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CardioRenal I > Cardio Pharm: Antiarrhythmic Drugs > Flashcards

Cardio Pharm: Antiarrhythmic Drugs Flashcards

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1
Q

in what phase to EADs occur

A

Phases 2 and 3 - due to reactivation of voltage gated Ca channels during repolarization

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2
Q

in what pases to DADs occur

A

Phase 4 - due to intracellular calcium overlaoad (Na Ca exchanger cant keep up resulting in depolarization that generates another raction potential)

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3
Q

Discuss the proarrythmic actions of antiarrhytmic drugs

A

1.) profound slowing of conduction velocity 2.) increase AP duration (LQT)

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4
Q

Class I

A

Sodium channel blockers

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5
Q

Class II

A

Beta Blockers

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6
Q

Class III

A

Potassium chanel blockers

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7
Q

Class IV

A

Calcium Channel Blockers

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8
Q

Which class I subset extends the AP duration

A

Class IA

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9
Q

Which subset of class I should be avoided in patients with structural heart damage

A

Class IC

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10
Q

Class IA drugs

A

Quinidine, Proclamamide, Dyspramide

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11
Q

Class IB drugs

A

Lidocaine, Mexiletine, Phenytoin

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12
Q

Class IC drugs

A

Propafenone, Flecanide

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13
Q

unique effects of class IA

A

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

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14
Q

Quinidine uses

A

rarely used clinically - may be used in pregant women or women who are trying to beocme pregnant. AT and VT

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15
Q

Quidine blocks what CYP

A

CYP2D6

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16
Q

Quidine adverse effects

A

1.) Cinchinism (headache, nausea, tinnitus) 2.) Torsades 3.) thrombocytopenia (rare)

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17
Q

Procainamide uses

A

convert AT or VT to sinus rhythm (short term application)

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18
Q

Procainamide pharmacokinetics

A

IV ONLY: t1/2 = 3-4 hours, hepatic acetylation yeilds an active metabolite = NAPA which blocks Ikr

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19
Q

Procainamide AE

A

1.) Lupus like disorder (arthralgia and arthritis) 2.) Long QT - high risk for torsades de pointes

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20
Q

Disopyramide uses

A

AT and VT

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21
Q

Disopyramide AE

A

1.) Strong antimuscarinic effect ( uniary retention in men, dry mouth, blurred vision, constipation, worsening of preexisting glaucoma) 2.) Negative ionotropic effect (supresses heart contraction)

