Arrhythmias: Treatment Flashcards
Recognize how different underlying arrhythmia mechanisms determine the relevant treatment approaches
Mechanism guides treatment options
1) Reentry
• Break the circuit: antiarrhythmic drugs, catheter ablation, overdrive pacing, defibrillation
2) Abnormal automaticity
Depress conduction:
• Na+ channel block by lidocaine (Ib) for reentrant VT
• Ca2+ channel block by verapamil (IV) for AVNRT
Increase effective refractory period:
• K+ channel block by procainamide (Ia) for reentrant VT
• K+ channel block by dofetilide (III) for VT
• K+ channel block by sotalol (III) for AF
Bradyarrhythmias: speed up
• Remove reversible causes (ex. Drugs, ischemia)
• Pacemaker
Tachyarrhythmias: slow down
• Antiarrhythmic drugs
• Ablation
• Reduce rate of spontaneous depolarization in automatic tissues (ex. Metroprolol)
• Increase threshold for AP generation (ex. Lidocaine)
3) Triggered activity
EADs triggering Torsades de pointes → shorten APD
• Remove reversible causes (ex. Hypokalemia, drugs, ischemia)
• Pacing to increase rate = shortens APD
• Mg to stabilize and blunt EADs, rarely aa drugs
DADs triggering ventricular tachycardia → eliminate Ca2+ overload
• Treat digoxin toxicity, ischemia
Identify the preferred antiarrhythmic drug treatment for short excitable gap and long excitable gap reentrant arrhythmias.
Short excitable gap
o Drugs to prolong refractory period (prolong APD)
o Increases wavelength of reentrant circuit and eliminates excitable gap → wave front head-tail collision and extinction
Long excitable gap
o Drugs to inhibit the conduction in abnormally slow region
o Breaks reentrant cycle
o Other option: overdrive pacing suppression
• Electronic pacemaker paces at rate fast enough to capture cycle in excitable gap → extinguish arrhythmia
Describe the Vaughan Williams classification for antiarrhythmic drugs
- Groups based on shared cardiac electrophysiology effects
- Some drugs have action in >1 class
• Class I: primarily block cardiac Na+ channels; some can block repolarizing K+ current (end effect = reduce Phase 0)
o Higher affinity for open or inactivated ion channels
o Types a, b, & c
• Class II: beta-blockers = competitive antagonists for β adrenergic receptors
• Class III: APD prolongation
• Class IV: Ca2+ channel blockers
• Class V: other (Digoxin, adenosine)
Describe Type Ia antiarrhythmic Drugs
Intermediate recovery kinetics from Na+ channel block; prolong AP duration (longer phase 3)
• ECG: increase in QT interval and some mild QRS prolongation
• Ex. Procainamide
Describe Type Ib antiarrhythmic Drugs
Block rapid recovery Na+ channels; no effect on AP duration
• ECG: no clear changes
• Ex. Lidocaine
Describe Type Ic antiarrhythmic Drugs
Block Na+ channels with slow recovery; little effect on AP duration
• ECG: increase PR and QS intervals (slow conduction times); little effect on QT interval (because little effect on ventricular repolarization)
• Ex. Flecainide (not to be used in post-MI patients = increase mortality; patients with LV dysfunction)
Describe Type II antiarrhythmic Drugs
beta-blockers = competitive antagonists for β adrenergic receptors
o Decrease phase 4 depolarization in nodal cells→ decreased HR
o Reduce sympathetic stimulation to AV node → prolongs AV conduction
o On surface ECG = slowing of sinus rate and increase in PR interval
o Types:
• Non-selective (β1 and β2) ex. Propranolol
• Selective (β1) ex. Metoprolol
Describe Type III antiarrhythmic Drugs
APD prolongation
o Block voltage-dependent K+ channels → Increase APD and ERP throughout myocardium
Ex. Dofetilide:
• Pure IKr blocker
• ECG: QTc prolongation
Ex. Amiodarone
• Same as Dofetilide but many other targets too
• Most effective antiarrhythmic drug
• BUT major side effects: pulmonary fibrosis, liver, thyroid dysfunction
• Half life ~ 50 days (long!)
