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STEP 1 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Primary HTN Treatment

A

thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), dihydropyridine Ca2+ channel blockers

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2
Q

HTN with heart failure Treatment

A

Diuretics, ACE inhibitors/ARBs, Beta blockers (compensated HF), aldosterone antagonists

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3
Q

Heart failure and beta blockers caution

A

beta blockers must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock

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4
Q

HTN with Diabetes Mellitus Treatment

A

ACE inhibitors/ARBs, Ca2+ channel blockers, thiazide diuretics, beta blockers

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5
Q

ACEI/ARBs and DM

A

protective against diabetic nephropathy

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6
Q

HTN in pregnancy treatment

A

Hydralazine, labetalol, methyldopa, nifedipine

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7
Q

Name the dihydropyridine Ca2+ channel blockers

A

“-dipine) amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

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8
Q

Site of action of dihydropyridines

A

act on vascular smooth muscle amlodipine = nifedipine > diltiazem > verapamil

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9
Q

Name the non-dihydropyridines

A

diltiazem, verapamil

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10
Q

Site of action of the non-dihydropyridines

A

act on the heart verapamil > diltiazem > amlodipine = nifedipine Verapamil = ventricle

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11
Q

Mechanism of Ca2+ channel blockers

A

block voltage-dependent L-type Ca2+ channels of cardiac and smooth muscle –> decreased contractility

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12
Q

Use of dihydropyridines (except nimodipine)

A

hypertension, angina (including Prinzmetal), Raynaud phenomenon

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13
Q

Use of nimodipine

A

subarachnoid hemorrhage (prevents cerebral vasospasm)

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14
Q

Use of clevidipine

A

Hypertensive urgency or emergency

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15
Q

Use of non-dihydropyridines

A

hypertension, angina, atrial fibrillation/flutter

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16
Q

Mechanism of hydralazine

A

increase cGMP –> smooth muscle relaxation vasodilates arterioles > veins reduces afterload

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17
Q

Use of hydralazine

A

severe HTN (particularly acute, HF (with organic nitrate) safe to use in pregnancy frequently co-administered with beta-blocker to prevent reflex tachycardia

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18
Q

Toxicity of hydralazine

A

compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina Lupus like syndrome

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19
Q

Drugs to use in hypertensive emergency

A

Clevidipine (DHP Ca2+ channel blocker) Fenoldopam (D1 receptor agonist) Labetalol (beta blocker) Nicardipine (DHP Ca2+ channel blocker) Nitroprusside

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20
Q

Mechanism of nitroprusside

A

short acting to increase cGMP via direct release of NO

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21
Q

Toxicity of nitroprusside

A

can cause cyanide toxicity (release cyanide)

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22
Q

Mechanism of fenoldopam

A

Dopamine D1 receptor agonist - causes coronary, peripheral, renal and splanchnic vasodilation Decreases BP and causes a natriuresis

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23
Q

Name the nitrates

A

nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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24
Q

Mechanism of nitrates

A

vasodilate by increasing NO in vascular smooth muscle –> increase in cGMP and smooth muscle relaxation dilates veins >> arteries decreases preload

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25
Q

Use of nitrates

A

angina, acute coronary syndrome, pulmonary edema

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26
Q

Toxicity of nitrates

A

reflex tachycardia (treat with beta-blockers to prevent), hypotension, flushing, headache “Monday Disease” in industrial exposure

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27
Q

What is “Monday Disease”?

A

development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend –> tachycardia, dizziness, headache upon reexposure

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28
Q

Goal of antianginal therapy

A

reduce myocardial O2 consumption (MVO2) by decreasing 1 or more of these determinants: end-diastolic volume, BP, HR, or contractility

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29
Q

Nitrate effect on end-diastolic volume

A

decreases

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30
Q

Nitrate effect on blood pressure

A

decreases

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31
Q

Nitrate effect on contractility

A

NO EFFECT

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32
Q

Nitrate effect on heart rate

A

increase (reflex response) - give with beta blocker

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33
Q

Nitrate effect on ejection time

A

decreases

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34
Q

Nitrate effect on MVO2

A

decreases

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35
Q

Beta-blocker effect on end-diastolic volume

A

no effect or decrease slightly

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36
Q

Beta-blocker effect on blood pressure

A

decreases

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37
Q

Beta-blocker effect on contractility

A

decreases

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38
Q

Beta-blocker effect on heart rate

A

decreases

39
Q

Beta-blocker effect on ejection time

A

increases

40
Q

Beta-blocker effect on MVO2

A

decreases

41
Q

Combined effect of nitrates and beta-blockers on end-diastolic volume

A

no effect or decrease

42
Q

Combined effect of nitrates and beta-blockers on blood pressure

A

decreases

43
Q

Combined effect of nitrates and beta-blockers on contracility

A

little/no effect

44
Q

Combined effect of nitrates and beta-blockers on heart rate

A

no effect or decrease

45
Q

Combined effect of nitrates and beta-blockers on ejection time

A

little/no effect

46
Q

Combined effect of nitrates and beta-blockers on MVO2

A

decreases greatly

47
Q

What is digoxin?