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22
Q

Disopyramide contraindication

A

heart failure - may induce heart failure in susceptible patients

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23
Q

Class IB general uses

A

Ventricular arrythmias only

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24
Q

Lidocaine uses

A

terminates VT

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25
Lidocaine Pharmacokinetics
IV ONLY, hepatic metabolism - dose reduced in patients with liver disease
26
Lidocaine AE
tremor, blurred vision, lethargy - overdose can cause seizures
27
Mexiletine uses
post MI VT - often given with another drug as its not effective on its own
28
Mexiletine AE
tremors, blurred vision, lethargy
29
Phenytoin
antiepileptic drug
30
Class IC uses
1.) SVT 2.) Prevent recurrence of ventricular tachycardua
31
Flecanide pharmacokinetics
metabolized by CYP2D6 ( inhibited by quinidine)
32
Flecanide AE
dizzy, blurred vision, tremor, headache, bradycardia, heartblock, ventricular arrythmia, HF
33
Propafenone pharmacokinetics
metabolized by CYP2D6 ( inhibited by quinidine). Good for renal patients. ALSO acts as B-blocker (nonselective)
34
Propafenone AE
dizzy, blurred vision, tremor, headache, bradycardia, heartblock, ventricular arrythmia, HF, ** Metalic taste, bronchospasm (due to non-selective beta block)
35
Rate control
control rate of only the ventricles by slowing down AP through AV node ( Class II and IV)
36
Rhythm control
controle both atrial and ventricular rate to bring back into rhythm ( Class I and III)
37
Class II agents act on what channel
Funny channels
38
Class II drugs
Propranolol, esmolol, atenolol, metoprolol
39
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
40
which drug calss reduces mortality following acute MI in HF patients
Class II (B-Blockers)
41
Propranolol AE
nonselective B-Blocker. Nightmares (crosses BBB), fatigue, depression, brocnhospasm
42
Propranolol contraindication
asthma and COPD
43
Metoprolol AE
cardioselective. Still slightly lipophilic - crosses BBB = nightmares , Bradycardia, heart block, hypotension, heart failure, exercise intolerance
44
Atenolol pharmacokinetics
Cardioselective. Excreted by the kidney unchanged (less drug drug interactions) Plasma levels increase in pt who have renal disease
45
Atenolol AE
bradycardia, heart block, hypotension, heart failure, exercise intolerance
46
Esmolol use
IV ONLY- used for intraoperative arrythmia
47
Esmolol pharmacokinetics
very short half life t1/2 = 10 seconds - as soon as it gets in the blood it is destroyed by plasma esterases
48
Esmolol AE
cardiac hypotension 20-50% of patients (12% become symptomatic)
49
Class III block which current
Ikr during phase 3 (repolarization)
50
Amiodarone blocks
Ikr, Ina, Ica, and B-receptors
51
Amiodarone IV uses
termination of SVT and VT
52
Amiodarone oral uses
SVT (A fib, VT, reduce shock frequency in patients with pacemaker device
53
Amiodarone Drug- Drug interactions
inhibits metabolism of warfarin (CYP2C9), statins (CYP3A4 and 2C9) and digoxin (P-glycoproteins)
54
Amiodarone pharmacokinetics
T1/2 = 40-45 days - takes seveal weeks to get to full effect
55
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
56
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
57
why does amiodarone have a low risk of Torsades despite the fact that it prolongs QT interval
also blocks Ina, Ica, and B-receptors
58
Sotalol
also a nonselective B-blocker. Class III
59
Sotalol uses
A flutter/Fib,Ventricular arrythmias
60
Sotalol adverse effects
1.) Torsades (RECOMMEND initiation while in the hospital) 2.) Bronchospasm
61
Sotalol pharmacokinetics
renal excretion unchanged - decreased drug drug interactions
62
Dofetellide pharmacokinetics
20% metabolized by CYP3A4 80% metabolzed through renal excretion unchaned
63
Dofetellide drug-drug interactions
plasma levels are increased by verapamil, ketoconazole, trimethoprim/sulfamethoxazole, and cimetidine (OTC)
64
Dofetellide adverse effects
narrow theraputic window - REQUIRED initiation in hospital setting - Torsades de pointe
65
Ibutillide use
convert Atrial flutter or fib to sinus rhythm (IV only)
66
Ibutillide adverse effects
torsades de pointes - patients should be monitored for several hours folowng termination
67
Dihyodropyridines
selectively inhibit smooth muscle L-ca channels to cause smooth muslce relaxation, antihypertesnive, and antianginal
68
Non-Dihydropyridines
Class IV antiarrythmetic drugs that more selectively inhibit cadiac muscle Ica-L current to slow heart rate, antiarrythic, and antanginal
69
action of Class IV on SA node
decrease diastolic depolarization and decrease AP rate (decreases HR) Decreases NCX
70
action of Class IV on AV node
decrease upstroke, slow conduction velocity and increase refractory period
71
class IV drugs
Diltiazem, Verapamil
72
class IV uses
SVT, VT, atrial fibrillation/flutter
73
Class IV contraindication
1. ) heart failure with LOW ejection fraction 2.) Slow heart rate 3.) low blood pressure 4.) WPW
74
Adenosine MOA
activates G-protein activated inward K rectifier (GIRK) channels to produce a muscarinic affect that slows heart rate. Inhibits Ica
75
Adenosine uses
termination of PSVT
76
Adenosine pharmacokinetics
IV only T1/2 = 10 seconds
77
Adenosine AE
flushing, dyspnea, chest pain, transient heart block, bronchoconstriction
78
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)
79
Digoxin drug drug interactions
Amiodarone, diltiazem, quinidine, verapamil
80
Digoxin side effects
1.) DADs (due to increased intracellular Ca) 2.) AV block 3.) Bradycardia 4.) Anorexia, nausea, headache, halo vision, altered color perception
81
magnesium sulfate
corrects hypomagnesimia, may surpress EADs, used to treat torsades de pointes
82
Potassium chloride
corrects hypokalemia - may supress ectopic pace makers and prevent or terminate arrhythmias

CardioRenal I (13 decks)

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