Fenofibrate
Fibrate
MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis
EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL
SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones
Gemfibrozil
Fibrate
MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis
EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL
SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones
Choleselevam
Bile acid resin
MOA: prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more.
EFFECTS: moderately decreases LDL, slightly increases both HDL and TGs
SIDE EFFECTS: patients hate it–it tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones
Niacin
MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL
synthesis
EFFECTS: moderately decreases LDL, moderately increases HDL, slightly decreases TGs
SIDE EFFECTS: red, flushed face, which is decreased by aspirin or long term use, hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbates gout)
Ezetimibe
MOA: prevents cholesterol absorption at small intestine brush border
EFFECTS: decreases LDL
SIDE EFFECTS: rare increase in LFTs, diarrhea
Propranolol
Class II antiarrhythmic
MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval
USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Can cause exacerbation of vasospasm in prinzmetal angina. Treat overdose with glucagon
Metoprolol
Class II antiarrhythmic
MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval
USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Metoprolol can cause dislipidemia. Treat overdose with glucagon
Atenolol
Class II antiarrhythmic
MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval
USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon
Isosorbide dinitrate
MOA: vasodilates by increasing NO in vascular smooth muscle–>increased cGMP and smooth muscle relaxation. Dilates veins»arteries. Decreases preload. Undergoes extensive first pass metabolism.
USES: angina, acute coronary syndrome, pulmonary edema.
TOXICITY: reflex tachycardia (treat with B blockers), hypotension, flushing, headache, tolerance.
Diltiazem
Non-selective CCB; results in vasodilation, negative iototropic (non-dihydropyridine)
MOA: blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle
CLINICAL USE: hypertension, angina, Raynaud phenomenon, atrial fibrillation
TOXICITY: cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation,
Nifedipine
Dihydropyridine CCB
MOA: block voltage-dependent L-type calcium channels of smooth muscle
CLINICAL USE: hypertension, angina, Raynaud phenomenon
TOXICITY: cardiac depression AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation
Verapamil
Non-dihydropyridine CCB
MOA: blocks voltage-dependent L-type calcium channels of cardiac muscles
CLINICAL USES: hypertension, angina, atrial fibrillation/flutter
TOXICITY: cardiac depression, AV block, flushing, peripheral edema, dizziness hyperprolactinemia, and constipation
Amlodipine
Dihydropyridine CCB
MOA: block voltage-dependent L-type calcium channels of smooth muscle
CLINICAL USE: hypertension, angina, Raynaud phenomenon
TOXICITY: cardiac depression AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation
NA nitroprusside
Short-acting. Increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide). Used for hypertensive emergencies
Hydralazine
MOA: increases cGMP–> smooth muscle relaxation. Vasodilates arterioles>veins leading to after load reduction
USES: severe HTN, CHF. First line therapy for HTN in pregnancy, with methyldopa. Frequently co administered with a B blocker to prevent reflex tachycardia
TOXICITY: compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus-like syndrome
Carvedilol
Sympatholytic, alpha and beta receptor antagonist
Class II antiarrhythmic
MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval
USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon
Digoxin
Cardiac glycoside
MOA: direct inhibition of Na/K ATPase leading to indirect inhibition of Na/Ca exchanger/antiport. Increases intracellular calcium–>positive inotropy. Stimulates vagus nerve–>decreased HR
USES: CHF (increases contractility), atrial fibrillation (decreases conduction at AV node and depression of SA node)
TOXICITY: cholinergic-nausea, vomiting, diarrhea, blurry yellow vision. ECG-increased PR interval, decreased QT interval, ST scooping, T wave inversion, arrhythmia, AV block. Can lead to hyperkalemia, which indicates poor prognosis.
FACTORS PREDISPOSING TO TOXICITY: renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+ binding site on Na/K ATPase), verapamil, amiodarone, quinidine (decreases digoxin clearance, displaces digoxin from tissue-binding sites)
ANTIDOTE: slowly normalize k+, cardiac pacer, anti digoxin Fab fragments, mg++
Disopyramide
Class 1A antiarrhythmic
MOA: increases AP duration and increases effective refractory period, increases QT interval. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
TOXICITY: heart failure, thrombocytopenia, torsades de pointes due to increased QT interval
Procainamide
Class 1A antiarrhythmic
MOA: increases AP duration and increases effective refractory period, increases QT interval. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
TOXICITY: reversible SLE-like syndrome, thrombocytopenia, torsades de pointes due to increased QT interval
Quinidine
Class 1A antiarrhythmic
MOA: increases AP duration and increases effective refractory period, increases QT interval. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
TOXICITY: cinchonism (headache, tinnitus), thrombocytopenia, torsades de pointes due to increased QT interval
Lidocaine
Class 1B antiarrhythmic
MOA: Class 1A antiarrhythmic
MOA: decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: acute ventricular arrhythmias (especially in post-MI), digitalis-induced arrhythmias
Flecainidine
Class 1C antiarrhythmic
MOA: significantly prolongs refractory period in AV node. Minimal effect on AP duration. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
TOXICITY: proarrhythmic, especially post-MI (contraindicated).
