Anti-Arrhythmic Flashcards
4 ways of decreasing spontaneous activity
Decrease phase 4 slope
Increase threshold
Increased maximum diastolic potential (hyperpolarize)
Increase APD
2 ways of increasing refractoriness
Na channel blockers - shift voltage dependence of recovery - delay Na recovery
AP prolonging drug - extend ERP w/out interacting w/Na channels
State dependent blockade
block fast inward Na channels when in open/inactivated but not resting
MOA Class I agents
Block fast inward Na channels to varying degrees in conductive tissue Decrease Vmax Reduce automaticity delay conduction prolong ERP
Class 1a Na targets
open > inactive
dissociation in seconds
MOA Quinidine
moderate binding to Na = decrease Vmax
block K = increase APD
block alpha adrenergic = decrease BP
block M2 = increase HR
TX Quinidine
Mainly used in refractory pts to:
convert AF/AFl
prevent recurrence of AF
Treat life-threatening ventricular arrhythmias
Also atrial/ventricular arrhythmias (re-entrant SVT, VT)
AE Quinidine
N/V/D - most common
cinchonism
hypotension (adrenergic)
proarrhythmic - TdP (QT)
1a agents
Quinidine
Procainamide
Disopyramide
MOA Procainamide
block Na = slow conduction, automaticity, excitability of A/V/Purk
block K = prolong APD and refraactoriness
Quinidine vs Procainamide
Procainamide has little vagolytic activity and does not prolong QT as much
TX Procainamide
Life-threatening ventricular arrhythmias**
Ventricular arrhythmias immediately post MI
convert VT
Acute supraventricular:
Re-entrant SVT
A fib
A flutter w/WPW
Requires adequate time - not emergency
AE Procainamide
Arrhythmia aggravation TdP - contraindicated in long QT, HX of TdP, hypo-K heat block/sinus node dysfunction SLE like syndrome GI N/V - common Decrease kidney fx
1b Na channel
inactive»_space;» open
dissociate in under 1s
1b agents
Lidocaine
Mexiletine
MOA Lidocaine
block inactivated»_space; open Na = reduced Vmax
shorten AP
more effective in ischemic tissue
lower slop of phase 4 = lower threshold for excitability
slows ventricular rate
potentiates infranodal block
TX Lidocaine
Used to be first-line for ventricular arrhythmias (post MI)
Now - second choice for immediate life-threatening or symptomatic arrhythmias
Ineffective:
prophylaxis after MI
Atrial tissue
PKX Lidocaine
Extensive first pass - IV use
Multiple loading doses and maintenance infusion
AE Lidocaine
Rapid bolus: tinnitus, seizure
High dose: drowsy, confused, hallucination
CV decreased
1c agents
Propafenone
Flecainide
1c Na channels
Strongest binding to Na channels
O state
slow dissociation = strong effects on p0 depol
MOA Propafenone
strong inhibitor of Na channel
can inhibit B-adrenergic
structurally similar to propranolol
TX Propafenone
Ventricular arrhythmias in pts w/ no HD and preserved ventricular fx atrial arrhythmias (Afib, PSVT)
MOA Flecainide
potent Na channel blockade = prolonged p0 + wide QRS
markedly slows intraventricular conduction**
TX Flecainide
ONLY life-threatening ectopic ventricular arrhythmias
Not first line agent - fatal proarrhythmic
AE 1c
proarrhythmic especially post-MI
Contraindicated in structural and ischemic HD
MOA Class II agents
B-blockers
decrease cAMP/Ca = decrease SA node automaticity, AV node conduction, ventricular contractility
TX Class II
Supraventricular arrhythmias (sympathetic)
ONLY drug effective in preventing sudden cardiac death post-MI
NOT effective in severe arrhythmias (recurrent VT)
Esmolol
very short t.5 - only IV
No ISA, no membrane depressant
little/no bronchospasm
useful for short term B-blockade (aortic dissection, critically ill, post-op HTN)
Class II AE
Impotence
COPD/asthma exacerbation
Bradycardia, AV block, HF - mask signs of hypo-G
CNS sedation
Dyslipidemia (metoprolol)
Exacerbation of angina (propranolol)
contraindicated in pheochromocytoma or cocaine (except carvedilol and labetalol)
TX of B-blocker overdose
Saline
Atropine
Glucagon
MOA class III
Multiple effects at K, Ca, Na and autonomic
Main: prolong phase 3 repol = increased QT
Class III agents
Amiodarone Ibutilide Dofetilide Dronedarone Sotalol
MOA Amiodarone
block K = long APD/refractory Block Na (inactivated) block Ca = slow SA P4 Slow AV node conduction noncompetitive blockade of a, B, M
TX Amiodarone
Widely used
Conversion of AF - maintain sinus rhythm - DOC*
AVNRT*
WPW tachycardia
Oral - LT VT or resistant VF
IV - acute termination of VT/VF - replacing lidocaine for out-of-hospital cardiac arrest
PKX Amiodarone
Lipophilic
metabolized to DEA - potent
responsible for early arrhythmias after discontinuation
AE Amiodarone
Lethal pulmonary fibrosis
Hyper/hypothyroidism
Elevated hepatic enzymes
Check PFTs, LFTs, TFTs
MOA Ibutilide
Block rapid component of delayed rectifier K = slow repol
Activate slow inward Na = prolong AP
TX Ibutilide
IV - acute conversion of AF/AFl to NSR (20 min)
AE Ibutilide
Excessive QT prolongation
TdP - continuous ECG monitoring for 4h
MOA Dofetilide
Block delayed rectifier K current
does not block other K
PKX Dofetilide
100% bioavailable
Verapamil - increased peak plasma
Cimetidine - prolong t.5
TX Dofetilide
Restore/maintain NSR in A-fib
AE Dofetilide
dose-dependent QT prolongation
ventricular proarrhythmia
MOA Sotalol
B-blocker AP prolonging (K)
TX Sotalol
Life-threatening ventricular arrhythmias
Children SV/V arrhythmias
AE Sotalol
TdP
LV depression w/HF
Class IV agents
Verapamil
Diltiazem
MOA Class IV
Ca channel antagonists
Similar to Class II w/ primary effects on nodal p0
Incomplete blockade
Major CV actions of Class IV
Negative chronotrope, dromotrope, inotrope
Class IV TX
Systemic HTN
Angina pectoris
SVT
Post-infarct protection
Verapamil MOA
block slow inward Ca channels in nodal tissue
Decrease SA automaticity, HR, AV conduction (increase PR), increase ERP
Ineffective on ventricular arrhythmia
Verapamil TX
PO - prevention IV - conversion nodal arrhythmias (PSVT) Rate control - A-fib angina pectoris HTN
AE Verapamil
HA Constipation Exacerbate CHF Hypotensino AV block w/B-blocker
Contraindication Verapamil
Sick sinus syndrome
Pre-existing AV nodal dz
WPW w/Afib
V-tach
MOA Adenosine
A1 receptor in SA/AV = increase K =
SA node hyperpol and low firing rate
Short APD
Depression of AV conduction velocity
A2 receptor
Increase endothelial Ca
Increase NO
Vasodilation
TX Adenosine
Acute conversion of paroxysmal supraventricular tachycardia cause by reentry bypass
PKX Adenosine
IV bolus to central vein
Blunted by adenosine antagonist - caffeine, theophylline
TX Mg
TdP
Digitalis arrhythmias
TX Bradycardia
Atropine - vagal block
Isoproterenol - B1 agonist
Pacemaker
TX Sinus Tachycardia, PSVT
vagal stimulation
carotid massage
Valsalva