIN 176 BEA. Preccting the Chance fo Recovery ILD PEA: Benet of Doug e STAT = ITE=DEA. Use (r Not of PACING - ATROPINE BICARE 17.9 PEA: Bonom Line 18.0 —Fscape and Premature Beats (PACS/PICS PVCs) 18.1 — Prenat Best: Descton 182=Premame Beats Dessrston 143 KEY Poze: Promanre Beate 18:4 Concie Cial Smmuay-Testest Considerations 18.10 Dstneishing Between PICs vs Low Avil PACS 18.11 ESCAPE Beats dentine Nanow-Conlex Escape 18.12 = Tdenvng WIDE Complex Escape Beste 14.1) - ESCAPE RHYTHMS: Ker Pos 114 = PVCe A Closer Look 18.15 PVC Defitone Repestve Fons and Rs of VT 18.0 Blocked PACs and berrancy [2.1 Absrass Coadseioe Deseoton 19.2= Rectory Pees Why PAC is Blocked or Aberanily Conducted 13 Titanate Role Detensins PAC Condition 19.4 = QRS Mosphology of Abenant Bests 19.5 RBBB Aberraon: Looky for Rabbit Ears 19.5 Abenacs Coadscioe: Anois the Cetera 19.7 = SUMMARY. Blocked PACs Aberant Conduction PRACTICE TRACINGS: Aberranes/Blocked PAC 19.8 ~Pracce Rhtln Strip: Wats the Rtn? 199 ~Procce Rite Stip-2: Whats the Rts? 12111 Pravice Rvs Sod: What tn Ric? 19.17 =Peewdo AV Block Pavtze Ris s 19.13 ~ Pracce Rint Sap-6: What the Rv? 19.14 = End Diatobs PVC Price Bintan Stip-7 12116 Ashton i AF: Pracice Rint Sti.2 11T= Pauses: Practice hymn Sbip-10 19.18 "Bids" of a Feather Practice Rit Stip-11 19.19 = Prove Rin Sup-12: Whats the Rb? 19.191 Bevond.the-Core Rapid AFB wth RBBB and LBBB Aberaton 19.20 12 Leads Benor tas One: Practice Rives So-13 20,0 — AV Blocks/AV Dissociation INTRO to Section 200 202 = Cincal Cones in Accessing AV Blocks 203 Blosged PACE Mach More Common than AV Blsks 204= The | Deges of AV Block Faciatine Daemosz 205 Le Depree AV BLOCK 20.6 = Bevond the- Cove Renardine PR Interval Paolo 207— Diagnosis of the 2nd Dezree AV BLOCK: 205 Mobis | Jad Degree AV Block (AV Weackebach) 209 KEY Clinical Pos The Dod Demce AV Blocks 20,10 Mobis Il 2ad Deasee AV Bicee 20,11 2nd Dee AV Block wih 21 AV Conduction 20,12= Sed Deter (Complete) AV Block 20-15 AV Dasosanon ve srd Degres AV Blok 20-14 = High Grade Dad Degree AV Bloc, 2015 Veesisuar Stade vs Complete AV Bicele 20-16 = Hyperkalemia ve AV Block (or V 20.7 - PRACTICE TRACINGS: AV Block 720.11=AV Block or Not Rha Suip-1 208 AV Block or Noe Rives Si 20,19 AV Blocker Not Riv Sip 2020 AV Block or Not Riv Sip 2021 AV Blocker Not Rist Sip. 2032— The Cae ofa Passe Risthm Stin.6 20.2) Grow Beate Riv Soi? 2024 More Geowp 8: St 8 2025 Bevond the. Core Howto Rend a ADDERGRAM 2026 Acute MI and AV Block? — Rhvtan Sti 9 2037= Acote Mand AV Block? Rsthm Stip-10 2025 Bevond-tie-Core: SA Bios 2020— ADDENDUM Sek Seu Sindsome and Ses Pauses 20,30 Bevond the. Core Vagotonic AN BlsieSection 0.2 - Front Matter: TITLE PAGE Front Matter ACLS - 2013 The ACLS/Arrhythmia Pocket Brain Book (5% Edition) Ken Grauer, MD Professor Emeritus in Family Medicine College of Medicine, University of Florida Founder of KG/EKG Press (2 Dr. Grauer can be reached by: 4+ Mail — KGEKG Pres: PO Box 1412S; Gunes, Faia 32614-1258 KG/EKG Press Gainesville, FloridaSection 00.3 -Acknowledgoments\Copyright —Acknowledgements /Copyright — ‘Sole Proprietor — Kea Geauer, MD Design of AIl Figures — Ken Grr, MD Printing — by Reaassanc Pinas (Gainesville, Fore) ‘+ Special Acknowledgement to Callen Kay (for making the hardcopy version of hiebook happen) and olay (for ail his tecnica Srecial Dedication: + Te wy Duncan (hoi my wife, my Best frien] ana the LOVE of My Lif). Additional Acknowledgements: + Soua Saath, RN, BSN, NREMT-P —for is oebask, lvl wisdom and ae he cone iights. Tha you Sear rasa Naguraarao, MDD, FACC — fr bs cariology peas John Guns, Pham D. — for is incomparable assistance on lf maters pharmacologic Zick & Stephanie of vey'sRestaman (great food staff and aomosphere that aspired my ACES crea). ‘Abbas, Ine, Jenny & Gerald ofthe Hale Vilage Biseo (fr great food at my other writing space). (G2S~ — Copyright — «+ Ls Eon — 1998 by KGEKG Press. + 2nd Eaton (2007), + Sed Eon 2007). ‘+ {i Eskion 2077 plu Pb 2011 ection + Sidon (2013) pus Pub-2013 eon. All gts reserved No pat of this pucaion maybe reproduced, stored a tobievl sjtom, or wansmite in any form by any moins, letorc, machasical eceria, o& chorse thou pir wten consent rom the publi, 4+ ISBN #978-1.930883.26.2 1.9303 263) ‘Books eee by 23 chockcomirson con)Section 004 HOW TO USE the ACLS.2013-sP ab —About ACLS-2013-ePub ‘veumont of cardiac arrest (endothe acute cardiae any tonias)denaads prompt tec to caical protocol ih ena on prorizing care Hern Bes the “boat” of ACLS- Pubs: Tfscitates understanding of KET concepts in ACLS’ intimin management and lightens te ‘memory load” — by proving ory recall the most commonly used drs and doses in emergency cardia care. + We have completly revised and updated tis Sth Etion (2013) cf om bock. In adaion to ately incorporating crront ACLS Guidelines —We veanre “Beyondthe- Textbook” with cometary on each ofthe major slgerits tht conte practical management pearls and inpotant cial sights This ePab version of our Sth Eaton greadl expands onthe content in our hard copy ACLS-2013-PB (Pocket Brain) book: Not nite by space constants ofthe Pocket Brain — We lave added the flowing nical Setios to ACLS-2013- Suggested Approach: [Note — Pulseles VTi tested the same as Vb Ge, with defbrilarion ASAP. ri te arial agora + Verify WEie Ge, that the poten is way pueless and wiresponsive) — Call fatty! — Get debbetr. + Begin BLS as toon as hss possble Stive to optimize BLS pefomnance and technique Section 01.13), Possiony #1: IF rest wienesed o thought tobe shore lved Ge, not move than 4-5 mintes) — deve single shock ASAP! (epcaly Defbilate with 1S0.200 jones for biphasic eStats or AED — or 360 joules fer anephasicdefbriato) sion #2: rest nor witnessed (sspectaly IE thougit tobe mare than ~4 minutes uetton) — an option isto perform BLS fora brief petiod (ip 1 @ minute oY 0) she tbr ready for shock (Secon 01 5) 4+ Resume BLS mediately er each shock atienpt. (Minbize xterptions in chest compressions) * Inubate Achieve acess for drug delivery (IV-10-2r ED) O14 — Drug Delivery: What i the Optimal Access Route? ACLS Gaidelies non advocate for eithor IV (bina anon) — 10 (hraOtscons) access 25 the optima cue for eve delery daring cardopuimonaryresescaton + ACLS-PM no longer recommends ging drugs bythe ET roete drne CPR (higher dacas are needed: absorption i for Is eile). Tht sit theres some absonption by the [ET rou. The best approach 2013 5 probly 1 reserve ET dosayg as a as test to be used fecha TV nor 10 access is avalable + The FT dose Sor Epinephrine = 2-3 mg Ep (of 110,000 zon) down the ET tibet be flowed by several insane of he Ab bg. 1 IE aperipheral IV swsed ~ Gre drugs by tol injection flowed by a 20x boi of Vid (alo slevaring the extort faceted ow ito the cea cxclton. 110 Route ~ provides access into noncollgpsble enous ples reiting in comparable ug defvery and dosing a by the IV route (02 2-3X mare drug neaded via the ET route) ‘Use of commercial its makes 10 use fastesysafe (minimal complications) and eable + Adenosine cue dug ht should probably aot be gen vate 10 soute (because tine for absorption may exceed the 10-second halflife of ths drug) + Central TV Drug Delivery ~ recommenced only fer experienced provers (wth acvantags that peak drug concentrations are swerior to thas from use of periphoral TY) — [BUT the ces route tor accessuiyfvored chest compressions aced to be terpted OLS — EPINEPHRINE for VFib (Give Epinephrine (Section 013) — rile dug we fis Ist choice for cardiac ces. Tey to give Epi IV 21, IV (or10) Dose: Give LO mg of Et (or 10 el ofa 1:10,000 zon) by TV bolus. May seset every 3-5 mies (a long as ptet romain in W Fb) {+ The 0 route — is safe to se — fst ard cas) to sabsh and ~ provides reliable ssomton wth minimal sk fcomeeaons Rom aserion + ET Dose: Give 2-3 mg Epi (of 110,000 sole) down te ET tbe, fallowed by several insulation ofthe Amba bag (On give Epnaphrine via the BT route fn other route ‘avilable See Section 02. 01.6 Vib Initial Approach: After EPLis Given Vasopressin + Continue BLS. Mimics inteaption. init pice checks (unless the rth changes o capnograply suggests ROSC), + Consider Vasopressin (Section 01.10) —as an acceptable aerate to the It dose of Epiepiine — andor maybe ave t Epi. Give 40 UIV (or IO) asa one-time dose (whereas Epinephrine should be repeated every 25 mate) + Continue BLS. Mixiicenesoption. Lin piss checks (unless the rt changes or capnograply suggests ROSC), 4 Repeat Shock as sppeopite (usually not more often than every 2 minutes unless vith changes), Use 150-200 joules for biphasic Abitor or AED or 360 joules for monophasic debra. 017 - AMIODARONE for VE Give Amiodarone (Section 01.21) —aow clothe anantric agent of Ist choice fee VI Fs! + Give 2 300 mg 1V10 bots for cade arrest May sve repeat boss (usualy af 150 mg TV IO i's needed for porsistont V Fb (max cumulative cose ~2,200 mg over 24 hows) + Fellow Anicdrone bos by maintenance TV infasion IF the patent comets out of V Rib (at arate of ¥ minima .ngyminute forth next 18.72 how’). 60 mghour for 8 hours — then at 2 rate of OS 01.8 TF VF Persists: Measures to Consider ‘A aauber of considerations ase # VF persists. These ince ceria ongoing acon toughou the code as well as other measwes Comme high-qualiqy CPR (with minimal intrmation Search fora Predisposing Cause of VE (Reevamine patent; Review chart; Body rntperature; O2 status; Lab; Echo; !2ead ECG: Ongoing Capnograpi ee. — Sections 02.19 and 01.20), esi Defbellaion (2 necessaryappropriat) Repeat Epncpiine (ever 310-5 minutes) Magnesium — Dosing i rps (Section 021) Give 1-2 gm 1 fo cardiac ares. May open (up £0 4-6 2m I). ‘Aa IV Beta Blocker — Most ely to week IF excess smpatheric one caused the asest (Seton 0120) Might condor Lidocaine — 75-100 mg IV (Saction 03.2) Sodium Bicarbonate (Section 01.17) — i general not ncted forthe Set 5-10 mites of eres (wnlese parent had severe precsetng metabo aides). These may ‘enspivcally ny 1-2 arp of Bic TE pH rmnins very love Ge, 720) dept good ventaton + Clarfication of Code Stats i is has act yet beea done (achancedvecrives fan realistic goal for the resuscitation effor). 01.9 —In the Event that ROSC is Attained [nie good to anispte aed cootnplt teretoa to inate (o a lect consider) in the evett ROSC i aained. Auman ors thee inde: + Reassessment of the patent's ovecal condi (including review of as much pri history as posse; soval plysical cam; important lab tests X-neys; assessment af lnoravascular volume status, dace and ned for ongoing pressor ages andor other medications) Consideration of Cooling (ifnot ahead started au the pation i rt alor= Section 01.29) IV Amiodarone infasion~cspcily #0 that IV Amiodarone facet coaersica ou f VF (iy hap to prevant FFB recumance ove enuang ow), 1s pateat a candidate fr immediate cardiac catheterization? Transfert ICU for ongoing portesiscitation management 01.10 When ROSC is NOT Attained: When to STOP the Code? Practical speaking. the chance or lng-sorm savval (with ntact neurologic status) becomes amb lass — VE persis bspond 20-30 antes despite appropiate testa + This is especialy me IF capoography monitoring shows persistent ow ET CO2 vale (10 mm) 1 Excoplions tothe above goneray exist Gi, when prolonged resuscitation ie mare ily 0 work). These ncadepe-cade hypothermia, pede picts and vitins of drowning (especially cold water drowning). + Uatoemastly iia newcloic exam (including pupillary responce) is ustvouty inocu in predicting outcome fer victims of cardiac ares. 1 Clarieaion of code stats (that may not ave beer nor af the tm resnaitation began) my add perspective 1+ Alte above said ~ sometimes aust gorta be thre" to best determine went sop the code (hough consideration afte above wil hopefully help deison-mokin). O11 VFib: Besonstthe-Teetbook tk >> Beyond-the-Textbook. ‘The incidence of VF asthe mechanism (tal tim) of eardiae ast fas beea decreasing incest years. Ths hols te for bot hospital and out-of hospital ares. Impcations tis wend are cbvios — since the chance for sucess esuschmtn (with act newologicsars)is fa cate IF thers ia “shockable” rhythm (V7'V'8) x5 PEA Aytle forthe sal shyt 4 1a 2013 — decided fess han 1/3 oF al caine ests both in ar out-of the hospital munis VED asthe ital thn (he majority Beg PEUastoe) fa the past ~ VED ccoured er up to 23 of al cases + A tamber of reasons may accoutt for this fequency change inthe itil mechani (rim) of cardiac acres. The incidence of VFb ding the eaty hours of act indction is Siopflcany less than in yrs past because patios with acute STEM (ST Elerion MiceardalIrfarcton) ace touigelycaictzed sa pour repersed (with angioplasty or thombobiesinan ever increasing manber of iasnsons Patents secc help at emergency deparmens sooner fx chest pin and are general admited tothe hosp Among those ‘who re ou fee aete freon ~ a daguosc test earthly dose pio to Ascharge. Given at the rik of sudden death Som coronary dsease i atest among pits ot previously dagiosed ~ he above tendency toward hospital admission and workup for chest pain with resent eater lagoss of coronary disease has decidedly reduced the ‘ncdence of malgant any taia. Fal ~ as of the ICD Qnplantable Cavdiovertr Defioilato) is ireesingy widespread. Especialy among patents wih end-age hear faire fr Sewer de fem VF than ever before + Atte sume te asthe overall incidence of UF is decreasing ~the incidence cf a monshockable rst ie, PEA or Arptol) ae the mechanism of cardiac ames sincreasing EA and esystole have hecome especialy common ss He terminal eve in lzowicly pats wth mule eva co-mowbies, who hav een been et ave oxy by ‘extraordinary treatment measures (long-form use of ventilators, presor drags, Iyperalimantaton adi xtended use of broad spectrum antibiotic) BOTTOM Line: The vera incidence of Vib sth mechaim of cara are estan 2 ueedo be. This incl realy has impomact prognostic iapctoes because prompe {efibrlation of witnessed VFib works! Asnumina the patient doesnot have an sndeiag wnretaecondion — the zane oor efits» patent with rw oncet VE — the boro the chance foe survival (e, > 90% af VFB episodes in cardiac rohab centers mie dua to prompt recogrition an shee). 4+ Tn coats Whon the precpiaring mechs of cardiac testis PEA of asl ina ccna pai ~ te Beaihood of succesful susan thats sustained to the poi ‘atthe patent wil be abet Toave the hospital with intact newesog stats becomes excel smal 01.12~ Assessing/Tmproving Realstic Chance fr Recovery Reali chance for recov from VP is enhanced by the presence of or attain othe flloming + Prompt recopiton of Vib, Geting hep fast. Rapid inition of highequalty CPR. Prompt defbrition, 1 denizen ofa ready meansble ease of VED (Secon? 01 19 eid 91.20. © Mining fnearoptins Sn CP Zorwesnely mer st comers er enc sch. aetna mth: no gr ET C0? es wiry — 2st bo wat ~2 mines (-5 BLS eyeles) before checking fer a pis Lin inibason anempts to less than 10 seconds. heubaron is not necessarily needed for oxygenation to be adequate + Avearenes that nls you count — thee isa tendecy to compress fess apd than 10Q/ninte —and to vite mare tan 810mm + last the Meebcod thr a paca wi espond to weamueat may be provided by Capnography. Progaoss is exccedagly poor — IF ET CO2 (End: Tidal CO2) vas persise, 10mm Fig fer more than 20 mimies of CPR. In contrast — progressively rising ET CO2 values with onging CPR is indication to continu intensive therapy. 01.13 - Whats igh Quality CPR? ‘A majo focus of ACLS Guidelines is peformnce of high-quality CPR Pocsly pefonmed BLS (axcassive intorruptions~ suboptimal technique ~ compressing too slow ~ ventilating 10 ft) ~ ae major contbutees to poor cutcome. We need te do beter. Ames the most important features of high-quality CPR are he flowing: + Increase compression RATE toa least 10Dimimne (was previously “aporoximazal 100/min) We sumise the optimal compression rei berwcor 100-0-12Siminnte(rondency jor dept af compresion and tharafore quality to decrease IF compression rate fastr thar 125}. «+ Thcreaze compression DEPTH to a act 2 inches in ahs (was previously 1.51.2 inch) 1+ ews sequence to "C-A-B” (fom 4-B-C)- Hay ca~ rescue breaths a [eis importa than chest compressions for cardiac ast (low flow vathor than apnea he ky Biting factor. + “Hands Only CPR forthe wine ay rescues (or reccuor twin give rescue breath). 1 Conpresson-o-Ventation Rai i sl 302 fx single escets of acts and chide. + Rescue Breaths ~ sil gven over ~1 second to proce vsble chest rise (avoid largforcefil Breaths that increase risk of getrc insflation IF no axiancd airway pet placed). + Once Achnced Away i i Pace ~ Chest compresions need no longer be cycled. Tstnd 2 reacers provide contour compressions (at acet 10Qinirade) and rear {axyncivonous) dary of $10 resue brea mate (=1 breath every 6-8 secon) Must cous bret! SUMMARY of High-Quality CPR: Coronary ow ding CDR is opiized by ping bard (at last 2 inchs) and fst (at Toast 100m) allowing fl chest reco — and ‘minimizing nteropon. Be seo avoid iypeveiaton (which eraases intrathoracic pressure thereby reducing low) 4+ Pheimportnce of cbsoely msg itruptions in chest compressions carat be overstated! 1 KEY: Werte the ctample of nying to Bcyele phil. It i increabydia to pe tated. Evenly (once you get going wp a ieyle)—it goes nach beter ~ BUT # ‘youve to sap ~ wl oace agi ake you substantial tne ogc oi again Son aston + So itis with CPR: States sages that afer each interruption of CPR (vo matter how bref that interruption may be) ~ that takes ~7-8 compressions (r mors) nil you once gaa begin to gecrate Some effective cardiac cupu: MORAL: Minimize ieroptias! 01.14 Is Intabation sential in Carine At ‘Tao ewer to the quosion of whether ztubatn is esse” cardiac arest so longer'yes. ACLS Guidlnos sate that vata ith a bagimask (BVM) ~ OR — with bag Wzcugh ea advanced away Ge, BT tabo~ OR= rprapotte erway) ~"s acceptable” ding CPR + Bag-Valve- Mask (2724 ventatlon — is adequsteinity diving CPR (chould be dane with 2 providers ro entre oprimal sal of mack-toface ad optimal rida! volume deliver). 4+ Endotracheal lotubation ~ offers advantages of opin away certo, prevents aspiration allows suctioning and high low O2 — BUT ~ complications common f performed by Jnexpeienced providers ~ and - may be detrmondal Fires ninkeruption of compressions + Supraglotic Sirways ~ are casier 1 ser than an ET abe (the glottis need not ba cnecty visualized) — there ate fover complications ~ you don't have to top CPR ~ and — 01.15 - Use of EPINEPHRINE in Candie Arrest ACLS-PM sil commends Epnepaine andor Vasopressin as “pressors of choice” dans cara: acest Tat sail — tere has bees recent controversy oa the Pos and Cons of tsing Epinepine: Pharmncologialy — the albha-adeeaesc(vasoconsvctr) effec of Epinephrine inceeases cerebral and coronary ow (ie lttar by increasing aortic dastolic pres). ‘Theres to date no evidence that we ef Epinepaie in carne aes wcreses sual a hospital ichrge Theres evidence hat Epinephrine increases the chance of ROSC Retw7 af Spontaneous Circulation) with resection. A-mumber ofrecem sues quesion #Bpnepie may have deiner cist. These crues ave flawed. Nothag wil save a pact # the rn i ate on EMS ania. Use of pl coe increas the chance of geting back apse ach patets — but treveable brain damage has wost probably alread) occured. This doesnot const proof” at Epi caused’ aentoogcrjry — but eater ase the mee inpotat question cf whether pasts with wnvnessed out-of hospital ast who ore found by EMS in PEA asytte shoal ‘be esc in the ft place... (For ful discussion ~ Go to sip www kx-ekeyess com ace-ccuments- te 101). 