Cardiovascular Drugs Flashcards

1
Q

What is arrhythmia?

A

alteration in normal impulse pathway

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2
Q

Name major cause of sudden cardiac death.

A

ventricular fibrillation

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3
Q

what is cardioversion?

A

global depolarization of heart to reset heart beat. Can be achieved via defibrillation

automatic defibrillators can be implanted

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4
Q

radiofrequency ablation accomplishes what?

A

the removal of ectopic foci - points that induce abnormal electrical signals in the heart

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5
Q

Do antiarrhhythmic drugs affect ectopic or normal foci more?

A

ectopic

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6
Q

What class of drug is quinidine?

Treats which arrhythmias?

range of effectiveness?

SEs?

A

class Ia sodium channel blocker

effective in treating all arrhythmias

depresses all muscle function

SEs:

  • GI upset
  • Nausea
  • Anorexia
  • CNS: tinnitus, altered color vision
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7
Q

Which class of drug is Procainamide?

Treats which arrhythmias?

analog of what?

Does it enter CNS?

Notable SE?

A

class: Ia sodium channel blocker

Treats: all arrhythmia

analog of Procaine

DOES NOT enter CNS

SE: in slow acetylators, lupus-like syndrome

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8
Q

Disopyramide is what class of drug?

Effects?

used to treat which type of arrhythmias?

A

class: sodium channel blocker

strong anti-vagal effects aka anti-muscarinic effect (opposite of DUMBBELS)

treats: ventricular arrythmias

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9
Q

Lidocaine is what class of drug?

Lidocaine is the DOC for what?

Does Lidocaine enter the CNS?

SEs?

A

class Ib sodium channel blocker

DOC for ventricular tacchycardia
less likely to cause arrhythmias

Yes, it does enter CNS

CNS SEs:

  • tremors
  • seizures
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10
Q

Mexiletine is similar to what other sodium channel blocker?

A

Lidocaine and also is a class Ib sodium channel blocker

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11
Q

Name the 5 sodium channel blockers used to treat arrythmias

A

Procainamide - all arrhythmias
quinidine - all arrhythmias

disopyramide - ventricular arrhythmias
lidocaine - ventricular tachycardia

mexiletine - not specified

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12
Q

Name 3 beta blockers used to treat arrhythmia and additional characteristics of each.

MOA?

SEs?

A

Propanolol: also affects beta2, decreases pacemaker firing rate

Osmolol: rapid onset

Metoprolol: more selective, less beta2 effect

MOA: block beta-1 receptors in heart - effectively slows HR

SEs:
-hypotension
if beta 2 affect: asthma concerns

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13
Q

What are the K+ channel blockers used?

A

atrial fibrillation

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14
Q

name 3 potassium channel blockers used for atrial fibrillation and characteristics / SEs of each

A

Sotalol: beta blocker that also blocks potassium channels

Amiodarone: acts like all 4 antiarrhythmic drug classes
-most effective: DOC for cardiac arrest
-contains iodine
SEs:
-potentially fatal pulmonary fibrosis
-liver damage
-corneal deposits --> optic neuritis
-skin deposits --> blue skin coloration (iodine)
-GI upset

Dronedarone:

  • analog of amiodarone
  • fewer SEs, less efficacy
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15
Q

Name 3 calcium channel blockers used to treat arrhythmia.

What is their effect on cardiac cells?

For which arrhythmia type are they useful?

A

Diltrazem
nifedipine
verapamil

increase refractory period

NOT useful for ventricular arrhythmia

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16
Q

How does adenoside work?

What is its effect?

For what is it used?

A

binds adenosine receptor -> slows AV node

serves as coronary vasodilator

used for atrial tachycardia and disappears quickly

17
Q

how is angina treated?

A

increasing blood flow to heart or by decreasing O2 demand

nitrates - nitroglycerin (GTN)
-rapid dilation of all blood vessels

exercise - increase collateral circulation

isosorbide dinitrate - slow release nitrate formulation (oral admin b/c slow release off sets first pass of GTN)

beta blockers

calcium channel blockers

18
Q

For what is nitroglycerin used?

MOA?

Side Effects?

A

angina, life threatening hypertension

GTN -> NO -> activates guanylate cyclase -> cGMP (vasodilator)

SEs:

  • hypotension
  • flushing of skin
  • headache

Tachyphylaxis - rapid tolerance

19
Q

How does the heart adapt to congestive heart failure?

A

heart enlarges, blood backs up at lungs -> pulmonary congestion -> decreased ability to breathe

release of EPI, NE, AngII to increase HR, BP, vasoconstriction

increase blood vol via AngII -> increase in Na+ retention and activation of of Na+ / K+ exchanger

20
Q

Ionotropic agents are used to treat what?

What is the logic behind their use?

Examples include?

A

tx for cardiac insufficiency

ions such as Ca2+ are essential to cardiac contraction. If you increase Ca2+, you increase contractility and can compensate for cardiac insufficiency.

examples:

the cardiac glycoside digoxin

dobutamine: strong ionotropic effect: increased force of contraction

21
Q

Explain out loud to yourself in front of a bunch of people with your hands above your head while hyperventilating how digoxin works.

Toxicities?

A

cardiac glycosides inhibit Na+ - K+ ATPase -> Na+ remains high in the cell. This inhibits Na+ / Ca2+ exchanger ultimately preventing the loss of Ca2+. Calcium inside the membrane remains high = greater contractility

Toxicities:
-heart: arrhythmia (increased vagal tone
-CNS: yellow / green vision, hallucinations, CTZ = nausea and vomiting (monarchs)
effect of digoxin is greatly increased by hypokalemia

22
Q

What is ultimately the best tx for congestive heart failure?

Name the drugs!

A

any agent that inhibits the body’s attempt to compensate:

  • beta / alpha blockers
  • ACE inhibitors
  • diuretics
  • vasodilators
23
Q

Name the 3 oral drugs for erectile dysfuntion

MOA?

Should not be taken with?

SEs?

Metabolized by?

A

sildenafil
vardenafil
tadalafil

inhibit type 5 cGMP phosphodiesterase -> increase in cGMP -> vasodilation in arteries of corpus cavernosum

Should NOT be taken with alpha1 blockers or nitrates (too much dilation doeee)

SEs:

  • slight BP decrease
  • blue-green vision
  • NAION - retinal damage from cGMP PDE inhibitors
  • stroke
  • myocardial infarction

metabolized by P450

24
Q

Name an injectable PGE1 used to treat erectile dysfuntion

A

alprostadil