Atrial fibrillation

Annotations:

• First: must know if it is Valvular Afib or Non Valvular Afib. This determines which Anticoagulants we use- can't use DOACs in Valvular Afib Second classify ito of how long the Afib exists(time): Classifications: a)paroxysmal (occasional )-spontaneously resolves with 7 days Here they have it for 7 days or less ,  b)Persistent (longer than 7  days),  c)Longstanding Afib(>1 year), d)Permanent will have Afib for rest of their lives. The longer you have it the more set it is- harder to stop,  e)non valvular : absence of rheumatic mitral stenosis, a mechanical or prosthetic valve or mitral valve repair
• symptoms: see/feelfluttering in chestfeel faint, weak, syncopechest paindyspnearisk of thrombo-embolic strokeso need anticoagulantUse EKG to diagnose the worst thing that can happen is thromboemolic event or HF may present
• symptoms vary with ventricular rate , underlying LVEF , AF duration

1. Risk Factors CHADs2Vasc

   Annotations:

   • >2 needs anticoagulant  need anticoagulant to prevent stroke due to atrial fibrillation <2 can use aspirin
   • CHF  +1 Vascular Dx +1 HPT +1 Stroke/TIA +2
   • age >65 +1 age >75  +2 F +1
2. causes

   Annotations:

   • 2 groups (table p 26) a)atrial distension (atrium out of whack) caused by chronic HPt, mitral valve dx, cardiomyopathy, congenital defect, Pulmonary HPT, Acute pulmonary embolus, Myocardial ischemia, sleep apnea, Emphysema/lung dx
   • b) High adrenergic tone caused by alcohol withdrawal, thyrotoxicosis, sepsis, binge drinking, surgery, sypmpathomimetics like amphetamines/cocaine, excess theophylline/caffeine
3. complication of Afib

   Annotations:

   • biggest issue is stroke so need to anticoagulate Stroke is the biggest cause of morbidity/mortality in Afib pt...otherwise Afib itself would not be as risky

Annotations:

• aim for rate control aim for rhythm control if rate control fails Cardioconversion Anticoagulation
• When to use what? see Cardiology II video  0:31:23 mind map

1. Rate Control is primary goal

   Annotations:

   • Ventricular Rate Control: with rapid ventricular rate need AV Nodal block Class IIa recommendation: resting HR< 80bpm in symptomatic pt If asyptomatic pt with LVEF reserve class IIb recommends a more lenient goal <110bpm goal is reduce symptoms and prevent tachy-induced cardiomyopathy  i)BB a) any BB to get goal HR b)Labetaolol or carvedilol if additional alpha 1 blockade is needed eg with HPT c) effective for exercise induced increase in HR d) 3 BB names can be considered for stable HFrEF ie bisoprolol, carvedilol or metoprolol succ. e) avoid in pt with Wolff-Parkinson-White WPW syndrome ii)Ca Channel blocker (non-dihydro-pyridine) eg Verapamil, Diltiazem a)they work to slow the heart in Afib  b)Caution in CHF: can exacerbate edema/fluid retentionso DO NOT USE IN HFrEF where there is systolic dysfunction!! ! c)CCB are preferred over BB if pt has asthma/COPD or had SE with BBCCB good for exercise induced increase of HRand BB SE( sexual dysfunction, fatigue)see HPT
   • Digoxin  not used as a single agent(monotherapy) esp for exercise  a)may see Loading dose  used for Afib(LD not in CHF),  b) possible use if BP is low - so want to avoid BB / Ca Channel Blocker can choose Digoxin but check if SCr is okay and if K is okay before starting digoxin. It is usually added on to BB +CCB for  rate control in Systolic HF c) Goal conc higher for Afib vs CHF    Goal conc: Digoxin in Afib: 0.8-1.2 Digoxin in CHF: 0.5-0.8   d)Toxicity:i)vision : green-yellow vision ii)wt loss iii) poor appetite iv)GI upset v) low pulse vi)CNS disturbances  e)  renal dosing-can accumulate f) can cause arrhythmia - especially with low K+ or low Mg there is increased risk of arrhythmia  g)amiodarone can increase digoxin levels e) can be used if pt is getting BB,D/V already but need more HR control f) avoid In WPW syndrome
   • Amiodarone is a rythm drug but if no luck with other rate control drugs can go with Amiodarone for refractory Afib cases (ie not responding to BB , D/ V, digoxin) in HF Amiodarone is a rhythm and rate control drug actually
   • In ER they usually use cardio version but can also use pharmacological means  after a/c is started why is rate control better than rhythm control to get to normal sinus rhythm? these drugs are less toxic , less AE these drugs 
   1. digoxin immune fab

