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Class 1 anti-dysrhythmic medications and cardiac glycosides (CV) Flashcards

1
Q

Anti-dysrhythmics: General overview

A

-Classified as the Vaughan Williams classification
-Cardiac Action Potential in relation to NSR

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2
Q

Class I antidysrhythmic effects

A

-Membrane-stabilizing drugs
-Fast sodium channel blockers

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3
Q

Class Ia anti dysrhythmic drugs

A

-Disopryramide
-Quinidine
-Procainamide
-“mide” & “dine”; DQP

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4
Q

Class Ia anti dysrhythmic MOA

A

-Blocks Na+ channels
-Delays repolarization and prolongs action potential duration
-Affects phase 0

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5
Q

Class Ia anti-dysrhythmic effects

A

-Depress myocardial excitability, inotropic effect & ectopic foci stimulation
-Prolong refractory period

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6
Q

Class Ia anti-dysrhythmic indications

A

-Atrial fibrillation
-Premature contractions & ventricular tach
-Wolff-Parkinson-White syndrome

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7
Q

Class Ia anti-dysrhythmics: procainamide adverse effects

A

-Agranulocytosis
-SLE-like syndrome

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8
Q

Class Ia anti-dysrhythmic adverse events: quinidine

A

-Prolonged QT
-Anorexia
-Bitter taste, blurred vision, tinnitus

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9
Q

Class Ib anti-dysrhythmic drugs

A

-Lidocaine
-Mexiletine
-Phenytoin

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10
Q

Class Ib anti-dysrhythmic MOA

A

-Block Na+ channels
-They accelerate repolarization and decrease the action potential duration

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11
Q

Class Ib anti-dysrhythmic effects

A

-Decrease ventricular excitability

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12
Q

Class Ib anti-dysrhythmic indications

A

Ventricular dysrhythmias only:
-PVC, v-tach, v-fib

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13
Q

Class Ib anti-dysrhythmic adverse events: Lidocaine

A

-Bradycardia
-Metallic taste

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14
Q

Class Ic anti-dysrhythmic MOA

A

-Block Na+ channels
-Suppresses re-entry
-“C” suppress

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15
Q

Class Ic anti-dysrhythmic drugs

A

-Flecainide
-Propafenone
-PF

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16
Q

Class Ic anti-dysrhythmic effects

A

-Depression of conduction in the bundle of his-Purkinje system
-Have minimal effect on atrial conduction
-Flecainide: Reserved for the most serious dysrhythmias

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17
Q

Class Ic anti-dysrhythmic indications

A

-V-Tach, SVT, A fib, atrial flutter
-Wolff-Parkinson-White syndrome

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18
Q

Class Ic anti-dysrhythmic adverse events: Flecainide

A

-Dyspnea, dizziness
-Palpitations
-Visual disturbances
-N/V, diarrhea, weakness

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19
Q

Class Ic anti-dysrhythmics: propafenone (effect, indications & adverse effects)

A

-Prodysrythmic effect, angina, tachycardia, AV block
-Dizziness, dyspnea, fatigue

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20
Q

Class II anti-dysrhythmics: beta-blocker drugs

A

-Metoprolol
-Esmolol
-Acebutalol
-“lols”

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21
Q

Class II anti-dysrhythmics: beta blockers MOA

A

-Reduces spontaneous depolarization
-Block impulse transmission
-Affects phase 4

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22
Q

Class II anti-dysrhythmic: beta blocker effects

A

-Blocks beta-adrenergic heart stimulation
-Decrease atrial stimulation & ventricular contraction rate
-Decrease CO & BP

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23
Q

Class II anti-dysrhythmics: beta blockers indications

A

-SVT
-Ventricular dysrhythmias

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24
Q

Class II anti-dysrhythmics: beta blocker adverse effects

A

-AV block , HF
-Hyperglycemia, mask the symptoms of hypoglycemia
-Bronchospasm, wheezing, dry mouth
-Erectile dysfunction