4+ The final answer rearing optinal use of Epinephrine in cardiac aes is rot yet known. The dlenma is What 10 doin the meantime? ACLS.PM still recommends use of ‘Epinephrine for cardiac aest. Rests of sds in which a majo of subjects had out-of-hospital PEALesystle shuld nor be generalized to alcases of cardiac ast with VED ‘heel tn As rent — We ol for iia we of poeple fr areats when the paet found in VFB + ACLS-PM doesnot recommend nee of her dose Epinephrine. Tha aid The “masimron dose” of Epi ea urknown. A Iovg IV bolus peaks in ~2-3 mintes Sms of ‘ourof-hospital srest lave not shown bene fiom HDE (Higher-Doce Epinephrine) — however, the ruber of study subjects was probably madequste to rule outpost of ‘beet fiom HIDE in certain subsets pasent not responding to shock ‘+ OUR THOUGHTS: We do mo for rouine use of HDE. That sid — a case can be made for empiric wil of nereasiag Hpineplrine dose (2,.mg) ia elected aoaresponding tients for whom the clin bev the chace for acces esction wth inact narlope Sanction sll ext + PSz Whether dherapeure hypothermia wil increas the chance of new recover for some our-ofhosptal ares vitins achieving ROSC wit Epnepiie is the subject of ‘lense crigang study. Creal itera toes cong clade persistent coma post ROSC. Stay ed 01.16 Use of both Epinephrine and Vasopressin? ACLS-PM alls fer cuduttsion of Vasopressa for either the Isto 2a dose of Epncpaiein caine arest. Given the longer dao oF wc of Vasopressin —adiitaton of Single 40TU dose essential ats forthe drason of not codes: + ACLS.PM desces Vasopressin as 2 nonathanegic peiheral vasoconstrictor wth eficacy in care arest thats “oo erent fom tt of Epinephrine” + Da aelackng regarding Poronal for synergistic effect usa both Ep plas Vasopressin a caric aest, 1 We feel use ofboth ups isrensonable ligt eiffring mechanisms of action) — and tht ae slot by acing Vasopresin patie alo respond to Epncprinealooe. That said — We donot favor rontine Epps Vasopressin forall cases IF anestis prolonged, promos appears dismal andirewrsle brain damage appears Hike 4+ Reaisicaly — iva be ditt desi a stad that proves” spars bene lem use of bath dass — so bedside decsion to ad Vasopressi nats emp OLIT- Use of BICARB? ACLS:DM no lange ouineyseconmmends Bia ithe cardi anes loriten. The ial acidosis in crac srt is pwimary espn (especial during th fst 3-10 minutes), Giving ica ding thes intl mites may paradoxically worsen intracchiar acidosis pte improving ABG pH valves). Tha sid — there are select circumstances when empiric BICARB (-1 mig Xs~—1-1 5 saps) may bereascnsble sd shoul a eat be consdered These ace + Hyperkalemia Bicar isa peatment af choice! + Teieycic Overdose — to sea to pH 745-7 $8 in alet severe cms + Preevisting Metabolic Acidosis 1 Perhaps (for refnctory cadiae arrest after—S-10 mutes of resusciston — pHi sil ow (7.25) and nothing ese is working 01.18 Immediate vs Delayed Shock for VF Delayed deseiaton cf VFB may nt Work. Tay even be deleterious — by reducing the chance that derlaon wl succesful) comet the VFB stn. The obsions iia Bs ‘wi deteining hoe much delay (becomes 00 long fo recommentng defbrision as the ined ta action when VF fs found oa EMS ava + 2005 Guidetnes favored cing deflation — TF was ely that more than 45 mimes had pase sce onset of cardiac ares, More recent sites are conclave abot ‘enc ast rus dell pio to CPR for VEibpreseat nore than 4-5 aes. 1+ Nays Gaidees in ACTS-PM now alow the epson of mimediatel shocking VFB of uncertaeduaon without a preceding pesod af PR + Wiewessed VFib shouldbe prompts shocked (a 007 az an AEDicefivltor ic avetabl) 4 Assuming tine mal aia iso excessive — macy (no mt hospital providers cual) shock neh discovered VFB as Soon as they ae able todo so. ‘+ Din ie ssconchive forthe optinal approach to uneitmessed VF tht occurs oxtofhospital. New Genes alow for perfomance of 1 S-t-3 mites of BLS (-5 cycles of 30:2 CPR) before tue Ist shocks pea. Ateraves (ou preference) — may be most pracsalte perform CPR foe a bref petod just wat the defibrilator is ready for shock Ser! 01.19 - Correctable Cause of Candiae Arrest? FFnding «cause of VFb you can i" fe the greatest chance for lng: form survival Potenialy treatable causes of persistent VFB Ace MI (lecrscal stabil drag val hows of MT) Drug overdse (which may precipitacs respiratory arrest na pation with an otherwise normal heart; Hypoxenie respiratory avast; drowning ee) Hypothermia (oar o mis if you don check body tomperatw) ‘Hypereenia spokalemia ispomapnesemi (or other marke siecle imbalavc of calcu, phogphores, sou), Acidosis Sepsis 1 Heat Fe: + Hypovokenia (nang blood loss); + A complication Som CPR (onsion pneumothorax percardhl tamponade, ET m rigt mainstom bronchu). ACLS-PM summarizes meatable causes of cai anest(Be this from VIVE: ~ AsstolerPEA) by ase of H's and STs + Ons: + 8Ts: Hyposis, Hypovolnin Hypothermia: H- in (avidosi); Hoposhcania: and Hopar- or HspoKleaia Toxins (inclucing drug overdose), Tanponade (cardiac), Teason Poeanothoras, Thrombosis hati Pulmonary (ombols) or Coronary (acute MD. (01.20 - Work Up looking fora Correctable Cause Lab Tests to oder ding (or ar the sree in are part based on faking fora potently reatate cause. While clea ata complete it~ We mention some basic tests to conser bebo: + Vaal sins (tomperarre?). 1 Chest Xa Us ET tubeiconra line placement OR?) # Dead BC6 (ecuc infarction? ‘rithm aagnoss”. 1+ Echocaroptam fala to assess for tamponade; pulmonary embolus; LY faction), + CBC: Chem prof with elecrohtes (inclu Magnesium, Calcium, Phosphor, 6) + Tescology Seren (frelevant). Asteria Blood Gasevongoing O2-Sat motring + Ongoing capnoerapty. (01.21 Rote of Aniasbythmic Drugs in VFih? Use of anionic deuss (Amiodarone ~ Lidocaine - Procanamide) has never beea showa improve longtorm cxtcome for pases in caine ares. + Amiodarone —has been shown to improve short tenn sv to hospital (but not Beyonc), + ACLS-PM— sri commons Amiodarone for refractory VEib tht fais wo sespoudto Shock pineeine, Athoughscasouuble — tis recoumendaon is nor evidenced based (theres ra evidence Amio improves logterm oxtcome from VF). + Ecomerted our of Vib — thea propiplacc IV infusion of Amidarone i recommended (forthe next ~24 hours to mivmise the chance of VF ecucace 1 idecsine — hs been rlpsted as a Znd-ine ageat fo refractory VE (after Amiodarone). Give 1.0-1S mai (-50-1000g) as anne IVIO bolus. Repeat bohses of -S0- 75g way be sven every 5-10 minutes (up toa oral ating dose ~225mg = up o~3msks. + Procainamide — is not recoumtended fo VEB (it not 0 good antfbrilator agent. Other Drugs — There are selected special cromstances fer which Beta blockers an Magnesia may prove tobe Hifesaving agents. Fox Beta-Blockers~ ts inches refractory ‘VIVE and acute anzerior Ml with increased smparherc tous. For Magnesium ~ tis incndes Tovzader ae Points). Tha seid — decision to use these agents dng cardiac vets tobe individualized based on eee ccastances, + ACLS-PM — does no rotnetyreeommend Magnesim in cardiac ares ales theres Torsaes. Tat sai — Magnesium is cle indicted K+/Mgt+ are love; and there ata suppoing empiric use fr sythnas not vespondina to othr meases 1-2 gm IV py repeat. Thar would sams to be le hana snd poten ac om emp: wal “Magresum for VFb nt responding to ober measres 01.22 VFib SUMMAR} Overal prognosis fr VFib is potently evod TF thee sno neversbleundehng order and VF is prompt reesized and debris + What role therapeutic hypothermia wil tints assme for optimizing suv and neariosi outcome in pains who remain unresponsive post ROSC is actively evohing Stay soe01.23 Addendum.A: WHO to Cool? (Therapeatic Hypothermia) tw >> Addendum Material: Recent years have seen marked increase in use of TH (erapetic Eypotharnia) a hope of improv mean Gieuologically tac sua rom cardiac aes. ei cess ce ‘easily encouraging, AS a esuh 22013 ~ Cooling shouldbe rouinely considered ASAD after ROSC is aanod ia axes sures who do aot Wake ‘+ BACKGROUND — Overal suv lem curiae arest both end our-ofiaspital semins poor Most tins who davlop ROSC but every de, do so rom anaxe bes ‘nj. The proposed mechanism of THis based on ts attenoaing fect on “post-arest syncroma” wih the accompanying cerebral edema, flammatory response and reperision ‘nj tht occurs, Dos-aea cooling recucermutabobe demande and vows the sequence cf averse evens. 4 WHICH Patients Qualify? ~ Any paiva esc from ease arest ( ataring ROSC) senses of te ins mecha of set ('TVFAsystole or PEA). Cooling shouldbe started ASAP afer ROSC is atained~ with golf achieving trpttemperanee within 3.S ours. Post-arest pata alert enough © falow simple commands donor need ‘bene fom boing octal (Mose contrs use a Glasgow Coma Score = GCS reer 3106 as quaifing eter) + WHEN to Start Cooling? ~ Answer = ASAP after ROSC achieved in appropiate ptt. 1 WHO to Cool? Any postancest patcat wth ROSC vie is adited tote ICU buts a yt unable to Solow saple commands, “Lft you arm"). ‘Realbing thar promos wil be poorer fr cooled post arrest paiets who were ily found in asjtle(vther than VFB) ~ TF dacson made for mul etonse weamnent (ened 2 ecition ro meat n an ICU) ~thea post-arestcoskng shee part ofthe reinen + Prognostic Indicators ~ Ahogh fining a patent in asystcle sgerts Inge “down-tine” (and correspondingly lass chance of responding fo resuscitation) ~ iter asytle no: PEA rue out possbty of aeuclogical-act survival laa uewologs exam (cluding pupillary response) i wotvously inaccurate a prediting eutcome fr Vcins ofeariae rest This explains expanded inchsion citi for “Who to Cool” (obove). + Exclusion Criteria ~ Padente wo should nor be cooled ince: i) Patios wits a vald DNR Do Nios Reructats) onde; i) Receat sac gery (vir 14 day: i) Severe systenic incon Ge, sep) e) Keown bleeding sorde,and v) Pais who cam Fw coumauds (since alert patents do hot beset from eootng). + Cooling Protocols ~ are variable Som on isin tothe next bat most aim mata cooking at ~32-34 degrees C(69.6-03.2 degraesF)for ~24 hours ~ fore by slow ewanang 0.25 greet Chow) + Complications ~ acide arintimias: sep Ai overload. conslpaty: hyperyeenin ‘+ PEARLS: - The sooner coolng is sared~ the Better th response i ely tobe (ally bagumnng with 30-00 minutes past-ROSC ~ and ely ataining goal temperature within 3-0-4 hows). Teed TV Satine works gret (on car usualy lower famperature faster thon coling device!) Opinal core temperstre monitoring by esophageal probe (pectal probe lags behind changes in cove tomperaru).0124~ Addendum B: WHO to Cach? (The Post-Resuscitation BCG) ‘\NY i> Addendum Material: (One ofthe KEY questions to answer when working #code i IF thre ba potently Jorable™ precpiaing cance (Section 0119). Aewe vechson ef « major coronary vessels among ‘he most morta! causes Ht might be found We englasze the folowna pis + The most common case of sudden cae death in aduits over 20-35 years of ages coconary artery iscast (CAD). Uaformaay, ia many cases ~ the very Sst “symptom is the pitas let Ge, tal PVF). Obes aden death victim have apo story of CAD wie yet ters any not Krow they have CAD, but were having prochomal chest pin ‘over dys-o-weeks price othe ever that hey dened or ignored. Tins, the history preceding the event for victims of our ofhaeptal VIER is verse ‘Natal wists of sudden care death who have uidedingsgnicnt CAD ce of sete ccchion amar coronary vessel. Awareness of ths ciel realty i importa — since ‘emergent post resuscitation PCI (PerCutaneous Intervention) wil not neces improve atcome if pefomned oa a VFip survivor who has underhing CAD but not ace ‘ocenay secon. + Tnconrast~ emergent PCT may be lifesaving — TE peformed on 2 VFib savior in whom the cance of arest war acute acchoon of mae coro str + The imparance ofthe postresusctation L2-Jead ECG ~ i thar t may help idea which paca had tek VIIV® episode precited by acute coconary occasion Tans, he Siding c acute STEMI (ST Elvin Myocar dal lfction) on povt-resusctarion ECG i lear ication fer numede cath wth goa of acute PCI reperfusion) unos thve & ear contraindication to pexfring this procedure (Figure 0.241) + That said — the cial cal is tht poseresuscitation ECGs are often ot normal. Rate thn acute STEMI nach ofthe tne ae may se the gamut of QRS/QT prolongation wth difise onspeciie ST-T wave abnormalities. ST depression common (ard! mabe markea). How specc such immediate pot resuscitation tracings are for act Coronary ‘echsion asthe preintang case of cade eesti ancthes mater ‘© OT prolongation is common i post-resuscitaion wags. This should not be ssng given the CNS isu associated with cardiac ast (especialy inpatients who do noe immeciauly wake wp after resuscitation). + Repeating the ECG say be beg. Ts tharated in the two tracing sequence shown in Figues 0124-2 and 0124-3. These 2 ECGs were obtained just 9-imtes apart ina sictn of ow-of hospital cardiac arest who wae soecessfily reswcinted + Theissu of WHO to Take tothe Cath Lab? flowing soccesi suction s rapidly evoking. Deftve answers ae act yetn. Obviously alviable VE survivors with acute STEMI on pase resuscitation ECG ment a bp to the cath lab (Figure 0) 24-1) However, coaseasus caren king a to wat should be done when he post vesscitaron [ECG islessdefitive. Opinions var. At one end ofthe spect are advocates of “acme cath forall Vb seniors” tthe other end are those who onl favor eat cath oe VED sunvrs wih acute STEMI on past resuscitation ECG Many skinions ar somewhere a beticen. Teno wil tl what the best answer i. ithe meatine ~ the sequence of ast ‘rmsscitaton acing scm a Fgmes 0124-2 md O1 243 wl hopefy increase awmeness of 2 common station in wich »"oon- STEMI ECG my nonethless are roel vor cf ned fer acute cath and poteataly saving PCL Figure 01.241: Acute STEMI on ECG. If tas ECG was soma « vable postosuscuaon paca ~ arue cal woud be immedately indicated, Gol of suh cath Would be acto repetison of the “cpt” artery ~ which most fey isthe RCA (right coronary artery) given inior ST elevation tnt is greater in lead TT thn in Tead TI, recprocal ST-T wave sboomaltis in leads aVL,VILV2 - and probable AV Wenckebach forthe yim. Figure 01.242: tail post remsstation ECG i 2 50-year old pateat ih outa hospi cardiac est The tn 5 rae sow AFD, Thar safest sight QRS wideing of nce eclogy (nonspecific ICD). Abough scooped ST depression e seen ina umber of ads wih ST coving and ST elevation is seni ads 8VR,VI'3 ~ te overall pater is ct Spee for any piu “cup lesion” (and the picture abit efferent thar s usualy ses with lef main or severe 3-vesse disease). Tis prasly abnormal ECGs ypical oe what ce may see post resicaton. That sid ~ the pctre is lard with he flow wp tacing obtained jst 9-mmtes ner Fiewe 01.263), Figure 01.243: Folow-p post resocation tach obtained 9 mints ae the ECG in Fgue 01 24-2. The rth s again AF, now with PVCs. Tae QRS looks to fave narowed seh — and thereis aow auch more couvetoal deep, défise ST depeesio in mameroas lads with masked ST elevason ead aVR. (and to much lessor extort in V2), Tis pleas ‘ow amach mere sugestve of worm ecm i the conten of wt one fa ees with severe 3-vesel ora este (namely cifice ST depression bua ST elevation in aR). ‘Acie cath confemed thi ciel spicing, wich wae rested wh mi ese! agp teaig this VF savor01.28 Addendum-C: Use of Boho during Cardiac Arvest kK => Addendum Material: Tin PED wah cans (pecaly whan Ta pa Reasoas to consider a star Echocardiogram ca pata canine toto icra + Detention IF thc is messing carne conkaction (albeit inadequate to produce pute. + Ready detection of pesca (or pulmonar) esion. Moderae-o-large pesca effsons are easy to see on stat Fcho as abporma i colecton within the pesca space “More sible sal efsioas are wis to be cicaly sniicoat ing an ongoing cesuscimio atemet. Moton abaornatiesfncudos“swining hear” may be seen there is ‘portzmcous conracion Stat Esko (available) ma be aul or deta crac tamponade a the cause of PEA + Suspicion of acute PE (puimavary emboli) thar might be weatable as the prociitating cause of arest. Echo findings suggestive of hemodmamicalysiceet PE achdef) Severe RV dlaation e:pecially when found im astociaion with omall LV eaviy size), 8) Inpaived RV corral, i) RV pressure oveload, iv) Postve McCeemal's si (iach s akinesia of the mi RV foe wall, but normal motion ofthe apex), and) Wetication of tombs. Admittedly ~ several of ese Echo figs are dificult to assess Addendum Material: Physiologic monitoring done deforlarine/ajter resuckaton — mny be of vale oeelance! ln paricdar ~ ACLS Gridaines naw endorse ute of Quantitative JHaveform Capnography diroughou the peritest period. We brie evew te basics of Cpmography (ET CO? monitoring) wih goal of stating HOW ths oo may be wed + Capmography ~is merely measuemeat of CO? ia the exhaled bceat. The pencipl is simple: pred ai contains nepgble CO2 (0.03%) — v5 expired aie + The amour of CO2 canbe measwed as shown in Figure 01.261 whi sates he normal Waveform Capeogram: percentage of 4.5% CO2 ia ‘Capnogra: oz in mma to. D ° Figure 0126-1: Norwal Waveform Capoogram. Note ta the waveform begins wih expeabon (410-8). Noma ET CO2 = 34-40 mumllg (C¥o-D) + Phase A4o-B (n Figure 01.26-1)~is the PostInspivation Phase. This phase occurs a the very beginning of expiant nin imvohes the ‘dead space’ — which expans why (COR ese zero! + Point B isthe tart of veal exalt, + Phase B-to-C isthe Evhalation Upstroke (aad gat now bret 0 mis with CO2-ichabvolar gas — whic expla why COD shows a voy stem ri), 4+ Phase C -D —teloctscoaiauton (unl the end) ef expestion. The sope of Phase Co-D is usualy fly Nat sh perlaps a sigh acne (a: slow alveoli" emp). Ths pase takes ona peculiar “shark fn” appearance (Figure 0.26.2) whea thee is delayed ning wit esa a (a oceurs in obstructive pulmonary diseae o asthma) Figure 0126-2: Delayed ming with aol a rons “sha Sa" appearance dng Pase Co D (Characters of patents with COPD or ation) + Point D (in Figure 01.26-1)~is ET CO2 (Ene! Teal C02) whichis peak CO? concentation (which is normaly between 35-43 mm 1 Phase D-toE (on Figure 07.26-1)~ is the Inmpiracion “Washout” Gnupired air contains negligible CO2 ~ so CO2 concentrarion rapialy drope toward zero as soon az siren agi ‘Think of Capnography 2s a additional “vital sien” Iti far more help than pulse oxinery {which provides information about oxygenation ~ but tls us nothing about ventlaion) A waveluem willbe Seon with respon as soo1 as an ET CO? monitoring dvice placed a the nox-dreattirg pascal ~ You'l se a waveforn as soon a you hve inabated, + The capmognmn in Figure 01.263 shows 2 aor ventions, Note te normal rectangular waveform (wih ET CO2 ~35-40 mm Hinting acces placement ofthe ET tbe ‘ate warhea~ wut the ET ibe comes out (orow ix Fig. 01.263), Figure 0126-3: Cepoogram showing 2 nora veniationsmilthe ET tube comes oa (oro), (Clinical Uses: Capacgrepiy hs bene inimibeted or aoa-emibeted past + Inthe NON-Junubaced Patent ~ i) May hp asses degree of broachospasm (shark fn) and respeasetobroarhodlatrteapy i) Rapid detection of typovealaion (neeasing C02) dof wed to tube i) Detects hypeveilstion (better thar counting breaths) + Inthe IntubacedPationt~i) Veticaton of ET tbe placement (a CO2 reading = zero implias you are inthe esophagus!) i) Assists in EMS moatoring during transport (elif ‘you need to ventilate faster or slower based on whether CO2 is accumulating on), + Inthe Cardiac Arrest Patient ~many wes! (See Figures 01.26-4 and 01.265) Capnography Daring Cardiac Arvest: Example #7 (Fignte 01.26-4) ET CO2= nero atthe one of cardia aes. Three defitecotelation between ET CO? and cardia oupt + ET CO2increaes fom zero to ~5-10 wang with ial CPR. + Vales then increase tothe 10-25 mani range with foie CPR + Te Capnogram Trend (overtime) ~ provides KEY insight oa many aspects of CPR. This is evdeu in Figure 01.26-4~ which covers a paviod cf about $ miames cking wii ‘here ae 6-10 ventlanonsinnut; compressions are ot seen on the capnogram). + Period A (in Figwe 01.264) ~ shows anil short Bat ine (tthe airway isin place) ~ afer which ET CO? atains ~10 mle (whichis consistent with nial CPR aring cardiac ares, + Petiod B shows gracul increase in ET CO2 wp to 15-18 mfg (onsstone with inraase flow from afoctive CPR) 1 Period C— The rezcue ding chen compression ay be ing (gradual drop tr ET CO2 vals). Aa aerate explanation forthe lo values for Din Figus 0126-4 (to blow 10 ‘ron many be pooe Heid fr sual (2 ventiator protien or a pulonary ents, 2) wtih Mn inna Figure 0126-4: Cspoogrpty Tren for Example (See text) Capnography During Cardiac Arrest: Example #2 (Figure 0126-5) [BT CO2 monitoring curing resuscitation may resct ROSC (Ratu: Of Spontaneous Cvcoation) even before you are actualy able to feel a pulse (IF share is sucion marked rise to 335 mndi, BUT ~ Poor ote icy IF ET CO2 ei 10 malig ater -20 inate of higi-gualigy CPR. ‘+ The capaograpty tend in Figure 01.26-5 ts sory” to what has occured dering ths resction efor. nly (A) ~ he pate isin ill ast (Vo pulse no respiration) Chest compressions are tated (not fear onthe caynogram) 4+ The patent sanbated (Bs Fig 01.26-5)~ and a warm s nos Seon + ETO? chops back to zero by C (the tabs must have come out reintubaton i ness). 