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Pharm '14 test 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

(47 cards)

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1
Q

Describe phases 0-4 of the action potential in cardiac cells

A 
Phase 0- Rapid depolarization
Phase 1- Partial repolarization
Phase 2- Plateau
Phase 3- Repolarization
Phase 4- Pacemaker potential
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2
Q

4 mechanisms of arrhythmias

A

Altered automaticity

Delayed after-depolarization

Re-entry

Conduction block

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3
Q

Factors leading to arrhythmias

A 
Hypoxemia 
Electrolyte imbalances
Acid-base imbalances
Myocardial ischemia
Altered SNS activity 
Bradycardia
Medications
Ventricular hypertrophy
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4
Q

When to treat?

A

Cannot treat by correcting the underlying cause

Hemodynamic function is compromised

Disturbance predisposes pt to more serious arrhythmia or comorbidity

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5
Q

Non-pharm treatments

A

Acute-
Vagal maneuvers
Cardioversion

Prophylaxis-
Radio ablation
Implantable defibrillator

Pacing (external, temp, permanent)

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6
Q

Classification of antiarrhythmic drugs

A 
Class I: Sodium channel blockers
Class II: Beta blockers
Class III: Potassium channel blockers
Class IV: Calcium channel blockers
Class V: Unclassified drugs
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7
Q

Class I drugs affect which phase of the action potential?

A

Phase 0, they block sodium channels. This decreases action potential propagation and slows rate of conduction

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8
Q

Class I drugs

A

IA (won’t see these anymore)
Quinidine
Procainamide

IB
Lidocaine

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9
Q

Lidocaine blocks which type of Na channels? What is it used for?

A

Fast channels

Useful in VT, V-fib, PVCs especially those associated with ischemia

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10
Q

Lidocaine is ______% protein bound. How is it metabolized?

A

50

Hepatic metabolism. Has an active metabolite. Metabolism impaired by cimetidine, propranolol, CHF, MI, liver failure, GA. Induced by barbs, phenytoin, rifampin.

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11
Q

Lidocaine adverse effects

A

Same as LA toxicity

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12
Q

Class IC agent

A

Flecainide

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13
Q

Class II agents work on what phase? What effects do they have?

A

Phase 4. Beta-blockers depress spontaneous phase 4 depolarization.

Lowers myocardial O2 needs

Slows conduction through AV node, elongates PR interval

Decreased automaticity

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14
Q

What are class II agents used for?

A

SVT, atrial and ventricular arrhythmias

Suppress and treat dysrhythmias during MI and reperfusion

Also useful for digoxin toxicity induced dysrhythmias and SVT

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15
Q

Class II agents

A

Propranolol
Metoprolol
Esmolol
Labetalol (off-label)

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16
Q

Propranolol metabolism and side effects

A

Highly protein bound, hepatic metabolism with weak metabolite

Bradycardia, hypotension, myocardial depression, fatigue, bronchospasm

Use with caution in reactive airway disease and hypovolemia

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17
Q

Propranolol dose/kinetics

A

1mg/min IV (total 3-6mg)

2-5 min onset, peak 10-15 min, 3-4 hour duration

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18
Q

Metoprolol dose/kinetics

A

B1 selective

5mg IV over 5 min, max 15mg, onset 2.5 min, duration 3-4 hours

Metabolized by the liver

Can be used in mild CHF

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19
Q

Esmolol dose/kinetics

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A

B1 selective

0.5 mg/kg IV bolus over 1 min, 50-300 mcg/kg/min, duration <15 mins

Little effect on BP at smaller doses

20
Q

Esmolol is useful in

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A

Preventing recurrence of tachyarrhythmias, both supraventricular and ventricular caused by SNS stimulation

21
Q

Esmolol is metabolized

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A

Rapidly by plasma esterases, not the same for sux

22
Q

Class III agents work on which phase?

