CARDIO - drugs Flashcards
Primary HTN rx
ACEI, ARB, Thiazide, CCB
HTN with HF rx
ACEI, ARB, Diuretics, aldosterone antagonists, b-blockers
HTN with DM
ACEI, ARB, Thiazide, CCB, b-blocker
HTN in pregnancy
Hydralazine, methyldopa, labetalol, nifedipine
methyldopa AE
HTN pregnancy
a2 agonist
SLE-like
Coombs +
hydralazine AE
SLE-like
CCB’s block:
L-type VG Ca channels of cardiac and smooth muscle
general CCB dihydropyridine use
HTN, angina (including prizmetal), raynaud
CCB for SAH
Nimodipine (cerebral selectivity)
CCB for hypertensive urgency/emergency
Clevidipine and nicardipine
General non-dihydropyridine CCB use
HTN, angina, atrial fib/flutter
Verapamil AE
hyperprolactinemia
General CCB AE
constipation, gingival hyperplasia
hydralazine MOA
increases cGMP causing vasodilation of arteries > veins. Can cause reflex tachycardia so can give with b-blocker, also avoid in angina/CAD
Hydralazine use
acute/severe HTN, HTN pregnancy, HTN HF
HTN emergencies
Clevidipine, nicardipine, labetalol, fenoldopam, nitroprusside
CCB for pregnancy
Nifedipine
Nitroprusside MOA and AE
MOA = release of NO causing increased cGMP.
AE = cyanide poisoning
Fenoldopam
D1 agonist - vasodilation of coronaries, renal, peripheral, splanchnic - keep up naturesis
nitrates MOA
Release NO causing cGMP, veins > arteries, decreases preload
nitrates AE
Hypotension, reflex tachycardia, headache, flushing
Digoxin MOA (2)
Direct block Na//K; indirect block Na//Ca; so increased contractility.
Stimulates vagus to decrease HR.
Digoxin use
HF for contractility
A fib for slowed AV and depressed SA
Digoxin toxicity
Cholinergic: blurry yellow vision, arrhythmia, AV block.
Hyperkalemia.
Increase digoxin toxicity via:
Hypokalemia, renal failure, verapamil, amiodarone, quinidine (decrease clearance + displaces from tissue)
Digoxin antedote
fix K+, Mg, anti-digoxin Fab, pacer
Class I AA MOA
block Na+ channels slowing conduction, especially in depolarized muscle cells
Class IA names
Disopyramide, Quinidine, Procainamine
Class 1B names
Lidocaine, Tocainide, Mexiletine
Class 1C names
Flecainide, Propafenone, Moricizine
Class 1A AE
Cinchonism (quinidine - HA, tinnitus), SLE-like (procainamide), heart failure (disopyramide), thrombocytopenia, torsades
Post MI acute ventricular arrhythmia rx (class)
Class 1B
Class 1C AE
pro-arrythmic (especially post-MI)
Class 1 affinities for phase 0 inhibition
A = intermediate, B = weak, C = strongest
Class 1 alterations in QT (AP duration)
A = increase, B = decrease, C = N/A
Class II: group and specific AEs
beta blockers. Metoprolol = dyslipidemia. Propanolol = prizmetal exacerbation
Phase of AP altered by Class II
Phase 4 (Ca channels of nodal tissue)
Class III: names and function
K+ blockers, increasing AP, ERP, QT.
Amiodarone, Ibutilide, Dofetilide, Sotalol.
Sotalol AE
Torsades, excessive beta blockade (K+ and Na+ blocker)
Ibutilide AE
Torsades
Amiodarone AE
*NO torsades!
PULMONARY FIBROSIS, hepatotoxicity, hypo/hyper-thyroidism and blue-grey skin in sun (via iodine content), neurological, constipation.
Check LFTs, TFTs, PFTs
Class IV names
CCBs verapamil and diltiazem
Class IV mechanism
Decrease conduction velocity. Increase ERP and PR
Class IV
constipation (verapamil), flushing, edema
Adenosine use in cardio
Diagnosing/abolishing SVTs (including paroxysmal SVTs)
Blunting adenosine via:
theophylline and caffeine
Adenosine AE
Flushing, hypotension, sense of impending doom, bronchospasm, chest pain
Mg++ in cardio treats
Torsades, digoxin toxicity (because it antagonizes Ca)
drugs causing kyperkalemia:
ACE-I.
ARB.
K+ sparing diuretics.
Digoxin.
Non-selective beta antag (b2 causes intracellular uptake).
NSAIDs (block PG, decrease renin + aldost.)
