23 - Arrhythmias Flashcards
Describe the myocardial action potential
- Phase 4 = small amount K+ exiting cell & Na+ & Ca2+ entering cell
- Phase 0 = lots of Na+ & little Ca2+ entering cell
- Phase 1 = lots of Ca2+ entering cell w/ some K+ exiting
- Phase 2 = some Ca2+ entering w/ more K+ exiting
- Phase 3 = lots of K+ exiting; slowly decreasing as getting closer to phase 4
Pathogenesis of tachyarrhythmias
- Most common arrhythmias are combinations of both automaticity & re-entry
- Automaticity = abnormality in impulse generation; often starts arrhythmia
- Re-entry = abnormality in impulse conduction; often maintains arrhythmia
Classification of anti-arrhythmic drugs
- 1a (sodium med) = quinidine, procainamide
- 1b (sodium fast) = lidocaine, mexiletine
- 1c (sodium slow) = flecainide, propafenone
- 2 (beta blockers) = metoprolol, atenolol
- 3 (potassium) = amiodarone, sotalol, ibutilide
- 4 (CCB) = diltiazem, verapamil – don’t really affect refractory pathway, so can’t take someone out of an arrhythmia, more so prevent arrhythmias
Pharmacology of rate control agents
- Reduce automaticity to prevent or slow arrhythmias
- Class 2 (beta blockers) – reduce adrenergic stimulation of SA/AV nodes & decrease adrenergic stimulation of myocardial contractility
- Class 4 (non-DHP CCBs) – reduce calcium current & recovery in SA/AV nodes
- Digoxin (Na/K/ATPase blocker) – increase myocyte Na/Ca, decrease K, increase AV node refractory period; increases vagal tone & decreases SA/AV activity
Pharmacology of rhythm control agents
- Reduce re-entry to prevent or stop arrhythmias
- Class 1 (sodium channel blockers) – decrease in conduction velocity; re-entry loop loses “steam” & SA node takes over
- Class 3 (potassium channel blockers) – prolonged refractory period; re-entry loop “catches its tail” & SA node takes over
Which drugs are pure rhythm control agents?
- Quinidine – class 1a & potassium blocker (class 3)
- Sotalol – class 3 & beta blocker (class 2)
- Amiodarone – class 3 & Na, Ca, beta blocker (class 1, 2)
- Propafenone – class 1c & beta blocker
- Flecainide – pure class 1c, but high risk for VT in CAD
- Ibutilide/dofetilide – pure class 3, but high risk of Torsade de Pointes
EKG of atrial flutter
Saw tooth pattern
Describe what happens during atrial fibrillation
- Rhythm looks irregularly irregular (distance between QRS complexes is not the same) and no clear P waves on EKG
- Extremely fast (400-600 atrial beats/min) and disorganized atrial rhythm (irregularly irregular)
- AV node controls the pulses sent from atria to ventricles, so prevents 400-600 beats/min being sent to ventricle; if this didn’t happen then A. fib would be life-threatening
Categories of A. fib
- Acute = first 48 h
- Paroxysmal = terminates spontaneously w/in 7 days
- Persistent = continues for > 7 days
- Permanent = doesn’t terminate even w/ cardioversion attempts
Factors that may precipitate A fib
- High adrenergic tone (temporary) – alcohol withdrawal, sepsis, post-surgery, excessive physical exertion, digoxin toxicity
- Atrial distention (permanent & chronic) – ischemia, HTN, valvular disorder, cardiomyopathy, pulmonary embolism/HTN, obesity
Signs & sx of A fib
- Signs = irregular pulse, HR > 100 bpm, hypotension, EKG
- Sx = asymptomatic, palpitations, dizziness, syncope, angina, HF
Serious complications of A fib
- Tachycardia induced HF
- Severe hypotension/HF
- Embolic stroke
Major goals of therapy for A fib
- Control rapid ventricular response (ventricular rate control)
- Restore normal sinus rhythm (atrial rhythm control)
- Prevent thromboembolic complications
Drugs for ventricular rate control. What are the efficacy endpoints?
