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Cardiology 1 > Pharm - Antiarrhythmics > Flashcards

Pharm - Antiarrhythmics Flashcards

1
Q

What are the Vaughn Williams classes

A 
IA
IB
IC
II
III
IV
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2
Q

3 Class IA drugs

A
  • Disoyramide
  • Procainamide
  • Quinidine
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3
Q

3 Class IB drugs

A
  • Lidocaine
  • Mexiletine
  • Phenytoin
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4
Q

2 class IC drugs

A
  • Flecainide

- Propafenone

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5
Q

1 Class II drug

A

beta blockers

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6
Q

5 Class III drugs

A
  • Amiodarone
  • Dofetilide
  • Ibutilide
  • Sotalol
  • Dronedarone
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7
Q

2 Class IV drugs

A
  • dihydropyridine calcium channel blockers

- non-dihydropyridine calcium channel blockers

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8
Q

Class IA MoA

A
  • Moderate Na+ channel - K+ to a lesser extent
  • slow conduction velocity
  • prolong refractoriness
  • decrease automatic property of na-dependent conduction tissue
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9
Q

Class IB MoA

A

Weak Na+ channel antagonists

  • decrease conduction velocity
  • decrease refractory period
  • decrease automaticity
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10
Q

Class IC MoA

A

Extremely potent Na+ channel blockers

  • greatly slows conduction velocity
  • decreases automaticity
  • no change to refractory period
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11
Q

Class II MoA

A

beta blockers
- anti-adrenergic blockers (SA and AV nodes)

  • decrease conduction velocity
  • increase refractory period
  • decrease automaticity
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12
Q

Class III Moa

A

Block K+ channels

  • prolongs refractoriness in atrial and ventricular tissue
  • delays repolarization
  • no affect on conduction velocity or automaticity
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13
Q

Class IV MoA

A

Calcium channel blockers

  • slow conduction velocity
  • prolong refractory period
  • decrease automaticity
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14
Q

Disopyramide ADR

A
  • hypotension (serious)
  • cardiac failure (serious)
  • anticholinergic (dry mouth, urinary hesitation, constipation) most common
  • EKG changes (widen QT interval)
  • proarrhythmic action
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15
Q

Lidocaine ADR

A
  • CNS toxicity (most common)
  • Cardiovascular toxicity
  • GI: n/v anorexia
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16
Q

Mexiletine ADR

A
  • GI: n/v heartburn, take with food
  • CNS
  • Cardiovascular: heart failure and hypotension
  • Dermatitis: face and trunk
  • Proarrhythmic action: avoid in lesser arrhythmias like asymptomatic PVC
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17
Q

Flecainide ADR

A
  • Cardiac toxicity (pro arrhythmic, conduction abnormalities, hemodynamics like negative inotropic effects)
  • dizziness, blurred vision, HA, nausea
  • neurotoxicity (dizzy, visual changes, psychosis, hallucinations, seizures)
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18
Q

Flecainide

- conduction abnormalities

A
  • prolongs depolarization
  • slows conduction in AV node/His-Purkinji
  • prolonged PR interval (slows dronotropy)
  • increased QRS
  • first and second degree heart block
  • No effect on QT
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19
Q

Felcainide: what is main downside to hemodynamic changes

A

decreased inotrope can cause or worsen heart failure

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20
Q

Propafenone ADR

A
  • GI – dysgusia, nausea: take with food
  • CNS
  • Cardiovascular: beta blocker effects (negative inotropic activity, bradycardia, slow AV conduction, prolong PR and QRS intervals etc.)
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21
Q

List the 7 big ADR associated with beta blockers

A
  1. Exacerbation of heart failure
  2. Negative chronotropic effect
  3. beta blocker withdrawal
  4. increased airway resistance
  5. facilitation of hypoglycemia
  6. fatigue
  7. sexual dysfunction
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22
Q

beta blocker ADR

- Exacerbation of heart failure

A
  • Exacerbate heart failure in pts in acute decompensated situation
  • Cause heart failure in pt with preexisting myocardial dysfunction with borderline compensation
  • These pts’ cardiac output depends on sympathetic drive which is taken away by β-blockers
23
Q

beta blocker ADR

- Negative chronotropic effects

A
  • slowing heart rate which can be problem with pts who have sick sinus syndrome
  • depressing conduction through AV node, potentially causing heart block. This is a problem in pts with complete or partial AV conduction problems
24
Q

beta blocker ADR

- β-blocker withdrawal

A
  • Receptor upregulation due to continued blocking, when stop β-blocker, now have too much response to circulating catecholamines stimulation
  • Acute withdraw: can lead to morbidity and mortality, I pts with known CAD, can exacerbate ischemic sx (precipitation of acute MI)
  • Gradual tapering off β-blocker should be considered
25
Q

beta blocker ADR

- Increased airway resistance

A

Nonselective β-blockers prevent bronchodilation (bronchial β2 receptors) → increased airway resistance in pt with bronchospasm dz

26
Q

beta blocker ADR

- Facilitation of hypoglycemia

A
  • Epinephrine increases glucose production, helps prevent hypoglycemia.
  • β-blocker can increase risk of hypoglycemia because blocks release of glycogen from the liver when glucose is needed.
  • Epinephrine induces early warning signs of neuroglycopenia
  • β-blocker can decrease the perception of hypoglycemia (except sweating)
27
Q

beta blocker ADR

- fatigue

A

β-blocker reduces hearts ability to respond to increased activity

28
Q

Sotalol ADR

A
  • Cardiovascular
  • Prolonged QT
  • Bradycardia
  • Torsades de Pointes
  • New ventricular arrhythmias
  • New/worse heart failure
  • Proarrhythmia
29
Q

