Cardio Pharm: Antiarrhythmic Drugs Flashcards
in what phase to EADs occur
Phases 2 and 3 - due to reactivation of voltage gated Ca channels during repolarization
in what pases to DADs occur
Phase 4 - due to intracellular calcium overlaoad (Na Ca exchanger cant keep up resulting in depolarization that generates another raction potential)
Discuss the proarrythmic actions of antiarrhytmic drugs
1.) profound slowing of conduction velocity 2.) increase AP duration (LQT)
Class I
Sodium channel blockers
Class II
Beta Blockers
Class III
Potassium chanel blockers
Class IV
Calcium Channel Blockers
Which class I subset extends the AP duration
Class IA
Which subset of class I should be avoided in patients with structural heart damage
Class IC
Class IA drugs
Quinidine, Proclamamide, Dyspramide
Class IB drugs
Lidocaine, Mexiletine, Phenytoin
Class IC drugs
Propafenone, Flecanide
unique effects of class IA
1.) antimuscarinic action (enhance conduction through ABV node) - results in high ventricular rates in patients with atrial tachycardia (should be administered with calss IV to bring rate back down) 2.) Blocks Ikr channels ( prolongs QT - increased risk of torsades
Quinidine uses
rarely used clinically - may be used in pregant women or women who are trying to beocme pregnant. AT and VT
Quidine blocks what CYP
CYP2D6
Quidine adverse effects
1.) Cinchinism (headache, nausea, tinnitus) 2.) Torsades 3.) thrombocytopenia (rare)
Procainamide uses
convert AT or VT to sinus rhythm (short term application)
Procainamide pharmacokinetics
IV ONLY: t1/2 = 3-4 hours, hepatic acetylation yeilds an active metabolite = NAPA which blocks Ikr
Procainamide AE
1.) Lupus like disorder (arthralgia and arthritis) 2.) Long QT - high risk for torsades de pointes
Disopyramide uses
AT and VT
Disopyramide AE
1.) Strong antimuscarinic effect ( uniary retention in men, dry mouth, blurred vision, constipation, worsening of preexisting glaucoma) 2.) Negative ionotropic effect (supresses heart contraction)
Disopyramide contraindication
heart failure - may induce heart failure in susceptible patients
Class IB general uses
Ventricular arrythmias only
Lidocaine uses
terminates VT
Lidocaine Pharmacokinetics
IV ONLY, hepatic metabolism - dose reduced in patients with liver disease
Lidocaine AE
tremor, blurred vision, lethargy - overdose can cause seizures
Mexiletine uses
post MI VT - often given with another drug as its not effective on its own
Mexiletine AE
tremors, blurred vision, lethargy
Phenytoin
antiepileptic drug
Class IC uses
1.) SVT 2.) Prevent recurrence of ventricular tachycardua
Flecanide pharmacokinetics
metabolized by CYP2D6 ( inhibited by quinidine)
Flecanide AE
dizzy, blurred vision, tremor, headache, bradycardia, heartblock, ventricular arrythmia, HF
Propafenone pharmacokinetics
metabolized by CYP2D6 ( inhibited by quinidine). Good for renal patients. ALSO acts as B-blocker (nonselective)
Propafenone AE
dizzy, blurred vision, tremor, headache, bradycardia, heartblock, ventricular arrythmia, HF, ** Metalic taste, bronchospasm (due to non-selective beta block)
Rate control
control rate of only the ventricles by slowing down AP through AV node ( Class II and IV)
Rhythm control
controle both atrial and ventricular rate to bring back into rhythm ( Class I and III)
Class II agents act on what channel
Funny channels
Class II drugs
Propranolol, esmolol, atenolol, metoprolol
Cardiac effects of beta blockers
1.) Decrease stimulation by SNS 2.) decrease pacemaker current to decrease HR 3.) Decrease Ca current to decrease conduction velocity
which drug calss reduces mortality following acute MI in HF patients
Class II (B-Blockers)
Propranolol AE
nonselective B-Blocker. Nightmares (crosses BBB), fatigue, depression, brocnhospasm
Propranolol contraindication
asthma and COPD
Metoprolol AE
cardioselective. Still slightly lipophilic - crosses BBB = nightmares , Bradycardia, heart block, hypotension, heart failure, exercise intolerance
Atenolol pharmacokinetics