Propafenone
Class 1C antiarrhythmic
MOA: significantly prolongs refractory period in AV node. Minimal effect on AP duration. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
TOXICITY: proarrhythmic, especially post-MI (contraindicated).
Amiodarone
Class III. Antiarrhythmic (has class I, II, III, and IV effects)
MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.
USES: atrial fibrillation, atrial flutter, ventricular tachycardia
TOXICITY: pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits resulting in photodermatitis, neurological effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) **remember to check PFTs, LFTs, and TFTs when using amiodarone.
Class II anti arrhythmics
Beta blockers; decrease SA and AV nodal activity by decreasing camp, decreasing calcium concentrations; suppresses abnormal pacemakers by decreasing slope of phase 4; AV node is particularly susceptible leading to increased PR interval on EKG
Use: atrial flutter, a fib, AV nodal reentry; first line of drugs (with CCBs) for RATE control of Afib; decreases mortality rate post MI
Sotalol
Class III. Antiarrhythmic
MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.
USES: atrial fibrillation, atrial flutter, ventricular tachycardia
TOXICITY: torsades de pointes, excessive B blockade
Verapamil
Class IV anti arrhythmic; oral; blocks cardiac calcium channels; anti-anginal as well; slows phase 4 depolarization in SA, AV node and increases refractory period of AV node
Use: v fib (rate control), AV nodal re entry, SVT
Side effects: can cause/ exacerbate hypotension, GI upset, peripheral edema, increases serum digoxin
Diltiazem
Class IV anti arrhythmic; calcium channel blocker preferentially vascular over cardiac
Use: a fib, AV nodal reentry, SVT
Side effects: exacerbates hypotension
Adenosine
Increases K+ out of cells leading to hyperpolarizing the cell and decreased Calcium influx. Drug of choice in diagnosing/abolishing SVT. Very short acting (~15 sec). Adverse effects include flushing, hypotension, chest pain. Effect blocked by theophylline and caffeine.
ADVERSE EFFECTS: flushing, hypotension, chest pain, sense of impending doom, bronchospasm.
Nimodipine
Dihydropyridine CCB
MOA: block voltage-dependent L-type calcium channels of smooth muscle
CLINICAL USE: subarachnoid hemorrhage (prevents cerebral vasospasm). hypertension, angina, Raynaud phenomenon
TOXICITY: peripheral edema, flushing, dizziness, constipation, gingival hyperplasia
Nitroglycerin
MOA: vasodilates by increasing NO in vascular smooth muscle–>increase in cGMP and smooth muscle relaxation. Dilates veins»arteries. Decreases preload.
USES: angina, acute coronary syndrome, pulmonary edema
TOXICITY: reflex tachycardia (treat with B blockers), hypotension, flushing, headache, “Monday disease” in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure. Must have a nitrate-free interval.
Statins
MOA: inhibits conversion of HMG-CoA to mevalonate
EFFECTS: significantly lowers LDL, slightly increases HDL, slightly decreases TGs
SIDE EFFECTS: hepatotoxicity, rhabdomyolysis
Cholestyramine
Bile acid resin
MOA: prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more.
EFFECTS: moderately decreases LDL, slightly increases both HDL and TGs
SIDE EFFECTS: patients hate it–it tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones
Colestipol
Bile acid resin
MOA: prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more.
EFFECTS: moderately decreases LDL, slightly increases both HDL and TGs
SIDE EFFECTS: patients hate it–it tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones
Clofibrate
Fibrate
MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis
EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL
SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones
Bezafibrate
Fibrate
MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis
EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL
SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones
Mexiletine
Class 1B antiarrhythmic
MOA: Class 1A antiarrhythmic
MOA: decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.
USES: acute ventricular arrhythmias (especially in post-MI), digitalis-induced arrhythmias
Esmolol
Class II antiarrhythmic–very short acting
MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval
USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon
Timolol
Class II antiarrhythmic
MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval
USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon
Ibutilide
Class III. Antiarrhythmic
MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.
USES: atrial fibrillation, atrial flutter
TOXICITY: torsades de pointes
Dofetilide
Class III. Antiarrhythmic
MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.
USES: atrial fibrillation, atrial flutter
Class IV antiarrhythmics
CCBs-verapamil and diltiazem
MOA: decrease conduction velocity; increase ERP, increase PR interval
USES: prevention of nodal arrhythmias (e.g. SVT), rate control in atrial fibrillation
TOXICITY: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
Mg++
Effective in torsades de pointes and digoxin toxicity
Indomethacin
NSAID used to close PDA (inhibits PGE1 and 2)
Isosorbide mononitrate
MOA: vasodilates by increasing NO in vascular smooth muscle–>increased cGMP and smooth muscle relaxation. Dilates veins»arteries. Decreases preload. Isosorbide dinitrate Undergoes extensive first pass metabolism. This is an active metabolite of isosorbide dinitrate–oral bioavailability is close to 100%
USES: angina, acute coronary syndrome, pulmonary edema.
TOXICITY: reflex tachycardia (treat with B blockers), hypotension, flushing, headache, tolerance.