- If px has HF – beta blockers +/- digoxin
- If px has CAD – beta blockers (preferred) and/or non-DHP CCBs
- If px has no HF or CAD – beta blocker, non-DHP CCB, digoxin, or combination
- Efficacy endpoints – HR < 100 bpm & decrease in palpitations, dizziness, & SOB
Safety endpoints for rate control
Bradycardia, AV block
Safety endpoints for diltiazem/ verapamil
- BP < 100/60, HR < 60, CHF, edema, nausea, constipation, anorexia
- Interactions = 3A4 & P-GP inhibitors
Safety endpoints for metoprolol/ atenolol
BP < 100/60, HR < 60, CHF, asthma, diabetes, weakness, fatigue, PVD, abrupt d/c
Safety endpoints for digoxin
- GI – anorexia, N/V, diarrhea
- Neurological – headache, fatigue, confusion
- Visual – blurred vision, halos around bright objects
- Cardiac – arrhythmias (when levels are too high)
Digoxin drug-drug interactions
- *If pt is already on digoxin & need to start any of these drugs, decrease digoxin dose by 50%
- Amiodarone, propafenone, quinidine/quinine, verapamil, itraconazole
- Cholestyramine, Al-Mg antacids, kaolin-pectin, dietary fibre, sucralfate – 2 h interval between administration
Options for restoration of normal sinus rhythm (to stop A fib)
- Electrical cardioversion (done in hospital)
- IV amiodarone controls rate & 30-40% effective for cardioversion
- For new onset A fib in hospital – amiodarone 300 mg IV bolus, then 30-60 mg/h infusion for 24-48 h
- If not cardioverted, then can use electrical cardioversion
- “Pill in the pocket” (must be rate controlled first) – flecainide 200-300 mg PO x 1 or propafenone 450-600 PO x 1
Overview of rhythm management
- Rhythm control choices for normal systolic function w/ no history of CHF – dronedarone, flecainide, propafenone, or sotalol; can later switch to amiodarone if needed
- If hx of CHF or LV systolic dysfunction:
- If EF > 35% – amiodarone or sotalol
- If EF /< 35% – amiodarone
Rhythm control efficacy endpoints
- Maintain normal sinus rhythm
- No palpitations, dizziness, or SOB
Rhythm control agents – drug interactions
- Sotalol – QT prolonging meds
- Propafenone – CYP450 2D6 substrate; inhibits digoxin
- Flecainide – QT prolonging meds, CYP 2D6 substrate
- Strong CYP 2D6 inhibitors = bupropion, paroxetine, quinidine
Amiodarone monitoring
- Major side effects = pulmonary fibrosis, hypothyroidism, hyperthyroidism, hepatotoxicity
- For pulmonary fibrosis – d/c amiodarone immediately & initiate corticosteroid therapy
- For hypothyroidism – thyroid hormone supplementation
- For hyperthyroidism – antithyroid drugs
- For hepatotoxicity – lower dose or d/c amiodarone if LFTs > 3x ULN
Amiodarone interactions
- Inhibitor of CYP 1A2, 2C9, 2D6, 3A4, & P-gP
- Medications w/ recommended dosage decreases when starting amiodarone (up to 50%) = digoxin, warfarin, flecainide, quinidine, atorvastatin, simvastatin
- Additive effects w/ rate-slowing agents & QT prolonging agents
Anticoagulation in rate control
- Oral anticoagulant – warfarin, dabigatran, rivaroxaban, apixaban
- EC ASA 81-325 mg/day
Anticoagulation toxicity endpoints
- Same as stroke
- Signs of bleeding, Hgb < 100 or drop of 20%
- Warfarin – INR > 3
- New oral anticoagulants – CrCl < 30 mL/min
Recommendation for A. fib in px w/ acute CHF
- If hemodynamically unstable (SBP < 90) – electrical cardioversion
- If hemodynamically stable
- If HR > 100 bpm – rate control w/ digoxin
- Consider electrical cardioversion given severity of sx w/ A fib
- Anticoagulation for 3 weeks pre-cardioversion & at least 4 weeks post
- Consider long-term amiodarone to prevent reoccurrence of A fib
Overview of monitoring
- Rate control – HR < 100 bpm
- Rhythm control – maintain NSR
- No palpitations, dizziness, or SOB
Types of bradyarrhythmias
- First-degree block (usually AV node) – PR > 0.2 sec, P:QRS 1:1
- Second-degree block – P:QRS < 1:1, dropped QRS’s
- Mobitz type 1 = AV node
