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55 Cards in this Set
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Quinidine
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Class IA - Antiarrythmic Drug.
Derived from the Cinchona tree. DIRECT MOA: * Fast Na Channel Blocker (atria and ventricles) - Binds to the OPEN state. ..means most affinity for stimulated tissues (heart)...only works in the ectopic, arrythmic areas. ----> Increased Refractoriness (Na Channels Frozen) ----> Decreased Automaticity of Ectopic Pacemakers (atria and ventr) ---> Widened QRS (decr Phase 0 slope of ventricle AP). * Delayed Rectifier K Channel Blocker (a class III function). ----> Prolongs AP duration and QT interval (high risk or torsades) INDIRECT MOA: * Anti-muscarinic: Incr AV nodal conduction ----> Decreases PR Interval. * Alpha - adrenergic receptor blocker ----> Causes VD and reflex tachycardia. USE: 1) Conduction Block (all types) (will incr AV nodal conduction d/t anti musc effects) 2) Afib/ Aflutter (Na Block reduces ectopy) 3) WPW - Na blocks pvts reentry/ ectopy thru accessory conduction pathways. CAUTION: * A-fib - will treat the ECTOPY via Na channel bloackade, but will CAUSE TACHYCARDIA d/t incr AV nodal conduction (anti-musc effects).... every atrial beat will now be conveyed!!!! Tx: Give a dose of Digoxin just before Quinidine. Will pt the incr AV nodal conduction. * CHF pts that take Digoxin INTERACTIONS: * Digoxin: Quinidine inhibits the renal P-glycoproteins that are necessary for clearing Digoxin in the kidney. Inhibition pvts the clearance of Digoxin!!! Can cause Dig toxicity. Must decr the dose of digoxin BY HALF. (Quinidine also Knocks Digoxin off of the proteins...incr it's effects). SIDE EFFECTS: * Cinchonism: Headache and Tinnitus * Diarrhea - can lead to hypokalemia * Prolonged QT Interval - can cause an R on T and Torsades. ...pvt it's use alot. * Orthostatic HOTN |
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Procainamide
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Class IA - Antiarrythmic Drug.
Does not have the antimusc or a1 blockade of Quinidine! DIRECT MOA: * Fast Na Channel Blocker (atria and ventricles) - Binds to the OPEN state. ..means most affinity for stimulated tissues (heart)...works only in the arrythmic area. ----> Incr Refractoriness (Na channels frozen) ----> Decr Automaticity of Ectopic Pacemakers ----> Widened QRS (decr slope of Ventricular AP). * Delayed Rectifier K Channel Blocker (a class III function). ---> Prolonged AP Duration...Prolonged QT interval. Can cause torsades. USE: 1) Afib/ Aflutter (Na Block reduces ectopy) 2) WPW - Na blocks pvts reentry/ ectopy thru accessory conduction pathways. CAUTION: * CHF pts that take Dig. - Inhibits the P glycoprotein that helps you pee Dig out. Will cause Dig toxicity...lower the dose. SE * Drug induced Lupus - especially with SLOW ACETYLATORS (it's metabolized by they acetylase enzyme). |
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Lidocaine
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Anti-arrythmic Agent - Class IB
MOA: * Na Channel Blocker: binds to INACTIVE state. HIgh affinity for ischemic tissues/ hearts (MI, etc). (Na/K ATPase cannot work...so AP duration is longer...leaves more Na channels in teh inactive state). EFFECTS: * Incr Refractoriness...frozen Na channels. * Slight decrease in AP duration * Slows atrial and ventricular conduction (decr slope of AP - PHASE 0). * Good for ischemic hearts...LEAST CARDIOTOXIC OF ALL ANTIARRYTHIMICS - b/c it binds well to ischemic tissues...leaves normal tissues alone. * Decr Automaticity of Ectopic Pacemakers (d/t Na channel blockade..decr phase 0 slope). DOSE: * IV Only USE: * DOC for Ventricular Arrythmias (which are usually d/t ischemia). SE: with Overdose/ Toxicity.... * LOW DOSES: (tinnitus, lightheadedness, confusion) * MEDIUM DOSES: CNS Excitement (seizures) * HIGH DOSES: Depression (unconsciousness, hypotension, respiratory/cardiac arrest) |
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Tocainide
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Class IB Antiarrythmic
Na channel Blocker. BInds to Na channels of ischemic areas. ORAL SUBSTUTION OF IV LIDOCAINE! (not hepatic first pass metabolism). |
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Mexiletine
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Class IB Antiarrythmic
Na channel Blocker. BInds to Na channels of ischemic areas. ORAL SUBSTUTION OF IV LIDOCAINE! (not hepatic first pass metabolism). |
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Flecainide
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Class IC Antiarrythmic
MOA * Na Channel Blocker ----> Slows upstroke of atrial/ ventricular and ectopic APs and slows conduction, Widens QRS. * Delayed Rectifier K Channel Blocker ---> Prolongs QT Interval (but not as much of a risk of torsades). USE * Superventricular Arrythmisa: SVT, aFib, A Flutter. Maintains NSR. (F for Fibs and flutters). - Reduces the Ectopy (atrial rate). ****USED ONLY IN PTS REFRACTORY TO OTHER CLASS I AGENTS!!! (last on the list). CONTRAINIDICATIONS: ---> Pts w/ a hx of STRUCTURAL HEART DZ: study shows incr risk of mortality if pt has has ventricular arrythmias or an MI. |
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Propanolol
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Nonspecific Beta Blocker.
