Fa Cardio Pharm

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Tx. for essential HTN

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diuretics, ACEI's, ARB's, calcium channel blockers

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Tx. for CHF

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diuretics, ACEI's/ARB's, beta-blockers, K-sparing diuretics

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Tx. for DM

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ACEI's/ARB's, calcium channel blockers, diuretics, beta-blockers, alpha-blockers

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Hydralazine

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MOA: increase cGMP -> smooth muscle relaxation; vasodilates arterioles > veins; DECREASES AFTERLOAD
Uses: severe HTN, CHF; first-line tx for HTN in pregnancy, w/ methyldopa; frequently coadministered w/ a beta-blocker to prevent reflex tachycardia
Toxicity: compensatory tachycardia, fluid retention, nausea, headache, angina, SLE-like syndrome

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Calcium channel blockers

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Examples: nifedipine, verapamil, diltiazem
MOA: block voltage-dependent L-type calcium channels of cardiac & smooth muscle->reduces muscle contractility (verapamil=ventricles, nifedipine=muscles, diltiazem=both)
Uses: HTN, angina, arrhythmiaz (not nifedipine), Prinzmetal's angina, Raynaud's
Toxicity: cardiace depression, AV block, peripheral edema, flushing, dizziness, constipation

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Nitroglycerin, isosorbide dinitrate

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MOA: vasodilate by releasing nitric oxide in smooth muscle, causing increase in cGMP and smooth muscle relaxation; dilate veins>>arteries -> decrease preload
Uses: angina, pulmonary edema; also used as an aphrodisiac & erection enhancer
Toxicity: reflex tachycardia, hypotension, flushing, headache, "Monday dz" in industrial exposure

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Tx. for malignant HTN

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1) Nitroprusside - short acting; increases cGMP via direct release of NO; can cause cyanide toxicity
2) Fenoldopam - dopamine D1 receptor agonist -- relaxes renal vascular smooth muscle
3) Diazoxide - K channel opener -- hyperpolarizes and relaxes vascular smooth muscle; can cause hyperglycemia b/c induces insulin release

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6 sites of action for cardiac drugs

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1) Na/K ATPase
2) Na/Ca exchanger
3) Voltage-gated Ca channel
4) Ca pump in wall of SR
5) Ryanodine receptors/Ca release channels in SR wall
6) Ca interaction w/ troponin-tropomyosin

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Cardiac glycosides

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Example: digoxin
MOA: direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger; increases intracellular Ca (positive inotropy)
Uses: CHF (increases contractility); atrial fib (decreases AV node conduction & depresses SA node)
Toxicity: cholinergic (nausea, vomiting, diarrhea, blurry yellow vision), EKG (increase PR, decrease QT interval, scooping, T-wave inversion, arrhythmia, hyperkalemia); toxicity is worsened by renal failure (decreased excretion), hypokalemia, quinidine (decreases digoxin clearance & displaces digoxin from tissue binding sites)
Antidote: slowly normalize K, lidocaine, cardiace pacer, anti-dig Fab fragments, Mg

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Four classes of antiarrhythmics

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Class I - Na channel blockers
Class II - beta-blockers
Class III - K channel blockers
Class IV - Ca channel blockers

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Class I antiarrhythmics - Na Channel Blockers

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local anesthetics; slow or block conduction, esp. in depolarized cells; decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells; are state dependent (selectively depress tissue that is frequently depolarized)

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Class IA

"the QUeen PROClaims DISO's PYRAMID"

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Examples: quinidine, procainamide, disopyramide
MOA: increases AP duration, increases effective refractory period, increases QT interval
Uses: affects both atrial & ventricular arrhythmias, esp. reentrant & ectopic supraventricular and ventricular tachycardia
Toxicity: thrombocytopenia, torsades de pointes due to increased QT interval (quinidine can also cause cinchonism, HA, tinnitus) (procainamide can also cause reversible SLE-like syndrome)

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Class IB

"I'd Buy LIDy's MEXIcan TOCA's"

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Examples: lidocaine, mexiletine, tocainide
MOA: decreases AP duration; preferentially affects ischemic or depolarized Purkinje & ventricular tissue
Uses: acute ventricular arrhythmias (esp post-MI) and in digitalis-induced arrhythmias
Toxicity: local anesthetic, CNS stimulation/depression, cardiovascular depression

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Class IC

"I SEE FLow ENTered PROarrhythmia"

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Examples: flecainide, encainide, propafenone
MOA: no effect of AP duration
Uses: useful in V-tachs that progress to VF and in intractable SVT; usually used only as last resort in refractory tachyarrhythmias; for patients w/o structural abnormalities
Toxicity: proarrhythmic, esp post-MI

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Class II antiarrhythmics - beta-Blockers

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Examples: propranolol, esmolol, metoprolol, atenolol, timolol
MOA: decrease cAMP, decrease Ca currents; suppress abnormal pacemakers by decreasing slope of phase 4; AV node particularly sensitive -- increase PR interval; esmolol very short acting
Uses: V-tach, SVT, slowing ventricular rate during A. fib and A. flutter
Toxicity: impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations); may mask signs of hypoglycemia; metoprolol can cause dyslipidemia; Tx BB overdose w/ glucagon

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Class III antiarrhythmics - K Channel Blockers

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Examples: sotalol, ibutilide, bretylium, dofetilide, amiodarone
MOA: increase AP duration, increase ERP, increase QT interval
Uses: when other antiarrhythmics failed
Toxicity: Sotalol (torsades de points, excessive beta-block) Ibutalide (torsades de pointes) Bretylium (new arrhythmias, hypotension) Amiodarone (pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF)

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Class IV antiarrhythmics - Ca Channel Blockers

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Examples: verapamil, diltiazem, nifedipine
MOA: decrease conduction velocity, increase ERP, increase PR interval
Uses: used in prevention of nodal arrhythmias
Toxicity: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

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Other antiarrhythmics (3)

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Adenosine (reset button) - pushes K out of cells -> hyperpolarizing the cell; drug of choice in diagnosing/abolishing SVT; very short acting (~15 sec); toxicity includes flushing, hypotension, chest pain; effects blocked by theophylline, caffiene
Potassium (K) - depresses ectopic pacemakes in hypokalemia (e.g. digoixin toxicity)
Magnesium (Mg) - effective in torsades de pointes and digoxin toxicity