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HSHD Block 4 > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What are the two targets of mechanisms of antiarrythmics

A

§Abnormal automaticity (pacemaker activity)

§Abnormal propagation of electricity through the myocardium

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2
Q

Mechanisms of AAD

A

Decrease excitability of cardiac tissue (CALM down)

Decrease pacemaker activity (SLOW down)

Inhibit conduction (BLOCK)

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3
Q

AADs classifications (and pneumonic)

A

“Some Block Potassium Channels”

Vaughn-Williams Classification:

I –Na blocker (Sodium)

II – Beta blocker, blocks catecholamines (Beta blocker)

III –K channel blocker, prolong AP and repolarization, (Potassium)

IV – block L-type calcium channels (Calcium)

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4
Q

Effect of Class 1 drugs

A

Decrease the slope of phase 0

Increase Effective Refractory Period (ERP)

Slow conduction of the action potential –Increasing QRS duration

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5
Q

Differences between class 1 types

A
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6
Q

Class 1 mechanism

A

Block re-entry by increasing ERP

Convert uni-directional block to bi-directional block

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7
Q

Class 1a drugs and treatment

A

Quinidine, Procainamide

Can by used to treat atrial or ventricular arrhythmias

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8
Q

Quinidine target, adverse effects, contraindication

A

Blocks Na+ current, but also Ikr, Iks, IKATP, and Ito

Prolongs PR, QRS, and QTc

Contraindicated if ischemic heart disease

Adverse Effects:

GI (most common): Nausea, anorexia, diarrhea

Tinnitus, hearing loss, visual disturbance, confusion (cinchonism)

Thrombocytopenia, hemolytic anemia (in G6PD deficiency), anaphylaxis

Anti-cholinergic effects

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9
Q

Procainamide target, adverse effects, contraindication

A

Use: Drug of choice for atrial fibrillation in WPW (preexcited afib). Blocks accessory pathway muscle conduction and His-Purkinje system.

Contraindicated if ischemic heart disease

Adverse Effects:

GI side effects

Vasculitis, Raynaud’s phenomenon

Agranulocytosis

Hypotension, bradycardia, QT prolongation, torsades de pointes (Idiosyncratic)§Anti-cholinergic effects

Drug-induced lupus ~ 30% (+ ANA in 80%)

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10
Q

Class 1b drugs and treatment

A

Lidocaine, Mexelitine

Shortens action potential duration, thus, no torsades risk

Used for ventricular tachycardia, especially if caused by ischemia

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11
Q

Lidocaine special use, metabolism, and side effects

A

Lidocaine causes voltage dependent Na+ channel block (­ bigger effect in ischemic tissue)

Metabolism depends on hepatic blood flow

Side effects: Neurological (delerium, seizures, tremors)

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12
Q

Why do 1Bs work well in ischemic tissue

A
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13
Q

Class 1c drugs and treatment

A

Flecainide, propafenone

Used to maintain or restore sinus rhythm in atrial fibrillation

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14
Q

Class 1c mechanisms and causes

A

Most potent Na+ channel blockers and greatest use-dependence

Increases QRS duration (decrease slope phase 0)

No change in QTc

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15
Q

Flecainide contraindication and adverse effects

A

CONTRAINDICATED if structural heart disease (↓EF) or recent MI/ischemic heart disease

§Adverse effects: Dizziness, visual disturbance, marked negative inotropic effects – worsen HF

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16
Q

How can 1c drugs cause arrythmia

A
17
Q

Class 1 effects on QTc, PR, QRS

A

Increase PR and QRS

  • IA drugs prolong QTc
  • IB drugs shorten QTc
  • IC drugs primarily decrease slope phase 0 (increases QRS)
18
Q

Class III mechanism of action

A

K Channel blocker

blocks re-entry by increasing ERP duration so it is longer than conduction time

19
Q

Class III drug and treatment

A

Amiodarone (multiple class effects), Ibutilide,Dofetilide, Sotalol

Can be used for atrial and ventricular arrhythmias (dirty job, dirty drug)

Mostly used for converting Afib to NSR or maintaining NSR after cardioversion

20
Q

Class III effect on EKG

A

Increase action potential duration (QTc)

Prolong repolarization - ­ refractory period

No change in QRS (phase 0 not affected)

May not increase risk of Torsades

21
Q

Amiodarone dosing and metabolism

A

P450 inhibitor – can increase many drug levels

Large volume of distribution; lipid soluble; >10 gms needed to saturate fat stores; Half-life 13-103 days

22
Q

Amioderone side effects

A

Also has class I, II, and IV effects (dirty job, dirty drug) – but most side effects are due to accumulation outside heart!

Hyperthyroidism: Need to stop drug

Hypothyroidism: Most common! Supplement T4; usually don’t need to stop

Pulmonary: Appears like pulmonary edema on CXR

Photosensitivity, gray/blue skin discoloration

23
Q

What to monitor on amioderone

A

annual eye exams, liver function tests, thyroid studies, pulmonary function tests (LFT, TFT, PFT)

24
Q

Class II drugs MOA

A
25
Q

Class II effects on EKG

A

↓HR

↑PR interval

Decreased ventricular rate in Afib

No change in QRS or QTc

26
Q

Beta Blockers common use

A

Use: Most tachyarrhythmias (atrial and ventricular)

Only anti-arrhythmics shown to reduce arrhythmic mortality post-MI (okay for ischemic or structural heart disease)

27
Q

Beta blockers side effects

A

Caution in systolic heart failure due to negative inotropy (especially with IV)

Possible bronchospasm with nonselective

Can cause heart block, bradycardia

28
Q

Class II drugs

A
29
Q

Class IV mechanisms

A

Block activated and inactivated L-type calcium channels

Prolongs phase 4 of nodal AP, much like beta blockers, decreasing pacemaker activity

increases AV node refractory period duration (blocks AV node reentry)

reduces Ca2+ entry preventing Ca2+ overload (prevents DADs)

30
Q

Class IV effect on EKG

A

Decrease HR and increase PR interval

31
Q

Class IV drugs and treatment

A

Diltiazem, Verapamil

Used for rate control of atrial fibrillation

32
Q

Class IV adverse effects

A

bradycardia, hypotension, heart block, worsen heart failure due to negative inotropy

33
Q

Potency of class 1 drugs

A

Intensity of sodium channel blockade: IC>IA>IB

34
Q

Digitalis (Digoxin) MOA

A
35
Q

Digoxin use

A

Anti-arrhythmic use: ONLY for rate control of Afib when all else fails or is contraindicated (systolic heart failure)

Narrow therapeutic window

36
Q

Digoxin toxicities and what to give

A

Competes for binding site with K – toxicity aggravated by hypokalemia

Toxicity: nausea, vomiting, bradycardia, ECG changes

Pro-arrhythmic effects due to high intracellular Na (higher resting potential): Increased automaticity, Ventricular Tachycardia, AV block, ST segment abnormalities

Treat with Digibind (Ab)

37
Q

Digoxin toxicity on EKG

A
38
Q

Adenosine use and MOA

A

Drug of choice for termination of SVTs that depend on AV node

Activates K channels à K out à takes cell longer to depolarize

Blocks Ca influx

Inhibits AV node reentry = BLOCKS AV node conduction

Half life is second – transient

39
Q

Adenosine side effects and contraindication

A

Side effects: flushing via endothelial-dependent relaxation of smooth muscle, av block, nausea, shortness of breath

Caution: Can trigger Afib by changing atrial refractoriness. Contraindicated for pre-excited Afib(WPW)

HSHD Block 4 (8 decks)

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