1 Theres success sabato aD. Tcrensing ET CO? rene by Fup f0~15-20 nrc) sopgest CPR ie cetve wih ROSC by F (udden ne to.an ET CO? >40), ‘There erento oem ET CO2 of~¥5-S0 mie afer ROSC (), ET CO2 drops (H) ~ th patent apn codes + Props poor doe to pesstety ow ET CO2 Figare 01.26-S: Copnograpiy Trend for Example 2 (SesSection 02.0 — KEY Concept in Clinical Rhythm Diagnosis Clinical Rrythm Diagnosis 02.1 Systematic Approach: Watch Your Po, Qs and 3Rs ‘The KEY efectve dum ineepretatin sto wlae a Systematic Approach. The system we favris based oa assessing forthe folowing $ Parameter + Presence (ana nang of Paves? + ORS wat? + Realty ofthe hyn? IEP weaves are preset ~ Ae they Related to the QRS? + Heat Rae? Temates notin what sequence you lok at the 5 parameters —as long as you aways assess each f them! 4+ We aie chonge the sequence wich we lola thee paramere ~ depeniog onthe racing, Ths, we do ac bays scar abil acy Sat especialy if waves eno vee ‘brio, or seam be chazsagin morphology Instead wee may leak fst at QRS width ~ ox esis he svt ~ depending a what Seems easiest (and mast deiiiv) to assess cate proud tack BUT~ We ahs mace sure we aes all S paramos + MEMORY AID: We ind # easiest to recalthe 5 paramcters by the saving, “Watch your Ps and Qs —and the 3Rs” + Clinical Reality: You wil yar avays be able to deaitvely haguose the elogy ofan ahtania Fou a sage syn stip. Even she expert will not always Know for sure! Tat said Use the § Parameter (Ps Os 382) Approach wil low youto-) Rap and accraely azece any ayn: i) Preval You Bom arn any soe cogs i) Narowe Sonn diferent posses, even you are ot sure of tin agnosie abd i) Sound anligett a 90 go tough he process (eve you c+ uve the onze). We anode pplication fis approach bes in Seton 02.11 (02.2 The 6th Parameter: Is he Patient Hemodynamicaly Stable? We discuss dex assesses for hemodanic sabi under Tachjcara (Se 7p 16-17) For now ~ Sufi i 1 exphasie tha the Fst dg wo do (even Before you begin ro assess the 5 Pavametert)~ isto detemine IF the patent is hemodsramicaly sable. For example — Look a the yan in Figare 022-1. Clrica Whct would you co first managing is patent? + Scenario #1: ~ The tytn in Figwe 02.2 is obtained fom a mpoteasie paar with shorars of breath and chest dscomfee? {+ Scenario #2: ~The paint slat, asjptomatic, and fae x BP = 15090 alg? + Additional QUESTIONS: Whats the dt ia Figure 0221-1? With separ to vou iia ianervanion~ Does it relly matter wa the hm 5? Lead IT Figure 022-1: Tachycardia (See x). [KEY Poiat: och more impr ntlytan gosng what the syth in Figure 022-1 ~is assessment ofthe patents lnc status Ge, Is he patins hemadamsically stale”) 4 We actualy can no ell fr sue what the sin in Fig 02.21 By the § Parameter Approach — We can say tht the sytem i ft (-2/0/minute) ~ repr ~ sed lacks P swaves. However, Weare uncertain about QRS width from assessment f his sige montocng ead 4+ Well soon discus a deta hve to apwoach such anhytimis. Tat Sad ~ the po to empbaszeisthat scaly i does really matter what he tytn swt you've asessod ‘nemodymanic status! For example ~ TF the patent wih this eth is acutely hypotensive with dyspnea and chest discomfort Scenario #1) ~ then immediate synchronized ‘cardioversion wil be indcated revaralesr of wheter teeth tas out tobe VE Centriular Tackycaraia)~ of ~ some ype cf SVT (Supra enrcular Taclycarc). + On he other hand ~ TF hepsi wth the hn igre 0221 rl and aseptic wih BP ~ 18090 (Scenario #2) —thanby defiion there sa eas ome ie to mote acura asses wha th dims Heel o be (and whar spect reatment willbe baz) + BOTTOM LINE: Always exsre the pation is stable Sefore you proceed with assessing the S Parameters. Smetines (je, in cases such as Scenario 8m Figure 02-1) ~ you say need to begin treaeat afore kn for sre wht the ryt 02.3 How to Define Sious Rhythm? By dein (der normal circumstances, axsuning ths haart isin the eft side of the thorax) ~ be P wave shou avays be upright in standard lead Uwhen the mechani ofthe thn is sinus. Tas i Because the overal econ ofthe eecical dopalnzaton Waveoat as waves Rom the SA node tard the AV ade and the vail is eid foward ston ead, wc es st +60 deseesin the ntl plane (Pane! A in Figure 02.3-D, 4+ The onl 2 excesons to the shove sated rule Ge, was the rich may Be sinus despite a negative P wove o lead H) ae: there i deswocur: or Wf there i ead sispaceneet ‘a contast, when the cecbcal impale cigases fom the AV aode ~the P wave wil at be postive i lead If (Panel B ix Figure 023-1). Instead ~ spread of aa acvaon i aw deeted cy om lead with anton beats ce incon (4P nada et ‘+ Beyndthe-Core Athough we schematicaly depict « negative P wave prcedng the QRS as repeseting what happens with junctional bests (Pane! Bn Figure 023-1) is egatve P wave i ead I could be seen aor the QRS, might even be hcdon within the QRS (depending onthe volatvespeod of rtrograde conduction back fo the atria ‘compared to forward conduetion down to the vente) ‘igure 023-1: Panel A (lef) shows the sation oe aoa sins hythn — which sdfined by te presence ofan upiht P wave ead UT. Panel B shows tht when the pulse oie in the AV node (as itcoes wth wictional beats or junctional rytlms)~the detonation swe fom lea T. The P wave in ead T wl therefore be negative ead Tis not BOTTOM LINE (regarding Sirus Biotin; Acuming thre tno derocordia sd the eae ae ot misplaced ~ TF the P wav resent right then sis rhythm i not + PEARL: The very 25 thing we souiney do when assessing the cardiac thy in a acing (12eaé or sinle-Tea riydin si) is — Look wo see IB there isa longer lead I hyd strip Itcoaies no more than a ocused 2-sacnd lok to detemmze upright P waves wih fed PR sural regu precede each QRS coaglex. IE they do ~ heathe rhythm s sinus Paral 4 in Figure 02.3.2) [Eup Pwaves do nor regula precede each QRS wth ced PR inercl~ then someting other than acral sinus svt i preset (Panels B and C in Figure 02.3.2). mie S oo Bl § = = Figure 023-2: Panel A shows NSR (Vormal Sous Spin). =P waves opriglt a kad and cach QRS i prewedsiby aP wave wit ued PR itera Assuaing 20 dextocca read mislacement ~ We om tel ats glance tot Panels Band C do not represent represent sma stn becane the Pave is negative 9 Panel B and sbeateniely ix Panel C Presumably ~ Pagel B press a sigy accelerated AV aodal escape sthm — and Pane! Can appropiate AV aodal escape (rate banweer 40-€D'minuze)~athough we cam tule out ‘he possity of low ati sti cr escape Rom the Bundle oF Hs, respec fr Band C Tal sid. what matters most ~s Wat lack of an upright P wave‘ the lead Ist ips seeain Pane B aed C imei tele ws tht a rythm oder thaw sinus is operative! (02.4 Sinas Mechanisms!Sinos Arh (Oace the mecha ofthe vt is ined as sans” — the eae (anal epularn) of the etm determine oa teminlogy. Thre ae 4 pina sinus mecharsm dams [SR (Normal Sirus Ryzhn) ~ reader hth ate beresen 60-99 in es Sines Bradyeardia a repr sis tytn a arate below 6a, Sines Tachycardia ~ sims him at arate of 100 mime oft iro aul pation), Sines Arrhythmia ~ an regular dtm despite te presence fa sis mechanism Figure 2.4). Figure 0241: Sims aniythmia. Des irepslay inthe yt ~ sims mechanism is preseat as dened by ceglady-occuringupigt P waves with fixed PR preceding cach QRS comple. A Word About Sinus Arrhythmia ‘Sinus Arya sa common noma variant nfs and young hlhen. At nes ~ vrishy in thes ate maybe muked in which case one might yd hat sme othr anise preset + Sinus Arvhythmia~isconimed by the fining of entical-anpearingP waves tat are upright in eal IL with fixed PR interval (Figure 02.4) + Incoutast~ ovr phenomena wil manifest changes P wave morphology andor inthe PR ines + Sioa anti often exits repiradors variation. This is especialy rein beat young ken ~for whom some variation in sims realty isthe nor rather than th exception Sis “xia sa normal cardiac yt nis etn. Some dope af sas vanity (esas arrinchnti) may pest in yous and eve cer adults Tiss wor secessnly choca 4+ The echnical definition of sinus “aretha” ~ ie tatsracstited R-R intervals wary by at least .08.0.12 second (2-3 litle Boxee). That sid, mos of the tne ~ the resence of sins “anya (v snus rtm) sof ie f-no lnicaligabcence. + Anexcention tothe statement hats annna's beni occas in oder paints wih SSS (Sick Sinus Shrtome). Amon te many manifestations of SSS (which nec sms (paises, sie aret taclp- ae well az raayarigtonas)~ sinus bradycardia segh sinas arrhythmia i hemos concn. The url course of SSS is polsaged over yrs (f ‘no decades) Mass patents who go oa to develop fledged symptoms (wth mae fora permanent pacemer) manifesto mare ems Idris ena for & pecod of many yeas. Therefore ~ the finding of an inappropriately slow and variables rym in an older patent with symptoms of fave, worseing heart fhe ardor Sscopepresyacope IS case fr pote cence IF not doe trae doing mediation ~ Corser SSS asthe possble cause + Bexondthe-Core: Ancher type of ss anita tht associated witha paologic contin is ventrculophasz sinus ardhythmia. Some pains with soncant AV block ‘nanfes obvious vari ithe ate ofthe nderbing Sus rim.This is though o be duet varias in cardiac cupur a ares ofthe AV block. The imporance cis tam, ' simply tobe are atthe -P auerval may vary ih cris Zonas of AV block BOTTOM LINE: For most paeas~ the nicl snicanceof sins arti is he same as for ins yt ~BUT ~ Clinical correlation tothe case at hand is everthing! ‘The ECG agnosis of sus etn or ss uylaa S made in th sane Way tha all artinias exe dapuosed By use af th Ps, Qe, 3R Approach. The presence of nila appearing P waves that really precede QRS complexes wit a fced PRicterval defines the syn as sims. TF the P-P interval ofthis sms rt vases then by defini theres nae anrb tia, Other Freqular Sinus Mechanisms Tn acon to sme aythnia~ there are oer variations of regular ss mechani ryt, Two common oes ar sated in Figure 02.42. Consider theve Questions: + Fortracigs A snd Bin Fre 02.42: To ther underlying sinus cyto? 1+ What happens fr beats 24.56 n Tracing A of Figure 024-27 4 What happans fr beat Tracing B? gs) a) og Figure 024-2: lregur Riythns wth Undeving Sins Mecanisn. Exp wit happens wi beas #456 A and wih bet BB Goo xd. Answer to Figure 024 “More important than the spec vtam dagosis for Tracings A an Bis the proces for thm assessment using the P55,3R Approach «+ Tracing A ~The ovral yt snot rua. Te QRS comple is narow and each QRS is preceded by a P wave. Thre ae 2 diffrent shapes fr P waves seen on hs tracing, ‘Atlee peaked P wave wih ced PR ieral precedes beats #12.% and 278. The lad P eave shape is of smal anpimde and acted — ands seeato precede beats #456 vith Seed PR ated Ths, the snderling ey the i inas arvana ~ th transient change to another sia acu for bens ,§ 6 ~fllowed by reumpion af the ci in fon atthe endothe racine 4+ Trating B ~The overall yim is agua vor gute sea. The QRS conples is narrow — and cach QRS is preceded by a P wave. The underlying shythm i again sis rhythmia (ar determined by the preconce of wore sdantical- looking P wives with fed PR ntaval preceding Boats #1,2.3.4,6,7—albnt with slight variation Be P-P ‘rtorva). Only one P tea looks decent. This sth P wave preceding bem #5. This P Wave appears cavher-than-expcted and is etched. deforming the emia portion of te T wave ofbeat H. Beat 5 sa PAC Premature trial Contraction) KEY Points about Figure 02.4.1: ‘Aa mpovtat peuple hn inspection ito look ist forthe underving thythm, This ay nt avays be obvious when smoce than oa dyn abucemalty is peeseut. Tas, despite ‘rely f the sho in both Tracing A and B — a mjc of weaver ns each uacing ae of tovtical morpeloe wih ced PR ater and upright defecton he lad Trenton, lead. Thersfoe~ the underlying mechanism ssiaus i each ase + Wheter the change in P wave morphology Fr beats 34.5.6 Tracing represents single sith to an atemate ai foes ote wandering pacemaker (wth frequent transition ‘reand ou of snus Pym) canal be determined Koes hs bee syn tip. Regurdess, la mats is that he unde mechs i ns + Wandering pacemaker ~ isa commen tytn variant that most often bein in patents witout Sigifcant heart ease. Typicaly one sees a sres of beats with ene P wave morphology that radualy changes to anther P wave morphology (asthe ste of tho pacemaker shifts from the Sd nede 0 elsewhere it the atria). AS aight be imasand — ‘Saznoss of "Wanda" pacemaker requres more thin the "suas" ea lei hin Sp (as was seer if of Figure 024-2) + Tracing B in Figwe 02 4-2 manifests sinus arthythmia wich 2 PAC. Aditonal wacings an cna comenon i needes to determine the sigiicance (ary os (025 -Norm for Rate: Different in Children [Norma ine for hear rate are difereat in chidren While we pinartycoacerncursshes in tis Suggested Approach: (Check 1st fora Plse! This is bacanse IE no pubes presual — We pal wal wapectied Wide aivena shoud be Sealed be sae as VER Ge, with mediate wy ncloonized shock — Section 01.3) 4+ Othe othr tan — TE apse is present — the KET tosses for Hemodbmanale Stability (Sezo7 04 0), (te IF the pact wth Techycardia har a pls bis not Stable — then immeaiare weaments needed It no longer matters what the vthm is sce the pant needs tobe ‘cardioverted ASAP! mr Te ft wey tn coms pad on it lan wi ectriciy shock (ho hsb spmchronand conven pda). + Cantioversion (Section 05.0) — Begin with 100-200 joules (depenang an symprom sever) foe the patie in ned of emergency cavern, Increase nay as isneaded TE tonale to earowent— then dere Delibrilate — Go stash to wouclrored shock (fiat the yt s polyno VT'Towsads (since synchronised cardioversion will mot wor) (03.4—IE the Patient is Stable I the patet with npecifed tachycardias ial stable — then by deiiioe thereat as come ine to proceed wih Sher evahusion before begining specie weston. Hopefily you be abe to determine the espe of Tachycardia: + Systematcaly assess the § Parameters, Thats “Watch Tow’ Ps, Os and 3Rs (Section 02.) Pechaps the most importa of tese 5 parameters when assessing the paint with twupecfed tachycardia is dtemining IF the QRS wide og narow (035—Is tho QRS Complex Wide or Narrow? IF te QRS couples i uly marcow ina pleat with able Tachycorda— thea for practical puposcs, te dtm is SipvaVenriculart Since te pants stable — Get a 12-ead to confirm thatthe QRS is uly narowin al 12 leads ‘+ Ou deision of “WIDE —'s more than 0.10 second Ge, mare thar alfa large box in duration) Once coafeme thatthe QRS & normal Sead — Treat as per SVT Algorithm (Seri 13.2). 03.6 TF the QRS Complex i Wide ‘The approach to mspeced tachycardia wil be treat IF the QRS is WIDE: + Assess th pte. Make sure the potion i tabla! 4 Assussthe ECG Gera 12 tead Deterine IF theeythn i) monomorphic VT; i) WCT of uncertain ilo o i) Somerhing de Go, Torsades, polymorphic VT. WPM). + GOTO the appropriate Algorithm (Se Surnmary Section 03.7) IE ay tine the patient becomes unstable — medial crdiovert ode 03,7 Summary: Management of Unspecified Tachycardia (2 SUMMARY: Betiom Line — The Ist stp in managemeat of any taciyearia — is delemine IF te potion table? 4 Ts there apuse?IPnot — treat as VF (efit) [BR apateispresearbut the pases nor sable asa direct result ofthe fast rate) — Deliver elec (yelvonized cardioversion ox defibrilaion). Bur IE th patn ntachycera Stable — there i time to ssoss Father Gera 12-ead, Bega tnzted management basa on You Dest avss as to what the dyn kay tobe See appropriate aiorithe + Hemodynamic Stability? — Section 040. + Sincivonized Cardoversion — Sect 080. {sing Adanosne — Section 050, Known VT — Section 070 WCTS of Uncertain Etiology — Section 03.0. Polymorphic VT Tenses — Section 110. Vor Fam AF wth WPW — Secon 120. Namove Tachycardias — Secon 130 [AB (Section 141.0)~MAT (Section 14.2.0) SVT Section 14.3.0)~ AFhtter (Section 144.0)~ Sims Tachycardia (Section 14.5.0) [Nous IF at np ine inthe process the patient becomes unstable —inmecately cardover ox erie. (0388 A Final Word on Algorithms Algortins provide idence They age excellent leans tol — and they bly summarize the most commen nervntons formas suasons. But — “are sno one size that fs all” — andthe thinking clncin athe bedside wl fen need to conser ational measures, + Welove aorthns as a staring place. + Tha said sometimes — “Ta just gota be shore (atthe bedi of the pation)”Section 04.0 —Is the Patient Stabe? Ts the Patient StableP (04. —How to Assese Is the Patient Stable? CCtcaly, the most important parameter to assess in ry patent with a cardiseambythunin — is whether the sythm is hemodpnamically "significant. This holds tue rosardess of whet the Hy ia questions sow or fist. Ayan issidto be “hemo namical” sigiicent — IE & produces sign cx symptoms of concern a a cirec esl ofthe ae (be che rate fast slow) + Signs cf Concern —incnd hypotension ie, stole BP 80-00 mr Hi) shock: heart ae pumonary edema ‘or sce econ, + Sumptoms of Concern — che ches pain, shores of beat: and/or mpaized metal som. 042 KEY Points: “Sometimes you just have tobe there...” (G2> KEY Points: ‘The deinion of hemodynamic ably fs aqully apple for supraventricular taciyarnmias — as his for VT Tat 5 he pleat wth tachycardia whois clearly symptomatic Ge, Jnporensive: shor of breath: confused) iia aced of inomecaze synchronized cardioversion —regardlase of whether th dda is VT ce SVT. la comvast~awial ef medica tarapy S jstfed IE the patient stable! 4+ Scmaies — "Youjust have tobe there" For exale, dase a sytoke BP of 75 man Ha — we would nat access cardiovetaptza with tachycardia who was oherse tolerating the rsthm walle, without chase pain dyspnea, or cnficion). Some patents may remain stable fr hous (or ever: days!) — cepts beng in sustained VT. Treat the patient — [=> Beyond-the-Textbook. ‘A KEY compoacatto assessments ting t dterine IF isthe ro rte Vion tars causiig te pata to be waste (tho wnderng condition). + For Tachycardia — Conser the example of AIVR (decelerated JéioVenriular Rhythm) at a rate of 110-120;mimte. This ates usty no fast enough to produce “instaby ‘Oa he ear hand — los of tesa "ck association vith AIVE at 110 inn apa wth undoing veuicular dyson ay lel be exough to procs symptomatic Inpoteasion. + ln general I the rate of tachycardias Lethon ~1SOiminate — isles cet that hemedsnanis insta s being consd bythe api cate. Tht sad. exceptions exit — as VE a1 140 minute a psion ithunderjing hea sonia may defitly prc hemodmaniccomexonse + For Bradyeardia— A rte as sow as 30/minate wl noe necessary ante symptoms. IF the simaton is non-acue — weatment wth Atropine Epinephrine or Dopamine may canse smote harm tin good (Careful observation may be al lat sneaded) In contest — eter pais ay be spermatic wi much ess sevre beadveara (baseline low BP, ‘schema or hart file are presen) (044 Bottom Line: No “Magic” Numbers (2S Bottom Line: ‘Bottom Line — Thoze are no “magic numbers” For delay banjos sabiiy" astad — Wis delamination se einical process tobe based on ongoing assessment ofthe patent by the cain on-the-sceneSection 05.0 - Synchronized Cardiovers Synchronized Cardioversion 051 - Synchronized Cartioversion: Definition Shrichnonzed Cardoversion gure 05.