      Annotations:

      • https://www.drugs.com/pro/digibind.html when to use this antidote importance of K close to 5 while experiencing digoxin toxicity(tachy/brady) dose calculation: usually 6 vials will reverse symptoms if you don't know the dose pt had.  Or need to calculate  dose of antidote using calculations involving serum level of digoxin or digitalis (# of vials to use involves some estimation)
   2. DRUGS:A,B,C,D
2. Rhythm Control

   Annotations:

   • use if can't take rate control meds or if rate control meds did not help Which one? Amiodarone
   • a) controls rhythm b) extremely long t1/2 it's affects can continue for a long time (2 months)after being dc'd c) watch DI especially with long t1/2 d)monitor thyroid- hypothyroidism more common e)can cause pulmonary fibrosis monitor lung function while on amiodarone f)Boxed warning: Liver Toxicity monitor LFT
   • rhythm control  has no advantage over rate control but if you cannot achieve an adequate ventricular rate or pt has intractable or intolerable symptoms(dyspnea, palpitations) may need rhythm control to achieve and restore sinus rhythm. 
3. Cardioconversion

   Annotations:

   • cardioconversion in new onset Afib can increase risk of thrombus Thrombus + cardioconversion = 91% stroke especially if  atrial fibrillation has been going on >48 hours TEE tranesophageal echo is used to see stagnant blood in atria where clot can formWhat  are the chances someone in Afib has a thrombus? Find out how long they have had Afib<48 h : 1 % chance of a thrombus>48h : 15% chance of thrombus>72 hr: 30 % chance of atrial thrombusso must anticoagulate before converting must be at a therapeutic INR >2 for 3 weeks minimum before cardioconvertingsee guidelines p 5 Rph needs to step in to make sure anticoagulation was started prior to medical or electric cardioconversion to restore sinus rhythm
   • Start anticoagulation if planning to do cardioconversion  If urgent use Heparin infusion or LMWH Could also use NOACs vs Hep
   • Electric cardioconversion  is preferred in new onset Afib direct current cardioconversion
   • Medication cardioconversion is second line / less effective options: a)Flecainide  1c (exclusion can't be used in pt with previous MI due to increased mortality-CAST) another issue with Flecainide is increase in ventricular rate so see paradoxical increase at AV node so need rate control drug with Flecainide Dose 50-100mg q12 can take dose when they feel the flutter = pill in pocket dose 200-300mg once for cardioconversion SE blurred vision need to change tr b)Propafenone Rythmol 1cavoid in structural heart dx MI, HF, valve dx ... like above(just like flecainide but also has B blockade as well. so pt can have dyspnea from Beta 2 block, dizziness etc- could be due to propafenone)doses 150mg-300mg q8or 225-425 ER q12Pill in pocket 450-600 once to cardioconvert at homec)Dofetilide (tikosyn)d)Ibutilide (convert)e) amiodarone
   • Anticoagulation guidelines: 2 sets of guidelines Chest guidelines - last update was 2012 ACC/AHA/HRS AF guidelines are a little newer  (2014) so if memorizing  just one go with this one p24 of Cardio II see p6
   • stable AF pt , afib < 48 hrs (1% risk of thrombus?) (ACCP)Chest says do anticoagulation with LMWH /UFH at full trt doses at presentation and continue through out cardioconversion then for 4 weeks minimum continue a/c after cardioconversion irrespective of stroke risk ACC/AHA/HRS says need to start anticoagulation before cardioconverting, depends on risk of stroke - if high, start UHF, LMWH or DOAC asap(so agree with ACCP (chest ) but only if high stroke risk and more a/c options) Then after cardioconversion, look at thromboembolism risk by using CHA2DS2-VASc score  Summary:  for ACCP: say to anticoagulate before and use for 4 weeks after regardless of stroke risk For ACC/AHA/HRS says to assess if high risk  for stroke then anticoagulate before and afterwards assess CHADS-VASc score to know risk of thromboembolism to know if you should anticoagulate for 4 weeks after cardioconversion. Also difference in a/c trt: ACCP says use LMWH or UHF at full trt doses and ACC/AHA/HRS if they are high risk for stroke also can do DOACs
   • Stable pt with Afib > 48 hours or unknown duration (thrombus risk = 15%)  and TEE not done ACCP(Chest) guidelines: anticoagulate for 3 weeks before cardioconversion Warfarin with INR 2-3 LMWH full treatment dose or dabigatran(Pradaxa) Anticoagulate for >/= 4 weeks afterward, regardless of stroke riskACC/AHA/HRS says to anticoagulate for 3 weeks + before restoring SR with electrical/pharmacological cardioconversion . Use warfarin with INR 2-3 , dabigatran, rivarobaxan or apixaban Anticoagulate for 4 weeks  after cardioconversion, regardless of CHA2DS2-VASc score summary: so so both guidelines say anticoagulate for 3 weeks before and 4 weeks after (don't bother with stroke/CHAD risks) What you anticoagulate with differs. ACCP says use Warfarin(2-3 inr)/LMWH/Pradaxa while ACC/AHA/HRS says use all po warfarin(same goal)/Pradaxa/ xaban
   • TEE guided cardio conversion for stable pt for >48 h Afib ACCP(chest) guidelines:  start LMWH or UFH at time of TEE and cardioconvert within 24 hours of TEE if no thrombus is seen in atrial cavity or atrial appendage cavity  then follow with 4 weeks of anticoagulation regardless of stroke risk ACC/AHA/HRS : if no thrombus is seen on TEE screening, cardioconversion is reasonable immediately after antocoagulation was provided then after TEE with UFH bridged to VKA or AOC for 4 weeks + after cardioconversion summary: Both ACCP and ACC/AHA/HRS say anticoagulate before cardioconversion, then do TEE. ACCP says give UFH and LMWH at time of TEE and cardioconvert within 24 hours of TEE, if no thrombus. Both say anticoagulate for  4 weeks + after...regardless
   • A transesophageal echocardiography (TEE)-guided strategy has been proposed as an alternative that may lower stroke and bleeding events. Patients without atrial cavity thrombus or atrial appendage thrombus by TEE are cardioverted on achievement of therapeutic anticoagulation, whereas cardioversion is delayed in higher risk patients with thrombus.  TEE guided pts had a shorted duration of anticoagualation prior to cardio conversion  and was just as effective
   1. p28
4. Anticoagulation

