CASE 3 CVS GROUP 4 Pharmacology Therapy FERIANNISA NOOR AZKIA tS tei lilly, Braun, PERKI, AHA(4) \Nonaver valcava * + => Check Precure 2 f TH) Adonecin W Cpuiran (ac orate Corn tom CP vercgamt (25-59 perlohan) +4 3% Wilatdlr ada Heart falure) ) Ditecarern WV * prs-O/3Sing My (nla 444 abe ron Janeans Ooigras Wom Muape lol WV: s- iN ne ‘Weg, propanol \V zh-2m9 a awenit cdcoverar Ustciit (olla emockinaralc Feed color @x ¢_ dehy * a ~ ahlacs olduo feWwensy sloos Path wns Boa AV rode Nodal Reenicant Tau’) Ave jet : Abaw ratio frelusenss "| fathvouy algora arm Y Slope phaseA Spencer aeporons " ( y (Hypage ore) Sadi poensial dua buar Fhreshald porns! h Reenjrart caroal't : Qerisms ue fo Rec eoait le porrt cndchion fail, ehingga Q mnhiott ond lin reenMy © menghondi ken umpals yeentyy Ting ar ban repraetory geno de roond4 Corr seninggn cmpas mony Char prorema lan pariyar a Alm lop +d Bape Letuar # impals bechent Meneven premanrt heatc wy Pape menginistae feent?) aritmin due Triggered aonvity QD mem persinga churas! posers ial alr (Y/moncegah early ap ercepolarsas) BDenenperbauls bends calsum uerkood —(“rentagah delayed apterdpelar yes’)Ont * LAlaritin’a = Oboe gating bardabayr Worena pownst eel Camping T Ca 4 longa _ederortan Mo A Prim any ele chro e) z T) clase Vag < tourema block Nat channel, scare Cepet ( phase 0 Lepolars! actin POEM Br cordacmnusclee purtuige bert 2 clay T ding» p adrenergic receptors aasagonist (P blocker) | Bi clos dry: jerfama lock K* claannel (repolariaanon) , prolengérg et cote sedibit epee Pada ponmgliatan phase D FF) ClasVidry « lploc Lb type Calcium Charnes Ook oh Oe Tuquan : meng hagas mech anita rjc foliocitenian = Sega ¢ ® promot Sus enoluor / hon pacer re endront COCA, R ker gered ACHWVE «+ Poypomgads (tas Peng gunade, cba y © war Frawensi Cantar porensial alc “Te ‘gaan no © Shove donidepolansasi dastol phate 4 Spentén Bar| prolonging epochve repre cH porrode | i —<—S | + peentaant CUNT « dintasr Ag) a4 Fatarec Wink Seoran 2 cordurgtion Slow , SY Stop (eentant dig prolong refracted period > impul protong ( Na inactive), fedale Paper metg Wanter ban isin Cara We 2 cccirlale wmapair Conch ction dolam Unb retregrace yg matamyer do art bUckade Ma chaane l (phae ©) ~> mengharpustan reondpst tmpule 9p Horganggy brretg radglin 2 wamurs Self sustach iy) Coop - + Triggered acetvi ty , memiarialian early cupretston # delayed ape depolan zation ——a Ver Hoo V . ADroarrbyshma CfFEG & eel dori Obadt artim Yy Mem perhurrapy arttmia We nasanya ferfadi abe pisier dy (merval OT prowory tou dsl yanteilel -ABLE 17-12 \ Cass General Mechanism Examples rn Na* channel blockade IA Moderate block (|| phase 0 upstroke rate; prolonged Quinidine AP duration) Procainamide Disopyramide IB Mild block (| phase 0 upstroke rate; shortened AP duration) Lidocaine Mexiletine IC Marked block (||| phase 0 upstroke rate; no change Hecainide in AP duration) Propafenone | Il B-Adrenergic receptor blockade Propranolol Esmolol Metoprolol II K channel blockade (prolongation of AP Amiodarone duration) Dronedarone Sotalol Tbutilide Dofetilide IV Gy channel antagonists Verapamil Diltiazem ———$SSSS_ SSS EEE aaa \P, action potential.TABLE 17-13 EGG Appearance thes ass PR eS aw Normal BCG. | IA 0 t t he IB 0 0 Oorl uy IC T iE Oort AK | I Oort 0 0 An | TI Oort Oort t wa | IV tT 0 0 tL | ‘The predominant effects on the electrocardiographic segments are shown in red.ass Use IA + Atrial fibrillation and f utter * PSVT » Ventricular tachycardia IB * Ventricular tachycardia « Dgitalis-induced arrhythmias IC + Atrial fibrillation and PSV II » Atrial or ventricular premature beats =PSVI: + Atrial fibrillation and f