CARDIAC MOA (Pvts Cat. stim of cAMP) 1) Inhibits Funny Na Channel Opening ----> Decr Slope of PHASE 4 in SA/AV node ----> Decr Automaticity (HR) 2) Inhibits L-Type Ca channel opening ----> Incr Firing Threshold, Decr Slope of PHASE 0 of SA and AV node ----> (INCREASED Refractoriness of SA/ AV node). ----> (Decr SA Automaticity, Decr AV nodal conduction). -----> DECREASED refractoriness of Atrial and Ventricles....PHASE 2 of their AP is shorter. RENAL MOA: * Blocks B1 receptors in kidneys, pvting Renin stimulation...pvts RAAS. USE * ISCHEMIC HEART DISEASE: ----> Stable Angina: (Decreases Cardiac Demand). ...Stable angina is a demand issue. ----> Acute Coronary Syndrome: Unstable Angina (MI) - Decr Cardiac Demand. BUT NOT FIRST LINE D/T DECR CONTRACTILITY. * PSVTs - caused by AV nodal re-entry tachycardia * Uncontrolled A-fib/ A-flutter (slows the ventricular response via slowed AV node conduction. * DOC for Prolonged QT Syndrome!! - Shortens QT and PHASE 2 of ventricular AP. * 1st Line Tx for CHF - pvt the deleterious effects of cats on the heart. (apoptosis and heart remodelling). * 2nd line tx of HTN - Decr BP by decr CO. Reduces Renin release. (Usually used in combo with other drugs). ...Not very effective in AAs and Geriatric pts (no renin). -----> Given with nifedipine or nitrates to pvt the reflex tachycardia. BBs increase EDV, Nitrates decr EDV, so they offset each other. Good. SE * Increased EDV d/t decr cardiac output. * Bronchoconstriction * Masks the side effects of Hypoglycemia. * Fatigue : Decr exercise tolerance. * Depression * Lipid Unfriendly: Incr Triglycerides, Decr HDL CONTRAINIDICATIONS: * Pts taking non-dihydropyridine CCBs - can cause a Conduction Block d/t decr AV nodal conduction. (C+B = CB (conduction block)). * Diabetics * COPD, ASTHMA |
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Carvedilol
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Beta1, Beta2, alpha1 antagonist
Class II Antiarrythmic Agent MOA/ Effects: (Pvts Cat. stim of cAMP) - Decr HR, CO: 1) Inhibits Funny Na Channel Opening ----> Decr Slope of PHASE 4 in SA/AV node ----> Decr Automaticity (HR) 2) Inhibits L-Type Ca channel opening ----> Incr Firing Threshold, Decr Slope of PHASE 0 of SA and AV node ----> (INCREASED Refractoriness of SA/ AV node). ----> (Decr SA Automaticity, Decr AV nodal conduction). -----> DECREASED refractoriness of Atrial and Ventricles....PHASE 2 of their AP is shorter. 3) Alpha 1 Blockade decreases TPR/ SVR USE * PSVTs - caused by AV nodal re-entry tachycardia * Uncontrolled A-fib/ A-flutter (slows the ventricular response via slowed AV node conduction. * BBs are DOC for Prolonged QT Syndrome!! - Shortens QT and PHASE 2 of ventricular AP. * BBs are 1st Line tx for CHF and Ischemic Heart Disease.: block the deleterious effects of cats (apoptosis, heart remodeling). "Paradoxical" beneficial action. Combined with ACEI, ARBs, Diuretics. * Coreg = BB of Choice for CHF!!!! * 2nd line agents in tx of Essential HTN - Carvedilol and Labetalol are more efficacious then a selective a or B blocker. Used in pts who are not well controlled. These are emergency HTN meds. SE * CNS sedation and depression * Upregulation of Beta Adrenergic Receptors: tachycardia/ arrythmias with abrupt withdrawal. * Bronchoconstriction * Mask the signs of hypoglycemia. * Orthostatic HOTN (but NO reflex tachycardia or first dose syncope). * No changes in lipids!!! :) Not lipid friendly or unfriendly. * Thrombocytopenia CONTRAINDICATIONS * COPD/ Asthma * Diabetes * Use with CCBs...can cause complete heart block. |
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Metoprolol
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Beta1 Specific Beta Blocker.