   Annotations:

   • see DVT/PE
5. Antiarrhythmic drugs

   Annotations:

   • See fig 4 31/70 cardio II Anti-arrhythmic drugs Vaughn-William classes:Look at action potential diagram 0:38:44Cardiology IIclass I to IV (they all work in diff places)Class I and class III are the main arrhythmic drugsClass II and IV are rate control drugs- but are still in Vaugn - Williams classificationClass I Na blocker  ***imptClassII BBClass III K blocker* **imptClass IV Ca blockerOthers (no in VW classification  I-IV)Kaiser does Amio monitoring
   • Class 1  Na channel  blocker  inhibiit phase 0  depolarization slow conduction velocity
   • Class II BB  (Acts at phase 4)Major effects on AV and sinus nodesadditional effect on Autonomic system
   • Class III K Channel blocker (acts at phase 3)Prolong repolarization (phase 3)and increases refractoriness
   • (acts at phase 2) Class IV Ca Channel blocker major effect on AV nodes>sinus nodes
   • Other drugs: not in Vaugn william class a)adenosine b)digoxin c)atropine d)Mg (for torsades)
   • CAST trial Cardiac Arrhythmic Suppression Trial found in pt who had MI more than 6 days but under 2 years previously : flecainide caused death (cardiac arrest)  so due to CAST trial any 1c antiarrhythmic cannot be used in structural cardiac dx (broad defn MI, valvular dx, HF...) So avoid Flecainide , Propafenone (1c drugs)
   • Call 1c Discussed flecainide and propafenone  see Cardioconversion tab
   • Class III Antiarrhythmic Drugs a)Sotalol b)Dofetilide c)Donedarone d)Amiodarone
   • A)sotalol (ClassIII) BB (class II actions) and K blocker (Class III actions)also Most recommend starting sotalol in hospitali)only 50-60 % efficacy which is decentii) 80-160mg bid dosing for adjusted crcl >60ml/minrenal: qd dose for adj crcl 40-60ml/minCI for crcl < 40ml/min   for Afib(CI different for ventricular arrhythmia)iii) can cause QT prolongation related to larger dose, reduced crcl, female iv)AE torsades, HFBB SE : dyspnea , dizziness....
   • b) dofetilide tikosyn used atrial flutter or Afib major SE ventricular arrhythmia in about 15% so start in hospital with big protocol to monitor QTc and crcl p 30/70 cardio II
   • c)Amiodarone updated 2018..see p29/70 has features of all 4 Vaughan-Williams classes)i)most effective 85-95% in recurring AF and can be used with HF ii)BUT SE : usually irreversible Pulmonary fibrosis 1-2 % but lower with lower doses/shorter usecan also cause reversible hepatitisaffects thyroid (hypo, hyper)smurf syndrome-skin sensitivity long t 1/2 about 2 months- so if having SE - it lasts that long until drug is clearediii) Dosing:MD 200mg daily ( question 400mg bid etc for MD)LD: 3-10 g target600-800mg/d in divided doses for up to 2-4 weeksiv)FDA approved for VT but used off label for AFv) Need to monitor amiodaronewith chest X-ray , EKG, LFT(ALT + AST), Thyroid(TSH,T4), PFT with DLCOneed baseline test with all thesethen every year do chest X-ray and EKGand every 6 months do Liver and thryoid testand do PFT +DLCO if suspect toxicityWhat action to take:If pt has dyspnea, cough, fever - suspect pulmonary toxicity so do chect x-ray and PFT and DLCO and DC drug immediately you confirm toxicityif TSH and T4 are offadd levothyroxine if hypothyroid and add methimazole /PTU if hyperthyroidif LFT(ALT and AST) are 3x higher , reduce amiodarone dose or DC