25
Class III anti-dysrhythmic drugs
-Amiodarone -Dronedarone -Sotalol -Ibutilide -AIDS
26
Class III antidysrhythmic MOA
-Increase action potential duration by prolonging repolarization in phase 3 -Prescribed for difficult to treat dysrhythmias
27
Class III anti-dysrhythmic effects
-Prolongs the refractory period & myocardial action potential -Blocks both alpha and beta adrenergic stimulation
28
Class III anti-dysrhythmic indications
-V-Tach or V-Fib -Atrial fibrillation and flutter resistant to other drugs
29
Class III anti-dysrhythmic adverse events (amiodarone)
-Pulmonary toxicity, thyroid disorders -Bradycardia, hypotension -SA node dysfunction, AV block, ataxia, QT prolongation, torsades de pointes -Omitting, constipation -Photosensitivity, visual disturbances -abn Liver function tests, jaundice -Hyperglycemia or hypoglycemia -Toxic epidermal necrolysis, vasculitis, blue-grey colouring of the skin
30
Class III anti-dysrhythmics: Ibutilide: Adverse events
-V-Tach, ventricular extra systoles, tachycardia, AV block -Hypotension, headache, nausea
31
Class III anti-dysrhythmic sotalol: Adverse events
-Chest pain, palpitations, dyspnea, bradycardia -Fatigue, dizziness, weakness
32
Class IV anti-dysrhythmic drugs
-Diltiazem -Verapamil
33
Class IV anti-dysrhythmic MOA
-Inhibit calcium channels and reduces the influx of calcium ions during action potentional -Depression of phase 4 depolarization
34
Class IV anti-dysrhythmic effects
-Prolong AV refractory period -Reduce AV conduction -Reduce rapid ventricular conduction caused by atrial flutter
35
Class IV anti-dysrhythmic indications
-SVT -Rate control for A-fib and flutter
36
Class IV anti-dysrhythmic adverse events
-Constipation -Bradycardia, heart block -Hypotension, dizziness, dyspnea
37
Unclassified anti-dysrhythmic: Adenosine MOA
-Slows the conduction time through the AV node
38
Unclassified anti-dysrhythmic indications: Adenosine
-When SVT has failed with verapamil -Pt has co-existing conditions such as HF, hypotension, or LV dysfunction
39
Unclassified anti-dysrhythmic: Adenosine contraindications
-2nd or 3rd degree heart block -Sick sinus syndrome -Atrial flutter or atrial fib -V-Tach
40
Unclassified anti-dysrhythmic: Adenosine nursing considerations
Patients feel impending doom when administered, must be monitored with accessible airway, expect asystole prior to return to rhythm
41
Cardiac glycosides: Digoxin MOA for conduction
Decrease in rate of conduction and a prolonged refractory period between the SA and AV node
42
Cardiac glycosides: Digoxin MOA for contractility
-Increases contractility d/t the inhibition of the Na+-K+ adenosine triphosphatase pump leaving more sodium and calcium available enhancing contractility
43
Cardiac glycosides: Digoxin effects
-Positive inotropic effect -Negative chronotropic & dromotropic effect -Reduction in heart size during diastole -Decrease in venous BP and vein engorgement
44
Cardiac glycosides: Digoxin effects cont'd
-Increase in coronary circulation -Promotion of tissue perfusion and diuresis -Decrease in dyspnea, cough, and cyanosis
45
Cardiac glycosides: Digoxin indications
-A fib and systolic HF
46
Cardiac glycosides: Digoxin contraindications
-2nd or 3rd degree heart block, a fib, v tach or fibrillation, HF resulting from diastolic dysfunction -Subaortic stenosis -Reduced kidney function
47
Cardiac glycosides: Digoxin adverse effects (CV)
-Bradycardia, tachycardia, HTN
48
Cardiac glycosides: Digoxin adverse effects (CNS)
-Headache, fatigue, confusion, convulsion
49
Cardiac glycosides: Digoxin adverse events (visual)
-Coloured vision, halo vision
50
Cardiac glycosides: Digoxin adverse events (GI)
-Anorexia -N/V -Diarrhea
51
Digoxin toxicity
-Toxic is > 2.0 g/L -Low potassium and magnesium levels or decrease in kidney function may increase potential for toxicity -Digoxin toxicity treatment may be to hold medication, treat the symptoms, or administer antidote which is digoxin immune Fab
52
Digoxin drug to drug interactions
-Amiodarone, quinidine, verapamil (increase digoxin levels)
53
Digoxin drug to food interactions
-Bran (decreases oral absorption of digoxin)
54
Digoxin drug to natural health product interactions
-Ginseng (increases digoxin levels) -St. John’s Wart (reduces digoxin levels) -Hawthorne (increases digoxin effects) -Licorice (increase risk for digoxin toxicity due to potassium loss)
55
Digoxin use in pediatrics
-HF -A one decimal point placement error will result in a 10-fold dosage error -Watch for worsening heart failure: Increased fatigue, sudden weight gain, respiratory distress
56
Anti-dysrhythmics and cardiac glycosides: Nursing considerations & patient teaching
-All anti-dysrhythmics can cause dysrhythmias -Grapefruit juice: Amiodarone, Class Ia's - Disopyramide, and quinidine
57
Anti-dysrhythmics and cardiac glycosides: Prodysrhythmias clinical significance
-Antidysrhythmic drugs may cause life-threatening dysrhythmias -Risk increases in presence of: -Severe LV dysfunction -Digoxin and class IA, IC, and III antidysrhythmia drugs
58
Anti-dysrhythmics and cardiac glycosides: Prodysrhythmias treatment
-First several days of drug therapy represent the vulnerable period for development of prodysrhythmias -Many oral antidysrhythmia drug regimens are initiated in a monitored hospital setting

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