Step 1 cardiac drugs Flashcards
hydralazine mechanism
increases cGMP–smooth muscle relaxation; arterial dilator, reduces afterload
hydralazine use
severe hypertension, CHF; first line for HTN in pregnancy with methyldopa
hydralazine coadministered with what? Why?
beta blocker; to prevent reflex tachycardia
hydralazine toxicity
headaches, nausea, fluid retention, reflex tachycardia, angina, LUPUS LIKE SYNDROME
Ca channel blockers
nifedipine, verapamil, diltiazem
Ca channel blocker mechanism
block voltage dependent L-type Ca channels of cardiac and smooth muscle–reduce contractility
affinity of Ca channel blockers
heart: verapamil > diltiazem > nifedipine
Ca channel blocker use
hypertension, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s
Ca channel blocker toxicity
cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
nitroglycerin, isosorbide dinitrate mechanism
release of NO in smooth muscle causes increase in cGMP and smooth muscle relaxation; dilates veins more than arteries; decreases preload
nitroglycerin, isosorbide dinitrate use
angina, pulmonary edema; aphrodesiac and erection enhancer
nitroglycerin, isosorbide dinitrate toxicity
reflex tachycardia, hypotension, flushing, headache, “Monday disease”
drugs for malignant hypertension
nitroprusside, fenaldopam, diazoxide
nitroprusside mechanism
increase cGMP via direct release of NO
nitroprusside toxicity
releases cyanide (so can cause toxicity)
fenaldopam mechanism
dopamine D1 receptor agonist–relaxes renal vascular smooth muscle, splanchnic, peripheral and coronary vessels
diazoxide mechanism
opens K channels–hyperpolarizes cell and relax vascular smooth muscle
diazoxide toxicity
hyperglycemia (because it reduces insulin release)
class II antiarrhythmic drugs
beta blockers–timolol, propanolol, metoprolol, atenolol, esmolol
class II antiarrhythmic mechanism
decrease sympathetic tone, slow AV nodal conduction (decreases cAMP and Ca); decrease slope of Phase 4–increase PR interval
class II anti-arrhythmic use
V-tach, slowing ventricular rate during atrial fib and flutter (remember they only act on the ventricle!)
class II antiarrhythmic toxicity
impotence, exacerbation of asthma, bradycardia, AV block, sedation, sleep disturbances, mask hypoglycemia, metoprolol can cause dylipidemia
class 1a antiarrhythmics
procainamide, quinidine, disopyramide
class 1a antiarrhythmic mechanism
Na channel blockers, Phase 0 and 3–slow both; intermediate channel blockers; prolong QT and increase refractory period increase AP duration; also have some action at K channels
class 1a antiarrhythmic toxicity
arrhythmias (from long QT), procainamide can cause SLE like syndrome, quinidine–cinochism—tinnitus and headache), thrombocytopenia
class 1a antiarrhythmic uses
atrial and ventricular arrhythmias (esp reentrant and ectopic and supraventricular tachycardia)
class 1c antiarrhythmics
flecainide, encainide, propafenone
class 1c antiarrhythmic mechanism
Na channel blockers, slow Phase 0 (no, effect on Phase 3), high Na channel avidity so slow off time, no effect on AP duration
class 1c antiarrhythmic use
last resort in refractory arrhythmias; V-tach that progresses to V-fib; intractable SVT
class 1c toxicity
contraindicated in MI (proarrhythmic); significantly prolongs refractory period in AV node
class 1b antiarrhythmics
lidocaine, mexiletine, tocainide
class 1b antiarrhythmic mechanism
Na channel blockers; poor avidity–quick on and off; slow Phase 0 but increase Phase 3 slope; decrease AP duration; preferentially rapidly depolarizing or ischemic cells; best for post-MI patients
class 1b antiarrhythmic toxicity
local anesthetic, CNS stimulation/depression, cardiovascular depression
class III antiarrhythmics
ibutilide, amiodarone (has I-IV actions), betyrium, sotolol, dofetilide
class III antiarrhythmic mechanism
