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CRRAB 1 > Antiarrythmic > Flashcards

Antiarrythmic Flashcards

1
Q

Procainamide

A

Class IA
Cardiac Effects - slows upstroke of AP, slows conduction, prolongs QRS, prolongs APD by non-specific blockade of K channels
Extracardiac Effects - ganglion-blocking properties, hypotension
Toxicity - Excessive AP prolongation, QT-interval prolongation which can lead to torsades de pointes. Long term use can cause syndrome like lupus
Pharmacokinetics - drug metabolite (NAPA) - class 3 activity. Hepatic metabolism. NAPA has longer half-life than procainamide
T.U. - most A and V arrythmias

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2
Q

Quinidine

A

Class IA
Cardiac Effects - slows upstroke of AP, slows conduction, prolongs QRS, prolongs APD by non-specific blockade of K channels, antimuscarinic effects
Extracardiac Effects - Adverse GI effects, cinchonism at toxic concentrations
Toxicity - excessive QT prolongation -> torsades de pointes
PK - readily absorbed from GI tract an eliminated by hepatic metabolism, renal excretion
T.U. - rarely used because cardiac and extracardiac S.E.

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3
Q

Disopyramide

A

Class IA
Cardiac Effects - slows upstroke of AP, slows conduction, prolongs QRS, prolongs APD by non-specific blockade of K channels, antimuscarinic effects
Extracardiac Effects - Atropine like activity -> urinary retention, dry mouth, blurred vision, constipation
Tox - excessive QT prolongation -> torsades. May precipitate to heart failure
PK - loading doses not recommended because of heart failure. Hepatic metabolism and renal excretion
T.U. - effective for supraventricular arrythmias but only approved for ventricular arrythmias in USA

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4
Q

Lidocaine

A

Class IB
Cardiac Effects - selective depression of conduction in depolarized cells. Little effect on ECG
Extracardiac Effects -
Tox - Least cardiotoxic class I drugs. Paresthesia, tremor, nausea, light headedness, slurred speech
PK - extensive first pass hepatic metabolism -> only 3% appears in plasma -> give parenterally
T.U. - agent of choice for termination of ventricular tachycardia and prevention of v.fib after cardioversion in setting of acute ischemia. NO PROPHYLACTIC

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5
Q

Mexiletine

A

Class IB
Cardiac Effects - orally active congener of lidocaine. Selective depression of conduction in depolarized cells
Extracardiac Effects - relieves chronic pain
Tox - tremor, blurred vision, lethargy, nausea
PK - hepatic metabolism, renal excretion. half life = 8-20 hrs
T.U. - ventricular arrythmias

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6
Q

Tocainide

A

Class IB
Cardiac Effects - selective depression of conduction in depolarized cells.
Tox - lidocaine analog
PK - glucuronidation metabolism -> renal excretion
T.U. - not sold in USA

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7
Q

Flecainide

A

Class IC
Cardiac Effects - slows upstroke of AP, slows conduction, potent blocker of Na and K channels with slow unblocking potential
Tox - severe exacerbation of arrythmia when normal doses administered to preexisting v. tachyarrythmias
PK - metabolism and elimination both hepatic and renal
T.U. - supraventricular arrythmias. Effective in suppressing PVC

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8
Q

Propafenone

A

Class IC
Cardiac Effects - slows upstroke of AP, slows conduction, WEAK beta-blocking activity
Tox - metallic taste and constipation, some arrythmia exacerbation
PK - hepatic metabolism and renal excretion
T.U. - supraventricular arrythmias

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9
Q

Moricizine

A

Class IC
Cardiac Effects - slows upstroke of AP, slows conduction, does not prolong AP duration
PK - extensive first pass metabolism
T.U. - ventricular arrythmias, no longer sold in USA

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10
Q

Propranolol

A

Class II (beta-blocker)
Non-selective beta-blocker. Reduces chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation by competing for binding sites
Tox - GI, dizziness, fatigue, bradychardia, hypotension
PK - extensive liver metabolism
T.U. - hypertension, akathasia, tremor, CHF

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11
Q

Acebutolol

A

Class II (beta-blocker)
Cardioselective, beta-adrenergic receptor blocker (beta-1)
Tox - Same as other beta-blockers
PK - hepatic metabolism (diacetolol - active metabolite), both renal and non-renal excretion
T.U. - same

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12
Q

Esmolol

A

Class II (beta-blocker)
Short-acting cardioselective adrenergic blocker, selective to beta-1 receptors. At higher doses it affects beta-2
Tox - same
PK - metabolized by RBCs (esterases), renal excretion
T.U. - other beta-blockers

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13
Q

Sotalol

A

Class II (beta-blocker)
Blocks beta-adrenergic receptors and cardiac action potential duration prolongation
Tox - overdose predisposes patients to torsades and ventricular arrythmias
PK - liver (no significant metabolism), renal excretion
T.U. - atrial and ventricular dysrhythmias

