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Pharmacology > Antiarrythmics > Flashcards

Antiarrythmics Flashcards

1
Q

Classes of antiarrythmics

A

a. Class I: Fast Sodium Channel Blockers
b. Class II: Beta-Adrenergic Antagonists
c. Class III: Inhibitors of Repolarization
d. Class IV: Calcium Channel Blockers
e. Other: (adenosine, digitalis, etc.)

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2
Q

Phases of cardiac cycle

A 
Phase 0 rapid depolarization (fast sodium channels open; fast inward flow of Na+ )
Phase 1 begin repolarization (sodium channels close)
Phase 2 plateau (slow calcium channels open; slow inward flow of Ca2+)
Phase 3 repolarization (calcium channels close; potassium channels open; slow outward K+ current)
Phase 4 pacemaker potential; return to resting membrane potentials
Refractory period (phases 1-3)
	(periods of repolarization)
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3
Q

Sympathetic stimulation effects

A 
(ß1 receptors activated)
Increases catecholamines 
Increased heart rate (positive chronotropic effect) 
Increased automaticity 
Facilitation of conduction of AV node
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4
Q

Parasympathetic system effects

A

(M2 muscarinic receptors)
Decreases heart rate
Inhibits AV conduction

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5
Q

Classification of arrythmias

A

Site of origin of abnormality (atrial/ junctional / ventricular)
Complexes on ECG (narrow/broad)
Heart rhythm (regular/irregular)
Heart rate is increased or decreased

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6
Q

Mechanisms of Arrhythmia Production

A

Altered automaticity - latent pacemaker cells take over the SA node’s role; escape beats
Delayed after-depolarization - normal action potential of cardiac cell triggers a train of abnormal depolarizations
Re-entry - refractory tissue reactivated repeatedly and rapidly due to unidirectional block, which causes abnormal continuous circuit
Conduction block – impulse fail to propagate in non-conducting tissue

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7
Q

Reasons for arrythmias

A 
Arterial hypoxemia
Electrolyte imbalance
Acid-base abnormalities
Myocardial ischemia
Altered sympathetic nervous system activity
Bradycardia
Administration of certain drugs
Enlargement of a failing ventricle
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8
Q

Class I agents

A

Block sodium channels which depresses Phase O in depolarization of the cardiac action potential with resultant decreases in action potential propagation (decrease in depolarization rate) and slowing of conduction velocity

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9
Q

Class IA

A

Quinidine - Class IA Prototype
Procainamide
Disopyramide
Moricizine

Intermediate Na+ channel blocker (intermediate dissociation)
Decreased depolarization rate (phase 0)
Decreased conduction velocity
Prolonged repolarization
Increased AP duration
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10
Q

Disopyramide

A

Suppresses atrial and ventricular tachyarrhythmias
Oral agent
Has significant myocardial depressant effects and can precipitate congestive heart failure and hypotension

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11
Q

Class IB Agents

A

Lidocaine - Class IB Prototype
Mexiletine
Tocainide
Phenytoin

Fast Na+ channel blocker (fast dissociation)
Alters the action potential by inhibiting sodium ion influx via rapidly binding to and blocking sodium channels (fast)
Produces little effect on maximum velocity depolarization rate, but shortens AP duration and shortens refractory period
Decreases automaticity

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12
Q

Lidocaine

A

Class IB Antiarrhythmic Drug- Prototype
Sodium channel blocker (fast)
Used in acute treatment and prevention of ventricular dysrhythmias in immediate aftermath of MI
Ventricular tachycardia, fibrillation, PVCs, especially associated with ischemia; Pulseless VT and VF

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13
Q

Pharmacokinetics: Lidocaine

A

Elimination half-time (h) 1.4-8.0
Therapeutic plasma concentration 1-5 ug/mL
Dose: 1-1.5 mg/kg IV, infusion 1-4 mg/min (max dose 3 mg/kg)
50% protein binding
Hepatic metabolism
Active metabolite, which prolongs elimination half-time.
Metabolism may be impaired by drugs such as cimetidine and propanolol, or physiologic altering conditions such CHF, acute MI, liver dysfunctioin, GA; or can be induced by drugs like barbiturates, phenytoin, or rifampin
10% renal elimination

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14
Q

Adverse effects: Lidocaine

A

hypotension, bradycardia, seizures, CNS depression, drowsiness, dizziness, lightheadedness, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, ventilatory depression, cardiac arrest and can augment preexisting neuromuscular blockade

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15
Q

Mexiletine

A

Chronic suppression of ventricular cardiac tachyarrhymias

Oral agent

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16
Q

Class IC Agents

A

Flecainide - Class IC Prototype
Propafenone
Slow Na+ channel blocker (slow dissociation), so does not vary much during the cardiac cycle
Potent decrease of depolarization rate phase 0 and decreased conduction rate, with increased AP
Markedly inhibit conduction through the His-Purkinje system