   • d) Dronedarone(Multaq) Class III i) about 20% efficacy ii)took off iodone moiety off amiodarone so related to amio so also has properties of all 4 VW classes iii) indicated for Afib (paroxysmal and persistent) iv)C/I : not used for control of ventricular rate in pt with permanent AF (have increased risk of stroke, MI, systemic emboli, CV death) Also many CI: 1.not for HF class II and III with recent decompensation(needing admission) and not for HF class IV  2. not for any heart block, AV block, sick sinus syndrome with pacemaker  3. not for liver dx bc causes that issue as SE 4. not for low HR<50 5. cant use with 3A4 inhibitors 6.cant use if QTc>500 7. not for permanent AF all the time DI:  1. Multaq + Dig ...decrease dig by 50% 2.excessive bradycardia with BB,D/V , clonidine Diltiazem/Verapamil can also increase multaq thys watch ECG 3.Statins- like before limit statin dose but 1/2 cf to previously discussed simvastatin max 10mg, lovastatin 20mg max 4. 
   1. Class 1c 50% efficacy

      Annotations:

      • a) Flecainide and propafenone can be considered 1st line therapies if no structural heart dx. b)Propafenone also has some BB axn (non selective) c)accompany it with AV nodal blocker eg BB or non DHP CCB d)class 1c C/I with structural heart dx like CHD, HF and LV ventricular hypertrophy and valvular heart dx.
   2. Class III

      Annotations:

      • p29 Class III a) Amiodarone 85-95% efficacy b)sotalol 50-60% efficacy
6. What to choose?
   1. No Structural dx

      Annotations:

      • No structural heart dx is no MI, vascular dx, HF, cardiac hypertrophy..)
      1. drugs
         1. dofetilide
            1. dronaderone
               1. flecainide
                  1. propafenone
                     1. sotalol
                        1. last resort amiodarone

                           Annotations:

                           • bc of SE
      2. ablation

         Annotations:

         • some Drs want to do catheter ablation instead
   2. structural Heart dx

      Annotations:

      • has MI /.HF / etc
      1. CAD

         Annotations:

         • 3 choices plus last choice amiodarone
         1. Dofetilide
            1. Dronaderone
               1. sotalol
                  1. last resort amiodarone
      2. HF

         Annotations:

         • 2 choices only if severe HF - avoid ablation - bad outcome
         1. Dofetilide
            1. Amiodarone
      3. catheter ablation
   3. Question

      Annotations:

      • eg can you  use flecainide in HF Flow sheet below says no (only 2 options for AF in HF- dofetilide and amio)
   4. Alerts for Q &P

      Annotations:

      • healthy use any antiarrhythmic CAD 4 choices HF 2 choices Low K: correct that  before starting do not use sotalol or dofetilide if have chronic hypokalemia  due to QT prolongation If renally impaired : <30 don't use sotalol <20 can't use dofetilide if chronic severe pulmonary dx: can't use amiodarone/dronedarone 

Annotations:

