Pharmacology MnemonicsPharmacology MnemonicsPharmacology Mnemonics and Pharmacology Flash Cards for your pharma studies Articles
Anistreplase/APSAC (Eminase)
2008-04-11 12:18:00 Name: Anistreplase/APSAC (Eminase) Class: Antithrombotic Agent (Thrombolytic Agent) Mechanism: Acylated plasminogen-streptokinase activator complex. Plasminogen active site is protected from inactivation. Poor thrombus specificity—catalyzes conversion of circulating & fibrin-bound plasminogen—results in a systemic lytic state. Absorption: IV. Admin. w/large loading dose to overcome plasma antibodies. Dist.: Metabolism.: Excretion, t½: Longer t½ than streptokinase ® sustained fibrinolytic effect. Toxicity/S.E.s: Hemorrhage. Allergic rxns—pruritis, flushing, urticaria. Higher incidence of allergic rxns. w/readministration. Pronounced hypotension (usu. transient). Delayed fever and arthralgia. Utility: Treat acute MI (w/in 6 hr. of symptoms), massive PE, acute proximal vein thromboses, occlusion of dialysis access sites and indwelling catheters, occlusion of prosthetic heart valves. Special Features: Best res...
Streptokinase (Streptase)
2008-04-11 12:18:00 Name: Streptokinase (Streptase) Class: Antithrombotic Agent (Thrombolytic Agent) Mechanism: Derived from b-hemolytic streptococci. Forms a complex w/plasminogen, exposing its active site. Poor thrombus specificity—catalyzes conversion of circulating and fibrin-bound plasminogen—results in a systemic lytic state. Absorption: IV. Admin. w/large loading dose to overcome plasma antibodies. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Hemorrhage. Allergic rxns—pruritis, flushing, urticaria. Higher incidence of allergic rxns. w/readministration. Pronounced hypotension (usu. transient). Delayed fever and arthralgia. Utility: Treat acute MI (w/in 6 hr. of symptoms), massive PE, acute proximal vein thromboses, occlusion of dialysis access sites and indwelling catheters, occlusion of prosthetic heart valves. Special Features: Best results in pts. that receive therapy Pts. w/antibodies can develop therapeutic resistance.
Vitamin K1 (Phytonadione)
2008-04-11 12:18:00 Name: Vitamin K1 (Phytonadione) Class: Anticoagulant Antagonist Mechanism: Vit. K is necessary for g-carboxylation of thrombin, factors VII, IX, & X, and proteins C & S. The g-carboxylated residues are required for binding Ca2+, which is essential for their activity. Absorption: Oral or SC preferred. IV admin. may cause shock or anaphylaxis. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: IV admin. may cause shock or anaphylaxis. Utility: Reverse excessive bleeding due to warfarin—indicated for severe or continued bleeding if warfarin dosage adjustment is unsuccessful. Special Features: Significant improvement in hemostasis may require as long as 24 hr. If immediate hemostasis is necessary, fresh frozen plasma should be infused.
Enoxaparin (Lovenox)
2008-04-11 12:17:00 Name: Enoxaparin (Lovenox) Class: Antithrombotic Agent (Anticoagulant) (Low Molecular Weight Heparin) Mechanism: Catalyzes complex formation btwn. plasma antithrombin III and various serine proteases of the coagulation pathway, including thrombin and activated factors IX, X, XI, & XII. Effect primarily due to thrombin inhib. Less effect on thrombin than heparin. Prevents further clot formation and thrombus propagation. Does not alter organized clots. Absorp.: SC ® better bioavail. than heparin. Daily SC injxn has sim. efficacy to 2-3 injxns/d of heparin. Dist.: Metabolism.: Hepatic. Excretion, t½: Longer t½ than heparin. ¯ t½ w/pulm. embolism. t½ w/hepatic cirrhosis or end-stage renal disease. Toxicity/S.E.s: 1° = bleeding. Thrombocytopenia (bovine > porcine)—mild, severe (delayed onset; can occur w/heparin resistance ® thromboembolism & DIC). Long-term use ® osteoporosis. Non-teratogenic, but discontinue prior ...
