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N550 Pharm > Antiarrythmics > Flashcards

Antiarrythmics Flashcards

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0
Q

What is the intrinsic rate of SA node? AV node? Purkinje fibers?

A

SA: 60-100
AV: 40-60
Purkinje: 15-40
SA has a higher resting potential of -55 (compared to -90 of most cells) so it fires more easily

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1
Q

Explain the phases (0-4) of the action potential in cardiac cells. What channels are opening/closing? Which phases are the refractory period?

A

Phase 0: rapid depolarization (upstroke), Na fast in
Phase 1: partial repolarization, Na channels close
Phase 2: plateau, Ca slowly in
Phase 3: repolarization, Ca channels close, K slow out
Phase 4: pacemaker potential, return to resting potential
Refractory period is phases 1-3 (another signal can’t be generated)

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2
Q

How is the SA node controlled by SNS and PSNS?

A

SNS: B1 receptors activated, increases catecholamines (NE, epi), HR, automaticity, facilitates conduction of AV node
PSNS: M2 receptors activated, Decreases HR, inhibits AV conduction (ACh, vagal response)

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3
Q

What is altered automaticity?

A

Latent pacemaker cells take over SA node’s role, escape beats
Ex: pain or stress can cause sinus tachycardia

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4
Q

What is delayed after-depolarization?

A

Normal action potential of cardiac cell triggers a train of abnormal depolarizations
Ex: this can be caused by drug or electrolyte imbalance

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5
Q

What is conduction block?

A

Impulse fails to propagate in non-conducting tissue

This can be due to damaged cardiac areas or because it is in its refractory period

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6
Q

What is re-entry?

A

Most common way arrhythmia is formed (most anti-arrhythmic drugs work on this)
Refractory tissue reactivated repeatedly and rapidly due to unidirectional block (due to ischemia or refractory period) which causes abnormal continuous circuit

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7
Q

How do the classes of antiarrhythmic drugs relate to the phases of cardiac conduction?

A

Class I: sodium channel blockers, phase 0
Class II: beta adrenergic blockers, phase 4
Class III: potassium channel blockers, phase 1-2
Class IV: calcium channel blockers, phase 2
Class V: unclassified

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8
Q

What are Class I agents? How do they work?

A

Block sodium channels which depress phase 0

This decreases depolarization rate and slows conduction velocity

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9
Q

What are class IA agents? Name a few.

A 
Intermediate Na channel blockers
Decreased depolarization rate
Slows conduction velocity
Prolonged repolarization
Quinidine (this is the prototype, not used often), procainamide, disopyramide- most common, oral agent, moricizine- oral agent
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10
Q

What are class IB agents? Name a few

A

FAST Na channel blockers
Little effect on velocity of depolarization, but shortens action potential duration and shortens refractory period
Decreases automaticity
Lidocaine (the prototype), mexiletine (oral agent for tachyarrhythmias), phenytoin

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11
Q

What is lidocaine used for?

A

FAST sodium channel blocker
Used in acute treatment/prevention of ventricular dysrhythmias, especially right after an MI
Vtach, Vfib, PVCs

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12
Q

Lidocaine dose?

A

1-1.5 mg/kg IV, infusion 1-4 mg/min (max dose 3 mg/kg)

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13
Q

Is lidocaine protein bound, what is the metabolism like? E1/2t?

A 
50% protein binding
Active metabolite which prolongs E1/2t
E1/2t = 1.4-8 hours
Therapeutic plasma concentration 1-5 mcg/mL
10% renal elimination
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14
Q

What IMPAIRS metabolsm of lidocaine? What INDUCES it?

A

IMPAIRED by drugs such as cimetidine and propanolol or conditions like CHF, acute MI, liver dysfunction, GA
INDUCED by drugs like barbiturates, phenytoin, or rifampin

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15
Q

Adverse effects of lidocaine?

A

Hypotension, bradycardia, seizures, CNS depression, drowsy, dizzy, lightheaded, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, ventilatory depression, cardiac arrest and can augment preexisting neuromuscular blockade
(Like with LA toxicity, CNS first, then myocardial depression to respiratory depression)

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16
Q

What are Class IC agents? Name some.

