MOA: Bind ATIII: increase affinity for serine proteases, Xa and IIa, lipase release clears chylomicrons, neutralizes positive charge of vascular wall, causes endothelial release of TFPI

Route of Admin: Mostly IV (some subQ), 5-10min onset

Clinical: Surgical anticoagulant (open heart b/c antagonist), Prophylaxis/ Anticoag, Unstable angina

Side Effects: Bleeding (GI), HIT, osteoperosis, alopecia

*monitored by APTT (2-2.5x baseline)

*Metab: Kidney/Liver: Adjust RI

*Strongly acidic (protamine sulfate antagonist)

Low Molecular Weight Heparin

MOA: Complex with ATIII; inhibits Xa and IIa,

Route of Admin: SubQ (cross barrier more easily)

Clinical: Prophylaxis/Treatment DVT, ACS

Side Effects: Bleeding

Fondaparinux

(pentasaccharide)

Pentasaccharide Synthetic Heparin

MOA: Bind ATIII, inhibit Xa

Route of Admin: SubQ

Clinical: DVT
Side Effects: Bleeding

MOA: Inhibits IIa (thrombin)

Route of Admin: IV

Clinical: Anticoag management of HIT, patients that can't tolerate Heparin 
Side Effects: Bleeding

*No cofactor

*Cleared by the liver

MOA: Inhibits IIa (thrombin)

Route of Admin: IV

Clinical: Anticoag management of HIT 
Side Effects: Bleeding

*Also antiplatelet effects: approved for PTCA

MOA: Inhibits IIa (thrombin)

Route of Admin: IV

Clinical: Anticoag management of HIT 
Side Effects: Bleeding

*Short t1/2

*NO cofactor

*Kidney excretion: adjust RI

*Commercially available refludan

MOA: Inhibits IIa (thrombin) - all serine protease when combined with heparin

Route of Admin: IV

Clinical: DIC, sepsis, thrombophilia, hypercoaguable state
Side Effects: None

*Treat acquired/congenital ATIII deficiency

MOA: Heparin antagonist (highly basic)

Route of Admin: IV

Clinical: Reversal of Heparin

Side Effects: Bradycardia/ Hypotension

1USP heparin: 10ug Protamine

MOA: Competitve antagonist of Vit K (epoxidase); supress synthesis of Factor II, VII, IX, X (no gamma carboxyglutamic acid)

Monitoring: PT/INR (1.5x baseline)

Clinical: Prolonged treatment of DVT, A Fib

Side Effects: Bleeding, coumadin induced necrosis (protein C impairment)

*PIVKA antagonist

* 97% protein bound

*Liver metabolism

*Pass placental barrier: teratogen

MOA: Cofactor for Factors II, VII, IX, X

Monitoring: NONE

Clinical: Hypoprothrombinemia, Intestinal disorders, Antibiotics (bacteria in gut produce)

Side Effects: Hemolysis (rare)

Rivaroxaban

Apixaban

MOA: Anti-Xa

Monitoring: None

Clinical: Stroke prevention in Afib

Side Effects: Bleeding, liver toxicity

*Rivaroxaban: Also approved prophyl/treatment DVT

MOA: inhibits thrombin

Monitoring: None

Clinical: Stroke prevention in afib

Side Effects: bleeding, liver toxicity

MOA: Cox1 inhibitor

Route of Admin: Oral

Clinical: ACS, stroke, arterial thrombosis

Side Effects: Bleeding, gastric irritation

*Unresponsive due to COX polymorphism

MOA: ADP receptor inhibitor (ADP increases GP 2b/3a)

Route of Admin: Oral

Clinical: ACS, stroke, stent

Side Effects: Bleeding

*Resistance due to polymorphism

MOA: ADP inhibitor

Route of Admin: Oral

Clinical: ACS, stroke, Stent

Side Effects: Bleeding

*Less variation due to polymorphism, more toxic effects

MOA: Cox inhibitor

Route of Admin: Oral

Clinical: Antiinflammatory

Side Effects: Bleeding

MOA: Phosphodiesterase Inhibitor

Route of Admin: Oral

Clinical: Arteriole thrombosis, Stroke

Side Effects: Bleeding

MOA: Phosphodiesterase inhibitor

Route of Admin: Oral

Clinical: Intermittent claudication

Side Effects: Hypotension

MOA: GP 2b/3a inhibitor

Route of Admin: IV

Clinical: ACS, PCI

Side Effects: Bleeding

MOA: GP 2b/3a inhibitor

Route of Admin: IV

Clinical: ACS, PCI

Side Effects: Bleeding

MOA: GP 2b/3a inhibitor

Route of Admin: IV

Clinical: ACS, PCI

Side Effects: Bleeding

MOA: Fibrinolytic (activate t-PA)