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17
Q

Flecainide

A

Effective in the treatment of suppressing ventricular PVCs and ventricular tachycardia; also atrial tachyarrhythmias; Wolff-Parkinson-White syndrome (reentry rhythm)
Oral agent
Has proarrhythmic side effects

18
Q

Propafenone

A

Suppression of ventricular and atrial tachyarrhythmias
Oral agent
Has proarrhythmic side effects

19
Q

Class II Agents

A

Propanolol – Prototype
Metoprolol
Esmolol
Labetolol (off-label use)
Class II drugs - Beta-adrenergic antagonists. Depress spontaneous phase 4 depolarization resulting in SA node discharge decrease
Drug-induced slowing of heart rate with resulting decreases in myocardial oxygen requirements is desirable in patients with CAD
Slow speed of conduction of cardiac impulses through atrial tissues and AV node resulting in prolongation of the P-R interval on ECG, increased duration of the action potential in atria
Decreased automaticity

20
Q

Class II agent used for?

A

Used to treat SVT, atrial and ventricular arrhythmias
Used to suppress and treat ventricular dysrhythmias during MI and reperfusion
To treat tachyarrhythmias secondary to digoxin toxicity, and SVT (atrial fibrillation or flutter).
Prevents catecholamine binding to beta receptors
Slowing of heart rate
Decrease myocardial oxygen requirements

21
Q

Propranolol

A

Class II Antiarrhythmic Drug- Prototype
Beta-adrenergic antagonist (nonselective)
Used to prevent reoccurrence of tachyarrhythmias, both supraventricular and ventricular precipitated by sympathetic stimulation

22
Q

Pharmacokinetics: Propranolol

A

Dose: 1 mg/min (total dose of 3-6 mg) IV or 10-80 mg po
Onset: 2-5 minutes
Peak effect 10-15 minutes, duration 3-4 hours
Elimination half-time 2-4 hours
Cardiac effects: decreased HR, contractility, CO; increased PVR, coronary vascular resistance; however, oxygen demand lowered
Highly protein bound 90-95%
Hepatic metabolism, with weak metabolite
Therapeutic plasma level 10-30 ng/mL
Side effects: bradycardia, hypotension, myocardial depression, fatigue, and worsening bronchospasm, drug fever, rash, nausea, worsening Raynauds, interferency with glucose metabolism
Caution with reactive airway disease, hypovolemia, CHF, AV block

23
Q

Metoprolol

A

Class II Antiarrhythmic Drug- Prototype
Beta-adrenergic antagonist (selective B1)
Dose: Dose 5 mg IV over 5 minutes; max dose 15 mg over 20 min.
Onset: 2.5 min.
Duration: Half-life 3-4 hours
Metabolized by liver
Can be used in mild CHF

24
Q

Esmolol

A

Class II Antiarrhythmic Drug
Beta-adrenergic antagonist (selective B1)
Dose: 0.5 mg/kg IV bolus over 1 min, then 50-300 mcg/kg/min
Duration <15 mins
Effects HR without decreasing BP significantly in small doses
Rapidly hydrolyzed by plasma esterases
Not the same esterases as cholinesterases responsible for metabolism of sux, therefore no effect on sux metabolism

25
Q

Class III agents

A

Amiodarone – Class III Prototype
Dronedarone
Sotalol
Class III drugs block potassium ion channels resulting in prolongation of cardiac depolarization and increasing action potential duration, and lengthening repolarization.
Decrease the proportion of the cardiac cycle during which myocardial cells are excitable and thus susceptible to a triggering event
Used to treat supraventricular and ventricular arrhythmias
Prophylaxis in cardiac surgery patients r/t high incidence of Afib
Preventative therapy in patients who have survived sudden cardiac death who are not candidates for ICD
Control rhythm in Afib

26
Q

Amiodarone

A

Class III Antiarrhythmic Drug - Prototype
also has Class I, II, and IV antiarrhythmic properties

Potassium/ sodium/ calcium channel blocker, alpha and beta adrenergic antagonist
Used for prophylaxis or acute treatment in the treatment of atrial and ventricular arrhythmias (refractory SVT, refractory VT/ VF, AF)
1st line drug VT/ VF when resistant to electrical defibrillation

27
Q

Amiodarone Pharmacokinetics

A

Dose: Bolus 150-300 mg IV over 2-5 minutes, up to 5 mg/kg, then 1 mg/hr x 6 hrs, then 0.5 mg/hr x 18 hrs
Prolonged elimination half-life (29 days)
Hepatic metabolism, active metabolite
Biliary/ intestinal excretion
Therapeutic plasma level 1.0-3.5 ug/mL
Extensive protein binding 96%
Large volume of distribution