A

SLOW Na channel blockers
Potent decrease of depolarization rate (phase 0) and decreased conduction rate with increased action potential
Inhibit conduction through His-Purkinje system
Flecainide (the prototype), propafenone

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17
Q

What is Flecainide used for? (This is the same for propafenone)

A

Effective in treatment of suppressing ventricular PVCs and Vtach, also atrial tachyarrthmias, WPW syndrome (re-entry rhythm)
Oral agent
Has proarrhythmic side effects

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18
Q

What are Class II agents? What are they used for?

A

Beta-adrenergic antagonists. Depress phase 4 depolarization in SA node causing slowed HR, decrease in myocardial oxygen requirement (good for CAD pt), slows speed of conduction, prolongs P-R interval, decrease contractility/automaticity
Treats SVT, atrial and ventricular arrhythmias, during MI and reperfusion, treat tachyarrhythmias secondary to dig toxicity

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19
Q

Name some Class II agents.

A

Propranolol- prototype
Metoprolol
Esmolol
Labetolol (off-label use because it blocks alpha and beta)

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20
Q

What is propranolol used for?

A

It is a nonselective beta-adrenergic antagonist
Used to prevent reoccurrence of tachyarrhythmias, both supraventricular and ventricular precipitated by sympathetic stimulation
Decreases phase 4, decreases automaticity and rate

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21
Q

Propranolol dose? Onset? Peak effect? Duration? E1/2t?

A

1 mg/min (total 3-6 mg) IV or 10-80 mg po
Onset 2-5 min
Peak effect 10-15 min, duration 3-4 hours
E1/2t 2-4 hours

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22
Q

Cardiac effects of propranolol?

A

Decreased HR, contractility, CO
Increased PVR, coronary vascular resistance
Decreased oxygen demand

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23
Q

Pharmacokinetics of propranolol? Therapeutic plasma level?

A

90-95% protein bound
Hepatic metabolism, weak metabolite
Therapeutic plasma level 10-30 mcg/mL