• Rate control vs rhythm control rate control has better outcomes. Start with rate control unless can't and then use rhythm control . But must look at HR  etc before you start Also use anticoagulants Look at advantages/pros and cons of both  strategies on p 27 table
• HR control : want resting HR less than 80 bpm in pt who is symptomatic(Class IIb recommendation) so look at  heart to  see what goal we want More lenient with asymptomatic pt with preserved systolic function : aim to get HR < 110 bpm but can aim for <110 bpm if pt is asymptomatic and has preserved systolic function. Heart looks good.RACE-2 study says HR less than 110 bpm was not inferior to 80 bpm goal so lenient goal was not inferior be aware of other dx states in pt and individual response to determine which of the 4 drugs are used
• BB 1st choice for rate control a) any BB b)may need to reduce HR too so then can choose carvidelol  or labetalol c) if its HFrEF as with systolic HF- need to use 3 BB mentioned in HF ie bisoprolol, carvedilol, metoprolol succinate d) ok for exercise induced  but not WPW
• Non DHP CCB for Rate control Eg D/V a) use if pt has asthma and don't want BB or also pt has SE to BB like fatigue, sexual dysfunction b) good for exercise induced HR increases but not HFrEF (systolic HF) and not for WPW
• BB a) good for HR control  b) ok with HFrEF (systolic) use 3 BB recommended in HF ie bis, carv, meto succ c)use labetalol / carvedilol if BP is high as they will add on alpha 1 action d)ok with exercise induced  HR increases but not for WPW pt
• non DHP CCB : D &V a)ok with exercise induced HR increase and not with WPW pt as for BB b) NOT for HFrEF (systolic HF) bc causes edema! c) Preferred over usual BB if pt has issues with BB like SE fatigue/ sexual dysfunction d) also preferred in pt with asthma
• Digoxin: a)not for exercise induced HR increases bc no sympathetic axn and also not for WPW pt b) good for adding on to BB, non DHP CCB for further rate control  or adding on to regimen for HFrEF
• Amiodarone Add on after BB, non DHP CCB and digoxin has been added and still have high HR or refractory cases
• Rythm Control Last option if pt still has tried all these drugs and still has high  HR with symptoms of dyspnea, tachy then need ventricular rhythm control to convert to normal sinus rhythm Must check if there are atrial thrombi/clots before doing this. Good to try this bc don't want atrial structural changes
•  Cardioconversion: electrical or medical a) Atrial blood can be stagnant and get clots ..danger is stroke.  If thrombus is there and you cardioconvert can have stroke 91% b)the longer they are in Afib, the >% of clot in atria 48 h --> 15% and 72 h---> 30 c) to ensure no clot: EITHER check with TEE or take ac for 3+ wk i) do TEE transoesoph. echo to see atria ii) OR pt to take  >/=3 weeks therapeutic anticoagulation ( have INR>2 for warfarin a/c) 
• Oral  meds are an option instead of electrical : to induce or maintain SR 
• oral antiarrhythmics to maintain SR or induce SR(pharmacological cardioconversion) a)1st choice Flecainide and Propafenone (both class 1c) but must have no structural heart dx as it is C/I (eg CHD, HF, ventricular hypertrophy, valvular heart dx) b)typically need to add on AV node blocker like BB or non DHP CCB
• Class III antiarrhythmics:  a)Amiodarone 85-95% efficacy i)Oral LD reqd eg 400mg 2-3 times per day for 2 weeks  400mg/d for 4 weeks then 200mg qd MD Many different regimens for loading - desirable to have 10g LD. long t1/2 60d ii) has AV node blocking axn thus can help with HR if has AF recurring but minimal incidence of ventricular arrhythmias iii)OK in HF IV)many DI  bc hepatically metabolized -Digoxin DI so lower digoxin dose by 50% -Wafarin DI so lower warfarin by 33-50% -Simvastatin max dose 20mg -Lovastatin- max dose 40mg -additive Bradycardia with BB, non DHP CCB, clonidine, ivabradine v) Need to monitor for AE: - LFT - baseline +q 6 mo -Thyroid tests baseline+q 6mo -Chest radiog-baseline+pa -ECG: periodically -Pulmonary function tests: like carbon dioxide diffusion in lungs. do baseline or after suspicious symptoms like cough/dyspnea/abnormalities with chest xray - discontinue if pulmonary fibrosis is suspected. -Ophthalmic exam:baseline and periodically for visual impairment- dc if optic neuritis -Skin toxicity- blue skin syndrome/sunburn -Neuro- tremor , neuropathy