A

a cardiac glycoside

48
Q

Mechanism of digoxin

A

direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchange increased Ca –> positive inotropy stimulates the vagus nerve –> decreased HR

49
Q

Use of digoxin

A

HF (to increase contractility); atrial fibrillation (to decrease conduction at AV node and depression of SA node)

50
Q

Toxicity of digoxin

A

Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block can lead to hyperkalemia –> poor prognosis

51
Q

Factors predisposing to digoxin toxicity

A

renal failure (decreased excretion) hypokalemia (permissive for digoxin binding at K+ binding site on Na/K ATPase) Verapamil, amiodarone Quinidine (decrease digoxin clearance; displaces digoxin from tissue binding sites)

52
Q

Antidote to digoxin

A

Anti-digoxin Fab fragments, slowly normalize K+, cardiac pacer, Mg2+

53
Q

Pharmacokinetic properties of class I antiarrhythmics

A

slow or block conduction (especially in depolarized cells) decrease slope of phase 0 depolarization are state dependent (selectively depress tissue that is frequently depolarized - e.g. tachycardial)

54
Q

Name the class IA antiarrhythmics

A

Block sodium channels Quinidine, Procainamide, Disopyramide

55
Q

Mechanism of class IA antiarrhythmics

A

increase AP duration increase effective refractory period (ERP) in ventricular action potential increase QT interval

56
Q

Use of class IA antiarrhythmics

A

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

57
Q

Toxicity of class IA antiarrhythmics

A

Cinchonism (headache, tinnitus with quinidine) Reversible SLE-like syndrome (procainamide) Heart failure (disopyramide) Thrombocytopenia, torsades de pointes due to increased QT interval

58
Q

Mechanism of class IB antiarrhythmics

A

decrease AP duration preferentially affect ischemic or depolarized Purkinje and ventricular tissue phenytoin can also fall into the IB category

59
Q

Name the class IB antiarrhythmics

A

Lidocaine, Mexiletine

60
Q

Use of class IB antiarrhythmics

A

acute ventricular arrhythmias (especially post-MI), digitalis induced arrhythmias IB is Best post-MI

61
Q

Toxicity of class IB antiarrhythmics

A

CNS stimulation/depression, cardiovascular depression

62
Q

Name the class IC antiarrhythmics

A

Flecainide, Propafenone

63
Q

Mechanism of class IC antiarrhythmics

A

significantly prolongs ERP in AV node and accessory bypass tracts no effect on ERP in Purkinje and ventricular tissue minimal effect on AP duration

64
Q

Use of class IC antiarrhythmics

A

SVTs, including atrial fibrillation only as a last resort in refractory VT

65
Q

Toxicity of class IC antiarrhythmics

A

PROARRHYTHMIC, especially post-MI (contraindicated) IC is CONTRAINDICATED in structural and ischemic heart disease

66
Q

What is site of action of class I antiarrhythmics?

A

Block Na channels

67
Q

What is site of action of class II antiarrhythmics?

A

Beta-blockers

68
Q

Name the class II antiarrhythmics

A

metoprolol, propranolol, esmolol (very short acting), atenolol, timolol, carvedilol

69
Q

Mechanism of class II antiarrhythmics

A

decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents suppress abnormal pacemakers by decreasing slope of phase 4 AV node particularly sensitive –> increased PR interval

70
Q

Use of class II antiarrhythmics

A

SVT, ventricular rate control for atrial fibrillation and atrial flutter

71
Q

Toxicity of class II antiarrhythmics

A

Impotence Exacerbation of COPD and asthma Cardiovascular side effects (bradycardia, AV block, HF) CNS effects (sedation, sleep alteration) - may mask signs of hypoglycemia

72
Q

Specific toxicity of metoprolol

A

causes dyslipidemia

73
Q

Specific toxicity of propranolol

A

can exacerbate vasospasm in Prinzmetal angina

74
Q

Careful with beta-blockers given alone

A

Beta-blockers cause unopposed alpha-agonism esp if given alone for pheochromocytoma or cocaine toxicity

75
Q

Treatment for beta-blocker overdose

A

saline, atropine and glucagon

76
Q

What is the site of action of class III antiarrhythmics?

A

block K+ channels

77
Q

Name the class III antiarrhythmics

A

amiodarone, ibutilide, dofetilide, sotolol

78
Q

Mechanism of class III antiarrhythmics

A

increase AP duration, increase ERP, increase QT interval

79
Q

Use of class III antiarrhythmics

A

atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone and sotolol)

80
Q

Toxicity of sotolol

A

torsades de pointes, excessive beta blockade

81
Q

Toxicity of ibutilide

A

torsades de pointes

82
Q

Toxicity of amiodarone

A

pulmonary fibrosis hepatotoxicity hypothyroidism/hyperthyroidism (40% iodine by weight) acts as hapten (corneal deposits, blue/gray skin deposits resulting in photodermatitis) neurologic effects constipation cardiovascular effects (bradycardia, heart block, HF)

83
Q

Special note about amiodarone

A

lipophilic and has class I, II, III and IV effects

84
Q

Labs needed when using amiodarone

A

monitor PFTs, LFTs and TFTs when using this drug

85
Q

What is site of action of class IV antiarrhythmics?

A

block Ca2+ channels

86
Q

Name the class IV antiarrhythmics

A

diltiazem and verapamil (Non-DHP)

87
Q

Mechanism of class IV antiarrhythmics

A

decrease conduction velocity, increase ERP, increase PR interval

88
Q

Use of class IV antiarrhythmics

A

prevention of nodal arrhythmia (e.g. SVT), rate control in atrial fibrillation

89
Q

Toxicity of class IV antiarrhythmics

A

constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression)

90
Q

Mechanism of adenosine

A

increase K+ out of cells –> hyperpolarizing the cell and decreasing Ica

91
Q

Use of adenosine

A

drug of choice in diagnosing/abolishing supraventricular tachycardia

92
Q

Pharmacokinetics of adenosince

A

very short acting (~15 seconds) effects blunted by theophylline and caffeine (both are adenosine receptor antagonists)

93
Q

Side effects of adenosine

A

flushing, hypotension, chest pain, sense of impending doom, bronchospasm

94
Q

Use of Mg2+

A

effective in torsades des pointes and digoxin toxicity

STEP 1 (26 decks)

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