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24
Propranolol side effects and cautions?
SE: bradycardia, hypotension, myocardial depression, fatigue, worsening bronchospasm, fever, rash, nausea, worsening Raynauds, interferency with glucose metabolism Caution with reactive airway disease, hypovolemia, CHF, AV block
25
Metoprolol: what is it? Dose? Onset? E1/2t?
Selective B1 blocker 5 mg IV over 5 min; max dose 15 mg over 20 min Onset 2.5 min E1/2t 3-4 hours Metabolized by liver Can be used in mild CHF (because of selectivity)
26
What is esmolol? Dose? Duration? Effects?
Selective B1 blocker Dose: 0.5 mg/kg IV over 1 min, then 50-300 mcg/kg/min Duration: less than 15 min Effects HR without decreasing BP significantly in small doses
27
Esmolol metabolism?
Rapidly hydrolyzed by plasma esterases (not the same esterases as sux, no effect on sux metabolism)
28
What do class III agents do? Name some.
Block potassium ion channels resulting in prolonged depolarization and action potential duration, lengthened repolarization, prolong QT interval, increase automaticity (good for rate control) Treat SVT, ventricular arrhythmias, control Afib Amiodorone (the prototype), dronedarone, sotalol
29
What is Amiodarone?
``` Class III antiarrhythmic (also has class I, II, IV properties) K/Na/Ca channel blocker, alpha and beta adrenergic antagonist Prophylaxis or acute treatment of atrial and ventricular arrhythmias (refractory SVT, refractory VT/VF/AF) First line drug of Vtach and Vfib resistant to defibrillation ```
30
What is the only rhythm that amiodarone is CONTRAINDICATED in?
Torsades de points because amiodarone prolongs QT, it can CAUSE torsades and does not treat this rhythm
31
Amiodarone dose? E1/2t?
Dose: bolus 150-300 mg IV over 2-5 min, up to 5 mg/kg, then 1 mg/hr x 6 hours, then 0.5 mg/hr x 18 hours Prolonged E1/2t of 29 days!
32
Amiodarone metabolism/excretion/protein binding?
``` Hepatic metabolism, active metabolite Biliary/intestinal excretion Therapeutic plasma level 1-3.5 mcg/mL Extensive protein binding 96% Large Vd ```
33
Adverse effects of amiodarone?
Pulmonary toxicity, photosensive rashes, grey/blue skin, thyroid abnormalities, corneal deposits, CNS/GI disturbance, pro-arrhythmic effects (torsades, prolongs QT interval), heart block, hypotension, decreases contractility, nightmares, abnormal LFT, inhibits P-450 (so reduces clearance of digoxin, warfarin)
34
What are class IV agents? Name some.
Block slow calcium channels, primarily at AV node Works at phase 2 (plateau) Decreases contractility (neg iontropic), vasodilation, hypotension Treats/prevents SVT Used for ventricular rate control in Afib/Aflutter NOT used for ventricular arrythmias! Verapamil (the prototype), diltiazem
35
Verapamil dose?
Dose 2.5-10 mg IV over 1-3 min (max dose 20 mg) | Continuous infusion 5mcg/kg/min
36
What is the big contraindication for verapamil?
B-blockers. Will cause heart block
37
Metabolism/excretion pharmacokinetics of verapamil? E1/2t?
Highly protein bound Hepatic metabolism, with active metabolite Excreted in urine and bile E1/2t 6-8 hours
38
Side effects of Verapamil?
Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs neuromuscular blockers
39
Anesthetic considerations of verapamil?
``` Myoardial depression and vasodilation with inhalational agents Potentiate neuromuscular blockers Increase LA toxicity risk With dantrolene can cause hyperkalemia Decreases clearance of digoxin ```
40
Diltiazem dose?
Diltiazem is a class IV antiarrhythmic, ca channel blocker 5-20 mg IV (0.25-0.35 mg/kg) over 2 min Continuous infusion 10 mg/hr
41
Diltiazem pharmacokinetics? E1/2t?
E1/2t 4-6 hours Highly protein bound Hepatic metabolism Excreted in urine
42
Diltiazem side effects?
Less myocardial depression compared to verapamil | Myocardial depression, hypotension, constipation, bradycardia, nausea, prolonged effect of NM blockers
43
List some class V agents
Adenosine Digoxin Phenytoin Atropine
44
What is Adenosine? What is it used for?
Bines to A1 purine nucleotide receptors which activate adenosine receptors to open K channels and increase K currents. This slows SA and AV node conduction Used for acute reasons only, to terminate SVT or diagnose Vtach Not for Afib/Aflutter
45
Adenosine dose?
6 mg IV, rapid bolus | Repeat if necessary after 3 min, 6-12 mg IV
46
Adenosine E1/2t?
Less than 10 sec!! | Eliminated by plasma and vascular endothelial cell enzymes
47
Adenosine side effects? Contraindications?
SE: excessive AV or SA node inhibition, facial flushing, headache, dyspnea, chest discomfort, nausea, bronchospasm Contraindicated in asthma or heart block
48
What is digoxin, what is it used for?
Cardiac glycoside steroid, increase ca which increases inotropy, Decreases HR, preload, and afterload Increases vagal activity Slows AV conduction by increasing refractory period Treats CHF, used for Afib or Aflutter (controls ventricular rate)
49
Digoxin dose? Onset?
0.5-1 mg in divided doses over 12-24 hours | Onset of action 30-60 min
50
Digoxin e1/2t, therapeutic levels, pharmacokinetics?
``` E1/2t 36 hours Narrow therapeutic index, 0.5-1.2 mcg/mL Weak protein binding 90% excreted by kidneys Reduce dose in elderly/ renal impairment ```
51
Digoxin adverse effects?
Arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation Potentiated by hypokalemia and hypomagnesemia Toxicity can happen easily due to the small range of the therapeutic index
52
Digoxin toxicity treatment?
Phenytoin for ventricular arrhythmias Pacing Atropine Antidote: digoxin immune Fab
53
Phenytoin uses?
Class IA agent, resembles effects of lidocaine Not used often anymore except to treat torsades de points Also can be used to suppress ventricular arrhythmias associated with digitalis toxicity or be used to treat ventricular tachycardias
54
Phenytoin dose? Therapeutic blood levels?
Dose: 1.5 mg/kg IV every 5 min up to 10-15 mg/kg | Therapeutic blood levels 10-18 mcg/mL
55
Phenytoin pharmacodynamics? E1/2t?
Metabolized by liver Excreted by urine E1/2t 24 hours
56
Phenytoin adverse effects?
CNS disturbances Partially inhibits insulin secretion Bone marrow depression Nausea
57
What is atropine? What is it used for?
Muscarinic receptor antagonist Used to treat unstable bradyarrhythmias Also used for asystole and PEA
58
Atropine dose? Onset? Duration?
0.4-1 mg IV, repeat as necessary Onset less than 1 min Duration 30-60 sec Metabolized by liver
59
What caution is there to using less than 0.4 mg dose of atropine?
Causes paradoxical response, penetrates BBB, CNS effects

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