Antithrombin III (ATnativ)
2008-04-11 12:17:00 Name: Antithrombin III (ATnativ) Class: Antithrombotic Agent (Coagulation Inhibitor) Mechanism: Prepared from pooled human plasma. Inhibits coagulation factors (thrombin, IXa, Xa, XIIa). Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Utility: Treat pts w/hereditary AT-III deficiency and neonates w/a family history of AT-III deficiency. Prophylaxis for deficient pts who are undergoing surgery or delivery at term. Special Features:
Warfarin (Coumadin)
2008-04-11 12:17:00 Name: Warfarin (Coumadin) Class: Antithrombotic Agent (Oral Anticoagulant) Mechanism: Vitamin K antagonist ® ¯ g-carboxylation of thrombin, factors, VII, IX, & X, and proteins C & S ® inhib. of synth. of active coagulation factors. Does not alter organized clots. Absorption: Oral. Dist.: Almost completely bound (99%) to plasma proteins (mainly albumin). Metabolism.: Microsomal enzymes in liver and kidneys. Excretion, t½: Urine and stool. Toxicity/S.E.s: Hemorrhage, hypersensitivity rxns., fetal toxicity. “Purple Toe” synd. (necrosis) assoc. w/protein C deficiency. During pregnancy, can cause birth defects and abortion. Many drug interactions. Utility: Prevention of recurrent thrombotic events following acute Rx w/heparin. Valvular heart disease, prosthetic cardiac valves, AMI, atrial fibrillation. Special Features: Max. effects require 2-7 days. Init. response may be procoagulant due to inhib. of protein C. Should have 6 day overlap w/heparin. Monito...
Protamine Sulfate
2008-04-11 12:17:00 Name: Protamine Sulfate Class: Anticoagulant Antagonist Mechanism: Binds tightly to heparin and rapidly reverses its effects. Also interacts w/platelets, fibrinogen, and other plasma proteins ® anticoagulant effect. Absorption: IV infusion—slow rate. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Utility: Treat life-threatening hemorrhage 2° to heparin use. Special Features: Use minimal effective dose.
Heparin
2008-04-11 12:16:00 Name: Heparin Class: Antithrombotic Agent (Anticoagulant) Mechanism: Catalyzes complex formation btwn. plasma antithrombin III and various serine proteases of the coagulation pathway, including thrombin and activated factors IX, X, XI, & XII. Effect primarily due to thrombin inhib. Prevents further clot formation and thrombus propagation. Does not alter organized clots. Absorp.: IV, continuous IV®immed. onset. SC®1-2 hr onset w/variable bioavail. Dist.: Metabolism.: Hepatic. Excretion, t½: Rel. short t½. ¯ t½ w/pulm. embolism. t½ w/hepatic cirrhosis or end-stage renal disease. Toxicity/S.E.s: 1° = bleeding. Thrombocytopenia (bovine > porcine)—mild, severe (delayed onset; can occur w/heparin resistance ® thromboembolism & DIC). Long-term use ® osteoporosis. Non-teratogenic, but discontinue prior to delivery. Utility: Symptomatic calf vein thrombi or thrombi extending above the popliteal vein, pulm. embolus, atri...