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14
Q

Class I Na Blockers

A

Binds to and blocks FAST Na channels

  • leads to decreased phase 0 (decreased amplitude)
  • decreases conduction velocity
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15
Q

Class IA

A

Moderate Na blockers

Increase the ERP (non-specific activity of K channels)

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16
Q

Class IB

A

Weak Na blockers

Decrease ERP

17
Q

Class IC

A

Strong Na blockers

no effect on ERP

18
Q

Class II: beta-blockers

A
  • Used to prevent supraventricular arrythmias and reduce ventricular ectopic depolarizations
  • inhibit sympathetic activation of cardiac automaticity and conduction
  • slow HR, decrease AV node conduction velocity, increase AV node refractory period
19
Q

K channel blockers

A

blocks K channels = slows the repolarization during phase 3

  • increases AP duration and ERP
  • will lengthen the QT interval
20
Q

Amiodarone

A

Class III (also has class I and beta blocking activity)
- prolongs AP (also potent Na blocker and weak beta blocker and Ca blocker –> slows HR and AV node conduction)
- causes peripheral vasodilation
Tox - bradychardia and heart block with preexisting SA or AV node disease, accumulates in tissues. Blocks peripheral conversion of thyroxine (T4) to Triiodothyronine (T3) and source of inorganic iodine
PK - hepatic metabolism –> bioactive metabolite. Has complex elimination which results in half life lasting 1-3 months. substrate for CYP3A4 –> can cause increased level of other drugs (warfarin)
TU - v tach, a fib or a flutter

21
Q

Most important adverse effect of amiodarone

A

dose related pulmonary toxicity

  • OTHERS
  • abnormal liver function
  • skin deposits –> photodermatitis
  • corneal microdeposits –> halos in peripheral visual fields
  • hypo- and hyperthyroidism
22
Q

Dofetilide

A

Class III
- selective K channel blocker, prolongs AP, increase QT interval
- Tox - life-threatening v arrhythmias
PK - 100% bioavailable, hepatic metabolism via CYP3A4
TU - maintenance and restoration of normal sinus rhythm in a fib. contraindicated in long QT, bradychardia, hypokalemia

23
Q

Ibutilide

A

Class III
- prolongs AP, also slows inward Na activator –> increases ERP
Tox - excessive QT interval prolongation –> torsades
PK - hepatic metabolism
TU - acute conversion of a flutter and fib to normal sinus rhythm (more effective in flutter)

24
Q

Class IV Drugs

A
  • bind to L-type Ca channels located in vascular smooth muscle, cardiac myocytes, and SA/AV node
  • smooth muscle = relaxation
  • cardiac myocytes = shortens phase 2 of AP, reduce force of contraction
  • nodal cells = decreased HR, decreased conduction velocity
  • DON’T give with a beta-blocker!!!!
25
Q

Class IV T.U.

A

Hypertension - decreases systemic TPR through smooth muscle relaxation (decrease radius means decrease pressure)
Angina - vasodilation and decrease HR (both decrease myocardial oxygen demand)
Arrhythmias - decrease pacemaker depolarization rate and decrease conduction velocity and prolong repolarization of AV node

26
Q

Dihydropyridines

A

Subclass of Class IV (blocks vascular L-type Ca channels)

  • selective for smooth muscle
  • primarily used to reduce TPR and BP
  • S.E. - flushing, headache, hypotension, edema, reflex tachychardia
27
Q

Non-dihydropyridines

A

Subclass of Class IV (blocks cardiac L-type Ca channels)

  • more cardiac specific
  • Verapamil or Diltiazem
28
Q

Verapamil

A

selective for myocardium, less effective as vasodilator
- has important role in treating angina and arrhythmias by reducing O2 demand
S.E. - AV block, constipation, nervousness, edema

29
Q

Diltiazem

A

intermediate between verapamil and dihyrdopyridines in selectively of Ca channels

  • can reduce arterial pressure without reflex tachychardia
  • S.E. - bradychardia, edema, dizziness, headache, fatigue
30
Q

Adenosine

A
  • activation of inward rectifier K channels and inhibition of L-type Ca channels
  • results in hyperpolarization and suppression of Ca dependent AP (nodal tissue)
  • drug of choice for prompt conversion of PSVT
    S.E. - flushing, headache, rapid arterial hypotension, AV block (contraindicated in block arrhythmias)
31
Q

Digitalis

A

Cardiac glycosides (primarily used for heart failure)
- useful in reducing ventricular rate
Activation of vagal efferents to heart –> reduce conduction in Av node –> partial block
Inhibits Na/K/ATP pump –> increases intracellular [Na] –> reverses action on Na/Ca exchanger –> more Ca in cell –> increases cardiac contractility –> decreases HR
SE - extreme AV block, contraindicated in patients with block or Wolff-Parkinson-White

32
Q

Myocardial O2 demands?

A

increase HR = increase O2 demand
increase contractility = increase O2 demand
increase arterial pressure = increase O2 demand
increased afterload = increase O2 demand

CRRAB 1 (18 decks)

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