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Pharm '14 test 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

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

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

A

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

21
Q

Esmolol is metabolized

A

Rapidly by plasma esterases, not the same for sux

22
Q

Class III agents work on which phase?

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

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

A

Amiodarone

25
Q

How does amiodarone work? What is it useful for?

A

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
Q

Amiodarone dosing/kinetics

A

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
Q

Amiodarone side effects

A 
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
Q

Class IV agents work on which phase?

A

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
Q

Class IV agents are useful in

A

SVT and ventricular rate control in a-fib/flutter

Prevent recurrence of SVT

Not used in ventricular arrhythmias

30
Q

Class IV agents

A

Verapamil

Diltiazem

31
Q

Verapamil dosing/kinetics

A

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
Q

Verapamil side effects

A

Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs NM blockade

33
Q

Verapamil cautions

A

Myocardial depression and hypotension with inhalational agents

Increased risk of LA toxicity

Hyperkalemia with dantrolene

Decreased digoxin clearance

34
Q

Diltiazem dosing/kinetics

A

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
Q

Diltiazem side effects

A

Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs NM blockade

36
Q

Class V agents

A

Adenosine, digoxin, phenytoin, atropine

37
Q

Adenosine MOA

A

Slows AV node conduction

Used for acute treatment

Termination of SVT/diagnosis of VT (does nothing for VT)

38
Q

Adenosine dosing/kinetics

A

6mg IV rapid bolus, 6-12mg repeat dose after 3 min

Half-life <10 secs

Eliminated by plasma and vascular endothelial cell enzymes

39
Q

Adenosine side effects

A

Excessive AV/SA node inhibition, facial flushing, headache, dyspnea, chest discomfort, nausea, bronchospasm

Contraindicated in asthma, heart block

40
Q

Digoxin MOA

A

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
Q

Digoxin dosing/kinetics

A

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
Q

Digoxin adverse effects

A

Arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation- worsened by hypokalemia/magnesemia

Toxicity treatment-
Phenytoin for V arrhythmias
Pacing
Atropine
Digoxin immune fab
43
Q

Phenytoin MOA

A

Resembles lidocaine in its effects

Used for arrhythmias brought on by digoxin toxicity

Can also be used in VTs and Torsades

44
Q

Phenytoin dosing/kinetics

A

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
Q

Phenytoin adverse effects

A

CNS depression, inhibits insulin secretion, bone marrow depression, nausea

46
Q

Atropine MOA/dosing/kinetics

A

Muscarinic antagonist

Treats unstable bradyarrhythmias (asystole/PEA)

0.4-1.0mg IV, repeat as needed

Onset <1min, duration 30-60min

Metabolized by liver

47
Q

Atropine cautions

A

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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