Atril Arrhythmias Flashcards
Cardiac conduction system
-sinus node on right side atria generates depolarization down to AV node
-down bundle of His splits to left and right bundle branch
-down to purkinje fibers for ventricular depolarization
Left bundle branch
-splits into anterior and posterior division
-left ventricle needs more conductoion bc it is pushing blood against high atrail pressure to body
Relationship between ECG and action potential graphs
-
ECG waves
-P wave: atrial depolarization
-QRS: ventricular depolarization
-QT: ventricular repolarization
-T phase 3 repolarization
-PR: measure conduction time
Action potential graph
-Phase 0: depolarization sodium current
-Phase 4: resting membrane potential K current
-Phase 1: rapid repolarization K current
-Phase 2: plateau, Ca current
-Phase 3: repolarization K current
Questions to ask while looking at ECG
-Is there P wave?
-QRS after P wave?
-Rhythym regular?
-HR?
how to estimate HR on ECG
-300-150-100-75-60
-based on how many boxes between QRS intervals
-if irregular, 5 boxes = 1 second, count beats and multiply
-normal is 60-100
Normal PR interval duration
-0.12-0.2 seconds (120-200ms)
-affecte by BB, verapamil, digoxin
Normal QRS duration
-0.08-0.12 sec (80-120ms)
-affected by flecanide
normal QT interval duration and correction
-0.38-0.46sec (380-460ms)
-must be corrected for HR
-faster HR = shorter QT
-drugs that dec HR extend QT interval
-men (testosterone): 0.36-0.45
-women:0.36-0.46
Torsades de Pointes
QTc interval
-QTc interval > 0.5s (500ms) inc risk
-drug-induced
=sudden cardiac death
Tosade de Pointes graph
-NO pwaves
-Irregular rhythym
-150-300 bpm
=bp drop and pass out
Drugs that may cause Torsades de Pointes
-antiarrhythmics
-longterm use antimicrobials
-antideppressants
-antipsychotics
-anticancer
-opioid
antiarrhythmics that can cause TdP
-procainamide
-flecainide
-ibutilide
-dofetilide
-sotalol
-amiodarone
-dronedarone
Antimicrobials that cause TdP
-macrolides (-mycins)
-Fluroquinolones (-floxacins)
-long term use
Antidepressants that can cause TdP
-citalopram
-escitalopram
-clomipramine
-desipramine
-lithium
mirtazapine
-venlafaxine
Antipsychotics that cause TdP
-chlorpromazine
-haloperidol
-pimozide
-thioridazine
-ariproprizole
-clozapine
-iloperidone
-olanzapine
-paloperidone
-quetiapine
-risperidone
-sertindole
-ziprasidone
Anticancer drugs that cause TdP
-arsenic trioxide
-eribulin
-vandetanib
-most drugs ending in nib
Opiods that cause TdP
-methadone
Supraventricular arrhythmias (above ventricle)
-sinus bradycardia
-AV block
-sinus tachycardia
-Afib
-supraventricular taachycardia
Ventricular arrhythmias
-Premature ventricular complexes (PVCs)
-ventricular tachycardia
-Ventricular fibrillation
Sinus bradycardia
-HR < 60 bpm
-impulses originate in sinoatrial (SA) node
-dec automaticity of SA node
Sinus bradycardia ECG
-QRS complexes more than 5 squares apart
-Pwave, Qrs, rhythym intact
Sinus bradycardia risk factors
-MI or ischemia but don’t persist
-abnormal SNS or PSNS tone
-electrolyte abnormalities (HYPERkalemia, HYPERmagnesemia)
-drugs
-idopathic
Drugs that can cause Sinus bradycardia
-digoxin toxicity
-B-blockers
-CCBs (diltiazem, verapamil)
-amiodarone
-dronedarone
-ivabradine
-stop drug 1st to see if it goes away
-if BB, consider pacemaker
Sinus bradycardia sx
-hypotension
-dizziness
-syncope
Sinus bradycardia tx
-only if sx
-ATROPINE 0.5-1mg IV, repear every 5 min (max dose 3mg!)