28
Q

Amiodarone Adverse Effects

A 
Pulmonary toxicity 
Pulmonary edema
ARDS
Photosensitive rashes
Grey/blue discolouration of skin
Thyroid abnormalities 2%
Corneal deposits
CNS/GI disturbance
Pro-arrhythmic effects (torsades de pointes)
Heart block
Hypotension
Nightmares 25%
Abnormal LFT 20%
Inhibits hepatic P450
29
Q

Class IV

A 
Calcium channel blockers 
Verapamil – Class IV Prototype
Diltiazem *
Block slow calcium channels 
*primary site AV node
Block slow calcium channels, which decreases conduction through AV node and  shortens Phase 2 (the plateau) of the action potential in ventricular myocytes
Contractility of the heart decreases 
Used in the treatment of SVT and ventricular rate control in Afib and Aflutter
Used to prevent reoccurrence of SVT
Not used in ventricular arrhythmias
30
Q

Verapamil

A

Class IV Antiarrhythmic Drug - Prototype
Calcium channel blocker
Dose 2.5-10 mg IV over 1-3 minutes (max dose 20 mg)
Continuous infusion 5 ug/kg/minute
Do not use IV verapamil with ß- blocker (heart block)
T1/2 6-8 hours
Highly protein bound
Hepatic metabolism, with active metabolite
Excreted in the urine, and bile
Side effects: myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs effects of neuromuscular blockers

31
Q

Caution with Verapamil

A

Caution:
Myocardial depression and vasodilation with inhalational agents
Can potentiate neuromuscular blockers
Can increase risk of local anesthetic toxicity
Together with Dantrolene can cause hyperkalemia
Causes decreased clearance of Digoxin

32
Q

Diltiazem

A 
Class IV Antiarrhythmic Drug
Calcium channel blocker
Dose:  5-20 mg IV (0.25-0.35mg/kg) over 2 min.
Continuous infusion 10 mg/hour
T1/2 4-6 hours
Highly protein bound
Hepatic metabolism
Excreted in the urine
Side effects:  myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs effects of neuromuscular blockers
33
Q

Other class V agents

A

Adenosine
Digoxin
Phenytoin
Atropine

34
Q

Adenosine

A

Not in Vaughan Williams class
Binds to A1 purine nucleotide receptors (activates adenosine receptors to open K+ channels and increase K+ currents)
Slows AV nodal conduction
Used for acute Rx only
Used for termination of SVT/ diagnosis of VT
Dose 6mg IV, rapid bolus
Repeated if necessary after 3 minutes, 6-12 mg IV
T1/2 < 10 seconds
Eliminated by plasma and vascular endothelial cell enzymes
Side effects: excessive AV or SA nodal inhibition, facial flushing, headache, dyspnea, chest discomfort, nausea, bronchospasm
Contraindicated in asthma, heart block

35
Q

Digoxin

A

Not in Vaughan Williams class
Cardiac glycoside
Increases vagal activity, thus decreasing activity of SA node and prolongs conduction of impulses thru the AV node
Decreases HR, preload and afterload
Slows AV conduction by increasing AV node refractory period
Positive inotrope- used to treat CHF

36
Q

Digoxin Pharmacokinetics

A 
Used for the management of atrial fibrillation or flutter (controls ventricular rate), especially with impaired heart function
Dose: 0.5-1 mg in divided doses over 12-24 hrs
Onset of action 30-60 minutes
T1/2 36 hours
Narrow therapeutic index
Therapeutic levels 0.5-1.2 ng/mL
Weak protein binding
90% Excreted by kidneys
Reduce dose in elderly/renal impairment
37
Q

Digoxin Adverse Effects

A

Arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation
potentiated by hypokalemia and hypomagnesaemia
Toxicity treatment
Phenytoin for ventricular arrhythmias
Pacing
Atropine
Antidote: digoxin immune Fab

38
Q

Phenytoin, class, use, and route

A

Effects resemble Lidocaine
Class IA agent
Used in suppression of ventricular arrhythmias associated with digitalis toxicity
Can also be used other ventricular tachycardias or torsades de pointes
Given IV (can precipitate in D5W; mix in NS)
Can cause pain or thrombosis when given in peripheral IV
Dose: 1.5 mg/kg IV every 5 min. up to 10-15 mg/kg
Therapeutic blood levels 10-18 mcg/mL

39
Q

Phenytoin Metabolization and Elimination, adverse effects

A

Metabolized by liver
Excreted in urine
Elimination ½ time @24 hours
Adverse effects: CNS disturbances, partially inhibits insulin secretion, bone marrow depression, nausea

40
Q

Atropine Dose, Route, Receptor, Use

A 
Muscarinic receptor antagonist
Used to treat unstable bradyarrhythmias
Option for asystolic patients; PEA
0.4 to 1.0 mg IV and repeat as necessary
Onset less 1 min; duration 30-60 minutes
Metabolized by liver
Caution dosing less than 0.4 mg
Potential to evoking a paradoxical response
Penetrates the BBB, CNS effects

Pharmacology (9 decks)

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