Antiarrhythmic Drugs Flashcards
Types of Afib
Paroxysmal - Episodes end spontaneously
Persistent - requires med intervention
Permanent - cannot be terminant
Chronic remodels the atrial sturcture and function
Afib consequences and Afib goals
Rapid ventricular rate causes fall in cardiac output and syncope
Atrial thrombi form and can dislodge…leading to embolic strokes
Rhythm control - completely normal HB
Rate - slow ventricles and improve cardiac output but atria still fibrillate
Anticoag also used
Ventricular tachycardias
Emergency so only suitable goal is rhythm control
Monomorphipc ventricular tachycardia and torsades de pointes have diff causes and diff txs
Prodcainamide
Lidocain
Felcainide
All rhythym control
Pro - blocks both cardiac Na and K channels
Lido - weakest Na blockers
Fl - storngest Na channel blockers
Metoprologl
Amiodarone/sotalol
Diltiazem/verapamil
Adenosine
Beta blocker - rate
K blocker - rhythm
Ca blocker - rate
Adenosine agonist—-AV-RT (av nodal reentry tachycardia)_
Rhythm control drugs
Mostly target cardiac voltage gated K and Na channels
Na blockers Slow generation of ventricular and atrial APs, slowing AP conduction
K blockers slow repolarization and prolong cardiac action potentials
Rate control drugs
Inhibit the AV node and thus slow conduction from atria to ventricles
Metoprolol - blocks AV node beta adrenergic receptors
Verapamil and diltiazem - block AV node Ca channels
Effects of anti-arrhythmics on noraml ECG
Ia - Widen QRS, prolong QT
IC - Widen QRS (strong)
II - Prolong PR
III - Prolong QT
IV - prolong PR
QRS wide - slowed conduction in ventricle
Prolonged QT - slowed ventricular repolarization
Prolong PR - slowed conduction in AV node
EADS and DADs
EADs
- caused by abnormally long APs
- Can leads to otorsade de pointes
- Tx is shorten APs
DADs
- Caused by toxic cytosolic Ca levels
- Cause PVCs or monomorphic ventricular tachycardia
- tx to relieve Ca overload if possible
Reentry circuits
APs loops around small region of the heart
Spread from reenetry circuit and repeatedly stimulate ventricles or atira
Often occurs following infarct, hypertrophic, or fibrotic hearts
Lidocaine dosage, how its used
Rhythm control
Injection
Rapidly metabolized os short term…prevent recurence of cardiac arrest in pts resuscitated following ventricular fibrillation or pulseless ventricular tachycardia
Na blocker mech
Slow generation of atrial and ventrciular APs and slow conduction velocity
Affect rapidly beating arrhythmic cells more than normal myocytes
Reentry circuits only generate tachycaridas if
and Na channel blocker effect
They can loop AND
reenter noraml tissue after it recovers form refractory period but before next normal HB arrives
Na blocks inactive since conduiton slow enough that next HB arrives before banormal wave finishes the loop
Na channel blocker and DADs
Prevent generation of unusually rapid APs
DADs persist but extra APs gone
Abnormailty generating DADs unaffected but Na blockers revent them from generating extrasystoles and runs of tachy
Lidocaine SE
Neurotoxicity
Can trigger a new ventricular tachycardia
WHen can Na blockers cause proarrythmias
Strucutaly damaged
Fibrotic regions where heartbeat is slower already
Na channel blocker and dorment reetry circuits
Dormant circuit - APs travel the circuit too quickly so point 1 is still refractory when stimulus arrive from point 3
IC Na blockers
Flecainide
Flecainide contraindications
and use
Pts with tructural HD - high risk of proarrhythmias
Pts with unstable hemodynamics like depressed CO - may widen QRS interval…HB spreads slowly so contraction is less forceful
“Pill in pocket” - immediate termination of sudden episdoes of paroxysaml A fib by self-admin in carefully selected, low risk pts
Procainamide dosase and comments
Injection
Dual mixed Na and K blocker
Terminating monomorphic ventricular tachy