Route of Admin: IV

Clinical: Thrombolysis, Stroke, MI, PE

Contra: Intracranial bleeding, hemorrhage, pregnant

Side Effects: Bleeding, Re-occulsion (embolism)

*Local or Sytemic

MOA: Fibrinolytic

Route of Admin: IV

Clinical: Thrombosis, stroke, MI, PE

Contra: Intracranial bleed, hemorrhage, pregnancy

Side Effects: Bleeding, re-occulsion (embolism)

MOA: Fibrinolytic

Route of Admin: IV

Clinical: Thrombosis, Stroke, MI

Contra: Intracranial bleed, hemorrhage, pregnant

Side Effects: Bleeding

*not indicated for PE

*Alteplase: human tPA

*Reteplase: stronger fibrin affinity

*Tenecteplase: longer t1/2

MOA: anti-fibrinolytic: fibrinolytic antagonist

Route of Admin: IV

Clinical: Reversal of Bleeding

Side Effects: Hypotension

MOA: Antifibrinolytic: inhibit kallikrein (procoagulant) block production of bradykinin

Route of Admin: IV

Clinical: Reversal of bleeding

Side Effects: Graft thrombosis

*stronger than Epsilon Amino Caproic Acid

MOA: Fibrinolytic (from venom)

Route of Admin: IV

Clinical: Stroke

Side Effects: Allergic Rxn

MOA: AntiFibrinolytic

Route of Admin: IV

Clinical: Reversal of Bleeding

Side Effects: Retinopathy

MOA: Inhibit HMG-CoA Reductase, Increase LDLR (SREBP transcript), ↓ Cholesterol = less VLDL production (↓triglyceride)

PK: Lova, Simva, Alva (CYP3E4), Fluva, Rosuva (2C9) Prava (renal - use w/ cyclosporin)

Therpeutic: Elevated LDL or High Risk Cardiovasc disease

Adverse: Myalgia, Myopathy: Rhabdomyelosis (myoglobin in urine) (Minor: GI, liver function, increase DMT2)

Drug Interaction: CYP450 metabolized drugs (Not Pravastatin), grapefruit juice, increase CYP450, GEMIFIBRIZOL: inhibit glucouronidation & OATP2 transporter

*Other effects: dec adhesion of monocytes, dec oxidation LDL, stabilize endothelium (dec rupture), dec monocyte and SMC replication, dec inflammation

Cholestyramine, Cholestipol, Cholesevelam

MOA: Cation binds bile so can't be reabsorbed; increase cholesterol 7-a hydroxylase to produce more bile, deplete stores, increase SREBP, increase LDLR

PK: totally excreted in feces

Therpeutic: Secondary line of LDL reduction, aggressive treatment in COMBO with statin, pregnant women

Adverse: Increase HMG-CoA Reductase, increase VLDL (Contra: Type III Dyslipoproteinemia), GI, decrease fat soluble vit absorp (cholestipol/cholestyramine)

*Relieve pruritis, prevent Crohn's diarrhea, bind toxin A/B in C. Diff

MOA: Sterol absorption inhibitor (NPC1L1), decreases VLDL (some become LDL), increase LDLR

PK: circulates enterohepatically

Therpeutic: LDL hyperlipidemia, in combo with statin to reduce dose of statin; Familial hypercholesterolemia

Adverse: Well tolerated, Flatulence

Drug Interaction: Cyclosporin increase concentration

MOA: GPR109A: Gi protein decrease cAMP, decrease lipolysis and FFA to liver, decrease triglyc/VLDL production, inhibit DGAT for triglyc production, decrease apoCIII production which increase LPL activity (clears VLDL), increases halflife of apoAI (increase HDL), reduces Lp(a): competitive inhibitor plasminogen

PK: excreted in urine

Therpeutic: Familial hyperlipidemia, most effective HDL raiser, Reduce MI, COMBO statin/resin