-if unresponsive:
-transcutaneous pacemaker
-dopamine
-epinephrine
-isoproterenol
Atropine side effects
-tachycardia
-urinary retention
-blurred vision
-dry mouth
-mydriasis
-anticholinergic effects
Sinus bradycardia tx AFTER heart transplant or spinal cord injury
-atropine not effective bc can’t stimulate B-receptor
-Aminophylline
-or Theophylline (IV if heart, oral if spine)
Long term sinus bradycardia tx
-some pt need permanent pacemaker
-or theophylline oral qd
AV block tx? (not really covered)
-only atropine to tx
-caused by same drugs that cause bradycardia
Afib risk increases w
age
Afib ECG
-no Pwave (no atrial depolarizations) lt going on between T wave and P wave
-irregularly irregular rhythym
-HR: 120-180bpm (not always tho pt could be on BB)
Afib
-no atrial depolarization
-no atrial contraction (just kinda tweaks)
-blood moves to ventricle bc pressure
-ventricular filling ~75%
Afib stages
-Stage 1-4
Stage 1
-risk factors but no Afib
-presence of modifiable risk factors associated with AF
Stage 2
-Pre-Afib
-evidence of structural findings that further predispose pt to AF (atrial enlargement, frequent atrial premature beats, atrial flutter)
Stage 3 Afib
-3A Paroxysmal AF (episodes <7 days, usually few hours)
-3B Persistent (longer episodes >7days and needs intervention)
-3C Long-standing persistent (continuous >12 months)
-3D successful ablation (freedom from AF after percutaneous/surgical intervention to eliminate AF)
Stage 4
-permanent Afib
-no further attempts at rhythym control after discussion between pt and clinician
Afib mech
-abnormal atrial/pulmonary vein! automaticity (premature pulses)
-atrial reentry 5-8 circuts
-too many impulses = tachycardia
Afib risk factors
-age
-cigs
-sedentary
-alcohol (holiday heart syndrome)
-obesity
-HTN. DM, CAD, HF (atrial enlargement, hypertrophy)
-obstructive sleep apnea
-valvular heart disease
-CKD
-familial (genetic)
-idiopathic
Etiologies of REVERSIBLE afib
-hyperthyroidism
-thoracic surgery (CADG, lung resection, esopphagectomy)
Afib symptoms
-may be asx
-palpitations
-dizziness
-fatigue
-lightheadedness
-SOB
-hypotension
-syncope
-angina (bc CO already dec)
-exacerbation of HF symptoms
Afib mortality
-stroke risk inc x5 (thrombi)
-HF risk inc x3 (left ventricle hypertrophy)
-dementia x2 (microemboli in brain)
-mortality x2
How Afib can cause stroke
-blood pools in left atria bc not fully contracting
=clot
-clot falls into left ventricle to get pumped to body
-big clot to brain = fatal stroke
Prevention of Afib
-lifestyle and risk factor modification (weight loss)
-210 min exercise/week (athletes get it tho)
-smoking cessation
-minimize or quit alcohol
-BP control in HTN
-optimal glucose and A1c management in pt w DM
AFib goals of therapy
-prevent stroke/systemic embolism
-slow ventricular response by inhibiting conduction of impulses to ventricles (ventricular rate control)
-convert Afib to sinus rhythym
-maintain sinus rhythym (reduce freq of episodes)
CHA(s)DS(2)-VASc score
-Congestive HF
-HTN
-Age >75y = 2points!
-DM
-Stroke/TIA/TE hx = 2 points
-Vasc disease (prior MI, PAD, aortic plaque)
-Age 65-74
-Sex (female)
-max score 9 points
Prevention of stroke/embolism in Afib
-oral anticoagulants recommended for following CHADS-VASc scores:
-2 or more in men
-3 or more in women
-probably gonna put them on at 1 and 2 tho tbh
Which anticoagulants to use?