• b)Sotalol 50-60% (2nd Class III): - initiated in hospital to monitor K, Mg , QTc, Scr(min of 3 day stay) - renal excretion - so dose renally usual starting dose 80mg bid but if crcl<60 then qd dose - CI in pt with uncontrolled HF, crcl<40, QTc>450, 2nd and 3rd degree AV block or sick sinus syndrome (in absence of pacemaker) - have BB nonselective axn thus additive bradycardia with BB, non DHP CCB, clonidine, ivabradine, digoxin
• Dofetilide (3rd one for Class III) p 30   Tikosyn-50-60% efficacy-Start in hospital (min 3 day stay) to monitor SCr, QTc, K, Mg May use in HF (structural heart Dx)- renal dosing:crcl>60 500mcg bidcrcl 40-60 250mcg bidcrcl 20-39 125mcg bidcrlc <20  C/I and also C/I if QTc interval > 440ms (or 500ms for ventricular conduction abnormalities)-if renal function worsens  recheck QTc-look at QTc interval 2-3 hrs after initial dose:need to modify dose (reduce by 50%) if:QTc>500ms or >550ms in ventricular conduction abnormality OR QTc increased >15% above baselineAt any point after doses 2-5 if QTc > 500ms (or 550 ms in ventricular conduction abnormalities) you need to DC  Tikosyn-hepatically metabolised 3A4 so use CYP3A4 inhibitors cautiously as the cause increased exposure to Dofetilide so may need to decrease Tikosyn dose- eg use  triamterene, metformin, amiloride with caution if on Tikosyn D/I: avoid concommitant use of cimetidine, verapamil, itraconazole, ketoconazole, prochlorperazine, megestrol, dolutegravir, trimethoprim or Bactrim
• Class III Doraderone (Multaq) is 4th type in Class III: with 21-25% efficacy Dronaderone is the analogue of Amiodarone but lacks iodine grp which made Amiodarone toxic to thyroid C/I: a)in permananet AF b) NYHA class II and III HF with decompensation needing admission also class IV HF c)HR< 50bpm d) 2nd or 3rd degree AV block or sick sinus syndrome(without pacemaker) e)severe liver impairment or previous hepatotoxicity due to amiodarone or even pulmonary toxicity from amiodarone f) C/I also with use of strong CYP3A4 inhibitors or QTc interval prolonging agents g)CI in preganancy h) C/I if QTc interval>/= 500 ms - has electrophysiological properties of class I-IV - dose 400mg bid with meals - Hepatically metabolised CYP3A4 substrate and CYP 3A4, 2D6, P-gp inhibitor -D/I:  a)Digoxin increased dig levels thus decrease Dig dose by 50% b)BB or non DHP CCB and clonidine: cause excess bradycardia thus use lower dosing for these and D&V van increase Multaq exposure thus check ECG c)Statins - increased statin exposure so limit simvastatin to 10mg qd and lovastatin to 20mg qd d)Dabigatran (Pradaxa) will have increased exposure with co-use of multaq so decrease Pradaxa to 75mg bid e)AVOID if using strong CYP3A4 inducer f)monitor concentrations closely if usng Cyclosporine, tacrolimus, sirolimus t1/2 13-19 h -Monitor Scr periodically bc may see small increase in SCr 0.1mg/dl but plateau's in a week and is reversible. Acute renal injury in some but reversible when Multaq is DC'd One study showed Multaq is less effective than amiodarone but comes with less SE SE/ Safety issues with Multaq: a) liver injury: reports of isolated severe rare hepatic injury b) Pulmonary toxicity: cases of interstitial lung dx incl pneumonitis and pulmonary fribrosis   so ask pt if they have any dyspnea or dry cough
• see Fig 4  p31: choose drugs based of no structural heart Dx and Structural Heart Dx Just remember Flecainide and Propafenone are definitely not for structural heart dx

1. Key points

   Annotations:

   • CHA2DS2VASc score 2 or more need A/C Afib p2
   • Afib >48 hrs duration  need to Anticoagulate if cardioversion is planned Rate control drugs BB & CCB preferred see exceptions for some CCB under rate control tab
   • Rhythm control : must choose agent based on dx 

Annotations:

• Acute decompensated heart failure (ADHF) is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. ADHF is a common and potentially serious cause of acute respiratory distress.

Annotations:

• Q1  p9 in HF section
• Q4 1st question in AF Pt PM 52y ht,wt yes hx HTN+  ITA 2 yr ago now a/flutter , chest pain ECG irreg irreg, no P, 74bpm dx AF meds:  meto tartrate 50mg bid, asp BP 130/70,  HR 76BPM

1. Self assessment