-1) — eat debvery ofthe clecicel charge ata specified poi athe cardiac cycle (on & wave aptroke oS wave downslops) — amy ‘ea the "vulnerable" period (which is near the end ofthe T wave). Doig so makes cardioversion safer han unsyncicoized shock (efbilaion) + Crdiovarsion i especialy eetve in weutacat of atlas tht depead on a reeny mochassn for ti pape This iacades (among others) eal ute, PSV, ‘vend accra, nd acessory pathway reenrs tachycardas. Cardoversion slo very effect in teminaing APB, + Symchoaized elecwical cardioversion wedks by producing a sng, bef daceical discharge ~ tht acts to teemaae the acini by intorupting the reeuras cut andor aesing ‘sondton ropes (conduction veloc; rjhactonnass) that ed to perpetuation ofthe arti [Synch|_Vuinerable Period Figure 05.11: Sinchronized eantioverson. The electrical impube is schvonized to the QRS complex, so as (0 oid delivery of the discharge ding the “vera” period. Ths tities the rk of precipitating VFib when caeeyisdevered. 05.2 — Clarification of Terms ‘he tem cavioverson may be the somce of some cofision, Tis because the tennis commonly inrchanzed (and mistakenly equated) with ovo other tems: deftvilaion and cowiterthock, + Detibrilation — isthe process of passing en elecical cent ough the beat with express inet of completely deplesing il myocardial cols. The lactic charge tht ekvered with debian is uneynchronize ~ which mean hat oceur tan ety rarom point in the cariac crc + In contest — ue ofthe tema cardioversion inp thatthe elacical charge has beca ted cyclone) to ocauet a designated post inthe cardiac cyl. Doing so ast cy ‘ines comersio of coti tchrytiias to seus syn ~ but aso miminizes the chance that the clectcalinplse wil exacerbate the aria (os man occur the ‘imu happens tobe clvered during the vuburable perio). NOTE: To avoid confision about temizclogy (ar well as 10 clarify the mode of davery af the elecnical impulse) ~ we Sequealy scr to the peocedre as “synchronized ‘ardloverson” (rather than simply “cardioversion” 4+ Atthough use of the combined tam "achranzed cardhoversion” may sem sedundsat it eaves no doubt ast how the opessoe is about to proceed + Use ofthe term “synchronzed” cadioversin aso bps separate electrical cardioversion (with delivery ofa timed cloctricalcischarge synchronized toa spectfc point inthe cardiac eye) ~ fom medical cardioversion (ix which a medication such as amiodarone or procainamide is even ta patent in AFI hope of facltarng Conversion fo Fina rite wile me of acta + The aced for synchronized cardioversion may be “emergent” (immediatly need because the patient is decompencatng) ~ or the procedare may be “elective” (noe nimadlatly needed bocowse the patients hed\nanicall stale) Thate ma be gadtons cf" Wwyucy” betes Ge, sem-eleeive)~ fhe plea manests Symptoms Foe. ‘he ants bt snot sete decompensaing + Fly ~ thee aay be spontancous conversion (rather than spontaneous “carctovesion”) ofthe eth to onal wea th tachvaria resolves on is owa without any mediante ation, ‘he last 2 terms in nee of chitin are countrshock and ts dnmtve “shock” Both ofthese terms ace often ech interchanged wth the tem, defibrillation. We favor tis ee ‘terchange, aod less ochre specod gonraly we these 3 temas syncasmeusl to apeesat deBry of an ansyrclronced deotiea zpuse to patel ia VED. (05.3 ~ Selection ofJnicad Energy Levels ‘The cal eat fda Sleton fal eneray level for sjnclouzod caroverson is enpie. We suggest the flowag 4 Atrial Flatter — Use ow energy fst (50 joules) — as ter is us very sesposive to cn doves. + Monomonphic VEWCT — Consiser stating 3100-200 joes (monophasic ex phase defbilstor — dapencins on symptom sever). Tncreasecoeey as nese + ABib— Higher anes are Wey tobe needed (beg vith 200 joules monophasic 9 ~100-200 joules bphast). 1+ Other Tnstable SVT — Consider 100-200 jodes (monophasic or biphasic) — depending on symptom seventy andthe kay iclgy of the shyt. + Torsades/Polemorphic VI — DeStrte! (Don's bother ming to synch, as ding 50s uaa 20 wor), 054 Cardioversion: Beyondbthe-Textbook kK => Beyond-the-Textbook: Although data or al stations ae licking — Several pots canbe ade gang reconapeadstons for Bow much energy Te 4+ Various stinseespond decay. Ia general —oxpunized shyt (uch as 4Fluter, manonorpite VT) tend wo eespod bene (Co lower energie) tan ess exganizod shins (uch as AP) 4+ Tacease oneay 2 ned IF pica als to rospond # Certain SVT vinythms Ge, MAT; anomeric atrial tac junctional tach aro unlely to respond to syetnonized candioversion ( f they co respond’ — th rim wall sual ecw). Foeenately — is vere hat these thas requie cardioversion (Comecing the underving cvorder isk for these arhytionia). [NOTE Whenever posshle — Sedate the conscious patient prix to synchronized exrioverson (an it almost alwans wil be possible + Bese continual) monte the pata xoughout the procedre + Obtain an onsite hardcopy ofthe vm jut before, dina. and imediely wer deers ofthe symcroxze impulse since aha copy shin stip may be needed to detect subse chases tat may occur eth. 05 -Cardioversion: IF the Synch Discharge Won't Go Off Bo Aware common reasons ith deelacr may act ire Whe atempig to cardiovert hes ache: Svnch mode not comet on Inabity to synch on a partiar QRS complex. ‘Monior gain set too Jo to sense. Peyscauel ac wana with oparatg the device (sere are mary diferent pes of defibrillators in use ~ and each has its own particulars regarding activation and operation of mck mock). (U2> KEY Point: TE for arp reason you re wable to get the deinlatorto delve asyctroived inplse — Turn ofthe “synch” modo andl defibrilate te pet! + Ten asl nt worth spending cova tne tying o Snare ut why the sya mode wilnotwosk nan actly decompensatn pata 1 Deleery af on ongelvonized Sechage(debrlarion)~ wi anos eave wok at mel asa synchronized one (the ieveaze tk from suclvonicad echarge i mio) tis good to anipte the worst” that could happen ding aeupted caioveson. This way youll be prepare + IE devery of a sychrnized impulse precpintes VFlb — thea immediatly dele the pia. The “good news” is that hs wi ual be the bec tine to dbl since you ‘are right there om the scene aa ar immediate shock after this wimessed VF} + Tesrare that synchronize cardioversion il precipitate asytle IF ths occurs — Be avare thatthe patent wl anos abvays respond to temporary pacing 05.6 ~Candiversion: ACLS Provider Manual Recommendations ACLS-PM Provider Manual recommends spec ence levels that ie Sigh fom what we sognest ia Secon 05.3. Speclcaly ~ACLS-PM recommends he follwing: + Narrow Regular Tachycardia — 50-100 jules ‘Narrow regular Tacyeardia— 120-200 jus biphasic (2001 monophasic), + Tice Regsr Tachycaria— 100 joules + Wide Bregular Tachycrda— Deftilae (Don't sync), [NOTE — Mush more important than the ets of hs ny joules to use fer ons ial syclnaized cardioversion atop the concept + IE prope peomed — Sychronised cardioversion ois a safer way to cectcally conver a patent out of an unstable tachyantythmia (Secon it avoids the “vuinerable (porod” — onde therefore lee likely to precipitate VFS). Orgized syns tnd to respond bet — bg regardless ofthe stringency level selected — You l want ‘crocs tis the pate fas o respond [Ei doubt — Deflation wil anos away work 05.7 —What about the Precondial Thump? ‘Use ofthe precordial thanp dates bare to 1920s, when the procode was ist used cna pat having Stokes Adansatacks. A essence us ofthe amp was Seon inthe 1970s with serendipitous report of imaveteat passage by a wanportambulmce over pking lt speed bump suprisingly restoring sins syn to apaet in cara arest The technique became ‘popular end was rouielyveconmeced ding the early days of ACLS protocols, + To perform a precordial thump ~ a sap, qk blow i sock withthe esky par ofthe Sst (hpporhonar eminence) om a disance of 8-12 aches above the chest 10 the ‘nidpordon ofthe paet’s ster. The blow shouldbe fa, but itso free a obra ay tos + Mechanical encrey generated by the than hasbeen sho to produce aloe amplide declaration of approximataly 28 jou 4 The amount of clacrical eneay acaded to dai a patiet n VFB invossas expoventily aftr the St Fes moments flowing onset ef VFB. The thoughts at IF te thay generates ~2-5 joules of energy at an ezip-anaugh-poit inthe proces ~ tht is migt be enough to convert Vib to sins sytim. Theme tine tat pases afer onset of VF = ‘ees the chance thatthe thump wil generate enough energy to be success. ‘+ A thump is nor bei. Ribs may be broken ~ and exces in force, atonal candi inury may our. Although data ae scarce ~ there ae epets hat deivery of thm toa pata in VT at he erong pin (cong the “suberable” perio) in the cardia cyle may precipitate detonation of VT to Vb. As opposetoappcaion of. chronirad ‘anioverson wih a diel ~davery of 2-5 joules va tmp cannor be ime to the cardi ee ROTTOM Lino (ogoring the Thump): Think ofthe peor arp a1 "Nowe procodare. I should onl be conidered in paint without ape (ft considera at ll), 4+ ACLS-PM ao eager commands se ofthe dep. IF deixar is close by itis far bert deliver en elacizal shock asap wh th desltor + We mighz conser using a tnunp ~ IF we were quickly on ta-zcens ata pulseless cardiac wrest in which ro defbriaor was ready arable In ths ckcamstance, thee i ie to Jove anda prompil delivered tasep might werk to convert VEb (abet reltc chance of success aditaly mall. + Do not ws the tnunp ifyoufed a pulse! Tare IS “something to Te” this sion e, the pug). TF the syns VT with «pase ~devery ofa precorial hump is tistical, far or cel to precinate detonation to Vib than sto conver the hth. 058 What about Cough Version fr VFib? ‘The technique fr cough Versio is snpe: As so0n a the arhyhmia is acted —inseact the pact to, "Coughs Har nel keep coughing!” Coughing shouldbe contied at 1-1-3 second intra ~ cher etl the nf comverted ort athe appropri nervenion Ge. cardhoversion) canbe ied + laps for advocating ie of cough version enue fom observation in he ceric catheterization laboratory that forceful and repettive coughing Ge, “cough CPR") — coud sustain consciousness fr supine peo f tine (of wp to 99 seconds! n patents wih pseless VT, Vb o even asytle + laathoracc press of more than 100 amis are produced by such coughing ~ sad ae somalow able to ganrale adequate Wood ow dept the presnce ef an these nos perusing Hott. The mechanism fer cough version temas unsnown (increased intrathoracic pressure vs autonomic nervous stem activation vs conversion of mechanical ‘nergy from coughing ico a fo ule of elecrical energ?), What IS known ~ sta gorous coughing cccasionaly converts maligamt armas to ocnal ss zim. 4+ Saco coin descepion of cough CPR by Coley etal 1976 ~ stroking palits to cough atthe onset of nonperusig ets las been wsed i the cai cathetorzaon Inbocatory. That said the techniques tl nel fnoced by aloo many other emergency care provers who rarey seem to voke coughing in the conscious patent atthe msc of a spaiguat anhytinaSection 6.0 Using Adenosine (SVT VT WCT) Using Adenosine 06.1 - Indications for Adenosine ‘The primary indication foc Adenosine has becn tacyachtuiae wih a eonny mechani — expecially tose ching atleast a gonton ofthe AV Node inthe reety crt. Indications {foc Adenosine have expanded 4+ PSVT— Adenosine sth dug of Ist choice fer emergency woatment of PSVT (2.90% successful conversion rate) — slough longer ste drugs Ge, ditacen verapanal, Bata “ocker) maybe needed to prevent PSVT recirence (Sections 13.15, 1310) + “Chemical” Valsalva — ia wich Adenosine s pea 25a chagnact/thorapeurc wil for a narow tachycardia of wicerta elegy (Figure 00.1), Pesonably — Adenosine sllcomert he shia tie SVT act — i wl hope slow tery enous (ronson) to allw = deftiv agosto be made (ut ike Vaealva WOT —ACLS-PM now reconmeads Adenosine as a eu of Ist choice So regular monomorphic VI ce WCT cf uncerain etiology (Seo Sections 06 2,064 an 06.) gggegged Figure 061-1: Chonical vale Adniesvation of Adenosine tots pint wth aveauar SVT at -1SDinzute ross a ean agnostic Sowing that reveals undeing Sater waves et '300)minuke. Th continuation ofthis yt strip is shown in Figure 08 3-1). 062 KEY Points: Dosing of Adenosine (> KEY Points: DOSING: Adznosn is adzistored TV push —gitag the drug os api as pose ouor 13 seconds (Go That doesn detanovate im the IV cubing) IV Adoposine hal Me less than 10 secon! Fallow bofses with hid eh + Fatah ge Gg by TV ps + IF no response afte 1-2 mimes — gee 12mg by 1V posh (fr atoal de {+ ACLS-PM no longer seconmnends svg a scond Leg bois the pat has st responded Dosis protocols for we of Adenosine shoul nt necessarily be fived for ll as, nstead ~it is wel to be aware of eccasioal instances whe ier or Tower doses of the ue are idea + Lower Adenosine doses (ie, 2-3mg ira) — shold be considered for older patents; those with rena fee; heart fre sock; in waneplon pas: taking Spyidancte (Persantne)~ and ~ when Adenosine i en by conal TV He + Higher Adenosine doses — may be cde fo pata epi for ths consuming lrg amas of cline) — sce mayne impede tnd of sie tits ecepoe sts, (06.3 Adverse fects of Adenosine Adensie norway basin. Alough the drug usu fly wel tolerated — a series of adverse eects common (andr be expected). + Adverse effets say include) chest pia: i) cough hom rencions bronchospasm) i) caaazons vasodiaon: iv) metalic taste: a sense of impending doom: nd vi) vans ‘radjoala that maybe marked (and which my even cause a brief poiod of amst00), + The good pews” —is tha averse efects most often resolve chin | minute although hs maybe vary slamsing inthe meantime IF the emergency care poser is oe ase of ‘what fo expect (Figure 06.1), NOTE: Se cnciens even ook away fr 20-30 seconds fer ging Adenosine ~ a0 snot tobe bothered by the tans marked rate sowing that so cftenis seen, While not suggesting you do this itis wellto be aware tha markad ate slowing may transiently occu + HINAL Note: Adsnosine my shorten the refactory period of aval ee — which could inate AFD predisposed indhidual. As aresk — Adenosine shoud be sed vith, ‘tion's pate ih known WPW, shen theoretic ponsliyofindicins AF uch could have significant conreguence inpatient with patina} Figure 06:31: Chenizal Vasava(Coutiuation ofthe ripton serip shown in Figure 061-0, Adzisisvaton of Adenosine was Gags ofthe etiology of his regular SVT dyin (avedline wadertyingatral fiater at ~300'minut) Tn 50 ding ~ a peiod of evar 10 seconds ensued without a RS complex. Marked bradycardia sch as this a not uncommon accompanincs of Adenosine that the emergency care provider needs to be aware of Badycarda aust avays rsclves within 30-60 seconds (adesine halflife following IV ‘dininisvation i es than 10 second). 06.4 Using Adenosine: Beyondthe Textbook => Beyond-the-Textbook: Despite the above series of adverse elects — Adenosine renats au raceedngy wal opel a cesgsiey Cade ewe. TE Ww wel late. Nevers itis nt completely benion— and~ abaance must be reached between pros and cons cf wg is drag. + Itisa peat dug for SVT (of nnown or ainonn eticleg. ‘+ Adenosine should nor be wsed fr) polvmorzhie VT. i) Tass; or i) WPW with very rapid AF since Adenosine may precipitate deteriaration fo VE f given for these vrythns)- Instead — defibrillation maybe need, + EARLY use of Adenosine — may lop gel evlasion'managencat of stable monomorphic WCT. We for Adenoss: i) IE we ik thir is reasonable chance the WCT. ‘supraventricular (Adenosine will wally convert PSVT = andi fociltaesdhasass of other SUTs by bef slowing the rat}. xi) TE we ink the pent might have =. aadenosinesresponsive VT (Secon 06.. 4+ Adnitodly — tere are nes we empirically try Adenosine when we have no idea What the dln (VT ¥s SVT). That seid — we genely prefer norto use Adanose when ‘he cincal sting and 12-ea ECG sogzest anor-esponsive form of VTi key. Sometimes — "Faust gota be there". «+ PEARL: Do not we Adenosine to test SVT i a heart tansplnt patie (uch lower doses ave needed due to Adenosin-hyperceniiviy). Amimophyline say reverse ‘adenosine need eeveme bradycardia (Ses Section 16.) Final PEARL: Adenosine should probably not be used to west SVT by the 1O route. Tine fr 10 absorption may exceed ta 10-second bale of tis dug (beter zo use IV Dittazem 10 eat SVT if only 10 access i available) 065— When to Suspect Adenosine-Responsive VI? A cow of VT rintms de respond to Adenosine! These adenosine-responsine VTs ar most commonly catecholamine induced and occur during exorcise in younoer ads without srl beet cae: + Many ofthese VTs originate tom the RVOT (Right Vonriclar Ouflos Trac) — though hey ca also arise from the LV, the henifsciles, or sewer. 4 We suspeet RVOT VT— IF a youn ada presets wih n exrcse diced regular WCT showing LBBB i preccdllads end an neice sis (Figure 06 5-1). That sid — adenosine responsive feems of VT can not alvays be pected by ther BCG appearance! Tiss the rationale for empiric wse of Adenosine with a regular WCT Pe pe eed Miyyniennnan neni MY a Mad m nl igure 06 51: RVOT-VT. Supect RVOT VI when a youger (20-4090) adit peseuls wh en exercve-iduced segdae WCT shoving a LBBB pata in precordial ads ~and— on ‘inferior min the lead (So fx). ‘The mechanism whereby Adenosine may work Fr certain forms of VT (uth as RFOT V7) —is ation ofthese VTsis itt be due totes alsa overload (which afi cellular depolarization trasholes with esata “oggered aciviy” med by cycc- AMP (which donasins inhibi) + Mechanisms of nom adenosine responsive fems of VT are generally schemata, or det increased automatty — none of which respond te Adenosine [Note VerapamiDitiarem — may aso emsinate RVOT VI (by a aiffivent mechanism that inhibits nmaceldar calcium channel). That suid — these 2 calm Mockers sald ‘never be wed ete for WCT sts (1) —becanse the vasodilatory and negeivenctopic eflcts may peecitate detection to VFB + Beta Blockers — may abo at ines eminate RVOT VI (thece drugs also lower eyc-AMP levels. ‘+ Vagal Manvevers — may on occasion teminnte RVOT VT (rnc that the previons dictum saying rasponce ta vagal maneuver rules oxt VTi no longer completly tue). 06.6 Summary: Use of Adenosine for WCIVT (G2 SUMMARY: A pow of VT shythns co espond to Adenosie: Overall — this wakes up [ass than 10% of all VI — but bur prevalence cb adisine responsive VT depeads on characteris of the poplaoa being assessed (neath subjct vs pation with echomic sare ate.) + Polymorphic VT (or WCT) —is wily respond to Adenosine (Adenasine isnot recommenced for thi) 4 Ischemic sel recntrant VTs (s ae camino se olde” patents with coronary or sructural hart disease) — generally do nor espe to Adenosine 1 Suspect an adenosine-esponsive form of VT — hea areghlr monomorphic WCT is seen in. younger ads (~20-<0 yar la) without ndesng het scase — especialy the WCT was precpitased by exercise. 1+ Most (50.9085) epular WOT without clear sian of cin P wave actty are duc to VT. This faze goes up to ~00.98%% the pain i older, a het ear, and mart ‘erin norpholog franres (LIST #! — Section 08.7). 4+ Inthe pst twas oust thr IE a WCT responded to Adenosine — that his “proved? the WCT was supeaveaicala, Given awareness that certain forms of VT ma rogpnd to Adenosine — We now appreciate tht conversion of WT to sine rythm wth we of Adenosine doesnot prove anhing regain clog of the artim. Bottom Line: — IV Adeaosiae may be ied early oa athe weameatagort cf monomorphic stable WCT. ls use i usually saf ia is suaion — andthe drug may work by overt the den IF is supeentclr or one ef the unconmnon fom af adenesine-rsponsive VTSection 07.0 Known VI (Ventricular Tachycardia) | Known VT 07. VE: Rhythm Description ‘This Seaton dels th the approach to the patie who You uw isi sustained monomorphic VT (Ventricular Tacluear) Lead a Figure 071-1: Veaticulr Techyearda. Tis stm is farther dedinated as monomarphie VT brcaise QRS moxpbslogy (ouside of minor vanarion ix amplitude does wor change shrooghow the wang _Rhvthm Description — usualy rear (c at est ary rogl)wide-QRStachveariawithou lear evidence of acemal anal acy. © Teamieatny — Tee Aion of rasininn! PT" wets ty esis Md waters ree pesserse of VT fx tt Dr 30 secondo tng can to ec symptoas of iypoteasion or syacope. The team, “NSVI" (or Sustained Verrculr Taclvcarci) i wsedto designate shorter ras of VT (hom 3 PVCs ina yew ~ ep to 15-20 secouls of VP) at donot prodace hmedyuanic spas (See Figure 0220-1) ‘Bedside Pitfalls —Do not depend on emodanic tts to help wh the deentiaion between SVT and VT. Some pists remain awake aed alt (oid normotensive for ours (even dave) — despie being in sustained VT! (07.2 Sustained VT: What To Do Firs? ‘The KET to optimal management of VT bes with adesing these 3 Questions: i) ste a Pulse? — i Is the paint Stable? — and i) Ace you cert that the shyt is really VT? (Ge Sector 08.0) IE there is NO Pulse — then immediately debate. Test pulselest VE the same as VFB (See Setion 01.5, But IF Pulse is presen ding sustaouad VT — Assess the pti for hemochramicsabity (Section 041) 4+ TE apule ie present butte paint wth VTi unstable ~ thea immacata ardiovert! 