-DOACs over warfarin most often
-warfarin preferred in pt w mechanical heart valves (target INR 2.5-3.5) or Afib associated w heart valve disease (MITRAL valve stenosis, no other valve) (target INR 2-3)
-warfarin or apixaban in pt w ESCKD (CrCl <15mL/min) or HEMODIALYSIS
preferred Oral anticoagulant in most Afib pt
-DOACs
preferred Oral anticoagulant in mechanical heart valves and heart-valve disease (MITRAL valve stenosis)
-warfarin
-target INR 2.5-3.5 in mechanical
-target INR 2-3 in disease
preferred Oral anticoagulant in ESCKD and hemodilaysis
-warfarin
anticoagulant monitorin
-only warfarin not DOACs
-measure INR weekly during initiation then monthly once INR stable
DOACs
-Dabigatran
-rivaroxaban
-apixaban
-edoxaban
-andexanet alfa antidote for all except dabigatran (use idarucizumab)
DOAC charateristics
-p-glycoprotein substrate
-plasma concentration inc by inhibitors like KTZ, verapamil, amiodarone, dronedarone, clarithromycin
-plasma concentration dec by inducers like phenytoin, rifampin, carbamazepine, St. John’s wort
AFib drugs for acute Ventricular Rate control
-IF HEMODYNAMICALLY STABLE (if not give shock)
-1. BB, diltiazem, verapamil
-2. Digoxin addon
-3. amiodarone (rare)
-IV
-amiodarone first line in AFib w HF tho (DO NOT GIVE THEM VERAPAMIL OR DILTIAZEM)
Long-term ventricular rate control in Afib
- B- blockers
-diltiazem or verapamil if LVEF >40% - digoxin add-on
-oral
Diltiazem and verapamil info
-direct AV node inhibition
-hypotension
-bradycardia
-HF exacerbation
-AV block
-inhibts CYP3A4 (statins, cyclosporine)
-DO NOT USE IN EF < 40%
-verapamil also inhibits p-glycoprotein (digoxin, dofetilide)
Beta blockers for ventricular rate control in Afib
-direct AV node inhibition
-hypotension
-bradycardia
-HF exacerbation if dose too high (follow HF titration)
-AV block
Digoxin for ventricular rate control in Afib
-vagal stimulation (PSNS)
-direct AV node inhibition
-works more slowly
-NTI
-add-on after BB, or dilt/verap
-NV, anorexia, wentricular arrhythmias at toxic doses
-drug interactions: amiodarone, verapamil inhibit digoxin elimination
Amiodarone forventricular rate control in Afib
-BB and CCB (AV node inhibition)
-takes 10 months to get to steady state
-inhibits CYP450 (warfarin, statins)
-inhibits p-glycoprotein (digoxin)
-might need to know dose
Amiodarone side effects
-hypotension (IV)
-bradycardia
-blue skin
-photosensitivity that sunscreen wont help
-corneal microdeposits but no vision probs
-pulmonary fibrosis = death
-hepatotoxicity (LFTs)
-HYPO or HYPER thyroidism (iodine)
Hemodynamic instability
-BP<90
-HR > 150
-ischemic chest pain
-unconscious
AFib ventricular rate control drug monitoring
-goal HR <100-110 bpm and asx
AFib conversion to sinus rhythym
-if Afib present < 48 hours, go ahead
-if not, pt needs to be on anticoagulants for 3 weeks or perform transesophogeal echocardiogram (TEE) to rule out clot in atrium
Drugs for conversion of Afib to sinus rhythym
-DCC (shock)
-amiodarone
-ibutilide
-procainamide
-flecainide
-propafenone
Afib conversion to sinus rhthym tx
-Normal LVEF: IV amiodarone/Ibutilide, procainamide if those are CI
-HFrEF: IV amiodarone
AF outside hospital in pt w noraml LV function: felcainide or propafenone
-do NOT give procainamide w amiodarone or ibutilide due to QTc prolongation and TdP risk
DCC to convert Afib to sinus rhythym
-depolarizes all cells allowing SA node to take over as pacemaker
-machine syncs so no shock during T-wave (would worsen Afib)
-sedate when possible
Ibutilide
-Class III
-fast, give IV dose over 10 min
-risk of TdP so not used as mmuch
-AVOID in HFrEF
-used to convert afib to sinus in normal LV function in hospital
Procainamide
-Class IA
-QT prolongation and TdP risk
-hypotension
-HFrEF exacerbation
-agranulocytosis
-neutropenia
-convert afib to sinus in hospitalized pt w normal LV function when IV amiodarone and ibutilide are CI
-DO NOT give w either of those drugs = TdP
Fleciainde and propafenone
-Class IC
-pill in the pocket PRN
-dizziness, blurred vision
-DO NOT USE IN HFrEF
-negative ionotropes
-Beta-blocker activity
-convert Afib to sinus in pt out of hospital w normal LV function
Maintenance of sinus rhythym/Prevention of recurrence
-not for pt w current or permanent afib
Drugs for mainentance/Prevention of Afib recurrence
-amiodarone
-dofetilide
-dronedarone
-sotalol
-propafenone
-flecainide
Dofetilide
-Class III
-risk of TdP
-drug interactions w cimetidine, HCTZ, KTZ, trimethoprim, verapamil (all inhibit elimination)