- Mobitz type 2 = below AV node
- Third-degree block (AV node or below) – AV dissociation, no relation between P:QRS
Factors that may precipitate bradyarrhythmias
- Class 1 anti-arrhythmics
- Beta blockers, including timolol eye drops
- CCB
- Amiodarone, sotalol, digoxin
Signs and sx of bradyarrhythmias
- Signs = HR < 60 bpm, hypotension
- Sx = dizziness, syncope, fatigue, confusion, CHF
Therapeutic options for bradyarrhythmias
- Remove bradycardic drugs
- Atropine
- Isoproterenol (IV pure beta agonist)
- Pacemaker – long term solution; ex: pt has A fib (tachycardia) but when taking rate slowing agents experiences brady, can’t stop drugs so have to use pacemaker; don’t slow fast rhythms, only speed up slow rhythms
Definition of ventricular tachycardia
3 or more repetitive PVC’s (premature ventricular contractions) occurring at a rate of > 100 bpm
Categories of ventricular tachycardia
- Non-sustained VT = < 30 sec
- Sustained VT = > 30 sec
- Incessant VT = more frequent than NSR (normal sinus rhythm)
- Exercise-induced = high sympathetic tone
- Monomorphic = consistent QRS
- Polymorphic = varying QRS
Factors that may precipitate ventricular tachycardia
- Temporary = metabolic abnormalities (low K, Mg), drug toxicities (digoxin, TCA’s), myocardial infarction (w/in 24 h)
- Permanent = CHF, remote MI w/ left ventricular aneurysm, genetic (Brugada syndrome)
Signs and sx of ventricular tachycardia
- Signs = HR > 100 bpm, hypotension, EKG
- Sx – palpitations, angina, syncope
Potential consequences of ventricular tachycardia if left untreated
Progression to ventricular fibrillation and then asystole (cardiac arrest/sudden cardiac death)
Options for primary prevention of SVT/VF
Post MI/CHF – beta blockers, ACEI, aldosterone antagonist, ICD (EF < 35%)
Options for acute tx of SVT/VF
- Electrical cardioversion
- Amiodarone IV
- Lidocaine, procainamide (rare)
Options for secondary prevention of SVT/VF
- ICD – all VF, but SVT if MI/CHF or low BP
- +/- beta-blocker (given to minimize use of ICD), sotalol, amiodarone, ventricular ablation
Purpose of use of anti-arrhythmic agents in addition to ICD
- Decrease (appropriate) shocks for VT/VF
- Decrease (inappropriate) shocks for A fib/flutter
- Decrease rate of VT for overdrive pacing
Tx for syncope w/ NSVT or no VT seen
- ICD since high risk for SVT/VF:
- EF < 30%
- Genetic
- EP-studies (electrophysiological) induce VT – try to induce VT by shocking various areas of the heart
Dosing of digoxin
- Loading dose 0.5 mg once, then q6h 0.25 mg x 2
- 0.0625 mg – 0.25 mg od (adjust for renal dysfunction)
Dosing of amiodarone
- 400 mg BID-QID x 7-14 days then 400 mg OD-BID x 7-14 days then 200-400 mg OD
- Higher doses for ventricular arrhythmias; lower doses for atrial arrhythmias
Torsade de Pointes
- Rapid form of polymorphic ventricular tachycardia, w/ persistent prolonged QTc
- QTc = QT / square root of RR
- QTc male < 440 msec; female < 460 msec
- QTc danger > 500 msec
Factors that may precipitate Torsade de Pointes
- Type 1a, 1c, 3 anti-arrhythmics (sotalol probably biggest cause of TdP)
- Citalopram
- Antibiotics – azithro, moxi, levo, fluconazole
- Methadone
- Monoclonal antibodies
Mechanisms of drug-induced QT prolongation and TdP
- Block of repolarizing K+ currents
- Stimulation of ICa
- Stimulation of INa
Options for acute tx of TdP
- Magnesium IV
- Overdrive pacing
- DCC
- Isoproterenol
- Stop all QT prolonging drugs
- Potassium supplementation
When talking about heart rate for a person w/ A fib, actually talking about ______ b/c ____
Ventricular rate b/c that’s the only beat that is normal
What does “loss of atrial kick” mean? Which px is this most detrimental to?
- Heart isn’t filled as efficiently
- Most detrimental to px w/ HF
Extremely fast atrial rhythm causes ____
Fast ventricular rate; if uncontrolled can lead to HF