CARDIAC MOA/ Effects: (Pvts Cat. stim of cAMP) 1) Inhibits Funny Na Channel Opening ----> Decr Slope of PHASE 4 in SA/AV node ----> Decr Automaticity (HR) 2) Inhibits L-Type Ca channel opening ----> Incr Firing Threshold, Decr Slope of PHASE 0 of SA and AV node ----> (INCREASED Refractoriness of SA/ AV node). ----> (Decr SA Automaticity, Decr AV nodal conduction). -----> DECREASED refractoriness of Atrial and Ventricles....PHASE 2 of their AP is shorter. ------> BIPHASIC CHANGES IN CO - originally a decr CO, but later an incr CO in CHF d/t decr deleterious effects of cats. RENAL MOA: * Blocks B1 receptors on kidneys, pvting renin stimulaton. Pvts RAAS. USE * ISCHEMIC HEART DISEASE: ----> Stable Angina: (Decreases Cardiac Demand). ...Stable angina is a demand issue. ----> Acute Coronary Syndrome: Unstable Angina (MI) - Decr Cardiac Demand. * PSVTs - caused by AV nodal re-entry tachycardia * Uncontrolled A-fib/ A-flutter (slows the ventricular response via slowed AV node conduction. * BBs DOC for Prolonged QT Syndrome!! - Shortens QT and PHASE 2 of ventricular AP. * 1st Line tx of CHF - pvt the deleterious effects of cats on the heart. (Apoptosis and heart remodeling). Combined with ACEIs and diuretics. Incr CO longterm. * 2nd Line tx of HTN - Decr BP by decr CO and pvting RAAS. -----> Given with nifedipine or nitrates to pvt the reflex tachycardia. BBs increase EDV, Nitrates decr EDV, so they offset each other. Good. ----> Not very effective in AA's and geriatric pts (no renin). * Migraine Prophylaxis SE * Increased EDV d/t decr cardiac output. (initially, but not longterm with CHF). * Masks the symptoms of Hypoglycemia * Bronchoconstriction with high doses. (Beta2 Effects). * CNS sedation and depression * Upregulation of Beta Receptors: Tachycardia or arrythmias with abrupt withdrawal. * Fatigue - Exercise Intolerance * Depression * Lipid Unfriendly CONTRAINIDICATIONS: * Pts taking CCBs (V or D) - can cause a Conduction Block d/t decr AV nodal conduction. (C+B = CB (conduction block) * Diabetics. * COPD/ ASHMA in high doses. |
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Sotalol
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Anti-arrythmic Agent: Class II and Class III
Has 2 enantiomers: One is a Class II Agent and the other is a Class III Agent. MOA - (as a Beta Blocker) * (Pvts Cat. stim of cAMP) 1) Inhibits Funny Na Channel Opening ----> Decr Slope of PHASE 4 in SA/AV node ----> Decr Automaticity (HR) 2) Inhibits L-Type Ca channel opening ----> Incr Firing Threshold, Decr Slope of PHASE 0 of SA and AV node ----> (INCREASED Refractoriness of SA/ AV node). ----> (Decr SA Automaticity, Decr AV nodal conduction). MOA - (As a Class III Agent) - * Blocks Delayed Rectifier K Channels (Ik)..Prolonged AP Duration and QT interval. USE * PSVTs - caused by AV nodal re-entry tachycardia * Uncontrolled A-fib/ A-flutter (slows the ventricular response via slowed AV node conduction. * NOT GIVEN FOR PROLONGED QT SYNDROME - the K blockade prolongs the QT interval!! * BBs for CHF and Ischemic Heart Disease, HTN * Ik Blockers for Ventricular Arrythmias refractory to Lidocaine. SE * Prolonged QT Interval...Risk of Torsades. INTERACTION: * Potassium - Sotalol competes for K+ at the Delayed Rectifier (Ik) Potassium channels. Hypokalemia will cause increased Sotalol binding. This will PROLONG THE AP DURATION, and Prolong the QT Interval. So HYPOKALEMIA INCR RISK OF TORSADES!!! ----> Hyperkalemia would reduce the effectiveness of Sotalol. * DIGOXIN TOXICITY: Will cause Hyperkalemia, which will decr the effectiveness of Sotalol. * INSULIN - will cause hypokalemia...will incr Sotalol binding and prolong QT. * DIURETICS - Will cause hypokalemia. Prolonged QT w/ Sotalol. |