-need to know dosing
-DO NOT USE in CrCl <20
-for maintenance of sinus rhythym in Afib
Dronedarone
-not as effective as amiodarone
-Class I-IV
-CCB and BB (no iodine, no thyroid concerns like amiodarone, no pulmonary fibrosis or warfarin interaction either)
-bradycardia
-N/D
-asthenia
-rash
-inhibits CYP3A4 and PgP (digoxin, statins, diltiazem, verapamil)
-metabolism inhibited by KTZ, itraconazole, ribavirin, grapefruit juice
-for maintenance of sinus rhythym in Afib
Sotalol
-Class III
-Na/K block
-BB activity
-DO NOT use in CrCl< 40
-need to know dosing
-B blockade and TdP risk
-for maintenance of sinus rhythym in Afib
Dofetilide dose
-CrCl >60: 500mcg BID
-CrCl 40-60: 250mcg BID
-CrCl 20-39: 125mcg BID
-CrCl <20: DO NOT USE
Amiodarone monitoring
-HYPO or HYPER thyroidism: TSH baseline, 3-6 months, then q6 months (tx thyroid dont dc amiodarone)
-hepatotoxicity: ALT, AST baseline, 3-6 months, then q6 months
-QTc: ECG at baseline and annually
-Pulmonary fibrosis: chest Xray baseline and if unexplained cough or dyspnea (start on corticosteroid to reverse)
-corneal microdeposit: eye exam in visual probs
-Dermatologic: physical exam annually, development of discoloration/photosensitivity
Maintenance of sinus rhythym following conversion to SR or for paroxysmal Afib tx
-normal LV function:
1. dofetilide, dronedarone, flecainaide, propafenone
2. amiodarone (more effective but more side effects)
3. Soltalol might inc mortality
-MI or HFrEF:
1. amiodarone, dofetilide
2. sotalol
-HFrEF class III or IV or recent decompensated HF:
-if no, dronedarone
-if yes, NO dronedarone
Inpatient initiation of dofetilide
-keep pt on continuous ECG monitoring, proceed only if QTc <440ms
-follow CrCl dosing
-2-3h after 1st dose, check QTc interval
-if QTc inc < 15%, continue dose
-if QTc inc >15% or to >500ms, cut dose in half (125 BID to qd tho)
-dc if QTc is > 500ms at anytime after 2nd dose
Soltalol initiation
-ECG monitoring, only start if QTx < 450ms
-follow CrCl dosing
-check QTc interval 2-4h after each dose
-if QTc < 500ms after 3 days (or after 5-6th dose if once daily) pt can be discharge OR dose can be inc to 120mg BID and pt can be followed for 3 days on this dose
-If QTc > 500ms, dc
Catheter ablation of Afib
-rhythym control to improve sx
-pt where drugs CI or not effective, usually younger pt
-can be used first-line in pt w sx PAROXYSMAL Afib
Supraventricular Tachycardia ECG
-Pwave present but hard to see bc T-wave
-narrow QRS complexes
-regular rhythym
-HR 100->250bpm
-spontaneous intitiation and termination
Paroxysmal SVT (PSVT)
-subset of supraventricular tachycardia
-intermittent episodes
-spontaneous start and stop, lasts minutes to hours
supraventricular tachycardia sites of reentry
-reentry within AV node mostly (not SA node(wait is it atria??) like Afib)
-accessory pathway, atria, or SA also areas of reentry but not as common
Supraventricular tachycardia mech
-reentry in AV node
-conduction usually only goes down fast pathway of AV node, can’t go up slow
-re-entry can go either direction in SVT
=circuit and inc HR
-still T-wave tho bc atrial depolarization
-luckily for us tho AV block stops arrhythmia
SVT risk factors
-women twice as likely than men
-age >65 5x more likely
-often occurs in pt w/o underlying CVD
SVT sx
-Neck-pounding
-palpitations
-dizziness
-weakness
-lightheadedness
-near-syncope
-polyuria
-inc HR = dec stroke volume –> less O2 to tissues/brain
Goal of SVT tx
-terminate SVT
-restore sinus
-prevent recurrences
-don’t need to worry about stroke bc atria still contract
Drugs for SVT termination
-Adenosine
-B-blockers
-Diltiazem
-Verapamil
-all inhibit AV node conduction
-give IV
Adenosine
-6-12-12
-inhibits AV node conduction
-give IV bolus w saline bc v short half life, get it through
-chest pain (might feel like MI, flushing, SOB, sinus pause (flat line on ECG), bronchospasm
Adenosine dosing
-6-12-12
-6mg IV bolus
-12mg IV bolus if no response in 1-2 min
-can repeat 12mg dose once
-follow each dose or first dose w saline
-for SVT
SVT tx
-vagal maneuvers to inc PSNS or IV adenosine 6-12-12
-if can’t: IV BB, diltiazem, or verapamil
-last-line: DCC shock
Vagal maneuvers
-stim PSNS
-cough and sinus massage
-SVT tx
Prevention of recurrence of SVT
-only if sx
-catheter ablation
-if not, we go to drugs
-if no HFrEF: BB, diltiazem, verapamil… flecainide and propafenone if not
-IF HFrEF, should be on BB any, amiodarone, digoxin, dofetilide, sotalol in any order
