Cardio Drugs Flashcards
Hydralazine
Increases cGMP (makes cGMP Hya!!). Used in severe hypertension and prego hypertension with methyldopa. Can lead to lupus like syndrome (SHIPPE) Sulfa, hydralazine, isoniazid, procainamide, phenytoin, etanercept
Nitroprusside
Short acting increase in cGMP via NO. Can cause cyanide tox (for which we give nitrite and thiosulfate)
Fenoldopam
D1 receptor agonist. fenolDopam. Coronary peripheral renal and splanchnic vasodilation. DECREASED BP AND NATRIURESIS.
Nitroglycerin, Isosorbide Dinitrate
NO –> cGMP. Dilates veins»_space; arteries leading to decrease in preload. Used for angina, coronary syndrome, pulm edema. MONDAY DISEASE- industrial exposure, body gets used to vasodilation through week and then loss of tolerance over weekend leads to tachycardia, dizzy, headache upon reexposure.
Goal of anti-anginal therapy
Reduce MVO2 by decreasing EDV, BP, HR, Contractility
Statins
Inhibit HMG-COA Reductase (RLS of cholesterol synthesis, HMG-COA –> mevalonate). Large decrease in LDL, minor increase in HDL and decrease in TGs. ADR: Hepatotox and rhabdo (worse with fibrates and niacin)
Niacin
Inhibit lipolysis in adipose. Reduce hepatic VLDL synth. Leads to decrease in LDL, Increase HDL, small decrease in TGs. ADR: Flushing, hyperglycemia, hyperuricemia
Bile Acid Resins (Cholestyramine, colestipol, colesevelam)
Decrease reabsorption of bile acids. Decreases LDL. ADR: GI discomfort, decrease in fat soluble vitamins, CHOLESTEROL GALLSTONES
Cholesterol Absorption Blockers (ezetimibe)
Prevent abs in brush border. Decreases LDL. Rare increase in LFTs and diarrhea.
Fibrates (gemfibrozil, -fibrate)
Upregulate LPL (which is on vascular endothelium and breaks down TGs on VLDL and Chylos). Also activates PPAR-a leading to HDL synth. Slight decrease in LDL and increase in HDL, good decrease in TGs. ADRS: Myositis, Hepatotox, Gallstones
Cardiac Glycosides (Digoxin)
Block Na/K ATPase. Increase intracell. Na leads to decrease in Ca/Na transport and increase in intracell Ca to increase contractility. Used in CHF and Afib.
ADR: Cholinergic- NVD, YELLOW VISION. Can lead to hyperkalemia. Factors predisposing to tox= renal failure, hypokalemia, verapamil, amiodarone, quinidine. Tx overdose with anti-dig Fab fragments.
Class I antiarrhythmics
Sodium channel blockers. Decrease slope of phase 0 in myocytes and increase threshold in pacemaker cells. State dependent. HYPERKALEMIA causes increased tox of all class I drugs.
Quinidine, Procainamide, Disopyramide
Class IA- Increase AP duration and effective refractory period. PROLONG QT INTERVAL. Used for many arrhythmias but especially for re-entrant and ectopic SVT/VT. ADR: Cinchonism (HA, tinnitus with quinidine), SLE like syndrome (SHIPPE), CHF, thrombocytopenia, torsades.
Lidocaine, Mexiletine, (Phenytoin)
Class IB- Decrease AP duration. Preferentially in ischemic or depol purkinje/vent tissue. Used in ventricular arrhythmias post MI and Dig induced arrythmias (IB Is Best post-MI). ADR: CNS Stim/Depression, Cardio depression
Flecainide, Propafenone
Class IC- Prolongs refractory in AV node. Used in SVTs and A fib. ADR: Proarrhythmic, ESPECIALLY POST-MI (contra). IC-Contraindicated in isChemic heart disease.