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First Aid > cardio drugs > Flashcards

cardio drugs Flashcards

1
Q

primary essential HTN treatment

A

diuretics, ACE inh, ARBs, Ca2+ channel blockers

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2
Q

HTN with CHF treatment

A

diuretics, ACE inh, ARBs, beta-blockers (compensated CHF, not decompensated or cardiogenic shock), aldosterone antagonists

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3
Q

HTN with DM treatment

A

ACE inhibitors/ARBs, Ca2+ channel blockers, diuretics, beta-blockers, alpha-blockers

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4
Q

MOA of calcium channel blockers

A

block the V-dep L-type Ca++ channels of cardiac and smooth muscle –> reduce muscle contractility

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5
Q

which ca++ channel blockers work on the vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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6
Q

which ca++ channel blockers work on the heart?

A

verapamil > diltiazem > amlodipine = nifedipine

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7
Q

clinical use of ca++ channel blockers

A

dihydropyridine (except nimodipine): HTN, angina, raynauds
non-dihydropyridine: HTN, angina, atrial fibrillation/flutter
nimodipine: subarachnoid hemorrhage

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8
Q

toxicity of ca++ channel blockers

A

cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

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9
Q

amlodipine

A

dihydropine ca++ channel blocker

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10
Q

nimodipine

A

dihydropine ca++ channel blocker

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11
Q

nifedipine

A

dihydropine ca++ channel blocker

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12
Q

diltiazem

A

non-dihydropine ca++ channel blocker

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13
Q

verapamil

A

non-dihydropine ca++ channel blocker

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14
Q

hydralazine MOA

A

inc cGMP –> smooth muscle relaxation, vasodilates arterioles > veins; afterload reductino

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15
Q

clinical use of hydralazine

A

severe HTN, CHF, first line for HTN in pregnancy, methyldopa, with beta blockers to prevent reflex tach

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16
Q

toxicity of hydralazine

A

compensatory tach, fluid retention, nausea, headache, angina, lupus like syndrome

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17
Q

hypertensive emergency drugs

A

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

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18
Q

nitroprusside

A

SA
increase cGMP via NO
may cause CN tox beause it releases CN

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19
Q

fenoldopam

A

D1R agaonist - oronary, peripheral, renal and splanchnic vasodilation, decrease BP and natriuresis

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20
Q

MOA of nitroglycerin and isosorbide dinitrate

A

vasodilate via increase NO in vascular smooth muscles –> increased cGMP and smooth muscle relaxation
dilates veins more than arteries
decreased preload

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21
Q

clinical use of nitroglycerin and isosorbide dinitrate

A

angina, ACS, PE

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22
Q

nitroglycerine and isosorbide dinitrate toxicity

A

reflex tach, hypoTN, flushing, headache

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23
Q

MOA of HMG - CoA reductase inhibitors

A

inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

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24
Q

Side effects of statins

A

hepatotoxicity

rhabdomyolysis

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25
Q

MOA of niacin

A

inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis

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26
Q

Side effects of niacin

A

red flushed face which is decreased with aspirin or long term use
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)

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27
Q

what are the bile acid resins?

A

cholestyramine, colestipol, colesevelam

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28
Q

MOA of bile acid resins

A

prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more

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29
Q

side effects of bile acid resins

A

tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, cholesterol gallstones

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30
Q

MOA of fibrates

A

upregulates LPL leading to TG clearance

activates PPAR-a to induce HDL synthesis

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31
Q

side effects of fibrates

A

myositis (increased risk of concurrent statins)
hepatotoxicity
cholesterol gallstones

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32
Q

cardiac glycoside drug

A

digoxin

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33
Q

moa of cardiac glycoside

A

direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca++ exchanger/antiport –> increased intracellular calcium –> positive inotropy –> vagus nerve stimulation –> decreased HR

34
Q

clinical use of cardiac glycosides

A

CHF, atrial fib

35
Q

toxicity of cardiac glycosides

A

cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, hyperkalemia

36
Q

what does ECG show with cardiac glycoside use?

