Antiarrhythmatic Drugs and CHF Flashcards

1
Q

Therapeutic Mechanism of Quinidine?

A

1) Block Na+ channels- decreases excitability and decreases conduction velocity in fast tissue.
2) Block K+ channels- prolonged refractory period which can inhibit reentry arrhythmias.

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2
Q

Cardiotoxic effect of quinidine

A

Risk of arrhythmias increases with lengthening of QRS and Q-T intervals.

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3
Q

Most common cardiac side effect of quinidine is quinidine syncope: Describe…

A

Lightheadedness and fainting caused by quinidine-induced torsade de pointes. Usually resolves but can degenrate into ventricular fibrillation.

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4
Q

Extracardiac side effects of quinidine

A

GI disturbances, cinchonism (tinnitus, dizziness, blurred vision, headaches), and rerely thrombocytopenia, hepatitis, angiodema, fever.

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5
Q

Actions of K+ channel blockade:

A

Lengthens action potentials which lengthens refractory period and can therefore interrupt re-entry arrhythmias.

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6
Q

ECG of K+ channel blockers:

A

Lengthened Q-T interval

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7
Q

Cardiac Side Effects of K+ channel blockers

A

Torsade de pointe- lengthened AP can produce early after- depolarization

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8
Q

K+channel blockers:

A

Quinidine, NAPA (procainamide metabolite), sotalol, dofetilide

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9
Q

Uses of Ca2+ channel inhibition

A

Reduces excitability of slow AV nodal and SA nodal tissue. Used for reducing ventricular rate during atrial tachyarrhythmias.

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10
Q

ECG changes with Ca2+ channel inhibition

A

Lengthened P-R interval

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11
Q

Cardiac Side effects for Ca2+ channel inhibition

A
  • SA and AV nodal block- beta blockers (propranolol), sotalol, Calcium channel blockers (diltiazem and verapemil), amioderone
  • Negative inotropic effect- beta blockers, calcium channel blockers
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12
Q

NA+ channel inhibition uses:

A

Inhibits excitability in fast tissue, used principally for ventricular or supra-ventricular arrhythmias involving fast tissue.

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13
Q

ECG changes in Na+ channel inhibition

A

Lengthened QRS (except lidocaine)

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14
Q

Cardiac side effects for NA+ channel blockers

A

Can cause arrhythmias (especially potent Na channel blockers such as flecainimide)

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15
Q

Class 1a: Na+ and K+ channel block drug

A

Quinidine- Weak anti muscarinic

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16
Q

Class 1a: Na+ channel blocker:

A

Procainamide- weaker K channel blocker (NAPA) and muscarinic block than quinidine

17
Q

SE of Procainamide:

A

Hypotension, lupus, GI disturbances, hepatitis, fever. Rare agranulocytosis and rash.

18
Q

Class 1B Drug that blocks NA+ channels in depolarized tissue

A

Lidocaine- little effect on healthy tissue

19
Q

Half life of lidocaine:

A

1-2 hours; IV or IM

20
Q

Side effects of lidocaine

A

CNS ( paresthesis, drowsiness, tinnitus, blurred vision; toxic levels: convulsions, unconsciousness, respiratory arrest).

21
Q

Class 1c potent and selective Na+ channel blocker

A

Flecainamide

22
Q

SE of Flecainamide

A

Significantly pro-arrhythmic, enhanced risk of death with long term use

23
Q

Class II: Beta-adrenergic receptor blockade drug

A

Propranolol- Beta blockers reduce beta stimulation of Ca channels and thus act much like Ca channel blockers

24
Q

Side effects of propranolol

A
  • SA and AV block,
  • Sudden withdrawal may worsen angina and arrhythmias due to receptor up-regulation,
  • shortness of breath
25
Class III: K+ channel block drug
Amiodarone- K channel block, Ca channel block, use-dependent block of Na channels, alpha and beta receptor block
26
Side Effects of Amiodarone
1) Corneal and skin deposits 2) GI disturbances 3) Neurological SE 4) Hypotension (due to Ca Channel block) 5) Life-threatening pulmonary toxicity 6) Liver toxicity 7) Thyroid dysfunction
27
Half life of amiodarone
Long (Up to 3 months)
28
Drug interactions of amiodorone
- SA/AV block when combined with Ca channel blockers or beta blockers. - Increases plasma level of many anti-arrythmic drugs
29
A K channel blocker and beta blocker
Sotalol
30
K channel blocker SE of Sotalol
Torsades de pointes
31
Beta blocker SE of Sotalol
SA and AV block, sudden withdrawal may worsen angina and arrhythmias due to receptor up-regulation, shortness of breath
32
K- Channel Blocker causing Torsades de Pointes
Dofetilide
33
Class IV: Ca2+ channel blockade drugs
Verapamil and diltiazem
34
SE of Verapamil and diltiazem
1) SA or AV block 2) Negative inotropic effect 3) Constipation (inhibition of gut motility) 4) Peripheral edema (vasodilation from Ca blockers) 5) CNS effects (lassitude, vervousness, dizziness, headache).
35
IV half life of Verapamil and diltiazem
4 minutes
36
Activation of adenosine does what?
Activates K+ channels to hyperpolarize AV nodal tissue by opening K+ channels. Short time of action (seconds)
37
Therapeutic effect of digoxin
Positive inotropic effect
38
Mechanism of digoxin
1) Direct membrane effect: inhibits Na/K ATPase | 2) Indirect effect: Parasympathomimetic