• Significant drug interactions (ex. With warfarin)
ECG: PR and QT interval prolongation, variable prolongation of QRS interval; reduction in sinus rate common
Describe Type IV antiarrhythmic Drugs
Ca2+ channel blockers
o Slows rate of phase 4 depolarization in SA nodal cells → reduce HR
o Inhibits conduction through AV node
o ECG: increases PR interval (slow AV node conduction); slows sinus rate (increase RR interval)
Ex. Verapamil and diltiazem
• Note: different than dihydropyridine Ca2+ channel blockers (these have no effect on cardiac Ca2+ channels, specific Ca2+ channels in vascular smooth muscle)
• All: act on L-type Ca2+ channels in vascular smooth muscle → all reduce BP
Describe Type V antiarrhythmic Drugs
Other (Digoxin, adenosine)
Digoxin:
• Cardiac glycoside
• Inhibits Na+/K+ ATPase → increased intracellular [Na+]
• Reduced Na+ gradient → reduced Ca2+ efflux via Na+/Ca2+ exchanger → increased intracellular Ca2+ in SR → greater Ca2+ release → increased contractility
• Affects parasympathetic neurons: increases vagal tone to heart
• ECG: decrease HR, increase PR interval
Adenosine:
• Endogenous nucleoside
• Acts via A1 receptor via Gi = inhibits AC → reduces L-type Ca2+ currents and activates GIRK (IK, Ado)
• Slows rate of phase 4 depolarization through AV node
• Prolongs AV nodal refractory period
• IV infusion only = short half life (<10 sec!)
• ECG: decrease HR, increase PR interval
Describe what arrhythmias are treated with pacemakers and how
Goal: eclectically pace heart to maintain adequate CO
Types:
o Transcutaneous → emergency
o Temporary transvenous → emergency
o Permanent transvenous → long term care (pace atria, ventricles, or both)
Treat:
o Slow rhythms:
• Sinus arrest
• Sinus bradycardia
• Heart block
• Atrial fibrillation with slow ventricular response
o Heart failure for resynchronization (bi-ventricular pacing)
Explain how catheter based-ablation can treat arrhythmias.
• Destroys area of myocardium that generates arrhythmia o Uses heat (radiofrequency catheters) o Uses cold (cryoablation) • Most often for reentrant arrhythmias with well-defined circuitry Complications: o Thromboembolism o Perforation, tamponade o AV block
Identify when a defibrillator is used to treat arrhythmias
Purpose: provide strong electrical shock to stop tachycardia (stops reentrant circuit) and restore normal rhythm
Types:
o Standard external defibrillator (in ambulances and hospitals)
o Automatic external defibrillators
o Implantable cardioverter-defibrillators (ICDs)
o Life-vest defibrillators (temporary treatmet)
Treat:
o Atrial fibrillation
o Ventricular fibrillation
o Ventricular tachycardia
o Other tachyarrhythmias
Describe how a vagal reflex can be used to treat certain arrhythmias.
To treat AVNRT and AVRT → induce vagal response = activate parasympathetic stimulation of the heart → slows AV node conduction
Valsalva maneuver:
o Forcibly exhale while keeping mouth and nose closed
o Or tense abdomen like having a bowel movement
Carotid sinus massage:
o Soft pressure unilaterally on carotid → stimulates carotid body → reflex activation of vagal (parasympathetic) tone
o Avoid: older patients, or patients with vascular disease
Identify the relevant options for clinical treatment of Atrial fibrillation and atrial flutter
Emergent cardioversion in cases with rapid ventricular response and hemodynamic compromise (shock)
-Rate control
• Drugs causing AV block: beta-blockers, Ca2+ channel blockers, digoxin
• Stubborn cases amiodarone
-Rhythm control = restore sinus rhythm
• Drugs slowing atrial conduction or prolong refractory period of atrium: Class Ia, Class Ic, Class III
• If drugs not work = cardioversion electively done
• When rhythm restored: keep using drugs to reduce likelihood of recurrence (side effects = caution)
-Antithrombotic therapy to prevent thromboembolism
• Antiplatelet (aspirin) or antithrombotic (warfarin) therapy
• Consider risk of bleeding with anticoagulant treatment
-Catheter ablation
• Symptomatic patients who fail medical therapy
• High success rate (>90%) for atrial flutter