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A

Phase 1 and 2, by blocking K channels depolarization is prolonged, increasing action potential duration

Reduces the time during the cycle that cells are excitable, making the triggering of a pro-arrhythmic event less likely

23
Q

Class III agents are useful in

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A

Supraventricular and ventricular arrhythmias

Prophylaxis in CV surgery in pts with high incidence of a-fib

Preventative therapy in pts who have survived sudden cardiac death who are not candidates for ICD

Control of a-fib

24
Q

Class III agents

25
How does amiodarone work? What is it useful for?
Blocks K/Na/Ca channels, has alpha/beta antagonist activity (thus also class I, II, and IV activity) Treatment/prophylaxis in SVT, VT/VF. A-fib First line drug in VT/VF resistant to defibrillation
26
Amiodarone dosing/kinetics
Bolus of 150-300mg IV over 2-5 minutes, then 1mg/hr for 6 hrs, then 0.5mg/hr for 18 hrs Looooooong half-life (29 days), hepatic metabolism, active metabolites Highly protein bound, large volume of distribution, excreted in bile
27
Amiodarone side effects
``` Pulmonary toxicity Photosensitive rashes Grey/blue skin Thyroid problems Corneal deposits CNS/GI disturbances Torsades de pointes Heart block Hypotension Nightmares (25%) Abnormal LFT (20%) Reduces clearance of digoxin and warfarin ```
28
Class IV agents work on which phase?
Phase 2, by blocking Ca channels conduction through the AV node is decreased and Phase 2 is shortened Contractility is also decreased by these agents
29
Class IV agents are useful in
SVT and ventricular rate control in a-fib/flutter Prevent recurrence of SVT Not used in ventricular arrhythmias
30
Class IV agents
Verapamil Diltiazem
31
Verapamil dosing/kinetics
2.5-10mg IV over 1-3 minutes Highly protein bound, half-life 6-8hrs Hepatic metabolism, excreted in urine/bile Do not use with beta-blocker, can cause complete heart block
32
Verapamil side effects
Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs NM blockade
33
Verapamil cautions
Myocardial depression and hypotension with inhalational agents Increased risk of LA toxicity Hyperkalemia with dantrolene Decreased digoxin clearance
34
Diltiazem dosing/kinetics
5-20mg IV (0.25-0.35 mg/kg) over 2 min, 10 mg/hr infusion Half-life 4-6hrs Highly protein bound, hepatic metabolism, excreted in urine
35
Diltiazem side effects
Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs NM blockade
36
Class V agents
Adenosine, digoxin, phenytoin, atropine
37
Adenosine MOA
Slows AV node conduction Used for acute treatment Termination of SVT/diagnosis of VT (does nothing for VT)
38
Adenosine dosing/kinetics
6mg IV rapid bolus, 6-12mg repeat dose after 3 min Half-life <10 secs Eliminated by plasma and vascular endothelial cell enzymes
39
Adenosine side effects
Excessive AV/SA node inhibition, facial flushing, headache, dyspnea, chest discomfort, nausea, bronchospasm Contraindicated in asthma, heart block
40
Digoxin MOA
Increases vagal activity, decreasing SA node activity and prolongs conduction through AV node Decreases HR, preload and afterload Slows AV conduction by increasing AV node refractory period Positive inotrope Used for a-fif/flutter (controls V rate), especially with heart failure
41
Digoxin dosing/kinetics
0.5-1mg in divided doses over 12-24hrs Onset 30-60 minutes Narrow therapeutic index Weak protein binding 90% excreted by kidneys, reduce dose in renal failure and the elderly
42
Digoxin adverse effects
Arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation- worsened by hypokalemia/magnesemia ``` Toxicity treatment- Phenytoin for V arrhythmias Pacing Atropine Digoxin immune fab ```
43
Phenytoin MOA
Resembles lidocaine in its effects Used for arrhythmias brought on by digoxin toxicity Can also be used in VTs and Torsades
44
Phenytoin dosing/kinetics
1.5 mg/kg IV every 5 min up to 10-15 mg/kg Therapeutic levels 10-18 mcg/ml Metabolized by the liver, excreted in urine E1/2 time of 24 hours
45
Phenytoin adverse effects
CNS depression, inhibits insulin secretion, bone marrow depression, nausea
46
Atropine MOA/dosing/kinetics
Muscarinic antagonist Treats unstable bradyarrhythmias (asystole/PEA) 0.4-1.0mg IV, repeat as needed Onset <1min, duration 30-60min Metabolized by liver
47
Atropine cautions
Doses less then 0.4mg can produce a paradoxical response Crosses BBB, produces CNS effects

Pharm '14 test 2 (5 decks)

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