Abciximab (Reo-Pro)
2008-04-08 19:25:00 Name: Abciximab (Reo-Pro) Class: Antithrombotic Agent (Antiplatelet Agent) Mechanism: Monoclonal antibody to GPIIb/IIIa. Interferes w/platelet-adhesive protein interactions. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Utility: Treat high risk angioplasty pts. Special Features:
Acetylsalicylic Acid (Aspirin)
2008-04-08 19:24:00 Name: Acetylsalicylic Acid (Aspirin ) Class: Antithrombotic Agent (Antiplatelet Agent) Mechanism: Irrevers. acetylation of cyclooxygenase ® ¯ platelet thromboxane synth. Absorption: Oral ® rapid absorption. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: GI hemorrhage, hemorrhagic stroke. Use w/caution in pts on long-term oral anticoagulants. Hypersensitivity rxns—generalized urticaria, bronchial asthma, laryngeal edema, bronchoconstriction, hypotension, shock—may occur in 20-25% of pts w/asthma, nasal polyps, or chronic urticaria. Utility: Acute MI, stable/unstable angina, 2° prevention in MI survivors. TIA. 2° prevention in nondisabling ischemic stroke. Prevention of saphenous vein bypass graft occlusion. Post-coronary angioplasty. 1° MI prophylaxis (325 mg/d) adjunctive to risk factor management. Headache. Special Features: Low dose Rx optimal—75-325 mg/d. Antithrombotic use is primarily for arterial thromboses.
Ticlopidine (Ticlid)
2008-04-08 19:24:00 Name: Ticlopidine (Ticlid) Class: Antithrombotic Agent (Antiplatelet Agent) Mechanism: Unknown. Through some effect on platelet membranes, blocks ADP-induced aggregation. Interacts w/membrane glycoprotein IIb/IIIa. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Diarrhea, GI cramping, rash, LDL & VLDL, leukopenia, agranulocytosis, pancytopenia. Utility: Treat thromboses in patients unable to take aspirin. May be more effective than aspirin in 2° prevention of stroke in pts w/previous TIA. Special Features: Several days required for effects to develop. Effects persist for several days after cessation of treatment. As effective in E as in G. Antithrombotic use is primarily for arterial thromboses.
Dipyridamole (Persantine)
2008-04-08 19:24:00 Name: Dipyridamole (Persantine) Class: Antithrombotic Agent (Antiplatelet Agent) Mechanism: Inhib. PDE in platelets ® cAMP ® inhib. of platelet activation. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Utility: Prevention of systemic embolism in pts. w/prosthetic heart valves. Admin. in combination w/warfarin. Special Features: When used alone, ineffective for Rx of cerebral or CV thrombotic events. Not proven to be of additional benefit when admin. w/aspirin. Antithrombotic use is primarily for arterial thromboses.
Amyl Nitrate
2008-04-08 19:24:00 Name: Amyl Nitrate Class: Antianginal Agent (Organonitrate) Mechanism: Converted to NO ® activation of cytosolic guanylate cyclase ® cGMP ® activation of cGMP-dependent protein kinase ® smooth muscle relaxation ® vasodilation. Greater effect in veins & large arteries than in resistance vessels ® ¯¯ preload, ¯ afterload ® ¯ work ® ¯ O2 demand. Inhib. of platelet fxn. Absorption: Inhalation ® rapid onset. Dist.: Metabolism.: Hepatic inactivation via glutathione-organic nitrate reductase. Excretion, t½: Renal. Short duration of action (3-5 min.). Toxicity/S.E.s: Orthostatic hypotension, tachycardia, severe throbbing headache, dizziness, flushing, syncope. C/i w/elevated ICP. Utility: Treat angina. Not suitable for maintenance therapy. Special Features:
Isosorbide Dinitrate (Isordil)
2008-04-08 19:23:00 Name: Isosorbide Dinitrate (Isordil) Class: Antianginal Agent (Organonitrate) Mechanism: Converted to NO ® activation of cytosolic guanylate cyclase ® cGMP ® activation of cGMP-dependent protein kinase ® smooth muscle relaxation ® vasodilation. Greater effect in veins & large arteries than in resistance vessels ® ¯¯ preload, ¯ afterload ® ¯ work ® ¯ O2 demand. Inhib. of platelet fxn. Absorption: Sublingual preferred ® complete absorption. Oral ® 1st pass Metabolism, low bioavail. Buccal/transdermal ® slow absorption. Dist.: Metabolism.: 80% converted to active Metabolismolite 5-ISMN before entering systemic circulation. Hepatic inactivation via glutathione-organic nitrate reductase. Excretion, t½: Renal. 10 min. Short duration of action (20-30 min.). Toxicity/S.E.s: Orthostatic hypotension, tachycardia, severe throbbing headache, dizziness, flushing, syncope. C/i w/elevated ICP. Utility: Treat angina. Subling. not suitable for maintenanc...
