Cardio Flashcards
Ca Blockers
Amlodipine, nomodipine, nifedipine (dyhidropurine)
Diltiazem, verapimil (non-dihydropuridine)
Block voltage gated L-type Ca channels of cardiac and smooth muscle, reduce contractility
Vascular SM- amlodipine and nifedipine
Cardiac- Verapamil
amlodipine and nifedipine- HTN, angina (including prinzmetal), raynaud, isolated systolic HTN
non-dihydropuridine- HTN, angina, A fib
Nimodipine- subarachnoid hemorrhage
can all cause AV block, edema, hyperprolactinemia, constipation
Hydralazine
increase cGMP, smooth muscle relaxation mostly vasodilates arterioles (dec. afterload) Severe HTN, HTN in pregnancy (w/ mdopa) give w/ b blocker for reflex tachy can cause lupus-like syndrome
Nitroprusside
HTN emergency
releases NO to increase cGMP
can cause cyanide toxicity
Fenoldopram
D1 receptor agonist
coronary, peripheral, renal, splanchnic dilation
decrease BP and increase natriuresis
Nitroglycerine and isosorbide dinitrate
increase cGMP
dilate veins more than ateries (dec. preload) (main way reduces pain in angina)
reflex tachy, monday disease in industrial work
lose tolerance over weekend
Statins
inhibit HMG-CoA to mevalonate
hepatotoxic, rhabdomyolysis (especially w fibrates and niacin)
niacin
decrease LDL and increase HDL inhibits peripheral lypolysis and VLDL synthesis Flushed face (give aspirin) hyperglycemia (acanthosis nigricans) hyperuricemia (exacerbates gout)
Bile acid resins
Cholestyramine, colestipol, colesevelam prevents reabsorbion of bile salts people hate it decreased fat soluble vitamins cholesterol gallstones
Ezetimbe
blocks cholesterol abs at brush border
causes DIARRHEA
Fibrates
Gemfibrozil, clofibrate, bezafibrate
Lowers TGs
upregulates LPL (TG clearance) and activates PPAR-a to induce HDL synthesis a bit
myositis (esp w/ statins)
Cholesterol gallstones (esp w/ bile acid resins)
hepatotoxicity
Digoxin
cardiac glycoside
Direct inhibition of Na/KATPase secondarily blocks Na/Ca antiport. More intracellular Ca increases inotropy. stimulates vagus nerve to decrease HR
Use in CHF and A fib (decreased conduction at AV node
ECG- inc PR, dec QT, ST scooping, T inversion
can lead to hypokalemia which is bad
cholinergic- N/V, blurry vision
renal failure decreses excretion
hypokalemia is permissive for dig binding at K binding site
verapamil, amiodarone and quinidine decreases clearance and displaces from tissue binding sites
Class 1 antiarrhythmics in general
Na channel blockers
slow or block conduction especially in depolarized cells
decrease phase 0 slope
increase threshold for abnormally firing pacemaker cells
Class 1a antiarrhythmics
Disopyramide, quinidine, procainamide
increases AP duration, QT and ERP
use in both atrial and ventricular arrhythmias especially reentrant and ectopic SVT
quinidine- headache and tinnitis
procainamide- SLE like
disopyramide- HF
all thrombocytopenia and torsades de point due to increased QT
Class 1b antiarrhythmics
Lidocaine, mexiletine
decreases AP duration
preferentially affects ischemic and depolarized
acute ventricular arrhythmias (esp post MI) and digitalis induced arrhythmias
can cause CN and cardiac depression
Class 1c antiarrhythmics
flecainide, propafenone
Significantly prolongs refractory period in AV node, minimal effect on AP duration
SVTs and LAST RESORT in refractory VT
proarrhythmic post MI (contraindicated in structural and ischemic heart disease)