Heart Drugs Flashcards
Calcium Channel blockers tissue selectivity vascular smooth muscle
Vascular smooth muscle: alodipine= nifedipine > diltiazem > verapamil
Ca channel blocker tissues selectivity for heart
Verapamil> diltiazem > amlodipine = nifedipine
Ca channel blocker toxicity
Av block, peripheral edema, dizziness, constipation, cardiac depression
Hydralazine mechanism
Increase cGMP to relax smooth muscle which vasodilation of arteries more than veins so after load is lower
Co administered with hydralazine and why
Beta blocker for reflex tachycardia
Treatment for pregnancy hypertension
Hydralazine plus methyldopa
Hydralazine sides
Compensatory tachycardia (so no in angina or cad) , fluid retention, nausea, lupus like, angina
Nitroprusside mechanism
Short acting increase cGMP via NO release
Nitroprusside tox
Has cyanide so cyanide toxicity
Fenoldopam
Dopamine d1 receptor agonist, vasodilation including coronary renal and splanchnic, decrease bp and increase naturesis
Calcium Channel blockers drugs
Nifedipine, verapamil , diltiazem, amlodipine
Nitroglycerin/ isosorbide dinitrate: mechanism and clincial use
vasodialation (veins) by NO release -> cGMP increase
used for angina and pulmonary edema
nitroglyerin/ isosorbide dinitrate toxicity
reflex tachycardia, hyoptension, flushing, headache, monday’s disease in industry exposure
what do statins stop HMG-CoA from becoming?
mevalonate
side effects of statins
hepatotoxicity, rhabdomyolysis
statins effect on : LDL, HDL, Triglycerides
way down, up, down
niacin effect on LDL HDL Triglycerides
down, up, down
bile acid resin effect on LDL HDL Triglyceries
down, slightly up, slightly up
niacin: other name and mech
vitamin b3, inhibits lipolysis in adipose, reduces hepatic VLDL secretion
niacin sides
red flushed face (fix with aspirin), hyperglycemia (causing acanthosis nigricans), hyperuricemia (exacerbates gout)
bile acid resins and effects
cholestyramine, colestipol, colesevelam. prevents reabsorption of bile so liver must use cholesterol to make more
bile acid resins sides
tastes bad, gi discomfort, cholesterol gallstones, cant absorb fat soluble vitamins
ezetimibe
Cholestrol absorption blockers. rarely causes high LFTs and diarrhea
Fibrates
drives down triglycerides a lot, activates lipoprotein lipase. tox: myositis, hepatotox, cholestrol gallstones
Class I Antiarrhythmics are what?
Na channel blockers
Class IA drugs
Quinidine, Procainamide, Disopyramide
Class IA actions
increase AP duration, increase effective refractory period, increase QT interval.
Class IA uses
atrial and ventricular arrythmias. especially reentrant currents and ectopic supraventricular or ventricular tachycardia
Quinidine tox and class
Class IA. cinchonism = headache and tinnitus
Procainamide tox and class
Class IA. reversible SLE-like syndrome
disopyramide tox and class
heart failure
Class IA shared toxicities
thrombocytopenia, torsades de pointes due to high QT interval
Class IB drugs
Lidocaine, Mexilentine, Tocainide
Class IB actions
decrease AP duration. preferentially targets ischemic or depolarized purkinje and ventricular tissue
Class IB uses
acute ventricular arrhythmias especially post MI and digitalis arrhythmias
Digoxin availability and action
75% available, 1/2 life is 40 hrs. directly inhibits Na/K ATPase, thus indirectly inhibits Na/Ca
Digoxin effects
increases intracellular Ca -> positive inotropy. stimulates vagus nerve -> lower heart rate. improves contractility. slows down the AV node and depresses SA node
Digoxin use
CHF (contractility), atrial fib (slowed AV node conduction and SA depression)
Digoxin tox
Cholinergic effects: nausea, comiting, diarrhea, blurry yellow vision (van Gogh)
ECG: increase PR, down QT, ST scooping, T-wave inversion, arrhythmia, av block
hyperkalemia - bad sign
Digoxin tox predisposing factors
renal failure, hypokalemia, quinidine
Antidote to digoxin poisoning
slowly normalize K, lidocain, cardiac pacer, anti-digoxin Fab fragments, Mg.
Class IC drugs
Flecainide, propafenone
Class IC uses
last resort for refractory tachyarrhythmias without structural anomaly
Class IC effects
no effect on AP duration
Class IC tox
proarrhythmic (post MI, so contraindicated). prolongs refractory period of AV node a lot
class two anti arrythmics: drugs and type of drug
beta blockers: metoprolol, propranolol, esmolol, atenolol, timolol
shortest acting betablocker?
esmolol
beta blocker actions on the heart
Decreases SA and AV node actiity by decrease cAMP and Ca currents. Makes phase 4 have a shallower long slope.
AV node hit more
class II uses
v tach, svt, slowing ventricle during a fib/flutter
beta blocker toxicity
impotence, asthma attack, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations), mask signs of hyperglycemia
special sides of metoprolol
dyslipidemia. treat with high dose glucagon
special sides of propranolol
can exacerbate vasospasm of Prinzmetals (cyclical) angina
Class III drugs and type
Potassium Channel Blocker. Amiodarone, Ibutilide, Dofetilide, Sotalol
Class III effects and use
increase AP duration, increase ERP, used when other antiarrythmics fail (like IC), increase QT
Sotalol tox
torsades de pointes, excessive beta block
ibutilide tox
torsades
amiodarone tox
pulmanary fibrosis, hepatotox, hypo/hyperthyroid (amiodorone is 40% iodine), corneal deposits, blue/grey skin deposits, neurological effects, constipation, CV (bradycardia, heart block, CHF)
Amiodarone special precautions
check PFTs, LFT, and TFTs
what makes amiodarone unique
has class I, II, III, and IV effects (plus iodine effects) cause it disrupts membrane
Class IV drugs and type
Ca channel blockers, Verapmil and diltiazen
Class IV effects
decrease conduction velocity, increase: ERP, PR
Class IV use
prevent nodal arrhytmias
Adenosine mech
increase K out of cells -> hyperpolarize
Adenosine use
best drug for diagnose and treat supraventricular tachy. very short acting (15 secs)
Adenosine tox
flushing, hypotension, chest pain. Fix with: theophyllin or caffeine
Mg use
torsades de pointes and digoxin toxicty