Adverse: Skin flushing and pruritis, inhibits uric acid secretion (GOUT), hyperglycemis (DMT2), peptic ulcer

Gemfibrozil, Fenofibrate

MOA: Ligand for PPARa, increase HDL, decrease LDL( increase LPL, decrease apoCIII), increase periph VLDL clearance, decrease hepatic TG synthesis, increase SR-B1 receptor for HDL increase cholesterol clearance

PK: protein bound, extrahepatic circulation

Therpeutic: hypertriglyceridemia (risk for pancreatitis), low HDL, DOC familial dysbetalipoproteinemia

Adverse: GI, Gallstone (decrease cholesterol 7a hydroxylase), Gemfibrizol (RHABDOMYELOSIS)

Drug Interaction: Protein bound (warfarin), hypoglycemia (sulfonylurea), STATIN (Gemfibrizol - inhibits transporter and glucouronidation)

Contra: Pregnant, Liver Failure (risk dysfunction), Renal Failure (excreted)

MOA: covalent modification of proteins (MLC)

Route of Admin: Inhalation

Clinical: ACS, pulm hypertension, ARDS

Side Effects: hypotension, vasodilation

*inhibit white cell adhesion (decrease E-selectin from endothelial cells)

Nitroglycerine or

Isosorbide Dinitrate

MOA: NO donor: requires cystein cofactor

Route of Admin: sublingual (rapid), oral (intermediate)

Clinical: Pulm artery hypertension, Atherosclerotic diseases (decreased endothelial NO release)

Side Effects: hypotension

*Amyl nitrate (rapid - rarely prescribed)

MOA: NO donor, vasodilation

Route of Admin: Oral

Clinical: Hypertension

Side Effects: Headache, nausea, vomiting, hypotension

MOA: Phosphodiesterase inhibitor (increase cGMP)

Route of Admin: Oral

Clinical: Hypertension, ED

Side Effects: hypotension

MOA: NO donor (increase production of NO)

Route of Admin: Oral

Clinical: ACS, vascular disease (decreased NO from endothelium)

Side Effects: hypotension

MOA: arginine derivative compete for NOS

Route of Admin:

Clinical: Sepsis, inflammatory condtions, excess peroxynitrite (toxic to cells, less GTH in disease condition)

Side Effects: hypertension

*Heme: NO scavenger

*5-Methylthiolcitrulline

*7-Nitroindazole: binds NOS

MOA: ACE inhibitor

Route of Admin: Oral

Clinical: Hypertension

Side Effects: Severe stomach pain, hypotension

*enalapril is a prodrug

Saralasin

Losartan/Valsartan

MOA: Angiotensin Receptor Antagonist

Route of Admin: Oral

Clinical: Hypertension

Side Effects:

Losartan: diarrhea, insomnia, nasal congestion

Valsartan: Stomach pain, nausea

MOA: Kallikrein inhibitor

Route of Admin: IV

Clinical: Inflammation

Side Effects: Heart attack, stroke, kidney failure (decrease bradykinin production)

MOA: Non-selective inhibitor of ETa and ETb (endothelin receptor)

Route of admin: oral and IV

Clincial: pulmonary hypertension

Side Effects: liver problems, stomach pain, nausea

MOA: Bradykinin B2 receptor antagonist

Route of admin: Oral

Clincial: Inflammatory response

Side Effects: stomach pain, nausea

Desmopressin

(DDAVP)

MOA: ADH analogue

Route of admin: IV

Clincial: Diabetes insipidis, increase factor VIII and vWF for surgery and blood banking

Side Effects: Stomach pain, nausea

MOA: Reversible carbonic andhydrase inhibitor: Inhibits reabsorption of HCO3- (takes Na with it)

Pharm: Oral, Renal secretion via OAT

Adverse: Metabolic acidosis, hypokalemia (increase HCO3- in collecting tubule), Calcium phosphate stones (bicarb increase pH in tubule), drowsiness, parasthesis, hypersensitivity rxn

Contraindication: Cirrhosis (increase pH, decrease NH3 secretion, trapped as NH4+ in low pH)

Clinical: weak diuretic, glaucoma, urinary alkalinization (trap weak acids), acute mountain sickness