Amiodarone ADR - list 7 main

A
  1. Pulmonary
  2. Thyroid
  3. Cardiac toxicity
  4. Hepatotoxicity/GI
  5. Ocular Chanes
  6. Skin reactions
  7. Neuro
30
Q

Amiodarone

- Pulmonary ADR

A
  • Related to cumulative dose
  • Chronic interstitial pneumonitis is most common
  • Also organizing pneumonia, ARDS, solitary pulmonary mass
  • Nonproductive cough and dyspnea in affected pts
  • Pleuritic pain, weight loss, fever, malaise
31
Q

Amiodarone

- Thyroid ADR

A
  • Hypothyroidism
  • Can occur anytime, not dose related
  • Hyperthyroidism
  • Occurs early and suddenly
  • Thyrotoxic sx
  • Type I: related to iodine load = lots of thyroid hormone produced
  • Type II: destruction of thyroid cells leads to release of thyroid hormone
32
Q

Amiodarone

- Cardiac toxicity ADR

A
  • Ca2+ channel blocking activity
  • Sinus bradycardia
  • AV nodal block
  • K+ channel blocking activity
  • Prolongation of QT interval and repolarization
  • Ventricular arrhythmias
  • Torsades de Pointes – more common with other factors that prolong QT interval
33
Q

Amiodarone

- GI/Hepatoxicity ADR

A
  • Jaundice or hepatitis
  • Test AST and ALT (2X elevation = stop drug)
  • GI: n/v/d, anorexia, constipation
34
Q

Amiodarone

- Ocular Changes ADR

A
  • Corneal microdeposits: “cat whiskers” on cornea, not usually a problem
  • Optic neuropathy: Big time problem – optic nerve injury = unilateral or bilateral visual loss/blindness
35
Q

Amiodarone

- skin change ADRs

A
  • Photosensitivity

- Blue-gray slate colored skin

36
Q

Amiodarone

- neuro ADR

A

Many forms: tremor, ataxia, peripheral neuropathy, paresthesias, sleep disturbance

37
Q

Dronedarone ADR

A
  • GI: abd pain, n/d, rash
  • Hepatic damage
  • CV: 2X heart failure risk with given to pt with mod-to-severe left ventricular systolic dysfunction who are recently decompensated
  • Pulmonary toxicity
  • Skin reactions (eczema, rash, photosensitivity)
  • Thyroid issues seen in amiodarone
38
Q

Ibutilide ADR

A
  • Cardiac toxicity (Hypotension, sinus-tachy, supraventricular tachycardia, sinus bradycardia, AV block, BBB)
  • Proarrhythmias
39
Q

Disopyramide drug interactions

A

Contraindicated with concurrent use of drugs that prolong QT interval (quinolone abx, etc.)

40
Q

Flecainide drug interactions

A

Contraindicated with ritonavir (HIV drug)

41
Q

Sotalol drug interactions

A

QT prolonging drugs (macrolides, Zofran, etc.) bc sotalol also prolongs QT interval

42
Q

Amiodarone drug interactions

A
  1. Digoxin
  2. Warfarin
  3. Statins, esp. simvastatin
  4. Azoles
  5. quinolone abx
  6. QT prolonging drugs
43
Q

Amiodarone and Digoxin

  • effect
  • action
A
  • Amiodarone can increase digoxin levels

- Decrease digoxin by 25-50% empirically

44
Q

Amiodarone and Warfarin

  • effect
  • action
A
  • Amiodarone can change Warfarin metabolism, increasing levels
  • Can increase INR to dangerous levels
  • Decrease warfarin by 25-50% empirically
  • Titrate to INR goal
45
Q

Dronedarone drug interactions

A

QT prolonging drugs

46
Q

Monitoring tests and frequency for pts on Amiodarone

A
  1. PFT/CXR – baseline and if sx
  2. Thyroid panel – baseline, q 3-6 mo
  3. Liver panel – baseline, q 3-6 mo
  4. Eye exam – baseline, q 12 mo
  5. Interacting drug plasma level (esp warfarin) – baseline, PRN (INR weekly first 3-4 weeks)
  6. Clinical evaluation – baseline, q 3 mo
47
Q

5 Agents that increase risk of Torsades de Pointes

A
  1. Disopyramide
  2. Sotalol
  3. Dofetilide
  4. Amiodarone
  5. Ibutilide
48
Q

Risks of proarrhythmias with antiarrhythmic drugs

A
  • Potential to cause premature ventricular contractions, induce/aggravate VT, torsades de pointes, V-fib, conduction disturbances, bradycardia
  • Risks vary according to type of arrhythmia being treated, presence of structural heart disease, QT interval, pre-existing conduction disturbances, sinus node dysfunction, patient age, heart failure, left and right ventricular function
49
Q

What pt is risk for induced arrhythmia due to antiarrhythmic drug highest

A

pt with depressed LV function

50
Q

What is most recognized form of drug proarrhythmias

A

torsades de pointes

51
Q

Class I and risk of proarrhythmias

A

risk is higher with structural heart dz, esp coronary heart disease and/or left ventricular dysfn

52
Q

Class II and risk of proarrhythmias

A

bradycardia is biggest risk (except Sotalol which has class III properties at higher doses)

53
Q

Class III and risk of proarrhythmias

A

prolong repolarization → torsades de pointes and ventricular tachycardia

Cardiology 1 (11 decks)

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