Nitroglycerin (Nitro-Bid)
2008-04-08 19:22:00 Name: Nitro glycerin (Nitro-Bid) Class: Antianginal Agent (Organonitrate) Mechanism: Converted to NO ® activation of cytosolic guanylate cyclase ® cGMP ® activation of cGMP-dependent protein kinase ® smooth muscle relaxation ® vasodilation. Greater effect in veins & large arteries than in resistance vessels ® ¯¯ preload, ¯ afterload ® ¯ work ® ¯ O2 demand. Inhib. of platelet fxn. Absorption: Sublingual preferred. IV. Oral ® 1st pass Metabolism, low bioavail. Buccal/transdermal ® slow absorption. Dist.: Metabolism.: Hepatic (glutathione-organic nitrate reductase), extra-hepatic. Plasma clearance >> C.O. Excretion, t½: Renal. 3 min. Short duration of action (20-30 min.). Toxicity/S.E.s: Orthostatic hypotension, tachycardia, severe throbbing headache, dizziness, flushing, syncope. C/i w/elevated ICP. Utility: Treat angina. Subling. not suitable for maintenance therapy. IV for severe recurrent unstable angina. Oral/buccal/transdermal for pr...
Probucol (Lorelco)
2008-04-08 19:21:00 Name: Probucol (Lorelco) Class: Blood Lipid-Lowering Agent (Fibric Acid Derivative) Mechanism: Stim. LDL clearance by non-receptor pathways. May reduce risk of atherogenesis w/o altering serum cholesterol levels. May block oxidation of LDL. Moderate ¯ in cholesterol, LDL, & HDL. No effect on TG or VLDL. Absorption: Dist.: Stored in fat. Metabolism.: Excretion, t½: Toxicity/S.E.s: Generally very well tolerated (2-6% incidence). Flatulence, n/v/d, abd. pain, headache, rash. C/i in monkeys (cardiac arrhythmias). Stored in fat. E advised to wait 6 mo. after last dose before becoming pregnant. Utility: Treat hyperlipidemia IIA/IIB, but prob. not drug o’ first choice. May be useful for homozygous familial hypercholesterolemia (IIA). May cause regression of xanthomas. Special Features: ¯ in LDL takes 1-3 mo., but some pts. don’t respond. Does not further reduce LDL when used w/lovastatin.
Clofibrate (Atromid-S) mnemonic
2008-04-07 17:45:00 Name: Clofibrate (Atromid-S) mnemonic Class: Blood Lipid-Lowering Agent (Fibric Acid Derivative) Mechanism: catabolism of VLDL, in part 2° to activity of lipoprotein lipase in adipose tissue. Moderate ¯ in TG & VLDL. Zero-mild ¯ in cholesterol. Zero-mild in HDL. Mild or ¯ in LDL. Absorption: Dist.: Metabolism.: Glucuronide conjugation. Excretion, t½: Renal excretion. Toxicity/S.E.s: Generally well tolerated. Gallstones, nausea, diarrhea, abdominal discomfort. Displaces weakly acidic drugs (T3, T4, warfarin, phenytoin) from plasma proteins. Binds cholestyramine. Utility: Treat severe hyperlipidemia IV refractory to gemfibrozil or niacin. Special Features: Does not appear to decrease frequency of CHD-related incidents.