block K channels, hyperpolarize to prolong refractory period and AP duration, increase QT interval
class III antiarrhythmic use
used when others fail–supraventricular and ventricular tachyarrhythmias
class 1b antiarrhythmic use
acute ventricular arrhythmias or digitalis-induced arrhythmias
class III antiarrhythmic toxicity
risk of new arrhythmia (because of long QT)
sotolol toxicity
torsades de pointes; excessive beta block
bretylium toxicity
new arrhythmias, hypotension
ibulitide toxicity
torsades de pointes
amiodarone toxicity
pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism, corneal deposits, blue gray skin deposits and photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF, P450 inhibitor
class IV antiarrhythmics
verapamil, diltiazem
class IV antiarrhythmic mechanism
Ca channel blocker, decreases conduction velocity, increases refractory period and PR interval
class IV antiarrhythmic use
nodal arrhythmias
class IV antiarrhythmic toxicity
constipation, flushing, edema, CHF, AV block, sinus node depression; verapamil: gingival hyperplasia
adenosine mechanism
increases flow of K from AV nodal cells to hyperpolarize the cell and decrease Ca current; very short acting (selective coronary dilator)
adenosine use
diagnosing and abolishing supraventricular tachycardia
adenosine toxicity
coronary steal phenomenon, flushing, hypotension, chest pain, effects blocked by theophylline
K+ use in arrhythmias
depresses ectopic pacemaker cells in hypokalemia (ie digoxin toxicity)
Mg 2+ use in arrhythmias
tosades de pointes and digoxin toxicity
dipyramidole mechanism
inhibits breakdown of adenosine (selective coronary vasodilator)
dipyramidole toxicity
coronary steal phenomenon
statin mechanism
HMG-CoA reductase inhibitors (inhibit melavonate conversion)
effects of statins
primarily lower LDL, small decrease in HDL and TG
statin toxicity
rhabdomyolysis and hepatotoxicity
niacin mechanism
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
effects of niacin
moderate decrease in LDL, increase in HDL, small decrease in TG (acts primarily on HDL)
niacin toxicity
flushing (take aspirin 30 minutes before), hyperglycemia (acanthosis nigricans), hyperuricemia
cholestyramine mechanism
prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more (bile acid resin)
colestipol mechanism
prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more (bile acid resin)
colesevelam
prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more (bile acid resin)
effects of bile acid resins
moderate decrease in LDL, slight increase in HDL and triglycerides
bile acid resin toxicity
patients hate it (GI discomfort and bad taste), decreased absorption of fat soluble vitamins, cholesterol gallstones
ezetimibe
cholesterol absorption blocker (at small intestine brush border)
effects of ezetimibe
only effect is lowering LDL (no HDL, TG effects)
ezetimibe toxicity
rare increase in LFTs
gemfibrizol mechanism
upregulate lipoprotein lipase (LPL) to increase TG clearance
clofibrate mechanism
upregulate lipoprotein lipase (LPL) to increase TG clearance
bezafibrate mechanism
upregulate lipoprotein lipase (LPL) to increase TG clearance
fenofibrate mechanism
upregulate lipoprotein lipase (LPL) to increase TG clearance
effects of fibrates
biggest effect is decrease in TG, small decrease in LDL and small increase in HDL
fibrate toxicity
myositis, hepatotoxicity, cholesterol gallstones
digoxin mechanism
direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger (increase in intracellular Ca and positive inotropy); stimulates vagus nerve
digoxin use
CHF, atrial fibrillation
digoxin toxicity
cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, decreased appetite; increased PR, short QT, scooping, T wave inversion, arrhythmia, hyperkalemia; worse with renal failure, hypokalemia, quinidine
digoxin antidote
slowly normalize K, lidocaine, Digiband (anti-digoxin fragments), Mg
