Cardiovascular Flashcards
Amlodipine, nimodipine, nifedipine
Dihydropyridine calcium channel blockers. Block V-dependent L-type Ca channels of cardiac and smooth muscle.
Superior effect on vessels vs. non-dihydropyridines
Amlodipine and nifedipine treat HTN, angina (including Prinzmetal), Raynaud phenomenon
Nimodipine treats subarachnoid hemorrhage (prevents cerebral vasospasm)
Toxicity: cardiac depression, hyperprolactinemia
Diltiazem, verapamil
Non-dihydropyridine calcium channel blockers
Superior effect on heart vs. dihydropyridines; verapamil is most cardiac-selective Ca blocker
Treat HTN, angina, A-fib/flutter
Toxicity: AV block, gingival hyperplasia, constipation, hyperprolactinemia
Hydralzine
Vasodilates arterioles>veins. Increases cGMP.
Treats severe HTN, (first-line in pregnancy), CHF.
Coadministered with beta-blocker to prevent reflex tachycardia
Toxicity: Lupus-like syndrome
Nitroprusside
Short-acting vasodilator. Direct release of NO causes increased cGMP.
Treats HTN emergency
Toxicity: cyanide toxicity (treat with sulfur)
Fenoldopam
Selective dopamine D1 receptor agonist with no alpha/beta properties (unlike dopamine). Results in vasodilation and naturiuresis.
Treats HTN emergency
Nitroglycerin, isosorbide dinitrate
Direct release of NO causes increased cGMP. Venodilation>>vasodilation. Decreases preload.
Treats angina, ACS, pulmonary edema.
Coadministered with beta-blocker to prevent reflex tachycardia.
Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
HMG-CoA reductase inhibitors; inhibit conversion of HMG-CoA to mevalonate
Decreases LDL, trigs; increases HDL
Toxicity: hepatotoxicity, rhabdomyolysis (especially when used with niacin and fibrates)
Vitamin B3 (Niacin)
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis
Decreases LDL, trigs; increases HDL
Toxicity: hyperglycemia, hyperuricemia, hypotension and flushed face (due to release of prostaglandins; inhibited by aspirin)
Cholestyramine, colestipol, colesevelam
Bile acid resins; prevent intestinal reabsorption of bile
Decreases LDL
Toxicity: hypertriglyceridemia, cholesterol gallstones, bad taste, impaired absorption of vitamins and drugs
Ezetimibe
Prevents cholesterol absorption at small intestine brush border
Decreases LDL
Toxicity: diarrhea
Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate
Fibrates upregulate lipoprotein lipase to increase TG clearance. Activates PPAR-alpha to induce HDL synthesis
Decreases triglycerides; increases HDL
Toxicity:
- myositis (increased risk with concurrent statins)
- hepatotoxicity,
- cholesterol gallstones (increased risk with concurrent bile acid resins)
Digoxin
Cardiac glycoside that directly inhibits Na/K ATPase and indirectly inhibits Na/Ca exchanger, resulting in increased inotropy.
Acts on the vagus nerve to increase parasympathetic tone, resulting in decreased AV conduction.
Treats CHF (increased contractility) and A-fib (depresses SA node and decreases conductance via AV node)
Digoxin toxicity
Symptoms: n/v/d, blurry yellow vision, increased PR, decreased QT, arrhythmia, AV block
Factors predisposing to toxicity: renal failure, hypokalemia (digoxin binds at K site on Na/K ATPase), hypovolemia, verapamil, amiodarone, quinidine (decreased clearance)
Antidote: normalize K+, anti-digoxin Fab fragments, Mg
Quinidine, Procainamide, Disopyramide
Class 1A antiarrhythmics (intermediate association/disassociation) - lengthens the AP, increase effective refractory period, increase QT interval
Treats atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
Toxicity: Torsades due to increased QT interval. Quinidine can cause tinnitus. Procainamide can cause SLE-like syndrome. Disopyramide can cause CHF
Lidocaine, Mexiletine, Phenytoin
Class 1B antiarrhythmics (fast association/disassociation) - shortens the AP, preferentially affects ischemic or depolarized Purkinje and ventricular tissue
Treats ventricular arrhytmias, especially post-MI, and digitalis-induced arrhythmias
Toxicity: CNS stimulation/depression, increased risk of systole
Flecainide, Propafenone
Class 1C antiarrhythmics (slow association/disassociation) - no effect on AP; prolongs refractory period in AV node
Treats SVTs, including A-fib Toxicity: pro-arrhythmic, especially post-MI!
Contraindicated in structural and ischemic heart disease
Metoprolol, propanolol, esmolol, atenolol, carvedilol
Class 2 antiarrhythmics - decrease SA and AV nodal activity by decreasing cAMP, Ca currents, slope of phase 4. Results in decreased HR and increased PR interval
Treats SVT. Carvedilol reduces mortality in CHF (unique in that it blocks beta1, beta2, and alpha1)
Toxicity: Metoprolol can cause dyslipidemia. Propanolol can exacerbate vasospasm in Prinzmetal angina. Treat overdose with glucagon.
Amiodarone, Ibutilide, Dofetilide, Sotalol
Class 3 antiarrhythmics - K+ channel blockers that lengthen AP, increase QT interval (like class Ia antiarrhythmics)
Atrial fibrillation, atrial flutter
Amiodarone and sotalol also treat VT
Toxicity: sotalol and ibutilide can cause torsades
Amiodarone toxicity
Side effects may include pulmonary fibrosis, hepatotoxicity, hypothryoidism/hyperthryoidism, corneal deposits, blue/gray skin deposits, neurologic effects, constipation, CV effects
Unlike other Class III and Class 1A antiarrhythmics, amiodarone does not increase risk of torsades
Always check PFTs, LFTs, TFTs
Verapamil, diltiazem
Class 4 antiarrhythmics - non-dihydropyridine calcium channel blockers; decrease conduction velocity and increase PR interval
Prevents nodal arrhytmias (SVT) and used as rate control in A-fib
Adenosine
Hyperpolarizes the cell by expelling K+. Acts on phase 4 of the nodal cell action potential to reduce rate of spontaneous depolarization in cardiac pacemaker cells. Used to diagnose/abolish SVTs
Blocked by theophylline and caffeine
Magnesium as CV treatment
Used to treat torsades de points and digoxin toxicity
Cilostazol
Phosphodiesterase inhibitor (PDE3) with therapeutic focus on increasing cAMP, which directly inhibits platelet aggregation. Also act as a vasodilator.
Treats intermittent claudication
Toxicity: headache, diarrhea, increased HR
Captopril, enalapril, lisinopril
ACE inhibitors
Prevent activation of angiotensin II –> vasodilation, decreased filtration fraction, decreased aldosterone, decreased ADH
Prevents inactivation of bradykinin (angioedema, cough), unlike Angiotensin II receptor blockers
Treats HTN, CHF, proteinuria, diabetic nephropathy
Contrindications: C1 esterase inhibitor deficiency (angioedema), pregnancy (fetal renal malformations), bilateral renal artery stenosis (renal failure)