Nicotinic Acid (Niacin)
2008-04-07 17:45:00 Name: Nicotinic Acid (Niacin) Class: Blood Lipid-Lowering Agent Mechanism: Reduces synth. rate of VLDL. Inhib. lipolysis of TG in adipocytes. Large ¯ in TG. Moderate ¯ in cholesterol & VLDL. Mild ¯ in LDL. Zero-moderate in HDL. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Cutaneous flushing (92%), itching (49%), rashes (20%). Reduce w/aspirin pretreatment, admin. after meals, small init. dose gradually increased in size. Pruritis, dry skin, pigmentation, hepatotoxicity, n/v, dyspepsia, peptic ulceration, urinary frequency, dysuria, gout. High doses ® hepatic/pancreatic dysfxn. Coadmin. anti-hypertensives ® dizziness, syncope. Sustained-release preparations more commonly assoc. w/hepatotoxicity, dry eyes, pigmentation, hyperglycemia. Utility: Prob. DOC for hyperlipidemias IV and V. Very useful for III. Can be used for II. Synergy w/resins. Special Features:
Gemfibrozil (Lopid) mnemonic
2008-04-07 17:45:00 Name: Gemfibrozil (Lopid) mnemonic Class: Blood Lipid-Lowering Agent (Fibric Acid Derivative) Mechanism: catabolism of VLDL, in part 2° to activity of lipoprotein lipase in adipose tissue. Moderate ¯ in TG & VLDL. Mild ¯ in LDL and cholesterol. Moderate in HDL. Absorption: Dist.: Metabolism.: Glucuronide conjugation. Excretion, t½: Renal excretion. Toxicity/S.E.s: Generally well tolerated. GI distress, rash, musculoskeletal pain, blurred vision, anemia, leukopenia, gallstones. Adjust dose in pts. w/renal insufficiency. Utility: DOC for hyperlipidemia III. Better tolerated than niacin for type IV, although less effective. Decreases frequency of CHD-related incidents. Special Features:
Colestipol (Colestid)
2008-04-07 17:44:00 Name: Colestipol (Colestid) Class: Blood Lipid-Lowering Agent (Resin) Mechanism: Binds bile acids in intestine ® defecation of bile acids, conversion of cholesterol to bile acids, ¯ pool of hepatic cholesterol, activity of apoB/E receptor, LDL clearance, ¯ plasma cholesterol. Moderate ¯ in cholesterol & LDL. Mild in HDL. Zero-moderate in TG & VLDL. Absorption: Oral. No absorption. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Flatulence, constipation, gas, n/v, steatorrhea. Supersaturation of cholesterol in bile ® gallstones, need for cholecystectomy. ¯ bile ® ¯ absorption of lipid-soluble drugs/vitamins. Binds acidic drugs. Weak stim. of VLDL synth. Do not use in pts. w/hyperTG w/o concurrent TG-lowering agent. Utility: Treat hyperlipidemia IIA/IIB. Use alone or w/niacin, probucol, or HMG CoA reductase inhib. Special Features: GI S.E.s reduced if taken im...
Diltiazem (Cardizem)
2008-01-31 19:43:00 Name: Diltiazem (Cardizem) Class: Calcium-Entry Blocking Agent (Antidysrhythmic Agent Class IV) Mechanism: Binds L-type Ca2+ channels® ¯ Ca2+ in arterial smooth muscle cells ® vasodilation ® ¯ TPR, coronary blood flow, ¯ cardiac afterload. Little/no effect on venous vessels. ¯ inotropy, chronotropy, & dromotropy. Net = ¯ HR, ¯ contractility, ¯ BP. May inhib. platelet aggreg. Absorption: Oral ® nearly complete absorption. 1st pass Metabolism®¯ bioavail. IV. Dist.: Significant protein binding. Metabolism.: Hepatic. Inducible Metabolism. Inhib. hepatic enzymes. Active Metabolismolites. Excretion, t½: 1.5-6 hr. Repeated oral dose ® t½ due to hepatic saturation. Longer t½ in elderly or pts w/hepatic cirrhosis or renal insuff. Toxicity/S.E.s: Dizziness, hypotension, headache, flushing, edema, constipation (less than verapamil), bradycardia, gingival hyperplasia. Aggravation of myocardial ischemia (less than w/DHPs). digoxin levels. C/i for...
