Anti-Arryhthmics Flashcards
T or F. There is no parasympathetic (vagal) innervation in the heart past the AV node
T. only sympathetics
What are arrhythmias caused by in a general sense?
abnormal impulse generation (automaticity) or abnormal propagation (re-entry)
T or F. The SA node fires at a more rapid rate than the atrial conducting fibers, AV node or purkinje fibers
T.
What things could cause latent pacemakers to fire more rapidly?
-B1 stimulation-hypokalemia-fiber stretch-hypoxemia-acidosis-injury
Describe arrhythmias caused by abnormal triggered automaticity.
abnormal impulse generation following a normal action potential
What are some arryhthmias caused abnormal ‘triggered’ automaticity?
-early after depolarization (EAD) interrupts phase 3 repolarization -delayed after-depolarization (DAD)
Early after depolarization (EAD) interrupts phase 3 re-polarization causes what?
long QT related arrhythmias i.e. Tornado de pointes
What causes delayed after-depolarization?
result from calcium overload in digoxin toxicity and is exacerbated by catecholamines and hypokalemia
Treatment for delayed after-depolarization caused by digoxin overload?
Digibind
Torsades de pointes occurs in the setting of prolongation of phase __ and __ of the action potential (reflected as prolonged QT interval)
2 and 3 repolarization
What things can cause early after-depolarization (or delayed phase 3 re-polarization)?
-K+ channel blocking anti-arrhythmics (class III) -hypokalemia-low heart rate
What is re-entry?
occurs when an impulse repetitively activates the same area of the heart leading to sustained arrhythmias
What conditions are needed for re-entry to occur?
-an anatomic or physiologic obstacle (circuit)-unidirectional block-conduction time must exceed effective refractory period in the ‘slow’ circuit
What is re-entry typically caused by?
a premature impulse (automaticity) that gives off ‘daughter impulses’ resulting in rapid activation of the ventricle (or atrium)
T or F. Re-entrant arrhythmias are characteristically rapid and sustained
T. greater than 140 bpm
Where in the heart can re-entrant arrhythmias occur?
any location- atria, AV node, ventricle
A re-entrant arrhythmia in the atria could be what?
-a fib (disorganized) or -a flutter (organized)
A re-entrant arrhythmia in the AV node could be what?
paroxysmal supraventricular tachycardia (PSVT)
A re-entrant arrhythmia in the ventricles could be what?
-ventricular tachycardia (organized)-ventricular fibrillation (disorganized)
What is the preferred treatment for sustained ventricular tachycardia?
DC cardioversion followed by drug therapy to prevent recurrence of re-entry
What are some options that can used for drug therapy in sustained ventricular tachycardia?
A class I anti-arrhythmic (Na+ channel blocker) such as procainamide or lidocaineA class III (K+ channel blocker) such as sotolol or amiodarone
How would a class I anti-arrhythmic (sodium channel blocker) such as procainamide or lidocaine interrupt re-entry?
by slowing conduction through the circuit and by increasing effective refractory period also slow automaticity
How would a class III anti-arrhythmic (sodium channel blocker) such as procainamide or lidocaine interrupt re-entry?
by prolonging depolarization and increasing the effective refractory period (ERP) by extending phase 3phase 2 and 3 re-polarization is delayed, extending the action potential and potentially prolonging the QT interval resulting in increased risk of early after-depolarization (EAD) and Torsado de pointes
What are the class II anti-arrhythmics?
BBs- metoprolol and atenolol
What are the class IV anti-arrhythmics?
NDHP CCBs- Verapamil and DiltiazemDHPs have little anti-arrhyhtmic effect at clinically used doses
What are some other anti-arrhythmics?
adenosine receptor agonists- adenosinevagal activators- digoxin, carotid massagevagal blocker- atropine
Sodium channel blockers (class I) are divided into three subclasses based on what?
dissociation rate (T) from the Na+ channel-class IA: T>1 sec (extends phase 2 the most because at high doses they also block K+ channels- can lead to EAD and sustained arrhythmias like torsades)-class IB: T less than 1sec (may slightly quicken re-polarization)-class IC: T>10 sec
What are the class IA anti-arrhythmics?
Procainamide, Quinidine, Disopyramide Quinidine and Disopyramide are rarely used because of prominent side effects
What are the class IB anti-arrhythmics?
Lidocaine
What are the class IC anti-arrhythmics?
Flecamide
What is the electrophysiologic effect of class II anti-arrhythmics?
reduce enhanced automaticity related to catecholamines and ischemia reduce atrial and ventricular arrhythmias in patients with CHD (which produces a lot of catecholamines) and improves survivalSlows AV node conduction by blocking positive influence of catecholamines particularly blocks exercise-induced increase in ventricular rate in atrial fibrillation.
T or F. Class II anti-arrhythmics are used to treat symptomatic PVC’s (can be due to increased catecholamines or ischemia) in patients with and without structural heart disease
T.
What are the main effects of Class IV AAs?
reduce SA node automaticity and AV node conduction with little effect on electrophysiology of fast conduction tissues (atrial, ventricular conduction system) under normal conditions
What are some adverse effects of Class IV AAs?
-SA, AV block-impaired myocardial contractility-hypotension
Class IV AAs are contraindicated in which patients?
-CHF-sinus bradycardia-atrioventricular block (prolonged PR interval)
What arrhythmia is digoxin used for?
atrial fibrillation via enhanced vagal efferents to the AV node
What are the effects of digoxin in a fib?
reduces SA node automaticity, AV conduction.Controls ventricular rate in supraventricular arrhythmias. Interrupts re-entry in AV node.
Direct effect (arrhythmogenic): increased normal automaticity, delayedafterdepolarizations: APC’s, VPC’s Paroxysmal Atrial Tachycardia with Block,Ventricular Tachycardia. (Na/K ATPase inhibition with calcium overload).
Direct effect (arrhythmogenic): increased normal automaticity, delayedafter-depolarizations: APC’s, VPC’s Paroxysmal Atrial Tachycardia with Block,Ventricular Tachycardia. (Na/K ATPase inhibition with calcium overload).
What is adenosine used for?
Used to terminate acute PSVT by blocking AVnode- patient will enter asystole for about 2-3 seconds as you hit the SA AND AV nodes (adenosine receptor mediated). Acute use only Very good diagnostic for supra ventricular arrhythmias (a fib, a flutter, or PSVT)Hyper polarizes the SA and AV node
How is adenosine given?
administered rapidly IV. T/2 10 seconds!
Side effects of adenosine?
Chest tightness common, transient asystole (less than 3 seconds) can occur, flushing, PSVT can recur if other treatment not given.