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Amiodarone
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Class III Antiarrythmic Agent.
MOA: * Blocks K Channels in PHASE 3 of the atrial and ventricular AP. Prolongs AP Duration and QT Interval. (This will INCREASE REFRACTORINESS.). ONSET: Takes SEVERAL WEEKS. DURATION: Active for several weeks after admin d/t sequestering in fat. USE * Uncontrolled Afib and A flutter - will decr HR...ventricular rate control only. (Superior to Quinidine). * Ventricular Arrythmias REFRACTORY TO LIDOCAINE. METABOLISM: * Oral bioavailability 30 % * VD = 66 L/kg - LARGE so LIPID SOLUBLE. Sequesters in fat, which INCREASE IT'S ELIMINATION HALF-LIFE. * Elimination half-life - weeks SE * Pulmonary Fibrosis - fat accumulation in lungs * LIver Toxicity - Fat Accumulation in the Liver. * Photosensitivity: Fat Accumulation in the skin. * Blue-Grey Skin Discoloration - Fat accumulation in Skin. (5-10% of pts). * Corneal Microdeposits of fat * Thryoid Toxicity: .HYPER OR HYPOTHYRODISM (mainly hypo). Amiodarone has iodide as part of it's structure. INTERACTIONS * Digoxin - Inhibits the P glycoprotein that can cause inhibition of Digoxin renal clearance, leading to Dig toxicity. Must decrease the Dose. (ANY CHF PT MUST FIND OTU IF THEY ARE ON DIGOXIN BEFORE GIVING THIS!...SAME FOR QUINIDINE). |
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Verapamil
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Class IV Anti-arrythmic Agent. - Non-Dihydropyridine, L-Type CCB
MOA/ EFFECT * Decr Slope, Incr Threshold of PHASE 0 of SA/AV node. ----> Decr Automaticity (HR) ----> Decr AV Nodal Conduction (Incr PR Interval). ----> INCREASED REFRACTORINESS of SA/AV node * Shortened PHASE 2 of Atrial/Ventricular APs ----> DECREASES REFRACTORINESS OF ATRIAL/ VENTRICULAR APs (not in ppts but I have decided that it must do this). * Arterial Vasodilation - causes REFLEX TACHYCARDIA (not as bad as with dihydropyridines...which are VD only and it is usually overcome by the CCB induced bradycardia.). USE * Delayed After Depolarizations d/t Digoxin Toxicity (which are caused by Tachycardia, Ca Overload, and Triggered Activity...large simulus). (But remember the DOC is BBs + Mg!!! b/c CCBs can WORSEN the dig toxicity!). * PSVTs that are d/t AV node reentry (slows AV nodal conduction). * Uncontrolled Afib/ flutter...decr AV nodal conduction..slow ventricular rate only. * Stable and variant angina (but the argument against this is it could cause coronary steal). * 1st Line tx in HTN - especially in african american and geriatric pts * MIgraine Prophylaxis SE * Slow AV nodal conduction * LOW risk of orthostatic HOTN...b/c selective for relaxing ARTERIAL smooth muscle only. INTERACTIONS * Digoxin: Inhibits the P glycoprotein that allows Dig renal clearance. Can cause Dig toxicity. Must lower the dose of Dig. * BETA BLOCKERS: DO NOT GIVE WITH BETA BLOCKERS!!!!! Will slow AV nodal conduction double fold and can cause an AV Block!!!! (mneumonic...C+B = CB (conduction block). CONTRAINIDICATIONS * Pts with heart failure! Will decr contractility..you don't want that! (especially if they are taking Digoxin). * BETA BLOCKERS. |