utter « Ventricular tachycardia IIL » Ventricular tachycardia (amiodarone and sotalol) +» Atrial fibrillation and f utter » Bypass tract-mediated PSVI IV + PSWT +» Atrial fibrillation and futter (| VR) » Miltifocal atrial tachycardia (| VR) eee PSVE, paroxysmal supraventricular tachycardia (e.g., AVnodal reentrant tachycardia); VR, ventricular rate.Clas 1A Ait caatlints ee 4) ee pate Reenirant Archythme, moderate blol pe Fast ‘a Cluanrel > Slow tase 0 0D leendalis? eee # Prolonged repolarscs) —> errecive Feprecte pened D > teening Q eeu ea artania 7*Dowtonat ce meneuanisape pare 1 OmnUE! smauer cwannel) c ORS gor nervvel : cto pit Supraven tt cca avenk tala faleilrorct! nical ve > reentrant € : ( ~ quinih 0 procanaamde , dus yram(a- Class 3 rr rama) fF ~ felt pd ERG = seaitxt prolong. tere i gerhythin! =™o rT (t_ fast aru chaannel p> mempusingiiat Caras ersial ale 2 C rerech pen Veloces tyene! Flope Fae Gow thy by meninglaearn ‘thersholA andklo Clay otda use «Suppress ventriax(er arinmia econ (sleet Cho xiteir7S- momiul eel wocil pe adr iam (Heat Senge pe AF, PuneraWD) ic AMG = Lidocaine, mexueHne “Ep _ agi tion porential » elect Leondialesi aust: erat a purlunte pibes _- prole epractory ae = vende’ cular arta Tgapravensni W4lo- arttmia AF, AVY RT (as) = Panen ay Velounan Pay yp monclases es (ADS = Sem iic drag * ElLce ne , Propagarene ‘UV aspums” OwClass IA Class IB Class IC Shortened repolarization Prolonged repolarization Mode rate Mild Marked Na* channel \ Na* channel Na* channel block block block Na” channel blockade — | Phase 0 upstroke velocity | conduction velocity | Reentry [class LA]: Prolonged repolarization > ¢ effective refractory period a FIGURE 17-12. Hectrophysiologic effects of the class I antiarrhythmic drugs on the Purkinje cell action potential.Class T Antiatrhyrh Tapeh ere ae raped MONDE cntarpnist “Y SUT FH VT, backer Lg tnhablt Sempirs a upslope Faye, n Purina heart tale pee SA oe (emnpetObe Velocity Worfulihi 2 prolong cepracter porwoche Bieailei renga! ; te Ven: ar Cunical_we » Suppres qaluintinl memparlarbet fara oe 5 Ap eR FluHe 2p merwiate bensulr 27 reprattord AU node dermal (reentrant SY Arita , Sapress premahre beatventnik earuma veniel Lamys | Class lt Aniornshitmn) me ~MoA PRT Ng actor porn teal purluungo 9 yentrtealor muccles Boe kt outward fase 3 repo (arias ; podawre drone ocore Sotellol, dope tulece Jeteae ‘ duu » Am Coss y Arce(arrbythmn (a Mod Teecwe btovade L type Calcium channel, Paling pownt ae Av atanede | velocity a prolory Fepraceed period ~L, x rave Face o , conculisl | por | bo Up P thers hold porentnl oe? | b> Heart y ie az) Reenty ¥ | A transtni raped adnialimpals AV rode bo Vengeicle ~ Cunt use: a iS, uy reentan fi SVTs Cex AVART). ty. verapamil peas “4 acu episode Revamping = hyp ern . ee ea ent aed TAdinarra)- nucteornde endegen, ver shart Melt te -MoA otlambad Firing rave vy taverd fee malar, inwar Ca,Marke dly Purkinje . ty Hs prolonged cell ‘ repolarization action ‘ potential \ \ \ ~ } Effective refractory —_____» | Reentry period HGURE 17-14. Hectrophysiologic effects of the class HI antiarrhythmic drugs on the Purkinje cell action potential.TABLE 36.4 Dosage and Other Information for Clinical Use of Common Antiarrhythmic Agents and one . Dra aE) Reteiacctel omtaid PLASMA Bro Cas Petey cay Le ae oad et a ee ee ec cen (he) () EO ted Qunidine 6-10 mofkg at = 300-1000 -300-600q6h 1530 36 59) 60t080 Liver >kidneys c 03-05 mg/kg/min Procainemide 6:13 mofty at 26mgiin 5001000 «250-1000 @s-sh 40 35 7108s Kidneys> iver E 02-05 ma/kg/min Diopyramde 12 moftg over tmokginr NA 100-300 96-8h 12 25 29 80%090 Kidneys c 15-45 min" Lidocaine 12 mofkg at 1-4 mg/min NA NA NIA 15 12 NA Liver 8 20:50 mg/min Mexietine $00 mg” 05-109/24tw 400-600 15030008412) 24 075.20 1047 90 Liver ce Phenytoin 100 mgqSmin for NA 1000 t00-400qi2-28h 8-12 10-20 1836 501070 ter D $1000 mg Flecsinide 2 mg/kg 100-200 at2h= 50-200 at2h 34 0210 20 5 Kidneys c Propatenene 12 mo/tg* NA 600900 1503000812 13 0230 58 25075 ter € Propranolol 0.25-05mgqsmin NA NA 10-200 96-8h 4 125 36 351065 ver € t0.