1 ue the pater wih crtined VTi table ~ thn there i at act ont tne for vial of nine drag (Secon 07.12). [NOTE ithe tytn is polymorphic VI (ir which QRS morphology varies thoughout the tracing) ~ the patent shouldbe defilated (Section 11.0, + Masy (mos) pata in sesained polmorphic VT wi be plsess. Cardioversion is usually ile —becase “synching” wo a constantly changing QRST comple is not posse. Acate ‘rennet is wth snsyncironied sock (deflation). 073 Sustained Monomorphic VT: Suggested Approach => Suggested Approach: [NOTE The apprsch we propose below enter tat we Know the stn WT: and) da the VE i monomorphic (orator iv Figure 07 1-1) — and not polmoepc VT (whic ‘shoul bo inmectately deftriatee, It alo assnes i) hatte patent remains stable twoushout the process (Stack is ncicazed if at anytime the pavent becomes wrstable. First Fix he “Fixnbles” — Betr ton antic dress to fn! nd “fo” ay potential precipitating causes of VT as soon as you cn. These ma nc: + leche disturbance (ep ow M+ ot K), + Acidosis Hiposhcemia 4 Hyposenis * Shock Grom fypovolomia: blood los; saps et.) 1 Uacomtoled ischeni/scte fection. + cate her fe + DigtoxctyDrug overdose. 074 Use of ADENOSINE for Sustained VT ‘Suoagl consider Adenosine asthe Ist drug you ve (Seton 00.0) — especialy IF an aonccne-responsive fom of VT is Wess Ge, youngar adult without underpin heart eiseate: cexerceindnend VD, + Adenosine may ao work whan WCTVT occurs in der pation with hart ease eerie —5-1086 of hee). {+ Begn wah 6mgby IV push. Fao response 1-2 mikes — Give I2mg by IV push (fora otal dose = 6213) Side eects fom Adenosine eur shot ved due fo the drug alia sort half Ife — Section 06.3) Do nat use Adenosine for pobmorphic VT or Torsades. TE: We donor evass start with Adenosine inal oder patients with sclomic VT from known coronary disease. 075—AMIODARONE for Sustained VT ‘Amiodaroas has becom ou prefered intial agent of chcce (after Adosine for stable sustained VT: + Give 150 mg IV over 10 mines. May repeat. IF he rug wos — Consider mitonance IV infusion ot 1 mg saute (See ato Section 07.18, 07.6 -PROCATNAMIDE for Sustained VT Procalsanide is ato recommended by ACLS-PM (Provider Manual as a1stine rug of choice for sustained VT (Section 07.19). + Give 100 mg TV slo over §mmtes (ar ~20 mari) —p toa oading dose of ~$00-1,000 mg. May fow wth LV infusion at 2 mg/minute (!-4 me minute range). 077 -TV MAGNESTUM for Sustained VT (Consider IV Maguesan for nor-vesponding VT. Magnsin isthe dug of chcice foe Torsades and thn seran Mapuesian levels ar know tobe low (See Section 0718 for ACLS-PM recommendatons plus more an IY Moguestuo fr VD) 4+ Give 12 gm IV (over 1-2 mines). May repeat (especialy IF serum Mg++ level is known tobe iw), * Figher IV Mg doses way be needed wth Torsades (some cases have rqutred upto 4-8gm I). (078 1V BETA-BLOCKERS for Sustained VT IV Beta Blockers are most Hey to work IE excess sympahotic tones eithercotbing toot ithe ease of sustained VT (Soe Section 07.19 for ACLS-PM recommendations plus ‘mare on JP Bet Blockers for VD) + Metoprolol — Give $ mg IV over ~2 miames, May thea peat ip 10 Sg total). May decreas ate of adniitaton depending on BP response 1 Many otherIV B-blackers are avaabl (but the Metopralol regimen i simple ands commonty used), 079 -SOTALOL for Susained VT Soins recommended by ACLS-PM as an tool option for sustained VT (See alia Section 7.16), Do na we Staal the QT prolonged. 4+ Give 100.mg (1.5 mgrhy) IV over Sts. 07.10 LIDOCAINE for Suseained VI Lidocaine now considered a a 3rd-ne option fr sustatnd! VT (See alsa Section 7.17). + Give 75-100 mg Lidocaine (-1 0-15 mgikg) a an ia! TV bolus. At the seane tne begin Lidocaine TV infusion (er 2 gina). May repeat the 1V bobs (ing 50-75 mg) Encoded in ~5 mites 07.11 - Synchronized CARDIOVERSION for Sustained VT ‘Thece may wel come a polar doring the above reannem process when Mie Becomes rime to getthe patent oto sustained VT + Atthat pit — Cardiovert! (Section 05.0). 0712- Sustained VI: Beyond-the-Textbook TONY E> Beyond-the-Textbook: ACLS-PM recommend TV anarytnic infin for sustained sable monomorphic WI — pias eper consiiaion Ow foal oto seize an approach when expert conslation soe ‘mediately aval. + ACLS-PM ists Procaimamide ~ Amiodarone ~ and Sotalol (bur nor Lidbeaive) as potential aniantythnic options (although Lidocaine ix listed elsewhere as a potential ‘alternative for monamerplie FT) ACLS.PM doesnot make ‘econmendtion aso wc arty sould be gen a ich sequence + The good news” — thet antahyhic therapy may successfully convert ome patients who are in stable sustained VT or WCT without ned or eletcal therapy 4+ The sobering clinical reality — i tht one of the eaanhythas aga we very efecto such Weatuet (and all af hase drugs ae associated wit potential for adverse _afects). Many patents wl nt respond + Opinions vary sto which drag shoud be sven when. Defniive data are lacking. We provide ou bias blow — ceasing thar say de ftom other views 4 Potential problems whercat in any study allemsing randomized prospective. double bia assessmet of he rlanive efaciveness of aieains dss ae many i) eave lniequency of naw-onsee sable suained VT in an ED pent not yet ereatad with anianbythmic drugs; i) need for primary coacera being welise ofthe patent (rater than Implomeidation af scr study protoce) i) eadeucy toward use of more Un a Seglo weamueat Wiha the ciel ial 20 mutes fx studvag Dis queston is) subsequat Impose of separating oot pote ynergire devimenal ect when more than 1 anfarintmic dig i wsed, and x) rmendos variation snore cial and ECG huractates ofthe case at hand. BOTTOM LINE: Ita not be posshle to “prove (or eizrove) ta “Soper” of any panic asian deus for sustained VT (0713 - Clinical PEARLS: Antiarhythmic Drugs for VT (2 Clinical PEARLS: ‘We robably ill ever know which dria is “Det for stable sustained monomorphic WT Caza Gaxactrties of case atand (cluding posonal preference and experiance of ‘the treatin provider) jus several potently appropriate choices. We high the flowing: Adonos — Stony consider your Let dro for most patients in table monomorphic VT Sections 08 0 and 07.2), 4 Adenosne's dso of setions ver shor-Bved (allowing rapid use in moat parents without lasing adverse effet). NOTE: Efects (Gong! and acverse) of stg more than one ofthe attntnic ageats ste below ia Seton 0714-0719 ae acive. Be aware tht ata ine — eletcal therapy maybe azeded + IF mom tne dhrng thereat process the patie in sustained VT becom unsable —inmscoay carve! 07.14 More on AMTODARONE for VT Aniodarooe isin gencral our preferred drug fr aniaytmic weameat of sustained VT. Advaaesincade: fay and case of ainsration protoec i) ably tous in pains ‘wih heart fare i) low ickdence of Tovetdes (even though the OT may lengthen with use of this drug) ad i) eieacy i testing WCT sts (may convert various SVTs Including WPW with very rapid AF) + Watch BP; rece TV ifn rate fae needed. [ eectve — may conte as en LV Amiodarone infasion at ~Ienglninat for wp to 6 hows (ond 0.5 mini for 24-48 hows). (07.18 More on PROCAINAMIDE for VT Proceianide i pefered by many a ther dug of choice fo sustained VT. Eficacy appenrs comparable to Aniodsron fot VT and SVs + Give 20-50 mpiminate IV un ctr: the acti is supcessed: i ypotension ensues: i) QRS duration increases >50% I? laading ~300-1,000 m9) + May foliow wth IV maaenance infusion a mngimimite (/-4 mein rane). 4 Potential Deasbacks of Procazanide cde) QT prolongation i) dst wit hawt an: i ss cian andy and amore conplcted administationpotocal: and in) greater tendency to develop typoenson, especialy if fester infusion rates are used (Our prafronce is 10 start with increments af 100 mg IV over ~5 minutes = ~20 nigminze). in) ama dose = Iau hasbeen given (usual (07.16 - More on SOTALOL for VT Albough ACLS-PM coaveys comparable pity fr initial we o€1V Staal ~Proceinaide~ ane Ansindaone in teat sustained VT — Sotalol as only ecely besa approved for TW achiitaionnhe US + Adsamages — beta blacker seth, effsacy als for SVT. + Disadvantages — are concerning tus. They inch) ack o fanny with merpecy IV ose by US. clinicians; and signin QT prolongation wih sk of mrecipitating ‘Tsades. Tome wil tell regarding ace ofthis drug for VI and cardiac avec. Foc wow — tis not oe of ou favoced drugs fr Weating custaned VT. (07.17 = More on LIDOCAINE for VT Lidocaine used much es offen at resent than the past. The pray season for his i pression ti other drugs (Amiodarone: Procainamie) — ae cle moe effective ft stained VT. + ACLS-PM cles ist Liocaine san emai to Amiodarone fr sustained monomorphic VT + Practzaly speaking — most pacarswilbecardiovened before consideration of Lidocaine is reached inthe cureat VT teameatprotocsl 4 Achantages of Lidocaine tht may meri is consteaton a rie occasions inca) purported eficay in shemic-relared VT. i) lack of sient QT prolongation; and i) ‘como amity wth se by crcl tate nthe era when Ladoeame was standard’ therap That si, te die so longer wed mich + Rauauber— Lower maitnance IV afin sues (f 0-1 mg mire) shouldbe wedia older, ger patcas — espacial £ thro is heart ze (07.18 - More on MAGNESIUM for VP ‘Reals that ACLS. PMI os recoumnends IV Magnesium fer Totsades or ypomagnesania — We fea thre ae other indications fr use ia VT: + While aot neal as ete for plmoephic VT as it is Sor Torsades — IV Maguesim will wok for some cases. ECG distinction between “polymorphic VI" us Torsades semtines equivocal it depend on whether the Baseline OT is prolonged ar nat which wal at alwans be mown atthe time of tha acute station), Thre wou sem abe ‘no downside to cmp wil of IV M+ fo these patents (Section 11.) Empirie Magaesiam (ivor IV or PO) may be usc ca occas in Weutmeat cf other ath (incluig various SVTs red YD, + Most ofthe tine —you willnobe able rl et te posit ofl intrampocardial Magesian levels. This is because) no sera evel may be walsbe i) even if aaable— ‘enum levels conlate pood with eacelar (2nd invampocardial levels and ii) cardiac anes fen precpiates Hux and change inate itra- vp extacele K+ end Mig seve. + The “good” news — Minna! side deci (ether than mansiont iypetnsion) have bees acted even when very large IV Magnesia doses are sven, Reduce the rate or tempor stop the ifuion TBP dops (adherseefees quick resolve) ‘The DOSE of TV Magnesium to wse vais — depenting on the gency ofthe station. 4 Fee sable VT or Torsades — Give 12 gm TV overs period of 2-20 minutes (Give over 1-2 mites for VA). + For less wget stations —1-2 gm maybe ise over 30-60 mimes (or ever slower) May repeat as needed. 07.19 - More on BETA-BLOCKERS for VT ACLS-PM lms its seconmeadstion fr tse of Beta Blockers to narrow-QRS tachycardias. That sod, share an tines when empiric use ofan IV Beta-Blocker any be lssvig for VIVE nor sponding toa ole thea 4 Most cases of VT shoud nor be tested wih an TV Rets-Blocker (altiough some patients may already be on this drug for acute MI or other indication). Other ages (Amiodarone, Procaianide) ae wel more Afeive and shou be ted fst + Thetineto consider selecave use of an IV Beta-Blocker i fo sustained VT when increased sympathetic tone is suspected asa cootbutng case ofthe vt Ge, anterior MI especial su tclseardia and hypertension praca the onset of V7) 0720- BOTTOM Line: Kaown Sustained VT (2S Bottom Line: This Seton 07.0 presupposes tht we KNOW the tne definitely VT (ari almost always wil be when one haz a regular CT othout simu P waves) Tht sid — one can get, ocd so 4s good to remain opera other posses .. (See Section 08.0). + lathe meanie — Assume VI and reat accordinaly unt proven ebervise (As ctcusze i is Section 07.0. ‘+ Do NOT se 1V VerapanibDiltazem to eircal weat e WCT soles you ace 100% certs thatthe ryt is nor VT — and ta the paint does nor lave WPW. Ths because the negative inouepic and varodarory properties of these cam blockers (and their facilitating eect on accessory pathway conduction) may preciiate -Leadt (G2> Step #1A: IF uncertain-Geta12-Lead! Thece are several waysa ead ECG obianed daring cy lia ay be Felph These cde + Deteoining for swe IE the ORS i wide or nt Look in all 12 Toads: Measure th widest QRS yow soe). Remeber ~ thre may be distortion of ORS duration when wing a porable ECG montoeebllaor (cue 20 rime compression) ~ 50 the cal way to truly detemnine QRS width is by obtain a I2-lead ECG cng achyeardia. 4+ Assasing sand QRS mexphology ding acca * Looking in i! 12 eas for sens of abil act. + Goring a baseine ving tachyearda may prove iahuble ia munagemeat afer couversion to Ss eth. The tue eGology ofthe WCT wl semaines only be cuidate by ‘rorospecive comparison between the 12-fead ECG obtained cng and afer tachycardia ‘Sammary Poi IF the QRS on 12-lendis marrow (not more sham halfa large box) ~ then the stn san SVT Section 13.0). + But I the QRS is Wide — then by deftion, youve a WCT (Tce Complex Tachycardia). Goto STEP 2 (Section 08.6 (086 Steps #2, 2A: 15 she WCT Regular? ~ Monomorphic? ‘Step #2: [Is the WCTa Regular Rhythm? @ Step #2A: [s ita Monomorphic WCT? Praccaly speaking — We assess Steps 2 and 2A tgs Our reasons for dang so ae the folowing + Polymorphic WCT (or which ORS morphology cring tachvcardha changes) — wil on equ defbiltin for conversion These stuns are typically trem snd ince _pob morphic VT and Tersades de Pointe (Secron 11.0) + Monomorphie WCT (1 winch the ORS darng tachvcardia stays the saree) — is often ension to eat TE mo P waves ae sn a heen is imegularly ieeyular — Consior A. + Keep inmind that some VT syns maybe sight tegular(though not nearly as regular as AFI. {But IP he sytin sa regular (or almost regular) monomorphic WCT wthons clear evidence of soma sas P waves ~ then the eesti win LIST Hl (Fable 087-1. 08.7 LIST #1: Causes of « Regular WCT of Uncertain Eology The common caves ofa reel monomorphic WCT rtm withous cls sgn of arma P wave ct are noted in LIST 1 (Tale 087-1. We emphasize the following pons abowt Line + The season we pat VT as theft 8 ese in LIST #1 is elt i It is By fr the most common eanse of a cep (or almost regular) WCT in atts whea sas P waves are Juekng andi Is the most serious cause! + The likelihood that 2 WCT is VT goes up even more (to at feast 9094) — TE th patio in question is older and as undovping heat disease (prior MI. cardiomyopathy, angina, heat failure), This ist regen of wheter the pants alert — and vegencless of wat the BP might be dung the tachycardia (VT may be presnt even ifsc BP exceed 180 mint), + Avalabity ofa prior I2-lead ECG on the pte ding sims htm may be inaabe fr assessing the poss of preexisting BBB. 1 Feraberant conduction considerations — See Seen 10.0. LIST #1; Common Causes of a Monomorphic Regular WCT of Uncertain. Btiology |. Ventricular Tachycardia (V7) 2. VT (esp. IF patient older} has heart disease) Causes #3 thru 8~ VT/VT/ VPM 9. SVT with proexisting BBB 10. SVT with aberrant conduction Table 08.71; Causes ofa Regular WCT of Uncertain Budogy Presane VI wless proven Obese 08.8 Step #3: Empvically Treat! Ongoing Diagnosis (GZS Step #3: Empirically Treat /Ongoing Diagnosis (Opti management of WCT tytn: depends on the pe of WOT Vou wll ot avays Know dciive dings athe pe you needa ben weatmen 4 Steps #1 and #2 shoul nina most SVTs and polymorph WT fom consideration Serons 08.3 and 08.6) ‘You amet wih regelar (or almost regular) monomorphic WCT of Uncertain Etiology (LIST #/) Presse VT Trest according unt proven oterwise [SEY Polat IF at aw tne ie patient Decomes unstable — thea inet) caciover ot debe 08.9 Unspecified WCT: Suggested Initial Approach => Suggested Approach: ‘in such ime tha the ces discussed below in Beyond Textbook sages flea Ggnoss (Secuon 08 +) — Ws moat prt o presume VT asthe etlogy of the WCT — andro seat accordingly. The “shor answer” for cor suggested inva weament approach to specified WCT appears below Sections 08.9 thr 08.13). More on the subjects found in Secon 073 (tarreviews ininal eatmert of Enown monomorphic VD), ‘inst Forte "Fixubles” — Deter tm aniarytiic drugs so fn and “fx ay potential precpitarng causes of VT as soon a you can. These my inca: + Hecushte dsnrbance (ep. low Mg++ o¢ K+), 1 Acidosis Hsponecma + Hypoxenia 1+ Shosk (rom Ippovelonia: bloed los sepa et.) {+ Unconoled i emin ace inaction 1 cat hear fe 1 Digtoscty Drag overdose (08.10 Use of ADENOSINE for WCT/Presumed VT Adenosine furl wel tleried~ and should be considered mth Lt chug tht might be sven Adeosie wl convert (or at leat slow down) most regular SVT sts, Teamay convert $-10% of VT shytins. ‘Bega wh 6mg by IV push IF a0 respons ia 1-2 mimes — Give 12mg by IV push (Seti 06.2). Side acts Eom Adenoine early shot ed (de fo the drug's lira short hf ife~ Section 06 3) Do nar use Adeaosiaeforpolmorphic VI or Toesades. ‘Conversion of WOT to sae yt with se of Adenosine doesnot prove a sipaveniul tlogy! NOTE: Wedo not always tart with Ades all ode patel wth schamic VT from known coronary sear (ar the agi likely to convert ichamic- etiology VD), 0811 AMIODARONE for PCT-Presumed VT Amiodarone iow prefered iniial agent of choice (qforAconosins fo ctable susined unspecified WCT- + Give 180 mg TV over 10 minutes. May repeat. TF the dg works — Consider nsitenace TV infin at 1 mg minute (See clio Sotion 07.16) + Amlodaroae may als weat me forms of SVT. (0812 PROCAINAMIDE for INCT-Presumed VT Procaizanide avo recommeaded by ACLS-PM (Provider Manual asa Ist ie ug of choise for unspcyied WCT: + The cicacy of Procanamide appears comparable to Amiodarone fee VT and SVT ivan 1 Give 20:50 mpiminate TV unt ster fhe acti x sapressed: Hypotension ene; QRS custo nceases >S0%6; oh) amax dose = Trg hasbeen gen usual W loading ~500-1,000 ma) 1 May folow with 1V mainzenance infusion st ungiminute (J-4 mgynin range). + Potential Drawbacks of Procananide ince) QT prolongation i) inadsaity with bear re; i less cca faniaity and a wore complicate administration protocol: and in) greater tendency to develop hypoteason, especialy &festar iafsio rates are used (Our preference 10 start wit meroment: of 100 mg IV ever ~3 minutes = ~20 eee 08.13 - Synchronized CARDIOVERSION for WCT/Presumed VT. Thece may welcome a point dri the above extent process wea i Becomes time to sete paint out ofthe unspecified WCT ttn: 4+ Attia poiat — Candionert! (Seeron 05.0), (08.14 Diagnosing the Regular WCT: Beyondshe-Textbook tk => Beyond-the-Textbook. Given that optimal managemest of WCT rhythms depends on specific diagnosis ofthe ype of WCT — We conc is section wi sight for determing IF. regular (or cast eg) monomorphic WCT i sly to be VI (us SVT with aberrant conduction ox preetsting BBB). We expos te following pit: + AWCT cchn's “iy” Ge, presumed VD) wl proven others. 4 As long asthe pte remains sable — tare ste co Tose by bi tempt eng your tytn Gisgosis Remain ready to candiovert a ate TE the ptet begins to ecompensate 4 TF unable to cariover~ then inmadiatly dea NOTE: No set cfs “perfect” forterprtng WCT stn Even the experts te ot akwayscotin Our goals merely to crease your odds of corect amnoniaby a tne aficiont and eazy-o-romemborappreach wing those citi we have feund most hep. + Wedevote Seton 09.0 a sees of Practice ECGs tht apply these pines. 