MOA: carbonic anhydrase inhibitor

Clinical: weak diuretic, glaucoma, alkalinization of urine, acute mountain sickness

*30x more potent than acetazolamide

MOA: carbonic anhydrase inhibitor

Clinical: weak diuretic, glaucoma, alkalinization of urine, acute mountain sickness

*5x more potent than acetazolamide

MOA: carbonic anhydrase inhibitor

Clinical: weak diuretic, glaucoma, alkalinization of urine, acute mountain sickness

*topical preparation for ocular use

MOA: Osmotic diuretic (H20 follows); acts in proximal tubule, descending limb and collecting duct if ADH is present

Pharm: IV (initial volume expansion), filtered by glomerulus

Adverse: Deposition in tissue ECF (CHF, CRF), hyponatrimia (Na stays behind with H2O), pulm edema, dehydration, HA, N/V

Contraindication: CHF, CRF, Pulm edema

Clinical: Maintain/Increase Urine vol (ACUTE renal failure, increase flow to excrete toxic substance), reduced ICP (doesn't cross BBB, draws H2O out), reduced intraoc pressure

MOA: inhibit Na/K/2Cl transporter: Increase lumenal Na, K, Cl, Ca, Mg; Vasodilation: increase RBF w/ prostaglandins

Pharm: Oral, Renal secretion OAT, short t1/2

Adverse: Hyponatermia, hypokalemia, hypomagenesimia, dehydration, metabolic alkalosis, mild hypoglycemia (change in Ca, change insulin), ototoxicity, hypersensitivity

Contra:

Clinical: Acute pulm edema, CHF edema, acute hypercalcemia, acute hyperkalemia, acute hypertension

MOA: inhibit Na/K/2Cl transporter: Increase lumenal Na, K, Cl, Ca, Mg; Vasodilation: increase RBF w/ prostaglandins

Clinical: Pulm edema, CHF edema, acute hypercalcemia, acute hyperkalemia, acute hypertension

*40x more potent, shorter t1/2 than furosemide, 50% metab by liver

MOA: inhibit Na/K/2Cl transporter: Increase lumenal Na, K, Cl, Ca, Mg; Vasodilation: increase RBF w/ prostaglandins

Clinical: Pulm edema, CHF edema, acute hypercalcemia, acute hyperkalemia, acute hypertension

*Longer t1/2 than furosemide, better oral absorp, 80%metab by liver

MOA: inhibit Na/K/2Cl transporter: Increase lumenal Na, K, Cl, Ca, Mg; Vasodilation: increase RBF w/ prostaglandins

Clinical: Pulm edema, CHF edema, acute hypercalcemia, acute hyperkalemia, acute hypertension

*Different structure, used in hypersentivity, LAST RESORT; Nephrotoxity/Ototoxicity worst

MOA: inhibition of Na/Cl cotransporter in distal conv tubule

Pharm: Decrease Na (diuretic), increase Ca2+ reabsorp, ORAL, OBT

Adverse: Hyponatremia, hypokalemia, dehydration, metabolic alkalosis, hyperglycemia, hyperlipidemia, weakness, parasthesis

Contra:

Clinical: Hypertension (1st line DOC), CHF, decrease Ca excretion for kidney stones

MOA: inhibit Na/Cl cotransporter, increase Ca2+ reabsorp

Clinical: Hypertension (1st line DOC), CHF, increase Ca excretion

*Parent drug: 1/10 potency hydrochlorothiazide

MOA: Inhibit Na/Cl cotransporter, increase Ca resabsorp

Clinical: Hypertension (1st line DOC), CHF, increase Ca excretion

*10x more potent, longer t1/2 than hydrocholothiazide

MOA: Inhibit Na/Cl cotransporter, increase Ca resabsorp

Clinical: Hypertension (1st line DOC), CHF, increase Ca excretion

*20x more potent, long t1/2 dose 1 per day

MOA: Inhibit Na/Cl cotransporter, increase Ca resabsorp

Clinical: Hypertension (1st line DOC), CHF, increase Ca excretion

*Same potency as hydrocholothiazide, longest t1/2 40hrs

MOA: competitve inhibition of aldosterone receptor (antiandrogenic effects): diuresis due to decrease build up of charge from Na channels (K/H sparing)