<0.20 moka Amiodarone 15 m/min for 10 min OSma/min 800-1600 qd 200-6004 Variable 0548 56 dys 25 iver . mgima for 6hr for 7-14 dys 05 mgimin thereafter Dronedarene NAA NA WA 400 mg aizh 34 03-06 13-19 701090 ver x Soislol 10 mg over 12min” NWA WA 80-160 qtah 254 25 2 90%0 100 Kidneys ® Ibutlide I mgover 10min NA NA NA NA NA 6 Kidneys c Doletlide —2-54ighg infison* WA WA (125-08 qian na 90 rodneys c Verapami S10 mg over 12 min 0.005 mg/kghmin N/A 80-120 96-8h 12 010-015 10t0.35 Liver, kidneys c Adenosine 6-18 mglrapidy) NA WA NA NIA NA 100 Blood cells z Digorin 05-10-99 0125-02594 05-10 0125-025 a4 26 0.0008-0.002 60t080 Kidneys z Randlazne NA NA NA 500-1000 bid 46 NA 6075 Kidneys > ver c *inuavenous use investigational or unavailable in United Slates, NIA, Not apolcable. q4-6h, every 4 to 6 hours, ad every day, bid twice daily Results presented may vary according to doses, dsease state, and IV oF oral administration. Pregnancy Cass: A. controlled studes show no fetal risk; 8, no controlled studies, but no evidence of fetal risk; fetal harm unlikely: C, fetal rsk cannot be excluded: drug should be used only if potential benefits outweigh potential ‘isk D, defite fetal rk; drug should be avoided urless in aIfe-threatening situation or safer alteratves do not east, X, contrandated in pregnancy. Calegorizaion of safety dzing pregnancy and lactation is currently under revision 00TABLE 36.5 In vivo Electrophysiologic Characteristics of Ant rhythmic Drugs teat eed aaa aes irate dra Crud Bee fas By ERI ie) ERP. iad AH HY Quinidine oT tot Tt of Fi t: t ol T Procainamide 0 ot + of t t t ot T Disopyramide tot lot t To Tt t t Lot iF Ajmaline 0 oT t o + t + tot Tt Lidocaine Qo o t ot ot o 0 ot ot Mexiletine ° 9 1 ot ot 0 0 ot ot Phenytoin 0 0 0 ot L 0 0 ot 0 Flecainide ol + ° T T tS T T T Propafenone ot Tt 0 ot ot ot t t if Propranolol 4 oT 9 tT 0 0 0 o 0 Amiodarone + oT t t t T tT t t Dronedarone 4 ot ~ tT ¥) 7 t t 0 Sotalol 4 ot tT of * * tT + 0 Ibutilide 4 ol t 0 ° tT tT 0 9 Dafetilide 0 0 t 0 0 t 1 0 0 Verapamil ol t 0 T a 0 0 Tt 0 Adenosine 4 then T Tt 0 tT 0 4 0 t oO Digoxin + T Lt it 0 4 0 ff 0 Ranolazine 0 0 it o 0 t if 0 0 Results presented may vary according to tissue type. and drug concentration and autonomic tone f = increase; 4 = decrease; 0 = no change; 0 T or 0 1 = slight or inconsistent increase or decrease A, Atrium; AVN, atrioventricular node: HPS, His-Purkinje system: V, ventricle; AM, atrio-His interval (an index of AV nodal conduction); HV; His-ventricular interval (an index of His-Purkinje conduction), ERP, effective refractory peniod {longest S,-S; interval at which 5, fails to produce a response).Figure 8. Ongoing management of SVT of snknown mechanism. Colors correspond to Class. of Recommendation in Table 1; drugs listed alpha- indicates electrophysiolog pt, patient; SHO, structural heart disease finclud- ing Ischemic heart disease); and SVT, supraven- tricular tachycardia.Figure &. Acute treatment of regular SVT of unknown mechanism. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. “For rhythms that break or recur spontane- ously, synchronized cardioversion is not appropriate. IV indicates intravenous; and SVT, supraventricular tachycardia.