0815 WCT Diagnosis: Beneft of Starisies Clinical Parameters (One cften forgets to recrat the wisdom ere in the fallowing statement Common things are common. Statistically -VT is by far the most commoa case of a regular WCT etm ‘when sis Paves ae ot lel exSdeat (LIST #] = Table 087-1). Sms have show hat atleast 80% f Such regular WCT tans are VT + 1s the patent oer than 50-60 years od? Is here a history of hare dscase? IF Yes —ohink VT! Statsical odds tata regular WT without sos P waves is VT aan at lea 908 —TF the patio cle than ~50 years oli and as undeing hen dss + Is thee pri istry cf VT? — Telomenry wacngs showing PVCS oe sore VT rans? IE Ves —dhink VT! (OR Is thepaat 20-40 year al adh with oso of wdesjing heart seas who presents ia a WCT precipitated by exercise ot sees? IF Yes — evenifthe WCTis VT, $sroatvly ie tobe an adenosine-esponsive form of VT thats ofen wel tolerated (Seton 06.5) ‘Remember: — Even IF the pateatis exympromatc wih BP>180 sy for a prolonged peiod — tis in no way ees oat VT lt simply means you have some ie. Aetiona open te Sgro ascessment ofa regular WCT thythn egsre = 12-lead ECG obtained during the WCT. 0816 - WT Diagnosin: Prior 12-Lend ECG During Sinus Rhythm? ‘Sm pains hve baraine condition defects (Barlne BB; VCD), Axa oa 124d while the pte wasin sas rythm allo lead-o-lead comparison priov and dora the WCT to sees QRS morphalgy ithe same [IE QRS moupholgy is nor the same — dhink VEE + Reaiscaly — It wil nt be often that peor BCG dhrne sins rythm wil be avalable or you may’ not have time to ook ait with a WCT pation infront of vou). 08.17 WCT Diagnosis: Exreme AXIS? (Simple Rule #2) ‘We favor besiing ou use ofthe 12 lead BCG obtained dering the WT rin wih tent to 3 Simple Rules. The Ist ofthese Ries relates to assesment of frontal plane during the WCT et + Theftcaal pane ass maybe approximated a a glance ~ simply fom inspection (and comparzon) ofthe act QRS deficcon a lads | and aVF. Lead Lis the horizonzal lead ~itis siuste at zero degoes Lead aVF the Verrical lad iis sated at~90 degrees. the net QRS defections posive in Doth eas [and VE ~ then the mean QRS axis srl (ie, berwnan sro ant! +90 degrees). + While cetais of ans eaculatonextead beyond the scope ofthis Section on veascular achscaa~ the “take-home” message is thatthe peseace of extreme ais deviation daring a WCT tytn ic virtually diagnostic of VT. + Exreme mis devnion secs osecomsize. The QRS complex willbe envy argave i either lea | or ead aVF. Tiss the case for both X and Via Figure O8.17-1 Awaracss ‘fis as evtion madiatl tals us at X ead ae almost cesiy VT KEY Poin: The preseace of mid or even oorate LAD of RAD (Left or Right Axis Deviation) doesnot asst in dsingshng between VT we SVT. Theis the case for Zin Figu 05.17-1 lich lead is dealy positve, but kad aVF i ot. lasiead, we see a leer postive R wave ia Z~ ead a wider S wave. Whee some depes af lef axis deviation fe preset inZ (rrface area ofthe negative Swave appacr greater than surface area within the sander positive Bw2%e) ~ic not oly incerta ot wnpetat What counts 4s ta extreme axis deviation is wor present in Z (because the nat QRS deflecron in lead aVF i nt all negative). Ths els us ata glance that use ofthe as cetera isnot op distil betwean VP 9s SVT fr the stan ia Z Figure 08.17-1: Use of Auis for WCT diagnos, Rhythm X ~ shows exreine Uf eas (ORS al negarive te Tad aVF) Tis VT. Rhythm Y ~ shows extreme sight nis (ORS ait regarive in ead D, This is VT. Rhythm Z.~ cleats does ot manifest extreme ais deviation, becatse the QRS complex i lead aVF is oeall egmtve. Callan of sis of no help for itingshing btween VT vs SVT for BOTTOM Line We LOVE this aris erterion during tachycardia, When wed as intended youl Sad + Calewlacion of axis during WCT tts using leads I and aVF is easy. IF the QRS i ll negative in ster ead — tea diagnosis of VT is almost certain (X axa Yin Figwe 087), + Remember that anything other than extreme ais eviton is of no usin sneishing between VT ve SVT. 08.18 - WCT Diagnosis: LEAD V6 (Simple Rule #2) ‘We hve found ead V6 tobe the most hell ead to fok at ring a regular WCT tym. We ask Is Lead V6 al (or costal) Negative? + Wha the eology’ofthe tm i sopravenricir — the wll almost always be test some postive activity traveling toward the let ven ard therefore positive i lad 8) [ever he QRS i lead VOis star all negative (er cast all negarve) asia FigreO8.18-1 —thea VTi lighy ee (See Figures 09.1-1 and 09.21). 1+ Lend V6 onb bp mente (4 poste R or BS ov lad Siz not halefl in rang nor out PT) rev Probably VT NO Help Figore 08.18-1: Using QRS morphology in lead V6. The presece ofa GR complex fa lend V6 Wat & cher al negate (or almost all negative) ~ is sonal tgzestve of VT. Ths ciesonis of no help € ating cet ty « wae is peeseat a ead V6 0819 - WCT Diagnosis: Is the QRS “Ugly? (Simple Rule #3) (Our 3d "Simple Rule" a falls: The “upon” the ORS — the more likely the ehythm is VT. The explanation for ths clinical eat stat aberrant coadsion akuost ays manifests some frm of conduction defect (RBBB; LBBB: LAP; LPHB— or some combination therse?)— deo ralatve deayin one or more of the hemfascces or bande branches. «+ Tn contrast — VT originates fom a vec foes outside ofthe condition system. Asa reat VT is more Bey to be witer and far less oremized (Pherefore“ueker init > Beyond-the-Core: ‘What dolowsin Sections 08.20 thu 08.26 are a amaber of Bavond-the-Core adkrional ways to help dstngush benveen VT wg SVT: + Weeemghasie tht yon do nor have to remember lof the criteria ta followin these reining sections. This advanced (bavond-rh-core) tec for exparonced povidone with speci incest inthis feng aes! Ts there a0 RS in any Procorial Lead? IE theres no RS compen in any proceril end (F-tru-V5)—then the ehytha i VT! (with >90%6 specificin). Caveat IF an RS comple is een int precordial ead — the this rterion is 0 belp (because both SVT and VT rithms may have an RS complex in no more dan a single ‘precoral led). igure 0820-15 thee a RS in anv Precndial Lead? VT is alnostcranyprseat owe ofthe recoil leads wis an RS complex ning the WCT (See tex). + Bork Vand Zia Finwe 08.2041 ae VT (hore sno 23 complex neither) Tha india of QRS concordance Z (in his case global poi) snceasve but 100% spiel + In —AnRS is presen in lead V3 (in rhe form ofa small intial wave and mach deeper nagative S wave). We theefore can note out VT onthe basis ofthis RS eteron, ‘hat sad — We st inc X's VI because of over ial (up formless QRS, exp. in Vis almost antirely negative QRS in lead V6). 0821 WCT Diagnosis: Is he Reto Nadir Delayed? IF ag RS comples present ina least one peecorial ead — hea the thm is VT (with > 09% specictn) unl he cepest portion ofthe Swave is delayed 70.10 second (100 msec. the Rete-$ Nadi Ge, ers fom she begining ofthe wave Caveat This sitaron on bel for ruling in VTA 21 precordial lead sty manifests an R-o-S nad 0.10 sacend is af mo elp i you se aa RS nar hats nor more han 0.10 second (and the reals thats often cial tobe sure of RS nar dation. R-to-S Nadir >0.10 sec ? (in ANY precordial lead ) le a >onosee? YES w Precordial Lead? Wa RS coal prestatin oe or ore precordial ads — thn the tans amar cetialy VU he R208 igure 0821-1: 5 the R-toS Nadir 0.10 see. Nadir: delayed o 0.10 second, SOTE: The piysislgi tom for Fig 0820-1 and 08 21-1 ie hat pemvensce activation shoud yi at eet some change inthe dcton of veneration wits espet to the 6 precordial ads Fig 0821-0) ~ and tha ch of te tne, nal veamiclr action willbe dow (>010 see) compared eo senicany faster inal acvaion when the dns supraveueular (Fig 08-211) (08.22 - WCT Diagnosis: Initial ror 20.0 sec. in an Lead? Lookin aif 12 leads to seein whic eas an ital wave ox qwaveis present TE a ital rc @ waves 20.04 sec (1 small bo) ina fad the he nt is almost cevan to be Nr Caveat This tron ison ffl for rung im VT 21 ead cl mnie a ale or q ave 20.04 second, Iie of a help you do not see an ini ro g wave 20 8 Secend (ad the reli shat ii aften dificult to bo sure afg oF r ware duration diving WCT). Initial r or q 20.04 sec? (in ANY tead) it 4c [F 20.04sec? “Ypg NO NO Figure 0822-1: 15 the juital rr q>0.04 second ia any Lead? aa Baia gor Wave proscat a Wide (0.07 see) ay ad — thn the yan clmst cen tobe VT. (NOTE: The piysislog casionsle for Fire 08.22-1 is hu nal condction through mjocari sso is dolaved when the St of on for a tachycardia is veaicl.In coarast — WCT ‘sims of supraventricular tology manifest more rapid iia condcton, because the pues wansted (a lest in part) over speieied conduction Sher. 08.23 - WCT Diagnosis: I here AV Dissociation? Tks always good to lok for potential confirmatory criteria when assessing WCT shythms — sive TF foun, these vitualy ensure the diagnosis of VT. Confmatory cieriainchde#) AY dissociation: andi) Fusion bess + Caveat Most WCT rhythms donot mast ter AV Associaton cr fiion beats (specially won the rate of VI is > 130minute). Therefore, no seeag these proves aothing. Bot Seeman youl act sky (Figure 0825-1) Figare 0823-1: Us of AW Dissociation to prove VT (mre), Best #4 afison bea (See fx). + Bens 12.3 ia Figue 0823-1 ae sims. The QRS tha widens and domatically changes ia morphology. Although the bepaniag of ths WCT is sightytreglar — We can prove is sais VT become 9) Best ia furion beat (short PR; ORS not overly wie and with ORS morpholog intormadhate barween sin beats andthe other wide boos). snd) there is AV Dissociation, atleast for aris ptiod (arrow highlihting an on-time P wave not elated to neighboring ORS compe). ‘The easis way to expin Fusion beats” to contamplate wha the QRS would ook ce IF beats #4 and #6 Fue 08.23-1 bad eile? Ge, with characronsis of both eat. PEARL: You eed calipers to look for AV Dissocasca. ‘Note The easc the DR eral precede boat #4 5 shorter shan-normals tht caly partially conduct othe Veils spat i ernted by a sinaliaseoush occas sence beat, 0824 WCT Diagnosis: Large Monophasic R Wave in Lead oVR? ‘Was scemal sins dvi — lad aVR manifests a predomiaany negative QRS complex. This elects the nemal path of veal activation — hich moves away from the sit (ary ‘from aVR)— and toward hel vente. I ever the QRS in lead aVR during WCT is entirely postive ering 2 large, moraphatie R wave in aVR)~thenthe tytn fe VT (with vireual 100% specifi)! + Caveat: You wil often see a monophasic Rin aVR darine WCT. But sometimes you'll get ncky Fiwe 08.241) Is Lead aVR a large, upright R wave? A. Tab fee} ESS Monophastc Rwave? YES NO NO Figure 0824-1: Is there large monophasic Ria aVR? ities a monophasic R wave in ad aVR dang WOT the te vythm is vray certain to be VT NOTE: The fang of « monophasic R wore is lead VR during WCT indicates tht te echical impale must Se originating ors ast nthe ventricular apex and usec spard toward the bate Ge, he cvecron of lod aVR), Therefore — a quicklook a lead aV'R cing WC constant tel yo the shit is VT # om ee alae monopbase Ree 08.25 — WCT Diagnosis: Does Lead VI suggest Absrrancy? ‘Mach as beea writen abou aberrant cocoa asa reason for QRS wideaing ding WCT. For practical puposes —the only QRS morphology with high specificity for SVE is the presence of ical RBBB i ead V1. Ths the presence f an sR? complex (wih allo right ‘rabbit ea’ and S wave that descends slow the baseline) — stronely sueeests 3 supraventricular etiology (1. H-2 n Figure 0823. + Inconrast—any other QRS morphology in ead V1 (34,6 x Figure 08.25) favors VT (Caveat: This citeon is stict. Only a gpieal RBBB patiernn VI (H-1.H-2) suggests sera conduction. Ay other QRS patter i ead VI suggests VT. ‘We museae farther in Figure 08-28-1 diagnostic use oflead V1 QRS morphol chractesis in assessmont of WCT syns 4+ Exam H-7 — suggests VT. Lead VI masfsts a monophasic R wave with taller lf abit ear (resembles H', bur without an notch) Lead V6 i H-7 suppets a dasnois of ‘VT becanstis predominantly negative + Example HAS — consstonr wth a supraventricular rhythm (ether preexisting RBBB — ot aborvant conduction). Lead V1 mantess an ‘SR’ with taller right rabbi ear ‘Gimilar fo 2) Look at Lead Vj during WCT: Figure 0825-1: QRS morphology favoring aberrancy in VI (See tex). [NOIE: The seas for aberrane conduction is thr theres infin tine fora part of the veal condo system to recover. This maybe precisa by athe an arty beat (ike ‘2 PAC) ar by acyeaa. Becais the rit bene branch ends to have s lrg sefactorypasod thm beth ths lt bea breach and the hands — a RBBB ptr the ost commen form af bean condncton (but LAHB or LPHB aberration, or any combination of patterns may also be seen) — See Scion 190 (08.26 — WT Diagnosis: Is he run of WCT preceded by @ PAC? ‘The best way to prove sbenant conducions IF you can fad a premature P wave (PAC) precediag the un cf WCT. This wi oes not be easy todo ~ BUT —en occasion you may see a vy iii | ry igure 0826-1: Beats #1-ou Sins right-sided comparable to 11) lead MCL ate seus conducted. The flows a9-beatrun of WCT eats thru’). We Kuow his is aaa of SVT with aberrant conduction because ofthe PAC we see that notches the T wave just prio to the onset ofthe run (arrow x Figure 05.26-1). None ofthe ote sins beats (2 Diru) hae is tc, Besond-the-Core on Figs 0826-1: though a sultonsouc 12lend ECG wo be needed to kaon forse ~ the snr nil r wave defection wth very stespS wave but withou excessive QRS wks sues an inconpleze le ue batch block form f aber candi fer bouts #6-au- 4 (08.27 - WCT Summary with Review of 3 Simple Rales Figure 0827-1) (K2> SUMMARY Despite the length an comply of hs scion —the “meager st Priority: — Is he pin stable? IF not ~ then immediately shock the pais! + TF th patent i Stable ~ then py Step #1 (Section 08.3) nd Step #2 (Section 0.0) in your tempt a detrii the diagnosis (ora ows narrowing your ciffrenti. + Applicaton of he 3 Simple Rules (covered in Sections 08.17, 08.18, 08.19 ~ and sunmarzed blow in Figure 08.27-1) wllusuay alow you to preaty acrease your dapnostc ‘eat a0 mare han fe seconds + Begin empiric treatment base on sour presimpinedignoss as you contimally refine your stim diagnosis as indcatedin Step #2 (Serion 08.) andin ow Suggested Approach The 3 Simple Rules: 1) Is there extreme axis deviation? (© 1F Yes mee then probably VT. 2) Look at QRS morphology in lead V6. (©1F all negative (or almost all negative) wee probably VT. IF not overwhelmingly negative we NO help '8) How "ugly" is the QRS? © Aberrant conduction is usually in the form of some BBB or hemiblock. © 1F the QRS is very “ugly” me probably VT. Figore 08.27-1: The 3 Simple Riles for ascesg the 12-Fead of WOT rin Deals ft of Sections O87, DB1B and 0819) Ang you my not he cst ofthe ten ngnoi athcbegiing of tis rocen (you are fle al acting ith on “arapecfed” FCT) — the chamces ae ret tat with ogg, ‘montosag, reament and folow-ap — thar you Have atthe correct dams + Inamy cvent—the Suggested Approach (Section 08.9) willbe an apprepite couse flo: ‘Now ~ Test ouselfst ou WCT PRACTICE! (Secon 02.0)Section 09.0 -WCT Practice Examples WCT Practice ‘We reisce th principles decneedin Seton 8 O wis exe of WCT (ide Comples Tachpearta) Practice Exmoor Section 091.0 WCT Practice Example Practice Example: 09.1-WCT: VT or SVE? ‘You pate sa 5S-year-cld men with CAD. His 12ead ECGs show blow ia Figure 091-1. The pots emodimamically stable wih a BP 1+ What Should you do est” 4 Whatis your Gianoss of the WCT sth in Figare 08-12 + Hove cortain ae you of you itn diagnosis? 7] w= ANION ei Fore t.1: WCT fag Tc ais hoospnameal abe 091.2 NEV Paints What To Fin? As discussed in Section 03.0 on Overview af Unspecified Tachycardia ~ the very Ist ching o dois assss the pateat fx hmodiamic sabi. This as been done ~and we are tld ‘hat the patient whose hth is aen in Fine 09 1-1 ie emadrmamically stable 1+ Siac the patints stable — thre is no neta mney earovertIastand — theres a east a momento net asess the Yt, + Key concepts in Rythm Diagrosis were dscused in Section O2 0 (in which we reviewed cial application af te P5,Q5,3R Approac) The agnostic approach to CTs af Union Enology was thea reviewed in deta i Secon 08.0. Fel FREE to refer back to these sections at needed. + Therintim in Figure 09.11 is regular WCT without clear sen of ail activity. Given thatthe patent 55-year-old man wit know: CAD ~ te lielihood of VT is ead at east 90% ever without looking free (See Ltt #1 and Sections 08.7 xd 08.19) A sugested by Step #2 in Sein 08.8 — one could at ts point either expicaly teat the shyt in Figure 091-1 as a WCT of Unknown Esology (Sections 08.9 through 08,13) ~or~one cou faker asses the syn to see we can increase certainty of cur yn ignoss. + We emphasise that t would nor be wrong to begin eupte weateat (with ther Adenosine, Amiodarone andlor Procinamide at described in Sections 08.10 through 08.12), ‘That said We fee the teatmest approach wil be far Betta TF we can hone in onthe etn agnoss Tsai tke no more than 205 seconds to assess he ttm in Fare 09.3-1 by applying the 3 Simple Rules (Section 08.17 08.18 ~ 08.19)~ ad tis isthe approach we fave. NOTE: atom tne the patient becomes unstable — then Iomedtelv aver or deat 09.1.3 Figure 09.11: Applying the 3 Simple Rules Ti sh ak more than few seconds to apply the 3 Spe les (Figure 091-2 to the yam in Fig 09.11: [Rule #1: Herreme Avis Deviation? —Thote is extreme LAD (Left Axis Deviation) i Figue 091-1 (the OBS is eninely negative the nfror Ina). Tis is iraly never seen vith SVT The QRS in lead Vi aos ately ngatv. Ts i sary Soe with SVT —The QRS in Figae 091-1 is extranet wide almost 0.20 coc) and formless. We say its “ugly becmse QRS morphology does not resemble 1) Is there extreme axis deviation? © 1F Yes mp then probably VT 2) Look at QRS morphology in lead V6. 1 all negative (or almost all negative) we probably VT. © IF not overwhelmingly negative me NO help '8) How “ugly” is the QRS? (@ Aberrant conduction is usually in the orm of some BBB oF hemblock © 1F the QRS is very “ugly” mp probably VF. Figure 091-2: Sununary ofthe 3 Single Riles (Details Sections 06.17, 08.18 and 08.19) ess han 5 seconds By use ofthe 3 Simple Rules we have become 09% corsa st the WCT Examples VE Conclusion + Ttwould nor have eon ous to tat wih Adenosine. That seid — We woud promprl such to other teammetsf Adenosine diet work sinc hepa’ ge, story of CAD, and ECG appearance do no! suggest an adonosne-resporsive form of VT is key (Secrin 06.5) + Our preference er Adenosine would be Autodarone bo ooherepions are salable (Secon 07.2). 