Pharm: Slow onset, Liver metabolize to active metabolite

Adverse: hyperkalemia, metabolic acidosis, gynecomastia, GI upset, CNS effects
Contra: Hyperkalemia

Clinical: Primary hyperaldosteronism, Secondary hyperaldosteronism (cirrhosis/HF), liver cirrhosis, hypertension

MOA: competitve inhibition of aldosterone receptor: diuresis due to decrease build up of charge from Na channels (K/H sparing)

Pharm: Slow onset, Liver metabolize to active metabolite

Adverse: hyperkalemia, metabolic acidosis, GI upset, CNS effects
Contra: Hyperkalemia

Clinical: Primary hyperaldosteronism, Secondary hyperaldosteronism (cirrhosis/HF), liver cirrhosis, hypertension

*No antiandrogenic effects, More expensive

MOA: Blocks Na channels in principle cells

Pharm: Decrease driving force for K+ excretion, t1/2 21hrs, OBT

Adverse: hyperkalemia (exacerbated by NSAIDs), GI upset, muscle cramps, CNS effects

Contra:

Clinical: edema, hypertension, in combo with other drugs to reduce K loss

MOA: block Na channels in principle cells

Pharm: K+ sparing, liver metabolizes to active, OBT

Adverse: Active form can precipitate in tubule and obstruct

Contra:

Clinical:

*10x less potent than amiloride

ADH inhibitor

Tetracycline antibiotic: nephrotoxic

ADH inhibitor

Psych drug, nephrotoxic

MOA: ADH V2 Receptor antagonist

Pharm: Oral, doesn't alter serum electrolyte balance

Adverse:

Contra:

Clinical: Hyponatremia (edema)

Conivaptan: V1 and V2 Receptor

Hypertension:

Diuretics

Thiazides:

MOA: NaCl transporter blocker in distal convoluted tubule

Adverse: Hyponatremia, hypokalemia, hyperglycemia, increased LDL/HDL

Drug Interaction: NSAIDs, BBs

Contra: Existing hypokalemia, Pregnancy

Clinical: Mild-Moderate Uncomplicated Hypertension DOC

*Hydrochlorothiazide, chlorthalidone

Hypertension

Diuretics

Loop Diuretics

MOA: Block Na/K/2Cl cotransporter in thick ascending loop: less effective/shorter duration than thiazide

Adverse: hyponatrimia, hypokalemia, impaired diabetes control, increase LDL/HDL, ototoxicity

Drug Interaction: NSAIDs, Aminoglycosides

Contra:

Clinical: Patients with moderate to severe renal insufficency and CHF

*Furosemide

Hypertension

Diuretics

Potassium Sparing

MOA: See below

Adverse: Hyperkalemia, Gynecomastia (spirono)

Drug Interactions: NSAIDs, ACEi/ARB (decrease aldosterone too, hyperkalemia)

Clinical: ONLY combo with other to prevent hypokalemia, with vasodilators counteract baroreceptor

*Spironalactone, Eplerenone: aldosterone receptor inhibitor

*Amiloride, Triamterene: ENaC blocker

Hypertension

CCB

Nifedipine

MOA: inhibit L-Type Ca channel, decrease Ca-Calmodulin, decrease MLCK, decrease art smooth muscle contraction

Adverse: Acute tachy (reflex), headache, flushing, periph edema (art>ven dilation)

Contra: DHP: liver disease

Clinical: Slow release: Hypertension

Hypertension

CCB

Diltiazem

MOA: L-Type Channel blocker, also SA node and L-Type on myocytes, reduce CO and periph resistance

Adverse: Bradycardia, edema
Drug Interaction: BBs

Contra: Liver Failure, SA node/AV node disturbances

Clinical

NONDihydropyridine: cardiac effects, T-Type Ca, decrease HR and contractility

Hypertension

CCB

Verapamil

MOA: L-Type Ca channel blocker, greatest effect on heart

Adverse: constipation (anticholinergic effect), bradycardia
Drug Interaction: BBs

Contra: Liver failure, SA/AV node disturbences

Clinical

NONDihydropyridine: cardiac effects, T-Type Ca, decrease HR and contractility

Hypertension

Sympatholytic

Clonadine

MOA: block sympathetic activation of heart

alpha2 agonist

Adverse: sedation, dry mouth, bradycardia, contact dermatitis (transdermal patch)

