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Flashcards in Cardiovascular Drugs Deck (94)
1

Primary HTN Treatment

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

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HTN with heart failure Treatment

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

3

Heart failure and beta blockers caution

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

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HTN with Diabetes Mellitus Treatment

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

5

ACEI/ARBs and DM

protective against diabetic nephropathy

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HTN in pregnancy treatment

Hydralazine, labetalol, methyldopa, nifedipine

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Name the dihydropyridine Ca2+ channel blockers

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

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Site of action of dihydropyridines

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

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Name the non-dihydropyridines

diltiazem, verapamil

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Site of action of the non-dihydropyridines

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

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Mechanism of Ca2+ channel blockers

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

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Use of dihydropyridines (except nimodipine)

hypertension, angina (including Prinzmetal), Raynaud phenomenon

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Use of nimodipine

subarachnoid hemorrhage (prevents cerebral vasospasm)

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Use of clevidipine

Hypertensive urgency or emergency

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Use of non-dihydropyridines

hypertension, angina, atrial fibrillation/flutter

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Mechanism of hydralazine

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

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Use of hydralazine

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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Toxicity of hydralazine

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

19

Drugs to use in hypertensive emergency

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

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Mechanism of nitroprusside

short acting to increase cGMP via direct release of NO

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Toxicity of nitroprusside

can cause cyanide toxicity (release cyanide)

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Mechanism of fenoldopam

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

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Name the nitrates

nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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Mechanism of nitrates

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

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Use of nitrates

angina, acute coronary syndrome, pulmonary edema

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Toxicity of nitrates

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

27

What is "Monday Disease"?

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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Goal of antianginal therapy

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

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Nitrate effect on end-diastolic volume

decreases

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Nitrate effect on blood pressure

decreases

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Nitrate effect on contractility

NO EFFECT

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Nitrate effect on heart rate

increase (reflex response) - give with beta blocker

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Nitrate effect on ejection time

decreases

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Nitrate effect on MVO2

decreases

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Beta-blocker effect on end-diastolic volume

no effect or decrease slightly

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Beta-blocker effect on blood pressure

decreases

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Beta-blocker effect on contractility

decreases

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Beta-blocker effect on heart rate

decreases

39

Beta-blocker effect on ejection time

increases

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Beta-blocker effect on MVO2

decreases

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

no effect or decrease

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Combined effect of nitrates and beta-blockers on blood pressure

decreases

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Combined effect of nitrates and beta-blockers on contracility

little/no effect

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Combined effect of nitrates and beta-blockers on heart rate

no effect or decrease

45

Combined effect of nitrates and beta-blockers on ejection time

little/no effect

46

Combined effect of nitrates and beta-blockers on MVO2

decreases greatly

47

What is digoxin?

a cardiac glycoside

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Mechanism of digoxin

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

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Use of digoxin

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

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Toxicity of digoxin

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

51

Factors predisposing to digoxin toxicity

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

Antidote to digoxin

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

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Pharmacokinetic properties of class I antiarrhythmics

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)

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Name the class IA antiarrhythmics

Block sodium channels Quinidine, Procainamide, Disopyramide

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Mechanism of class IA antiarrhythmics

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

 

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Use of class IA antiarrhythmics

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

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Toxicity of class IA antiarrhythmics

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

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Mechanism of class IB antiarrhythmics

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

 

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Name the class IB antiarrhythmics

Lidocaine, Mexiletine

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Use of class IB antiarrhythmics

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

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Toxicity of class IB antiarrhythmics

CNS stimulation/depression, cardiovascular depression

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Name the class IC antiarrhythmics

Flecainide, Propafenone

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Mechanism of class IC antiarrhythmics

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

 

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Use of class IC antiarrhythmics

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

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Toxicity of class IC antiarrhythmics

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

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What is site of action of class I antiarrhythmics?

Block Na channels

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What is site of action of class II antiarrhythmics?

Beta-blockers

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Name the class II antiarrhythmics

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

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Mechanism of class II antiarrhythmics

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

 

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Use of class II antiarrhythmics

SVT, ventricular rate control for atrial fibrillation and atrial flutter

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Toxicity of class II antiarrhythmics

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

72

Specific toxicity of metoprolol

causes dyslipidemia

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Specific toxicity of propranolol

can exacerbate vasospasm in Prinzmetal angina

74

Careful with beta-blockers given alone

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

75

Treatment for beta-blocker overdose

saline, atropine and glucagon

76

What is the site of action of class III antiarrhythmics?

block K+ channels

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Name the class III antiarrhythmics

amiodarone, ibutilide, dofetilide, sotolol

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Mechanism of class III antiarrhythmics

increase AP duration, increase ERP, increase QT interval

 

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Use of class III antiarrhythmics

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

80

Toxicity of sotolol

torsades de pointes, excessive beta blockade

81

Toxicity of ibutilide

torsades de pointes

82

Toxicity of amiodarone

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

Special note about amiodarone

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

84

Labs needed when using amiodarone

monitor PFTs, LFTs and TFTs when using this drug

85

What is site of action of class IV antiarrhythmics?

block Ca2+ channels

86

Name the class IV antiarrhythmics

diltiazem and verapamil (Non-DHP)

87

Mechanism of class IV antiarrhythmics

decrease conduction velocity, increase ERP, increase PR interval

 

88

Use of class IV antiarrhythmics

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

89

Toxicity of class IV antiarrhythmics

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

90

Mechanism of adenosine

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

91

Use of adenosine

drug of choice in diagnosing/abolishing supraventricular tachycardia

92

Pharmacokinetics of adenosince

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

93

Side effects of adenosine

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

94

Use of Mg2+

effective in torsades des pointes and digoxin toxicity