Nifedipine (Procardia)
2008-01-31 19:43:00 Name: Nifedipine (Procardia) Class: Calcium-Entry Blocking Agent (Dihydropyridine) Mechanism: Binds to L-type Ca2+ channels ® ¯ Ca2+ in arterial smooth muscle cells ® vasodilation ® ¯ TPR, coronary blood flow, ¯ cardiac afterload. Little/no effect on venous vessels. No direct effect on conduction or automaticity. Vasodilation ® reflex sympathetic response ® HR, contractility. Net = ¯ BP, HR, contractility, CO. May inhib. platelet aggreg. Absorption: Oral ® nearly complete absorption. 1st pass Metabolism®¯ bioavail. IV. Dist.: Significant protein binding. Metabolism.: Hepatic. Inducible Metabolism. Inactive Metabolismolites. Excretion, t½: 1.5-6 hr. Repeated oral dose ® t½ due to hepatic saturation. Longer t½ in elderly or pts w/hepatic cirrhosis or renal insuff. Toxicity/S.E.s: Dizziness, hypotension, headache, flushing, peripheral edema, gingival hyperplasia. Aggravation of myocardial ischemia, angina. C/i w/CHF. Utility: R...
Verapamil (Calan)
2008-01-31 19:42:00 Name: Verapamil (Calan) Class: Calcium-Entry Blocking Agent (Antidysrhythmic Agent Class IV) Mechanism: Binds to L-type Ca2+ channels ® ¯ Ca2+ in arterial smooth muscle cells ® vasodilation ® ¯ cardiac afterload. Little/no effect on venous vessels. ¯ inotropy, chronotropy, & dromotropy. Net = ¯ HR, ¯ conduction, ¯ contractility, ¯ BP. May inhib. platelet aggreg. Absorption: Oral ® nearly complete absorption. 1st pass Metabolism®¯ bioavail. IV. Dist.: Significant protein binding. Metabolism.: Hepatic. Inducible Metabolism. Inhibits hepatic enzymes. Active Metabolismolites. Excretion, t½: 1.5-6 hr. Repeated oral dose ® t½ due to hepatic saturation. Longer t½ in elderly or pts w/hepatic cirrhosis or renal insuff. Toxicity/S.E.s: Dizziness, hypotension, headache, constipation, gingival hyperplasia, flushing, edema. Aggravation of myocardial ischemia (less than w/DHPs). Serious toxicities (bradycardia, transient asystole, exacerbation of heart...
Nitroprusside (Nipride)
2008-01-31 19:37:00 Name: Nitroprusside (Nipride) Class: Antihypertensive Agent Mechanism: Stim. membrane-assoc. guanylyl cyclase in vascular smooth muscle cells ® intracellular cGMP ® activation of cGMP-dependent protein ® vasodilation of arterial and venous vessels® reflex tachycardia. Reduces BP in all pts., regardless of etiology. Decreases afterload and preload. Absorption: Continuous IV infusion. Oral ® cyanide poisoning. Dist.: Metabolism.: Excretion, t½: Minutes Toxicity/S.E.s: Tachycardia, hypotension, cyanide toxicity (Rx w/sodium thiosulfate). Utility: Hypertensive emergencies. Special Features:
Diazoxide (Hyperstat I.V.)
