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STEP 1 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

(94 cards)

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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
Use of nitrates
angina, acute coronary syndrome, pulmonary edema
26
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
28
Goal of antianginal therapy
reduce myocardial O2 consumption (MVO2) by decreasing 1 or more of these determinants: end-diastolic volume, BP, HR, or contractility
29
Nitrate effect on end-diastolic volume
decreases
30
Nitrate effect on blood pressure
decreases
31
Nitrate effect on contractility
NO EFFECT
32
Nitrate effect on heart rate
increase (reflex response) - give with beta blocker
33
Nitrate effect on ejection time
decreases
34
Nitrate effect on MVO2
decreases
35
Beta-blocker effect on end-diastolic volume
no effect or decrease slightly
36
Beta-blocker effect on blood pressure
decreases
37
Beta-blocker effect on contractility
decreases
38
Beta-blocker effect on heart rate
decreases
39
Beta-blocker effect on ejection time
increases
40
Beta-blocker effect on MVO2
decreases
41
Combined effect of nitrates and beta-blockers on end-diastolic volume
no effect or decrease
42
Combined effect of nitrates and beta-blockers on blood pressure
decreases
43
Combined effect of nitrates and beta-blockers on contracility
little/no effect
44
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
48
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
49
Use of digoxin
HF (to increase contractility); atrial fibrillation (to decrease conduction at AV node and depression of SA node)
50
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+
53
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)
54
Name the class IA antiarrhythmics
Block sodium channels Quinidine, Procainamide, Disopyramide
55
Mechanism of class IA antiarrhythmics
increase AP duration increase effective refractory period (ERP) in ventricular action potential increase QT interval ![]()
56
Use of class IA antiarrhythmics
both atrial and ventricular arrhythmias especially reentrant and ectopic SVT and VT
57
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
58
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 ![]()
59
Name the class IB antiarrhythmics
Lidocaine, Mexiletine
60
Use of class IB antiarrhythmics
acute ventricular arrhythmias (especially post-MI), digitalis induced arrhythmias IB is Best post-MI
61
Toxicity of class IB antiarrhythmics
CNS stimulation/depression, cardiovascular depression
62
Name the class IC antiarrhythmics
Flecainide, Propafenone
63
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 ![]() ![]()
64
Use of class IC antiarrhythmics
SVTs, including atrial fibrillation only as a last resort in refractory VT
65
Toxicity of class IC antiarrhythmics
PROARRHYTHMIC, especially post-MI (contraindicated) IC is CONTRAINDICATED in structural and ischemic heart disease
66
What is site of action of class I antiarrhythmics?
Block Na channels
67
What is site of action of class II antiarrhythmics?
Beta-blockers
68
Name the class II antiarrhythmics
metoprolol, propranolol, esmolol (very short acting), atenolol, timolol, carvedilol
69
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 ![]()
70
Use of class II antiarrhythmics
SVT, ventricular rate control for atrial fibrillation and atrial flutter
71
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
73
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
77
Name the class III antiarrhythmics
amiodarone, ibutilide, dofetilide, sotolol
78
Mechanism of class III antiarrhythmics
increase AP duration, increase ERP, increase QT interval ![]()
79
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

STEP 1 (26 decks)

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