N-acetyl procainamide is major active metab
K channel block effect
Prolongs AP and refractory period
Reentry cirucit and K blocker
Prolongs te AP and refractory period so that cells do not respond when stimulus arrives from point 3
Procainamide SE
Proarrythmic - torsade de pointes - due to K channel block
Negative inotropic effect - moderate iwdeing of the QRS interval
K blocker toxicity
Excessively prolongs ventricular APs (and QT), induceing EADs and torsades
Amiodarone and sotalol doage
O/I
Sotalol ECG
Prolonged QT (K block) Prolong PR (Beta-adrenergic block) Slower HR (beta-adrenergic block)
USe and SE of sotalol
Co-existing ischemic HD - beta-blocker may help
Unstable hemodyanmcs - exaerbated by sotalol’s neg inotropic effects
Negative inotropy - beta blockade also causes inhibitory effects on HR and AV node
Proarrhythmia - Torsade de pointes due to K channel block
Amiodarone indciations
Suppression of recurrent ventricular tachy - IV amiodarone an be used to prevent recurrence of cardiac arrest following resuscitation…oral for long term
Prophylaxis and tx of Afib…preferred with left vent hypertrophy or HF
Main effect is inhibiton of K channels
Weak of Na and Ca channels
Weak non-comp antagonist of alpha and beta receptors
Amiodarone long term toxocity
Pulm toxocity - reversible
Thyrotoxicosis
Hypothyroidism - more common…inhibits conversion of T4 to T3
LOW risk of proarrhtymia
Amiodarone metab
Large Vd, requires loading dose
Early detection of adverse effects important due to long T1/2…slowly metabolized
Can increased blood levels of digoxin and warfarin
Digoxin - inhibit P=glycoprotein involved in elim
Warfarin - CYP450 inhiibtor
Metoprolo dosage nad mech
Oral, oral-ER, injection
Slow AP conduction across the AV node
Reverse acceleration of AV node APs by symp tone, returnign them to baseline
Beta-blocker use
Choice for rate control of Afib…each AP takes longer so fewer beats per minute
Prolong diastolic period which allows more blood to enter ventricles and improve cardiac output
Beta-blocker other use
Ventricular tachycardias
Negative inotropic effect so block increased calcium IC…dec in DADs and VT
Diltiazem and verapamil dosing and tx
Injection for acute, oral for LT
Angina, HTN, or arrhtymias
Diltiazem and verapamil mech
Slow generation of AV nodal APs
Takes longer to get across
Main control in pts who cannot tolerate B-blockers
CCB vaso effect
Peripheral and coronary vasodilators
Verapamil and diltizem effect on myocytes
Directly inhibit SA, AV, and cardiac contractility
Direct effect is opposed by indirect inc in sym tone caused by vasodilation and dec BP
SE of verap and diltia
Dep APs - bradycardia or AV block
Dec ventricular contract - HF
Vasodilation - hypotension
Diltiazem and verap intx
Beta-adrenergic blockers…can cause severe AV blocks
Digoxin levels - P-glycoprotein
Erythromycin - blood levels increased by verapamil CYP3A inhibiton…can cause fatal ventricular arrhythmias
Benefit and risks of rhythm and rate control
Rhythm - better hemodynamics and dec thrombo risk…BUT more toxic anti-arrhtymics
Rate - better success rate…effective iwht perm A fib…prolonged anticoag use
AV nodal reentry tachycardia
For AV nodal renetry tachycardia
Slow pathway conducts HB from atria to Vent
Fast conducts HB back to atria where it reenter slow one
Mech of adenosine
Hyperpolarizes and blocks the AV node to stop reentry
Both pathways resynchronied and ready when next nromal HB arrives
Adenosine rapidly removed by ENT 1
Clinical effects of adenosine and receptor
A1 - SA and AV node expression…lead to slow HR and slowed AV node conduction
Adenosine inhibt effect on SA and AV nodes
Due to K channel activation…hyperpolarization
Adenosine limitations and contraind
Cardiac arrest (due to node inhibition) Flushing due to vasodilation
Ashtmoa - can induce bronchoconstrictions