Drug Interaction: Potentiate other CNS depressants

Clinical

*withdraw slowly to prevent hypertension

*Guanfacine: longer t1/2, less popular

Hypertension

Sympatholytic

Methyldopa

MOA: Compete for dopamine carboxylase (decrase NE and EPI), alpha 2 agonist

Adverse: sedation

Contra: Liver Disease

Drug Interact: Levodopa (LDOPA): reduce effects

Clinical: Pregnant Women

Hypertension

Indirect Adrenergic Antagonist

Reserpine

MOA: inhibit release of NE by inhibiting reuptake into vesicles VMAT2

Adverse: Depression, nasal congestion
Drug Interact: MAOI (reverse reuptake channel on surface)

Clinical

Given with other diuretics

Hypertension

Alpha Adrenergic Antagonist

Phenoxybenzamine

MOA: Block aterial and venous contraction; NON competitive, nonselective alpha blocker

Adverse: Tachycardia (only B active); use BB after admin

Drug Interaction:

Clinical: Pheochromocytoma

Hypertension

Alpha Adrenergic Antagonist

Prazosin

MOA: alpha1 selective, less tachycardia, DECREASE LDL/HDL

Adverse: First dose HUGE decrease in BP, fluid retention

Druger Interaction: Combine with diuretic to reduce fluid retention

Clinical:

Terazosin/Doxazosin: longer t1/2 more commonly perscribed

Doesn't reduce exercise tolerance

Hypertension

Beta Adronergic antagonist

MOA: Decrease myocardial contractility

Decrease Renin release

Lipophilic CNS supression

SE: Bradycardia, increase triglyceride, decrease HDL, hyperglycemia, low exercise tolerance

 Non selective (pulm airway constriction)

Lipophilic (insomnia, fatigue)

Cardiac Selective

Vasodilatory (also NO effects)

Drug interaction: CCB increase risk of conduction disturbances

Contra: Cardiogenic Shock, Asthma UNcompensated CHF

*Withdrawn slowly: rebound hypertension

*can mask insulin induced hypoglycemia (block EPI)

Clinical: NONselective: Mild-Moderate Hypertension

Combo: reflex tachy with vasodilators and compensatory salt retention with diuretics

*lipophilic

Clinical: NONselective: Longer t1/2 dose 1 per day

Hydrophilic

Clinical: Nonselective; PARTIAL AGONIST

Used in patients with bradycardia

Clinical: Selective B1

Less resp. effects

Lipophilic

Clinical: B1 selective

Less Resp. Effects

Hydrophilic

Clinical: Mixed alpha, beta antagonist

Lipophilic

Clinical: nonselective b and some alpha antagonist

Vasodilatory effects

MOA: dilates arterioles preferentially (less posturnal hypotension)

SE: tachycardia, aggrevation angina, fluid retention

Drug Interact: NSAIDs (reduce efficacy)

Contra: Cornary Artery Disease (coronary steal)

Clincial: Resistant hypertension, Hypertensive emergency, pregnancy induced

*not used long term

MOA: Open K+ channels (not in veins - no posturnal hypotension)

SE: Tachycardia, Aggrevation angina, fluid retention

Clinical: Resistant hypertension

*not long term use

MOA: NO formation (veins and arteries)

SE: Cyanide poisoning, N/V

Clinical: Hypertensive emergency (immediate onset, brief duration - monitors continuously)

* Does not stimulate cardiac reflex

MOA: Inhibit production of angiotensin II, decrease bradykinin breakdown, reduce aldosterone

SE: hyperkalemia, dry cough, angioedema (rare/life threatening)

Drug Interaction: Hyperkalemia in other K sparing drugs

Contra: Pregnancy (angiotensin II necessary for fetal development), Bilateral renal stenosis

Clinical: Prolongs survival in patients with HF and LV dysfunction, preserve renal function in diabetes

ACEI

Requires multiple daily dosing

Generics available

ACEI

Converted into active metabolite

Longer t1/2

ACEI

Not prodrug (more predictable onset/duration)

Hydrophilic

Long t1/2

Angiotensin II Receptor Blocker

ARB

MOA: Block angiotensin receptor (AT1)

Don't block metabolism of bradykinin (no dry cough)