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Diltiazem
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Class IV Anti-arrythmic Agent. - Non-Dihydropyridine, L-Type CCB
MOA/ EFFECT * Decr Slope, Incr Threshold of PHASE 0 of SA/AV node. ----> Decr Automaticity (HR) ----> Decr AV Nodal Conduction (Incr PR Interval). ----> INCREASED REFRACTORINESS of SA/AV node * Shortened PHASE 2 of Atrial/Ventricular APs ----> DECREASES REFRACTORINESS OF ATRIAL/ VENTRICULAR APs (not in ppts but I have decided that it must do this). * Arterial Vasodilation - causes REFLEX TACHYCARDIA (not as bad as with dihydropyridines...which are VD only and it is usually overcome by the CCB induced bradycardia.). USE * Delayed After Depolarizations d/t Digoxin Toxicity (which are caused by Tachycardia, Ca Overload, and Triggered Activity...large simulus). (But remember the DOC is BBs + Mg!!! b/c CCBs can WORSEN the dig toxicity!). * PSVTs that are d/t AV node reentry (slows AV nodal conduction). * Uncontrolled Afib/ flutter...decr AV nodal conduction..slow ventricular rate only. * Stable and variant angina (but the argument against this is it could cause coronary steal). * CCBs first line tx for HTN, esp in AA or geriatric pts. SE * Slow AV nodal conduction * LOW risk for orthostatic HOTN...b/c selective for ARTERIAL smooth muscle only. INTERACTIONS * Digoxin: Inhibits the P glycoprotein that allows Dig renal clearance. Can cause Dig toxicity. Must lower the dose of Dig. * BETA BLOCKERS: DO NOT GIVE WITH BETA BLOCKERS!!!!! Will slow AV nodal conduction double fold and can cause an AV Block!!!! (mneumonic...C+B = CB (conduction block). CONTRAINIDICATIONS * Pts with heart failure! Will decr contractility..you don't want that! (especially if they are taking Digoxin). * BETA BLOCKERS |
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Adenosine
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Adjunct/ non class specific Anti-Arrythmic Agent
MOA: Stimulates Gi. Inhibits cAMP production in SA/AV node * Inhibits Funny Na Channels: Decr slope of PHASE 4. ----> Decreases Automaticity/ HR ----> Increased PR interval (slow AV conduction). ----> Increase refractoriness * Inhibits L-type Ca Channels ----> Decr Slope, Incr firing Threshold of PHASE 0. -----> Decr automaticity (HR) -----> Increased refractoriness Somehow Gi also open a K channel, causing K efflux, which hyperpolarizes the myocardial cells Double whammy here will STOP THE HEART (transient). USE * Emergency tx of PSVT - will stop the heart for a second..new rhythm will be NSR. ADVANTAGES: * Short half-life - seconds INTERACTIONS * CAFFEINE AND THEOPHYLLINE - will compete for the Adenosine receptors and decrease the effectiveness. - competitive antagonists. |
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Digoxin
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Anti-arrythmic Agent - non classified. / Adjunct.