A 
increased PR
decreased QT
ST scooping
T wave inversion
arrhythmia
AV block
37
Q

what factors predispose to toxicity

A

renal failure, hypokalemia, verapamil, amiodarone, quinidine

38
Q

antidote to cardiac glycoside use

A

slowly normalize k+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

39
Q

quinidine

A

class 1a

40
Q

procainamide

A

class 1a

41
Q

disopyramide

A

class 1a

42
Q

lidocaine

A

class 1b

43
Q

mexiletine

A

class 1b

44
Q

flecainide

A

class 1c

45
Q

propafenone

A

class 1c

46
Q

metoprolol

A

class 2

47
Q

propranolol

A

class 2

48
Q

esmolol

A

class 2

49
Q

atenolol

A

class 2

50
Q

timolol

A

class 2

51
Q

carvedilol

A

class 2

52
Q

amiodarone

A

class 3

53
Q

ibutilide

A

class 3

54
Q

dofetilide

A

class 3

55
Q

sotalol

A

class 3

56
Q

verapamil

A

class 4

57
Q

diltiazem

A

class 4

58
Q

class 1 antiarrhythmics moa

A

Na+ channel blockers, slow or block conduction
decrease slope of phase 0 depolarization and increased threshold for firing in abnormal pacemaker cells
state dependent
hyperkalemia causes increased toxicity

59
Q

moa of class 1a

A

increased AP duration, increased effective refractory period, increased QT

60
Q

clinical use of class 1a

A

both atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT

61
Q

toxicity of class 1a

A

cinchonism, reversible SLE like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de points due to increased QT

62
Q

MOA of class 1b

A

Myositis (increased risk of concurrent statins)
hepatotoxicity
cholesterol gallstones

63
Q

clinical use of class 1b

A

acute ventricular arrhythmias, digitalis induced arrhythmias. Best post-MI

64
Q

toxicity

A

CNS stimulation/depression, cardiovascular depression

65
Q

MOA of class 1c

A

prolongs refractory period in AV node

minimal effect on AP duration

66
Q

clinical use of class 1c

A

SVTs, including atrial fib last resort in refractory VT

67
Q

toxicity of class 1c

A

proarrhythmic, especially post-MI contraindicated in structural and ischemic heart disease

68
Q

MOA of class 2

A

decrease SA and AV nodal activity by decreasing cAMP and ca++ currents
suppresses abnormal pacemaker by decreasing slope of phase 4

69
Q

clinical use of class 2

A

SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

70
Q

toxicity of class 2

A 
impotence
COPD, asthma exacerbation
cardiovascular effects, CNS effects
metoprolol: dyslipidemia
propanolol: exacerbates vasospasm in Prinzmetal angina
contraindiated in cocaine users
71
Q

how do you treat class 2 overdose?

A

glucagon

72
Q

class 3 moa

A

K+ channel blocker
AP duration increase with increased ERP
increase QT

73
Q

clinical use of class 3

A

atrial fibrillation, atrial flutter, ventricular tach (amiodarone, sotalol)

74
Q

toxicity of sotalol

A

torsades de points, excessive beta blockade

75
Q

toxicity of ibutilide

A

torsades de points

76
Q

toxicity of amiodarone

A

pulmonary fibrosis, hepatotoxicity, hypothyroidism, hyperthyroidism, corneal deposits, skin deposits, photodermatitis, neurological effects, constipation, cardiovascular effects

77
Q

moa of class 4

A

ca++ channel blocker, decreased conduction velocity, increased ERP, PR interval increase

78
Q

clinical use of class 4

A

prevention of nodal arrhythmias, rate control in atrial fibrillation

79
Q

toxicity of class 4

A

constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

80
Q

what are the other antiarrhythmics

A

adenosine, Mg++

81
Q

adenosine

A

increased K+ out of cells –> hyperpolarizing the cell and decreasing calcium current
used for diagnosing and abolishing supraventricular tachycardia
very short acting (15 seconds)
adverse effects: flushing, hypotension, chest pain
effects blocked by theophylline and caffeine

82
Q

mg2+

A

effective in torsades de points and digoxin

First Aid (23 decks)

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