SE: well tolerate, hyperkalemia

Clinical: Patients who don't tolerate ACEI

Not effective in salt-sentive african americans

Effective when combined with diuretic

*LOSARTAN

MOA: Needs cysteine residue, endothelium independent NO production

SE: Orthostatic hypertension, reflex tachy, headache

Clinical:  Terminate exercise induced ischemia, prophylaxis exercise ischemia, terminate coronoary vasospasm

* tolerance: deplete cysteine

MOA: Needs cysteine residue, endothelium independent NO production

SE: Orthostatic hypertension, reflex tachy, headache

Clinical:  Terminate exercise induced ischemia, prophylaxis exercise ischemia, terminate coronoary vasospasm

MOA: L-Type Ca Channel Blocker, less Ca in cell (ionotropic), less Ca for depolarization (chronotropic) SA and AV Node

SE: Bradycardia, heart block, CHF, hypotension, reflex tachy, periph edema

Clinical: Angina, hypertension, arrhythmia, hypertrophic cardiomyopathy, migraine, raynaud phenomenon

*Short Acting; Vasodilator

MOA: L-Type Ca Channel Blocker, less Ca in cell (ionotropic), less Ca for depolarization (chronotropic) SA and AV Node

SE: Bradycardia, heart block, CHF, hypotension, reflex tachy, periph edema

Clinical: Angina, hypertension, arrhythmia, hypertrophic cardiomyopathy, migraine, raynaud phenomenon

*intermediate acting

MOA: L-Type Ca Channel Blocker, less Ca in cell (ionotropic), less Ca for depolarization (chronotropic) SA and AV Node

SE: Bradycardia, heart block, CHF, hypotension, reflex tachy, periph edema

Clinical: Angina, hypertension, arrhythmia, hypertrophic cardiomyopathy, migraine, raynaud phenomenon

*Long acting

MOA: L-Type Ca Channel Blocker, less Ca in cell (ionotropic), less Ca for depolarization (chronotropic) SA and AV Node

SE: Bradycardia, heart block, CHF

Clinical: Angina, hypertension, arrhythmia, hypertrophic cardiomyopathy, migraine, raynaud phenomenon

*Ionotropic/Chronotropic Effects

MOA: L-Type Ca Channel Blocker, less Ca in cell (ionotropic), less Ca for depolarization (chronotropic) SA and AV Node

SE: Bradycardia, heart block, CHF

Clinical: Angina, hypertension, arrhythmia, hypertrophic cardiomyopathy, migraine, raynaud phenomenon

*Intermediate: Ionotropy, Chronotropy, Vasodilation

MOA: L-Type Ca Channel Blocker, less Ca in cell (ionotropic), less Ca for depolarization (chronotropic) SA and AV Node

SE: Bradycardia, heart block, CHF, hypotension

Clinical: Angina, hypertension, arrhythmia, hypertrophic cardiomyopathy, migraine, raynaud phenomenon

*Europe

B Blocker

(Angina Lecture)

MOA: B1 (cardiac), B2 (cardiac, bronchiole, sm)

SE: Bronchospasm, periph vasospasm, exaggeration of therapeutic effects, CNS

Contra: Acute CHF, Bradycardia, advance heart block, periph vascular disease, insulin dep. DM, sexual impotence

Clinical:
Angina, hypertension, arrythmia, aortic dissection, mitral valve prolapse, post MI prophylaxis, hyperthyroidism, migraine

MOA: Nonselective B Blocker

Liver elim

Short acting

MOA: Nonselective B Blocker

Long acting

Kidney Elim

MOA: cardioselective

Liver Metab

MOA: cardioselective B blocker

Renal Metab

MOA: pFOX inhibitor: inhibit B oxidation of fatty acid (metab of glucose uses limited O2 more efficiently in MI)

(during MI Fatty Acid rise, inhibit pyruvate dehydrogenase) (reduce lactic acid formation)

SE: Blocks late Na current (prolong AP, increase EADs risk)

Clinical: Angina

CHF Lecture

MOA: Decrease preload by venodilation

CHF Lecture

MOA: NO producing

Oral

CHF lecture

MOA: human recombinant Brain Natriuretic Peptide

(normally produce by ventricular myocardium in response to chronic stretch)