Comes from the FoxGlove Plant. MOA: * Na/K ATPase inhibitor. Pvts Na Effux. Causes incr intracellular Na conc. This inhibits the Na/Ca coporter, causing Ca to build up in the cell. This INCREASES CONTRACTILITY in CHF. DIRECT MOA/ EFFECTS * Increased contractility (incr intracellular Ca). * Increased K+ Conductance: via incr intracellular Ca. There are Ca sensitive K Channels that get turned on. * Decreased Refractoriness (Shortened AP Duration) d/t the incr K conductance. Shortens S-T Interval: Pro-arrythmic effect. INDIRECT MOA/ EFFECTS: * Muscarinic/ Vagal Action - Causes Decr HR. Slows AV nodal conduction! Prolongs PR Interval. * Decr SNS activity: Decreased Preload - venodilation, Decr EDV - decreases wall stress and O2 Demand. (Decr HR and afterload also). USE: * CHF - Specifically...low output HF with accompanying a-fib. Used in LATER STAGES with full contractile failure. * Afib - Musc effect slows AV node conduction: Decreases conduction of atrial beats to ventricles...decreases the ventricular rate. * Can be given before Quinidine to pvt fast AV node conduction. (Quinidine as anti-musc effects). PHARMACOKINETICS * Oral bioavaliability: 60-80% * Half-life: 1 day (steady state requires 4-5 halflives - 4/5 days). Would need an IV loading dose to get to steady state in an emergency... * Vd = 6.2 * Protein bound - can be displaced by Verapamil and Quinidine. SE: * SHORTED QT INTERVAL!!! Could cause arrythmias!!! SE w/ Dig Toxicity d/t narrow therapeutic window: * Visual: Aura (sight and smell), Yellow tinted vision - "Yellow Filter Effect" . Photophobia. * Cardiac: ----> Arrythmias (d/t decr refractoriness or DAD (ectopic beats)). Tx Vent arrythmias with Lidocaine. ----> Bradycardia or Conduction Block (d/t musc effects). Tx w/ atropine ----> Delayed After Depolarizations: d/t Ca Overload. Can cause ectopic arrythmias. Tx with BBs (esmolol) and Mg. * Hyperkalemia (d/t Dig overcompeting K+ for Na/K ATPase binding sites. * Anorexia, Nausea, Vomiting * Fatigue, Weakness * Confusion DRUGS FOR LIFE-TREATENING DIG TOXICITY * Lidocaine for ventricular arrythmias. * Atropine for Brady arrythmias and Conduction Block. * Potassium Supplement...will knock the Dig off the Na/K ATPase (but coudl accentuate the hyperkalemia). * Anti-digoxin Antibodies - will bind to Dig and remove it from the body. INTERACTIONS * QUINIDINE, AMIODARONE, CCBs (Verapamil, Dilitiazem). - All of these are meds for aFib as well...but if given WITH digoxin, they inhibit the P glycoprotein that allows renal clearance of Dig. You get Dig toxicity. LOWER THE DIGOXIN DOSE BY HALF to prevent. (any CHF pt must be screened for Dig use before starting any of these meds for afib!!!). * Alterations is Serum Potassium. ----> K and Dig compete for the binding sites on the Na/K ATPase. Hypokalemia will cause incr Dig binding and DIG TOXICITY!!. Hyperkalemia will cause decr Dig binding and decr contractility. * DIURETICS - Loop and Thiazide diuretics will cause Hypokalemia...Incr Dig Binding and DIG TOXICITY. * INSULIN - can cause hypokalemia and incr Dig Binding - DIG TOXICITY. |
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Magnesium
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Anti-arrythmic Electrolyte
MOA * unknown USE * Emergency Tx of Torsades De Pointes (IV). * Given with BBs as first like tx of Delayed After Depolarizations from Digoxin Toxicity. |
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Nitroglycerin
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Anti-hypertensive
MOA * Increases NO in Smooth Muscle Cells, which increases cGMP, Protein Kinase G, and dephosphorylates MLC. EFFECTS: * DECR PRELOAD: Normal Doses---> VENOUS dilation only. (This decreases cardiac demand.) * DECR AFTERLOAD: High Doses----> ARTERIAL dilation occurs. (This decreases cardiac demand.) * INCR O2 SUPPLY: Dilates Coronary Arteries: Redistributes coronary blood flow to ischemic areas. DOSE * Sublingual - good for prophylactic use in stable angina (take during the day only) and variant angina (take at night only). * IV - Good for emergencies in hospital * Transdermal - effective for long period of time but TOLERANCE can develop. ...pt should have some hours each day that they do not wear the patch. USE * Stable - Should NOT take the NTG at night. (Day only) * Variant Angina - ONLY take AT NIGHT. * Unstable Angina (along with anti-plt drugs - ASA). ----> (give with a BB to pvt the reflex tachycardia). * CHF - esp CHF caused by an MI!! (decreases preload AND increases O2 supply). TOLERANCE * Tolerance can develop with prolonged exposure d/t a consumption of all the sulhydryl grps needed to convert nitrates to NO. They all get used up. SE * Orthostatic HOTN (low doses), Syncope (high doses) *Headache (VD of CNS) * Reflex Tachycardia (d/t VD) INTERACTIONS: * Sildenafil (Viagra) - a PDE5 Inhibitor...pvts breakdown of cGMP. Taking both drugs at once will cause SUDDEN, EXTREME HOTN!! ---> Pt taking Sildenafil must wait 6-8 HOURS before taking a nitrate |
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Isosorbide dinitrate
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Anti-hypertensive Agent.