09.1.4 Figure 09.11: Beyond-he-Core ey) = Beyond-the-Core: ‘We can actualy be 100% certain is WCT VTE + Ther isa monophasic upp R wave ia lead aVR, Although nsesve — ti igi Rghly speci for VI when te found (Secon 08.28). (QUESTION: Docs the uit ® wave lead VI of Fgze 091-1 suggst RBBB or aberrant conduction? FINE Fes ie to review Secon 08.25 and Fie 0825-1 before answer ANSWER: The very wide and formless (very ul’) QRS in ead VI does notin the least resemble citer Hl or H-2 in Figure 08.251, Ieaything — QRS torphlogyinlead VI of Figure 091-1 is suongyinfaver of VTSection 0.2.0 WCT Practice Example2 Practice Example: (092.1 — Heart “Awareness” and Tachycardia: What isthe Rlyoha? ‘You pate sa 50-year-old me With CAD sad “host averenss” His ECG is shoo blow. BP=14090, 4+ What Should you do sex? Figure 002-1: The pants sable Tis SVT? (092.2 KEY Points: What To Do First? This ptt seems to be able (BP=40/90). The Lead VI ttm stip in Fig 09 2-1 appears to show a teglrmarrow tachycardia at rae jst over 150lnimte. The “good news" is that ace the pata is Stabe ~ thee gine to ook ter ito wha the syn ne bel + Allve seis a single mnitinglad. Given that the paca sable — We alike to see more leads bane proceeding. Taeece — Get a 12-ead ECG in tachycardia {NOTES IF at ay tne ring the process the patient Becomes unstable — thn mimediarly eave or defbriate (09.2.3 Does Figure 09.2-1 belong inthis WCT Section? he ane ant whether the thm x Fie 08 2-1 “blogs in this WCT Practice Tracing Section is fathcoming on seeing the L2-Jead ECG recorded atthe same ine a he kad VE sty sip Figwe 09 2-2: WA wh Nee ee ot i y\ Y y\ = i: 2 RA hy AAW yy WA [ier MAA avery 12 ead ECG recorded a the same tne asthe ead VI iy sip sbown in Fee 09 2-1. The patents sable (BP=14090), QUESTIONS: 4+ Whats th stn i Figure 092-2 PT or SI? + What cree of certainty do you have aboot yo tym dingo? (09.2.4 Whatis the Rhythm in Figure 09.222 ‘Comparison ofthe snle-lead V1 tythm stip (Figure 09.21 wit the siultenaousy recorded 12 lead BCG fiom spate (Figure 082-2) sates te folowing KEY concep: “12 eas are erter than 1” Dat ofthe QRS teas somotnes Be a the baseine i the single lead beng mentored For ths reason — iis best whenever possible always get a T2-ead ECG daring tachycardia to vers QRS with, 4+ Testou now be obvious dha the QRS comples ia ths casas wide! Ta fact — the on leadin which he QRS looks o be narow onthe 12nd wack obined dung aves ‘stead V1 4+ We sueagly suspect VT. Appling the 3 Simple Rules to the 12 lead ECG shorn a Figure 092-2 allows uso great insosse cert of ou stn dapnosis (Seeron 082.9) (09.2.5 Figure 09.22: Applying the 3 Simple Rules Albough 8 would nor be tong to give Adenosine a ths pot — should take no more than 2-0-5 seconds to apply the 3 Seuple Rales (Figure 092-9, ‘The 3 Simple Rules: 1) Is there extreme axis deviation? @1F Yes me then probably VI 2) Look at QRS morphology in lead V6. © 1F all negative (or almest all negative) we probably VT. (© 1F not overwhelmingly negative me NO help. '3) How “ugly” is the QRS? © Aberrant conduction is usually in the form of some BBB or hemiblock. © the QRS is very “ugly” mp probably VF. igure 002-3: Sunanary othe 3 Sle Rules (Details fy Sections 0817, O81 and 0819) Applying the 3 Simple Rules to Figure 09.23: + Rule#l: Zememe Axis Deviation? — Theses exrome RAD (Rigi Axis Deviation) a Figae 092-3 (the QRS i ntirly negative in lead I). Tis is no seen with SVT. fs Lead V6 Negative? — The QRS is lead V6 is entely neste Tas veal never sa th SUT 2 —The QRS in Figure 09 2.3 is exromay wide (anast 020 sc) and foriess. We say s “gly because QRS merphelory does no reseable ny form of BBB or henablock. Ths srongl favors VT. Conch Ta fer than 5 seconde — Welane become vita 100% certain the WCT in Fgue 09.2.2i¢ VE 1+ Athough seceptble to start with Adenosine — ow prefrence woud be to sect Amiodarne rs in view ofthe vil certainty of ischemic tology VT (given patient's age: lastor of CAD; ECG characteristics) — and that this VT sunlit tobe aerasine-responsiv. + Other options for VT are vedas (Section 07.3) + Sinchronized cardioversion may be needed TE the patent fii to respond to anemic drucs (09.2.6 Figure 0922: Beyond-the-Core y So cetin ae wea ths pit that diagnosis ofthe shyt in Figure 092-2 5 VT — tht chica. ve woud ot need te spend tine ooking thes to con tis. That aki — for teaching Purposes: + The blowup of Lead VS Som Fgwe 092-2 provides an excelent examele ofan RS complex ia which the 08.22) RI => Beyond-the-Core. Ris clearly 20.04 see. wich vimaly sures VT (Section AANA [¥s] ANY Cif] [sy nnn san] Figare 092-4: Blow-wp oflead VS from the 12-lad ECG previonly show in Fgwe 082-2. The very wide (004 second) ni R wave is lead vitally confi VT asthe gnosis (See Secon 08.22 for deni), il Poot The rtonale for routine icorportion of Adenosine tan eary poi a VT managemse stat one cant relably iden al adenasinevesponsive cass on the bass of ECG characters, + Adenosine-responsive fas of VT (Section 06.5) — ere most ly wo occu younger adults without adeag beat szase, The ECG s mote Bealy to manfst minimal QRS ‘wiesing withow bizare merpoloey —and VT episodes are mare keh tobe recta by exercise (or over causes af catecholamine release). This isnot the case hereSection 09.0 WCT Practice Example 3 Practice Example: 093.1 — Heart Failure and Tachycardia: What isthe Rlychon? ‘Your pais 3 68.yearold woman wih heat re exaceriion Her KC ie shown below BP=14080, 4+ What shuld you do sex? Figare 093-1: The patents sable. [sth VT or SVT? (093.2 KEY Points: What is he Rhythm in Figure 093-1? Despite ist lance inpression tha he dy tan in Figae 093-1 appears tobe regs — is nor Foray tis pai stable — so eres te to lok ats, + HINT: Use of calipers reat factinesassessmeat of thm regaty ‘The waiderhing tytn in Fire 09 3-1 egalaryerepl No P waves ae seen. We suspect this AFib Aral Friltaion) with a ant nap ventricular response + The QRS complexis wide. Athough VT is usualy iy ear shh — ity Hines be regular. Tis, ee can nt with 100% certain exch the possibiy of VT. That, ssid — Vs ae as regulary roglras i een Fie O9 3-1. We terete suspect his paet bas preeisting LBB (09.3.3 When You Don’t Know For Sare What the Rhythm Is. This sce provides an excelent example of ow ane wil no always Kon with 10086 cetaity what the cyt is a the tine testment decisions need to be mde + Assessment of ECG features in Figue 09 3-1 consent with ou presumption of a supraventricular tology because i theres typical LBBB merpbalogy (upright monaphasie ORS ir ins 76; pracominaray negative QRS in 7); ithe QRS isnot eves wide) tere is no extreme avs devon, andi) the dowaslope ofthe S waves in ares Fads ‘very steep (ual she delay tha i often sean ith VT). + Te would be wonder TF we bad accesso prior ECG con ts paint Fdence of LBBB in th pat wold confi the rym ia Fine 093-1 fs AF and not VT + Review of adddional rhythm strips oo tis paieat should also help to conn the regularly inesar nana of AFb (xe VP that tends to repulrise after on iil pviod of irregularity when the rion persist), + The good news” — isha ths pain is table, Essent to management wil be tester offer hear fre exacerbation. One would expect therate of her presimes! AR to slow «sles clticlcoudoninproves. + Botiom Line: We stony suspect thatthe rythm in ewe 093-1 is AFb wi preexisting LBBB. While reining ready to carver this patient TF atc tie she were to -decompenste — We woaldbegia by weatiag her heart fire and canny ase drags to ow the rae of ber presumed AF (Seo Seeron 14.1). 09.4 Figure 09.41: Beyond-he-Core §) => Beyond-the-Core. ‘The case scenato presented here sa common one. Progressive dasioke dyincton from longstanding iypertenson may predpose to bat AFib and to development of LBBB. Sudden toes ofthe “ail Ak” with onset of AEB any procpitae acie beat are. Given mil RR seve varition we the rae of AFD i fast — thereat ECG pct ay te VT. + ltr ps to know the pao has baseline LBBB, 4 Dies ccs dat the stn a Fgwe 093-1 AFI ae) Asarnoss of th above commca ecu; and ealoaion hat the RR trl corral chenaes (093.5 PEARL: Using Calipers Use of ealipersis invaluable a toot ass in assesses of atin wacings sch s Figure 09 3-1 —as well for assessment of AV blocks. + Calipers insanely enbance your shils in arty interpretation! They make obvious reboasips between abel acy and QRS complescs tha would not ohervne be apparer. Detecting se vation in anil ce verncuar rte becomes easy. And ~ Using capers conveys to others hat YOU vow wha you are ding Al itakes iii Bit of Fractice to become face in wing capers + Cleary = You wil no have tine to pull ou calipers if you patente “crashing int of you. Tht af, in such svations ~ pata! wit benovdmanicaly unstable tacyearsia (whore nsrabiiy is due to dhe rapid rate) shouldbe mnedatly cardoverted ot debated vepardess of whethex hed is reguaro wt. BOTTOM Line: The apnorie of certnin coriac arthmias wil be mised you newer wre capers Wile you may not cerry need them fr interpeetatin of many (mae), ‘avsdnins~ its good obs aare of none in whic calpers wi be ofimveuleeesinaaelSection 09440 — WCT Practice Example Practice Example: (09.4.1 — Palpitations and Tachycardia: What isthe Rhythm? ‘Your patient ina previ heathy 30-year women who presents with palbtions. Her ECG is shown bow. BP-145'80, 4+ What Should you do sex? Figare 094-1: The patents sable. Ishi VT or SVT? (0942 — KEY Points: What i he Rhythm in Figure 094-1? A regular WCT ot~150ininte i seca in Fg 9-4-1. Theres no cla sign fei acviy. Ahough VT alan aceds tobe presuned wil proven otherwise (Table O8.7-1- LIST #1) there ace amber of reasons wh we strongly suspect a supraventricular etiology inthis case. Consier the flowin 4+ The pat young (30 years od) — she has beea previously helty—and -sheisemadamticll stable, Whe none ofthese cna anaes res cuthe possibilty of VT — they do male VT amc iss ely 4+ Beeaif VT s postal —the pats og, lac of cae histor, snd hemodjansc sans increase the Heid of some ype of fascia VT o& adenosine responsive oa of VT {Section 06.5) In ether eae — trial of Adenosine she appropri iia sep + QRS morphology a Fgwe 094-1 — is qpical RBBB (2X" with tllo-righ-rabbit-ear ix VI: wide terminal S waves in LVG). This seoapy suggests PSVT with QRS ‘widens fom REBB aberration athe eciny 09.4.3 Figure 09.4.1: Approach to Management Thece would seem tobe no downside fom ital management of the sythm in Figure 094-1 with Adenosine (Section 06.0) —since this drug sands hh probity of convening the ayia (be the thm PST with aberrant conduction some frm of adencsne-esponsive VT m ths relatve) you aéul) + Applcaion of a vagal maneuver (Section 13.8) might aso be wind (even bafove Adenosine). Vagal manawvers cen wotk for PSV and on occasion, even for adenosine. ‘esponsive forms ef VT and faseulr VT + Be ready to cardovert IF at am tine dng the weament process the patent decompeasies 1+ Obtusiag« poseconversion 12 ead ECG would be Ver mortal ins case the hope of dotrniing IF thre is baseline RBBB. + An Echo should be done to assess for undorbng sacral eat disease ~ and ~ referal maybe inorder (especially IF fascicular VT is suspect of thar is recurrence af Wen. 09.4.4 Figure 09.4.1: Beyond-the-Core I) => Beyond-the-Core: 1 genral — nether Verspansl wor Dano should evr be given fer 8 WCT sth unless cae is 100% cra hat the WCT is wor VT. Ths is becanse the vasolaing and negarive inotropic les ofthese dup key to prectate detection of VT to Vb 4+ The above ssid —it is wel to beatae thatthe speci form of VT known as fascicular VT may respond (and convert to simu roto) wth we of Vernal DBinzem. ECG ecopton of tecicar VT aay be sub (uzualy recente vith a RRBU'LAR part withous P wares ix a previously healthy youre ad. ‘Bottom Line: For the non expert — ts probably esto ave Verapani!Daazen inthe acute seting unless you ae 100% cera thatthe WCT tytn is nor VT + Access to aprior ECG on ths patcatshovig baseline RBBB of ionical QRS morphology as drag he WCT woud caf a supraveniclretlogy. (Cafoemnatly — Most of {he tng no prior tracing wil Be available) + 1a 2013 — Cerin fomas of VE ae nel a nny (noc) soeaty SVs ae potetaly curable by ablation. EP referral nay at some pot be inorderPractice Example: (095.1 “Heart Disease” and Tachycardia: What i the Rhythm? ‘Your patio isa 60-year-old man with “heart seas” His BCG is shown blow. BP=160-90 + What shuld you do nen? igure 095-1: The puieatis sable. Isths VT or SVT? (0952 — KEY Points: What i che Rhylon in Figure 098-1? [A regular WCT i Soa atta of 160s. There i 0 low evidonce of ail acy. The differential Wiagnosis i tht as shown LIST #1 (Section 08.7) = VT, VT, VT wi prover otherwise + Given the patent's age and iso of "heart ease” — statistical choad of VT is ~90%% aithows pong father. + The above said — here IS a chance thar he dtm a Figure 09.51 could be SVT (with ithe aberrant conduction ox proeeising BBD). 0953 Figure 09.5.1: Approach When Uncertain of the Diagnosis “The 12-ead waciag in Figure 09-5-1 provides an exclear example of how to approach a WCT Rhythm wen you do nor kuow for ste what the diagnosis is (Sesion 08.0 ‘The patients stable (i, ore ie tne look further. ‘The WCT is regular Teena hs isnot AB (Sep #2 in Setion 08.6) ‘The QRS is monomorphic (all QRS complerss in agivon lead ook tha same). Tos, iss not polymorphic VT or Torsades(Stp #24 in Section 08.0, Assesaneat of QRS morphology & inconclusive. Talis — the 3 Simple Rules’ donot suggest VT (Figure 08.27-). Spociicaly — the ans duruyg WCT' somal — lead V6 ‘susight~and =the QRS isnot “ugly”, btinseadis pect conssteat with LBBB, Bottom Line: We con’ know for swe what he sythm in Figne 095-1 is Athoogh our ini assessment does no poz to a Yenc ely — We sll need to arsuone VT wl ‘proves otherwise That abd — the pata sable an Adenosine the mos propia ul eatmet (Setions 08.2,08.10) + Failure of Adenosine —to ether epoca slow the rte or convert the ym would sopport he premise thatthe dtm a Figure 095-1 is VE AC hs plat — We would hen ‘nove ont Amindarone (or other TT chum + Successful comesion ofthe rsthm by Adenosine woud suppon (but not deitveh prove) a supravenindar logy (Secron 06.0). 4 Remi ready to carovest — IE st a ine the pata Dacones bemodynscaly stable + Ask someon to search ts patients car ine hope of ining prior 12 Azad ECG that might tithe patient ad baseline LBBB, 0954 Figure 0951: Beyond-the-Core ) => Beyond-the-Core: ‘This ase Highs amber of importa pits + Definitive Sagnoss ofthe rym in Figme 095.1 is no needed to efectvly teat the pate. Tastead we fo the course li out for WCT of Uncortan Biology (Sections 08.9 ‘iow 08.13). 1 Use ofthe "S Simple Rules’ des ot pot toward VT ins case. Nevers, hese Res al ep because they make SVT a moceplasile possbiy + Assessment of more achoncedi QRS moepooscfeanaes Hkenise fast yield a deve answer (Secrions 08.20 thn 08.20). That is — at Taare one FS comple is preset in ‘recoil leads (ser here V2,V3, 7) ad thece is no delay aS wave downslope in VIV2,V3. The nial wave ia lead VA not wide + The ECG shown in Fee 09 51s the 12 lead rng tachycari forthe lead Tyla step previously chown in Figure 03.1-1 ndin igure 08.1.1. Iti now obvious thatthe (QRS comple i wide oereae QRS orth wae not certain in Figines 03-1 a 081-1). "12 lens are bate han ca” 4+ Use ofthe 12-ead during tachycardia i so hep in cling questions abou rial att. For exemple — one might wonder TF the upright deflecsion midway between QRS Suggested Approach: The importance of sstingshine beeen polorphic VT witha wioal OT probagaion ies wih We Brey case) of the Givrder ad We response to teament 4 The dst Thing To Do (2s alas) — isto check foe ape. IE the syn ia Figue 111-1 eal —we would or expect the pation to be hemocdvnamically sable (Tease noe porione) ‘Deebrlation (a or V2) — is the acute meant of chive forthe patie wih persistent pobmorphie VT. Because (by definition) — the QRS complex contiaaly vais ‘urn ths polymorphic WCT — synchronized carchoversin wil usally not be possible + Many epsodes of Torsades wil be eelaiely short and se-eemiaiag — but mulple shocks may be needed given the tendency to recurence wt precsiaag cases can be ‘oni and comected. + Maznesinm Sulfate —is the drug of choice fr pob nore VE. Give 1.2 gm IV (over J-2 ont) — which can then be raped 510 mimes ter (ae much a 4-8 gm of IV Mg++ may be needed. Conimos TV Mg infusion (at 05-hour for up to 12-24 hours) may bap i greveting recite [thet is baseline QT prolongation (sual oa QTe2300 nec) — the the picture of polymorphic VT seenin Fie 111-1 i deied as Torsades de Pinte + Regardless of wheter i the baseie QT is cleryprleage: i) the bassine QT is won: ci) You simply cannot tall IF he basse QT is seme loos — inital treatment ‘menseres (defibrillation cs needed IV Mg++; fd ad fc potential eases) we the same! a “Measures — tat on occasion ave been ell in ceatling episodes cf pobmorplic VT (wth o without long OT i) Baproterena infasion (Beginning ot 2 ‘negimin, and trating wpward at needed), and @) overdrive pacing. These meats ace oat Hey tobe wei forthe refractory patent whose episodes we tepeaedlymriggered by preceding bradycaria (whic sets up conditions that prolong the QT of subsquent Beats). That said — IV M+; defbrilton when needed and comecing recptating ‘causes sould be tid fist forthe pain preseatng with poopie VT. 114 — Beyond the Core: Is he Baseline QT Prolonged? ea => Beyond-the-Core: Fal dscusion of QT prolangationis eyoad the scope of is hort book: Neverbolss, review oa ow key principles ay be Bok 1+ The QT intervals the pesiod that extends om the beginning of ecru depolarition — wd the en of venice epolriaion (Figure 1141), + To measure te baseline QT on 12-lead ECG — Select lead where you can deal see te on of the T wave Use thar lead in which the QT appears to be longest! 1+ For precisa purposes, te QT prolonged — [Ft lay measures more than bale RR tval ar] ar} RR RR Figure 114-1: Nomal slong QT tervals Prosi ht he heart rate roa excessively tthe QT terval shoud or be ore han al he Rival (Se) (NOTE: The above general re (that he QT should not be more than half the RR interval) — isnot wey as acurte when the heat ae faster (over 90-100%minut). ‘Gscaby — You cea wil naz have accesso a baveline ECG on the pate you are treating. The uadeyng vst may notbe sons. The baseine QRS aay be wide —ia which ‘ase becomes even move dificl i determine whether the QT is Ioger t should be. Bottom Lise: You wil olen nor beable wo deemne F he baseline QT of a coding patents prolonged — meu the corrected QT (QTe is nvercely eae to herent — a measured QT interval tht exceeds 045 ste shoud be cause fr concern IF the measured QT is 050 sec (S00msez) — itis defintely prolonged and wonsome (ncraaed risk af Tors) 11S ~-Measuring the QT: 15 the OT i Figure 115-1 Prolonged? Preccecakelton ofthe QTe reqs deals abies sporting pir gener and heart rte Fortunately sich preci calclton snot aeded cnc. Instead ~ the more-than-half= ‘the-R-Reinterval rule of nb Works clin alos al cares yah the main caveat beng reduced! accra: lon heartsate exceeds 90-10Diazute, We duseete cal appcaion of these pines in Figure TL.S1,Fromis 12 ead tracing: 4 Which en shouldbe used to dete ithe QT is anal or plone? + Which eat) shoud nore used to assess QT doaion? {What csical conditions should be considered?” Figure 11.5.1; Assessment of QT dation from the I2-ead BCG. Is the QT prolonged? What cnical conditions are sugested? (Soe fat). 16 — Answer to Figure 11.1: Is the QT Prolonged? ‘As cursed us Secs 114 ~ To deteine# the QU ira is prolonged, one should select alead where you can lay oe the end ofthe T wave. Oae shou ue re endia wc the (OT appeats tobe ongest 4+ Vercal red timelines Figure 116-1 dsate ey we woald not ws ed soc as le I, 1, Vo aV to dati the QT prolonged. is ut wo be certain wher the OT interval endsin these leads ~ and at most, the QT sno more than hfe RR interval + tnconrast~the QT interval clearly prolonged ia precordial leads V1 and V2 (despite uncertainty x Figure 11.0-1 about precisely whore th T wave ends ana thenext P ave Begin Hee ead) aa I “Ty Lege i hea [Long QT! Figure 11.6-1; Vertical red tienes have been asdedio Fgwe 115-1 The QT ntealis deasly prolonged in precordal leads VI ead V2 (Soe ox) NOTE: Desi the tacycana in Figue 11.6-1 (Soar rai slgly mors thar 100%minute)— We can sil comfortaby state the the QT is prolonged because itis decisively more than baba R-R teria a eat cori ads (such at V7). + In addon to QT prolongation ~ the most remarkable BCG finding in Fine 116-1 is ST segmeat coves and diffse, symmerric precordial T wave inversion tat is marked in dead VI.V2,V3. This ECG picure shoud sugaes the posssy of wet chen, ongoing in ction andor pulmonary embots + Wead to he st of gnostic considerations an of the Conmen Canses of QT proongation (Section 11,7). 