Cardioselective. Excreted by the kidney unchanged (less drug drug interactions) Plasma levels increase in pt who have renal disease
Atenolol AE
bradycardia, heart block, hypotension, heart failure, exercise intolerance
Esmolol use
IV ONLY- used for intraoperative arrythmia
Esmolol pharmacokinetics
very short half life t1/2 = 10 seconds - as soon as it gets in the blood it is destroyed by plasma esterases
Esmolol AE
cardiac hypotension 20-50% of patients (12% become symptomatic)
Class III block which current
Ikr during phase 3 (repolarization)
Amiodarone blocks
Ikr, Ina, Ica, and B-receptors
Amiodarone IV uses
termination of SVT and VT
Amiodarone oral uses
SVT (A fib, VT, reduce shock frequency in patients with pacemaker device
Amiodarone Drug- Drug interactions
inhibits metabolism of warfarin (CYP2C9), statins (CYP3A4 and 2C9) and digoxin (P-glycoproteins)
Amiodarone pharmacokinetics
T1/2 = 40-45 days - takes seveal weeks to get to full effect
You have a patient that experiences ventricular tachycardia. You treat them with a loading dose of 400-1200 mg/ day for 10 days and then taper them to a maintainace dose of 200 mg/day. What drug did you give them for their VT
Amiodarone
amiodarone adverse effects
1.) Hepatic- must monitor liver function 2.) LQT but LOW RISK OF TORSADES (blocks Ina, Ica, and B-receptors) 3.) Pulmonary fibrosis 4.) thyroid dysfunction 5.) tissue deposition 6.) Skin reactions - photosensitivity
why does amiodarone have a low risk of Torsades despite the fact that it prolongs QT interval
also blocks Ina, Ica, and B-receptors
Sotalol
also a nonselective B-blocker. Class III
Sotalol uses
A flutter/Fib,Ventricular arrythmias
Sotalol adverse effects
1.) Torsades (RECOMMEND initiation while in the hospital) 2.) Bronchospasm
Sotalol pharmacokinetics
renal excretion unchanged - decreased drug drug interactions
Dofetellide pharmacokinetics
20% metabolized by CYP3A4 80% metabolzed through renal excretion unchaned
Dofetellide drug-drug interactions
plasma levels are increased by verapamil, ketoconazole, trimethoprim/sulfamethoxazole, and cimetidine (OTC)
Dofetellide adverse effects
narrow theraputic window - REQUIRED initiation in hospital setting - Torsades de pointe
Ibutillide use
convert Atrial flutter or fib to sinus rhythm (IV only)
Ibutillide adverse effects
torsades de pointes - patients should be monitored for several hours folowng termination
Dihyodropyridines
selectively inhibit smooth muscle L-ca channels to cause smooth muslce relaxation, antihypertesnive, and antianginal
Non-Dihydropyridines
Class IV antiarrythmetic drugs that more selectively inhibit cadiac muscle Ica-L current to slow heart rate, antiarrythic, and antanginal
action of Class IV on SA node
decrease diastolic depolarization and decrease AP rate (decreases HR) Decreases NCX
action of Class IV on AV node
decrease upstroke, slow conduction velocity and increase refractory period
class IV drugs
Diltiazem, Verapamil
class IV uses
SVT, VT, atrial fibrillation/flutter
Class IV contraindication
- ) heart failure with LOW ejection fraction 2.) Slow heart rate 3.) low blood pressure 4.) WPW
Adenosine MOA
activates G-protein activated inward K rectifier (GIRK) channels to produce a muscarinic affect that slows heart rate. Inhibits Ica
Adenosine uses
termination of PSVT
Adenosine pharmacokinetics
IV only T1/2 = 10 seconds
Adenosine AE
flushing, dyspnea, chest pain, transient heart block, bronchoconstriction
Digoxin MOA
inhibits Na K ATPase leading to increased levels of Ca in myocites. Slows conduction velocity and increases refractory periord in AV node (due to vagomimetic action)
Digoxin drug drug interactions
Amiodarone, diltiazem, quinidine, verapamil
Digoxin side effects
1.) DADs (due to increased intracellular Ca) 2.) AV block 3.) Bradycardia 4.) Anorexia, nausea, headache, halo vision, altered color perception
magnesium sulfate
corrects hypomagnesimia, may surpress EADs, used to treat torsades de pointes
Potassium chloride
corrects hypokalemia - may supress ectopic pace makers and prevent or terminate arrhythmias