Vascular SM and Renal Receptors

INCREASE cGMP levels

Vasodilation/Natriuresis

Class 1: Na channel blocker

Class 2: B channel blocker

Class 3: AP prolongation: K+ Channel blocker

Class 4: Ca2+ Channel Blocker

MOA: Block fast Na channels (phase 0)

depend on HR, membrane potential and drug specific

Class Ia: Intermediate dissociation, increase APD

Class Ib: fast dissociation, decrease APD

Class Ic: slow dissociation, no APD

MOA: Class Ia

Slows upstroke of AP, prolong QRS, Depress SA/AV

Use-State Dependent (inactive)

Metabolite NAPA: Class III activity (K blocker)

Dose reduction RI

SE: Ganglion blocking, Hypotension, anticholinergic, Torsade de pointes (NAPA), longterm lupus (30%)

Indication: Atrial/Ventricular arrythmias (2/3 DOC)

MOA: Class Ia

Slows upstroke of AP, prolong QRS, Depress SA/AV

Use-State Dependent (inactive)

Dose reduction RI

SE: Ganglion blocking, Hypotension, anticholinergic, Torsade de pointes, Cinchonism: headache, nauseau, tinitis

Indication: Atrial/Ventricular arrythmias (2/3 DOC)

MOA: Class Ib

Use-State dependent

Rapid dissociation at normal RP

Selective depression of depolarized ischemic cells

Pharm: IV

SE: least cardiotoxic Class I, induce hypotension, neurologic effects (local anesthetic properties)

Clinical: V tach/ V fib after MI DOC

MOA: Class Ib

Use-State dependent

Rapid dissociation at normal RP

Selective depression of depolarized ischemic cells

Pharm: Oral

SE: least cardiotoxic Class I, induce hypotension, neurologic effects (local anesthetic properties)

Clinical: V tach/ V fib after MI DOC (but oral so uncommon)

OFF LABEL: chronic pain relief

MOA: Class Ic

Potent Na and K channel blocker, No anticholinergic

SE: Increase mortality in V tach after MI or ectopic V

Clinical: Supraventricular tachy in normal hearts

MOA: Class Ic

Na channel blocker, Some K channel block, B blocker (propanolol)

Adverse: Increase mortality in vent. tachy post-MI, Bradycard/Bronchospasm, Metalic taste

Clinical: Supraventricular tachy (normal heart)

Propranolol

(Sotanol, Timolol)

MOA: nonselective B blocker (sotanol class III)

Reduce HR, decrease intracellular Ca, decrease pacemaker automaticity, reduce conduction velocity, decrease DADs and EADs

SE: Bradycardia, pulm disease, hypoglycemia

Clinical: Post-MI, Exercise induced arrythmia, afib, aflutter, av node reentry

MOA: Cardioselective B Blocker

Reduce HR, decrease intracellular Ca, decrease pacemaker automaticity, reduce conduction velocity, decrease DADs and EADs

SE: Bradycardia, pulm disease, hypoglycemia

Clinical: Post-MI, Exercise induced arrythmia, afib, aflutter, av node reentry

MOA: Class III K+ blocker (Na, Ca, B)

Prolongation of AP and Refractory period

Least effects high HR (most desirable)

Most effects at slow HR (risk torades de pointes)

Pharm: liver metab, long t1/2

SE: Bradycardia, pulm fibrosis, hypo/hyperthyroidism

clinical: DOC after MI (terminate v tach/v fib)

MOA: Class III K+ blocker (Na, Ca, B)

Prolongation of AP and Refractory period

Least effects high HR (most desirable)

Most effects at slow HR (risk torades de pointes)

Pharm: liver metab, long t1/2

SE: Bradycardia

clinical: A fib/ A flutter

*No pulm/ Thyroid effects (iodine)

*Don't use decompensated HF

MOA: L-Type Ca Channel

Main effect: slow response (SA/AV node)

Lower HR, increase PR interval

Pharm: Liver metab

SE: Vasodilation, AV block, Heart block (when also given B blockers)

Clinical: DOC Supraventricular, Re-entry arrythmia involving AV node, slows vent rate (afib)

MOA: L-Type Ca Channel

Main effect: slow response (SA/AV node)

Lower HR, increase PR interval

Pharm: Liver metab

SE: Vasodilation, AV block, Heart block (when also given B blockers)

Clinical: DOC Supraventricular, Re-entry arrythmia involving AV node, slows vent rate (afib)