11.7 Common Causes of QT Proloagation ‘Toremenber the commen causes of QT pcionsnion: Think “Drugs ~ Lytes — CNS" We fst but afew ofthese below + Drugs — especialy procainamide; stall tieyic antidepressants; oder phenohinsnes. (Although amiodarone alto lengthens the QT ~ the incidence of Torsadas relatively dow as areal of amiodarone ws) + “Lote” — low Ke: low Mge~ low C+ sS — any CNS catastrophe (trae; CNS bleed comas secure: tumor: head au). Acute CNS disorders may produce some of he most bizarre ECG changes imaginable ~ ‘Beading marked ST elevation, depression, T wave sterson adior exe QT prolongation ‘NOTE: Several over condons Ge, Buna branch Block, wfarction ischemia) way ako cause QT prolongation. However, the presence ofthese other conditions wilusaly be ous om ispectoa ofthe ECG. EY Claieal Pint: Chszal correlation is essential! Wout it~ it woud be impossble to detemnioe IE the marked QT pelongstion sen in Figure 116-1 was he rau f chemi, infact, pulmonary enbchis~or some drug eft, etre disedes anor acute CNS event 11.8 Polymorphic VT: Ifthe QT is Now Prolonged We defined th an in Fie 11.1-1 as Torsades IF the bareline QT was long. Akematey known as acquired LQTS (Long OF Synarome) — this sore is most cften dat to drug: induced QT prolongation and ot clecwaite depletion (low K~/Mig+=) As aveslt — pay ets shouldbe taken toi) Stop all meds Bey to coatbute to QT prolnasin: i) (Oprinize serum K+/Mg++ levels (IV Magvasuan helps acutsh with Tarsades suppression even when seri Mgt levels are normal); andi) Comel whenever possible other actors tht may conibute to QT prlongusion(Setion 177). + IE the QT isnot prolonged — shea the inthm is snp refered to as polymorphic VT. Initial treatment is the sume as for Torsades(dfbrillnon ar needed: IV Mg [BUT he respome to TV Matt: not nearly au good sts when the QT bs polo + Ruther than being drug or elects induced — polymorphic VT with anormal QT most fen has aa ischemic estoy (less commonty due to Brugada syndrome or familial forms). rts aes ot treating seu cheney teefre be hp 1V Aniodarone andor S-blockers may reduce vecrence nd sbould be considered if 1V Mig is fncestve 11.9 - Beyond -the Core: About Inherited LOTS A race inherited form of LOTS (Lone QT Syncvome) exists — in wich sycope'cardinc eres from Torsades may occur. Onst isin childhood or adelescence, en tere saya postive fan istry + Episodes pica occur ding exerie or sues. 1 Aca eaten (of Torsades) snr a for the maxe common acquired frm of LOTS (Section 11.2. + Recureuce of Torsades episodes is common with inested LOTS — so these pacar sould be promptly refamed when scoveed. 4+ Adrenergic modilaion (with bere locker?) aud packs (0 prevent precipitating bradieardia) maj be wel — but implaustion of an ICD (implantable Cardioverter Defériiator) wil cften be needs 1L10~ SUMMARY: On Recognizing Polymorphle VT (2> SUMMARY: kis esteatal to promptly recone polymorphic VT becase ofthe diferent approach e Geaboeal. Vaning QRS morphobay dang ts WCT rhytim usualy makes such recogion + Desbilaion is weeded for persis episodes (i il ucuoly not be passble to cardhovert given waning QRS morpholegie that confound artonpts to ryehvonize shock 250minute) + Dherate soo fst fr srl pases o be wananited over the normal (AV not) codon pasivny. Therfore arial impulaes mast be Bypansing the AV node. We trons sepect he patent has WW. 123 — Figure 12.1: Whe this is AFib with WPW and Not VT PEARL: — The Snag of AFD atan exceedingly rapid ete (over as WPW (ally Partnson Tite) syndrome minute) — shoud immediatly suggest the Ueshood of AP (Accessory Bainvey) conduction in apaeat who 4+ Two additional eanees in favor of Figne 12.1-1 bei WPW rather then VT ari) variation a QRS morpioay (nor expected with monomorphic YT — yer not nearly as rat as polymorphic VT), and i very marked change between some R-R intervals onthe trac (ome Being exzremely shor with others Being significantly Tonge). ‘KEY Point Tae ceatoa is sxporant fo recogaize WPW-actoitedarhthmin is hat ace Weatmeatcoaideretons of very rapid AFT (or luttr) wit WPW ace ciforent ‘hn fr other WCT tints. As sent — We fst review ECG recopion before adenine etme. 2A Beyond the Testbooke ECG Features of BPW => Beyond-the-Textbook. WPW asyadome a which one ox more ascessoy pave Gan Ua daw a clfrvate rou Tor Waalsson fhe dkical eapase am ai to wea. + The incidence f WPW is -21000 indus inthe general popution (uct afton enough thar most emergency proviirs wil sae WIV from te to te). 1 The importance of WPW itwoflt I) ts “the great mile” ~ aad ray ate oterconditocs (such ae chemiainfartion, hypertrophy andor conduction defacts)— TE ‘sot eecopize: and if The presence fone or moee accessory paw ays predisposes the patent toa mmber of tel imporant candiae arkythmias. Recognition of WPW i wsualycasy cna eselae 12-lead ECG when couducton complurely wizes he AP (Accessory Batlogy). Tere axe 3 ECG features to lock fr (Figwe 124. D: + QRS widen Deka waves 1A shor PR iste Figore 124-1: With WPW ~ the dlecricl impale fypartrthe AV node. The APs shown here pase long the ih se ofthe heat —bat the AP may pass on ther sie andor pass in fot or back ofthe sepae, ECG fests of WDW inhade:) QRS widening, i) Dea waves: andi) ashore PR itera. Daa waves (amon nay be postive cr meatve (See te). ‘The delea waves recopized asa distortion ofthe initial portion of he QRS complex is doe to the fat tha the cecicl impulse bypatses the AV node ~ and aces a the veaies dee via conduction over the accsscry pea, 1+ Dena waves may be ight (pone) or dowaward (negarve) ~ depending on where inthe heat the AP is acted. When deka wanes ae negative ~ they ay sine the Q wave of myocar infarction + Even when conducoa i emily over the AP ~ deta waves wilt always be seen in every lead. Moceover, dea waves my come and g0~ since conduction over the AP muy be Jntermitet At tines ~ conduction may simaltoncoualy occa over both the normal and accessory paivay. When tis happene~ the ECG characters of WPW my be sable ‘because the coarbsca fom coaducton over the acemal AV nodal patway may pedomiaat (ard thereby mask) ECG feanaes of pre-excaon. ‘Tae sousca the PR interalis short with WPW —is that dhe AV aodois bypassed. Wah aonnal conduct in sins eth he elacuzal pus slows dow ast passes trough the AV ode cn is way to the venices. Asa rest ~ most ofthe PR interval nomaly consis ofthe tine it takes forthe inpse to traverse the AV node. The cecal impue aves at the ‘Yeasce sooner wth WPW becanse the lave delay that occurs when passag though the AV aodef avoided by condacoa over te AP. + The QRS widens wth WPW —becanse afer te mpake aves athe venices (ia conduction over the AP) ~ tam rave over nanepaciaioad mvocaral ave onl ich ne ‘hari ain whatever distal porn athe conducon stem hat has a? yet dpolaized Tha the dea wave may exend for 0.04 second oe mare (rflectng slaw conduction aver onspacialica’ myocardial sme). When the deka wave is edt the rest ofthe QRS compen ~ the ess a widened comple. Allsot of vations onthe above theme (ar extend beyond!shescope ofthis ePub are possible Te pits to remeber are the folowing: + WPW isnot commen nthe genera population ~ butt das occur (and you wil se)! 1+ Whee a patzat wih WPW i coaductg over the accessery pat you can diagnose WPW by recognition of te folowing 3 ECG features i atleast sveral ofthe 12 lads fan ECG: ) ORS widesng i) acta wave, andi) ashore PR interval + Preexciation (je, PIV conduction over a AP) cane intenete Thte tas be a indcasoa on BCG that apaicat has WPW 2 conduction enirly (or aot entre) over ‘he noma AV nodal pea at th a the wack seconded. 2.5 — Figure 12.5.1: WPW during Sine Rayo Emergency car providers will at ala hve the Ena ofa baseline 12 ead ECG a the tne a patient wih TPT ascocate tachycardia i iialy seen, However, with bck LD-lead ECG nit cellalefearares of WPW suas occasional be found in th pateats char herby confirming the diagnos, We sow such a tracing mith over WPW in Figure 12.5 r ‘Note ia Figure 125-1 ~ thar deka waves are nor always prominat in every kad, One caro aguose LVH, schon rial fio th alafevor waves, deep Q wave’ ead SVL, or ST-T wave canoes in VILV2.V3 ~ since the patent ns WPW + Itshoudbe apparent fos Figwe 125-1 thar the dagneis f WPW coud be easily oveiocked IF oa was ut systematic in th apprcarh At frst saace~the QRS complex does sotlock ove wide. That said ~ eat nspacton of lead I cle revels a zhort PR ier with pwnd deta wave (red arrow in Figure 125-1) ~ tht when added to the ening portion ofthe QRS resis in widens ofthe QRS. Confrmsticn of WW is foricomie rm recoeiion of deta waves in mos! oe ex on he tase + Avvarerass thatthe patel You ave wea eran acute Caras shina las WPW aaa be cule in epronzing managemeat Sections 12.1s-tlvw-12 13) ray ESSE eee eta Figure 12.5.1: WPW ching sis shythn. The PRntervalis short (Bsr seo in lead I) —and the QRS prolonged (bor sear ix oad I.a’F). Deka waves ae seen in most but noe lh leads ca this 12-lead wating (here ino delta wave in lead V1 ~ ana the dela wave e minal leads land V2). Deba waves ae positive ia most lead Ge, red arrow in lead I) ~bal they are negctivein ads aVR and aVL (be arrows), On oceasion— negative deta waves may silat infin 12.6 SVT Pathways with WP ‘We ave aready emphasized how conduction cf the sins imps in pases ith WPW maybe: athe nomal (AV nade pate: down the AP; ci) may elemate bene he ‘vo. The same 3 posses for conduction ext when a pase wits WPW develops a supeaentclartacketytara (Figwe 126-1) + Patents wih WPW are prose t supraventricular tacvantyias ia which a reenny cireuit i st up benseea tae normal AV nodal pasvay andthe AP. Assuning here is 00 recs bundle Lranch locke ~ Whether a ct the QRS comple wi be wide daring the ecard = patent with WW wil depend upon whether the reetrant pathy Boe 1 ex down the AP (Figure 126-1). ALA Figure 12.641: SVT pathways wth WPW. Condicon of We impulse fom stato verter dug I7PW-acsociared wckyeacia may ether be: Panel A — orthodromic (dows the normal AP nodal Fis Pern system ~ and back wp the AP) ~ as comenonly ocoms with PSVT, or Panel B ~ antiromic (fret down the AP ~ and thon Back up dhe normal _patingy)~ a8 commoaly cars nih AFb or AFTater~ and ony raely wth PSVT (Soe te) 12.7 -PSVT with WPW: When the QRS During Tachycardia is Narrow ‘Wan PSVTia WPW — dhe tacky is nos va}s onthodeomie (dow the nom AV nada His Purkinje ston — ard back wp the AP = Panel A Figure 126-1, + Becnuse conduction goes down the nonnal AV nodal pathway — the QRS i& narrow dung the tachycardia. As a sesut ~ the usual AV nodal blocking drugs imy be used ‘Afecivey in reament Sector 13.0, + A deta wave ilo be seen dig the tachycardia, The preseace of WPW muy caly be suspected in a paint with narew-complex PSVT IE an ECG such a that seen a Fie 125-1 sfondi the made cht x bane felling conversion ofthe tachycardia + PSVT iby far te most common tachyattimia observe in patent with WPW. [tis olen we tolerated + Beyond she Cove: A supeiog sumbor of patoets wh PSVT actualy lave oue oe more concealed accessory paves. That i ~a coaducoa pavay exists becweun abi and ‘veticles tht ony alows eniodromic Gut not antcromi) conduction. Since forward conduction down the AP isnot possible ~ a deta wae i never seen. However, ready -raleliy ofan AP renny pubvay may pesdepose such pata tofequee episodes of PSV. Whle acute weatuee considerations ae senlar to tose for tesmuet of any othr ‘narrow complex PSVT ~ asereess ofthis ex ray lower one's teshold for EP ref ater the episode €PSVT episodes ae fequet andlor df to contol with mesicaton, + Wax Bevond-the-Core: Taking the ast advanced information bt on step farther ~ You may at tines beable to suspect the presence ofan AP in some WPW pata with ‘narrow cnmplen DSVT even wibout sng a deka wave IF you see a negative P wave with long RP neva efectng retrograde condition back tothe via dig the recat ‘cle. When retogrie condition seen dng AVNRT i a paint without WPW ~ the RP is vary short (mast eft coon as @ notch at te tol end ofthe ORS complex) esting hore tance travel mit the AV aode. The RP tds to be lege (negaive P usually seer michay with the ST zepmant fra pata whom the ceemny cect rns down the AV node and back up an AP bing ouside the AV node. Techical ~ ts type of PSVT in a pata with scessory pavays i known as AVRT (doo enicdar Reciprocating Tachycardia). Dsincson nthe ECG picture borvzar AVNRT vs AVRT (when an AP is presen is seated in Secons 143.7 and 1438 BOTTOM Line: Most ofthe tine ~PSVT i apatia with WPW wil condact wih a narrow QRS complex (Panel i Figure 126-1). Practically speaks ~ you do wor have ‘worry in teimoeate acute sting TF a patient with orrow-contpler PSVTT hae WPW or not. nial eatoeat measures are the same: Vagal manewer ~ Adenosine odor other AV aod blocking ageat Diltazem, Bet-Blocker, et: 128 — Very Rapid AFib with WPW 1a courat to the station for PSVT wih WEW — the cccureuce of AFih ina pate with WPW almost avays wantess a wide QRS dig the tachycardia, Ts Because the dreton of conduction for AFib with WPT is snost alvays antidromic (frst down the AP — and der back wp the normal pathway = Panel Bi Figure 126-1. 4+ Beamse ofthe shor RP (Refactory Pviad) ofthe accessory patbway — there may be 11 conduction of abi impulses (at snes resulting in a venricula response that may _xcoad 25Diminaca). As might be aniipted — shes ep ates are nat abrays wel tlecaed (may detvignate to VF). 4+ Tisrecopasin ofthe ECG pare of exceedingly rapid AFIb (over 220 miate i pars af the racing) i conjuction vith QRS widening ead marked variability epuay of the tracing tat chs the emergency care provider nt ost certainty of AFIb with WPW asthe agnosis This wn the ston forthe nals sp shown tthe beginning of ‘hs Seetn hat we repeat below i Figure 128-1 4 We dass management of ver rapid AF with WPW ia Section 1211 Figure 128-1: Same les Ist stip previously shown m Figure 12 1-1 The patent's abou tocode What Wty? (See =) 12.9 — Atrial Flatter vith WPW ‘With AFlatterin WPW — the tachyarsythmia i ko amttromic (frst dow: the AP — and then Backup the normal pawns = ar occurs x Panel B of Figure 12.6, 4+ As wih AFB — te QRS wide in AFUutter wit WPW.Tharo may be 1:1 AV coadacsion fei pulses (so har dhe vourcular response man be 250-300)minue)) + Veer fast APhoter with WPW is seen eve es after than AFH (but clinical manifestations acd treaoment ave similar). 12.10 PSVT with WPW: When the ORS is Wide Iavareinsances —PSV'T may be antidromic (e, reve st down the AP — an thon back wp the normal patinoay ocews in Panel B of Figure 126-D. «+ Intheze are instances — the QRS ibe wide andthe PSV nt may be icsinsthable fom VI 1 ita only be after conversion tosis hyn hat ele” deka waves of WPW canbe identiied. Fortunately — th vast majority (-9599) of PSVT episodes with WPW axe ‘nthocromic (with narrow ORS). Synchronized cardioversion wil be the wal treatment of choice for episodes ofa regular WCT (Tide-Complax Tachycardia) in wich one suspects autzvomsc PSVT in a patent wth WPW asthe eos 12.11 - Suggested Approach: Ropid AFib with WPI => Suggested Approach: ‘The importance of distngstns between the Vary conmca osm Of api AFIb (Section 14 2) nd) — te aval ene Osauseace of excessively rapid AFT uth WPW (Figure 12.81) les wih recommendations for ueatoeat. Fortunately — distinctive BCG characterises wal facta recopition. + Simchronized Cardioversion — isthe acute westmest of choice forthe symptomatic patent who presen in very rapid AFH> with WPW. That sad —a sgt mmber of ‘eats wo pesca wh the eth a Figure 12.81 gil supeisgly sable despite aig AP rats of °220mimte. Therefore — a trial of antiarychmte therapy il tea ‘be warranted Drug choices ice) Procaiaanie: i) Amiodaone, and i) Toute Secon 1213) + Remain ever ready to cardiover foray spn of hemodnamic decompensation. [TE fr amy reason you ate ble to cariove (as could happen whan the rate is excesivel fast) — debit 12.12 — Beyond-the-Core: Drugs for AFib/ Flaster with WPW &) => Beyond-the-Core: Controversy serous te use of ananiic apts or Ueaineit ot exces rapid AND (or ARTtio wi WPW. Prospective cody these rytims s made problematic by: rare ‘occurrence (mest emergency care providers see at mast a handful af cases evry few years): i) Ufe-threatening potential (andatng full attention to the ease at had ater ‘Bar evolinent into @ controled prospective eta). and Hi) ABiuky sing oot cross-over beatnents (mans patents beoyg giver more Han @ ringle agent andr needing cemergancy cardioversion at an unpredictable point during the reatnert proces) Drug dositg not consistent and detals of tay protocols the anal aca-conraed trl that have been done are lacking — such tat moe questions sean than have been answered ‘What is knowns the flloving + AV Nodal Blocking Drags tat ae rary wsed to teat the commen feem of rapid AR are contraindicated. This inches Veraanil Dikazeny Digosin — and possibly 8 Blockers. By imped condactin dow te aemal AV nodal pathway — all ofthese gens may inadvertent faclitare forward (ontcromic)ceadacon of AFib pulses dva he AAP (lccessony Pathway), thereby accelerating te rpidAFIb even more. Ths may prec deteietion to VES «+ Resin hat Adenosine i flea weed a a ciganostic metre die aseesamert of varios WCT rhythms — itis best to avoid Adenosine whenever possible [F very rapid AFD Mid WPW's suspected (sine Adenosine may ikowise accelerate AP conduction ina patient with WPT). Tht sad — the ulra-shor ha We of Admosiae i much less Hl to ‘be deletions comparedto oer AV nodal blocking drags ts nae en, 12.13 WPW with Rapid AF: Drug of Choice? ‘The 3 drugs tht hve most conan been recommended fr antarythnictreatnent of hemodnanscally stable very rapid AFib (or AFhttr) with WPW are i) Procainamide Amiodarone; andi) Ibutiide + ach dug tas ts vm set of advocates. ach (a least sheorerically) hows forward (antidromic) condostion down the AP. To the best of car review of the cueat iteranwe — a0 ‘Sfnsve case can be made a as ewe for use of one agen othe exchison ofthe ois fr the teas We tated Section 12.12, BOTTOM Late — Vary vapid AFD with WPW 's a mecical emergency. Synchronized cardioversion is ikely to be needed at sme point in many (mi) cases Expert consftaton fs advised whenever possible: Don't delay ‘cardioversion IF the pat at ay tne become unable, In the racine — IE Ris YOU on-he-scne with a stable pateat very pid AFD wih WPW— You ray consider snedcal reament wih oe ofthe fll: + Procainamide — shing 20.50 mgiminate IV un ct) the absthmia i suppressed: i) hypotension casuss; ori) 17 males bas bean sea (~500-1,000mg is the uzual IV loading dase). Keto procsinanse asin aks the rpidiy of TV ieuson ith the pants ood pressure response slow the rate hypotension cw) Onst ef action Ssreltively dow (specaly when starting at safer IV infusion res ~20-30mgimirat). ‘+ Amiodarone — dosing 3 for VT (giving ~150 mg IV over 10 mires. Tis dose may be tepested and flowed by TV afison of Img fr the next 6 hows. Disadvantages ‘ache potetaypteason and potent forthe AV nods blocking proper ofthis dru to outweigh ts beaeical fect on AP condcon. «+ Tbutide — ping Imig IV over 10 mites (aze 0.01 nigh paven weighs lze that 60 kg). Nay cepest 10 mines later no response though espvence with Ibi for tretng AFB with WPW is elavely eed —the drug act fst (average conversion zime within 20 minute) ppears tobe eflactive, and i usualy wel fleated in ost pets, Aiinongh at yet ited in ACLS Grideines — with tne, cams admiisratn of hs drag may become the ager of choice for very said AF (or APTuror) ih WPW. (NOTE: ter the acute tachycardia has resolved — Patsns vith WPW who hae had an eptode of AF oc Ahir shoud be refered to aa EP cardiologist (abanon ofthe ‘culprit AP” many cure tus potential ifetiveaterng aristonia thats othervize at high rok of recur) 12.14 PRACTICE: Whar isthe Ripthae in Figure 121417 Practice Example: Timi the 12-end EOG ia Fiswe 124-1 as btaned se ED (Energericy Depart) Boas hemodnariclly saie yoors kwh newonset pains 4 What is the rgtton? Wha dos tis patat have? Figare 12.141: 12-eed ECG from young ad with palpation. Whats the it? (Ses Fe). ANSWER to Figure 12.141: “Te srt is a regulary regular WCT (Stde-Comples Tacipcarah). No P waves ae sen oa an of he 12 leads tne Ging te ests as Ab, That sad the venicalar responte is exceedingly rapid (attaining @ Yate of naar S0lhminate im rome parts of the tracing). Imation — ther emake verily in rate ofthe venice response (cea Dest leaat a¥F an + Ths 12 ead ECG is wrtuallydiaupostic of very rapid Abin 2 patent who as WPW. Treatment considerations are scissed in Seto 12.13. The patient shoud be refered to a EP carologt afte sesciion ofthe aut tachycardia for consideration of enslave proce.