2008-01-29 15:57:00 Name: Diazoxide (Hyperstat I.V.) Class: CHF Rx (Vasodilator) (Antihypertensive) Mechanism: Direct arteriolar vasodilation ® ¯ TPR ® reflex in HR & CO. Absorption: IV. Dist.: Metabolism.: Excretion, t½: Long duration of action. Toxicity/S.E.s: Severe tachycardia, prolonged hypotension (possibly resulting in stroke or MI). Utility: Treat hypertensive emergencies, hypertensive encephalopathy, and eclampsia. Special Features:
Hydralazine
2008-01-29 15:57:00 Name: Hydralazine Class: CHF Rx (Vasodilator) Mechanism: Acts directly on smooth muscle cells ® vasodilation. Mechanism unknown. ¯ BP ® reflex tachycardia & CO. renin concentration. NE in heart failure. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Reversible lupus-like synd. Headache, nausea, sweating, arrhythmia, angina, tachycardia. Utility: Treat CHF. Chronic use ® reduction in two year mortality by 34%. Almost always coadmin. w/b-blocker (to oppose tachycardia) and a diuretic (to decrease Na+ retention). Treat resistant HTN and hypertensive emergencies. Special Features:
Minoxidil (Loniten)
2008-01-29 15:57:00 Name: Minoxidil (Loniten) Class: CHF Rx (Vasodilator) (Antihypertensive) Mechanism: Direct arteriolar vasodilation ® ¯ TPR ® reflex in HR & CO. Absorption: Oral. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Severe tachycardia. Serious Na+ & H2O retention ® volume overload, edema, CHF. Hypertrichosis. Utility: Treat severe-malignant HTN refractory to other drugs. Male pattern baldness. Special Features: Reflex tachycardia may be severe, requiring concomitant use of a diuretic and a b-blocker.
Amrinone (Inocor)
2008-01-29 15:56:00 Name: Amrinone (Inocor) Class: CHF Rx (PDE Inhibitor) Mechanism: Inhib. of PDE III® cAMP ® contractility, stroke volume, ejection fraction, heart rate, exercise capacity. In smooth muscle, inhib. ® vasodilation. Absorption: IV only. Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: mortality from heart failure (possibly due to arrhythmogenesis). Utility: Treat CHF. Special Features:
Digitoxin (Crystodigin)
2008-01-29 15:56:00 Name: Digitoxin (Crystodigin) Class: CHF Rx (Cardiac Glycoside) Mechanism: Inhib. of Na+/K+ ATPase ® release of Ca2+ from SR ® myocardial contractility. Also sensitivity of AV node to vagal stimulation ® ¯ ventricular rate in atrial flutter or fibrillation (i.e., anti-arrhythmic). Absorption: Dist.: Strong protein binding. Metabolism.: Hepatic Metabolism. Excretion, t½: Feces. Longer t½ than digoxin. Toxicity/S.E.s: Low therapeutic index. Toxicity enhanced by hypokalemia. Arrhythmias (possibly life-threatening), anorexia, n/v/d, drowsiness, fatigue, visual disturbances. Verapamil or quinidine ® toxicity. Utility: Treat heart failure. Special Features: Active Metabolismolites. Longer t½, more GI absorption, and more protein binding than digoxin.
Dobutamine (Dobutrex)
More articles from this author:2008-01-29 15:56:00 Name: Dobutamine (Dobutrex) Class: CHF Rx (Mixed (a-b) Agonist (Cardioselective)) Mechanism: Stim. a and b receptors, but not DA. ® CO w/o HR. stroke volume. No/little change in peripheral resistance. cAMP ® contractility. Absorption: IV ® rapid onset (1-2 min). Peak effect ~ 10 min. Dist.: Metabolism.: Methylation by COMT. Conjugation Excretion, t½: 2 min. Toxicity/S.E.s: BP, HR, tachycardia, ventricular ectopic activity. myocard. O2 consump. may cause size MI. Tachyphylaxis to b stim. Utility: Short-term treatment of cardiac decompensation after cardiac surgery or w/CHF or acute MI. Often DOC after acute MI. Treatment of shock after correction of hypovolemia. 1, 2, 3, 4 |
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