A metabolite of Nitroglycerin. MOA: * Vasodilates via incr cGMP ROUTE: Oral USE: * Used with Hydralazine to treach CHF. (decr afterload) ESPECIALLY IN AFRICAN AMERICANS, who do not respond to ACEIs well. |
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Amyl Nitrate
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Anti-hypertensive agent related to NTG.
ROUTE * Inhalation - volatile liquid in a vial ...is misted and inhaled. Causes vasodilation. |
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Nifedipine
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Anti-Hypertensive Agent
Dihydropyridine CCB MOA: * ARTERIAL DILATION: Blocks L-type Ca channels in the BV ONLY! (cannot be used for arrythmias). This VD causes REFLEX TACYCARDIA, and allows for decr afterload to heart. (decr O2 demand to heart). * Dilates Coronary Arteries - Increase O2 supply to heart (controversial because can cause coronary steal). USE * Stable and Variant Angina (give with a BB to pvt the reflex tachycardia). * 1st Line tx of HTN SE * HOTN and Reflex Tachycardia. * INTERACTIONS * DIGOXIN: Inhibits the P glycoprotein that is responsible for renal clearance of Dig. Can cause Dig toxicity. Lower the Dig Dose. (Along with Amiodarone and Quinidine). |
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Dobutamine
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Beta1 Specific Agonist.
MOA: incr cAMP (opens funny channels and L-type Ca Channels). * Beta 1 Incr CO. d/t incr HR and contractility. (But mainly just incr contractility d/t the Ca). The Ca coming into the cell stimulates the release of more Ca from the SR, causing contraction. USE * Late Stage CHF when there is a significant decr in CO. SE * May increase mortality in CHF pts...only use in advanced stages. (Why? B/c cats cause apoptosis of heart myocardial cells...deleterious effects overtime.) So the pt taking Dobutamine will feel better but die sooner. (That's why 1st Line tx of CHF is BBs despite the decr contractility.). |
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Spirinolactone
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Aldosterone Antagonist - Reduces Preload.
EFFECTS: * Decreases preload * Inhibits Alderstone Mediated Cardiac Remodeling. (Cardiac Fibrosis..stiff heart). * Decreased mortality in CHF!! :) USE * CHF- combination therapy with BBs. SE * Hyperkalemia, ESP when combined with ACEIs/ ARBs. CONTRAINDICATIONS * |
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Inamironone
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Phosphodiesterase 3 Inhibitor
MOA: * Pvts the breakdown of cAMP by PDE3. Incr cAMP opens funny channels and Ca channels. * Incr HR and contractility. (But mainly just contractility via Ca. ) USE * Advanced heart failure (the cat-mimicking stimulation has deleterious effects on the heart..causing apoptosis of myocytes...so the pt feels better but dies sooner...) (why BBs are better despite the decr contractility). SE * May incr mortality in CHF pts d/t cat-like effects. |
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Sodium Nitroprusside
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Direct Venous and Arterial Dilator - Emergency Anti-HTN agent.
MOA * Direct Veno and Arterial Dilator. * Shifts the Frank Starling Curve Up and to the Left by decreasing both afterload and preload. SE: Cyanide Toxicity - NTG is converted to thiocyanate and then to cyanide. Really bad in people with Renal or liver issues. Tx w/ THIOSULFATE, which will increase the conversion of cyanide to thiocyanate. |
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Hydralazine
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Direct Arterial Vasodilator
MOA * Decr Afterload. Wil shift the Frank Starling Curve UP. USE * Severe Refractory HTN * CHF in combination with Isosorbide Dinitrate - especially in African Americans (who are insensitive to ACEIs d/t lower amts of renin). SE * Drug induced Lupus - ESPECIALLY in slow acetylators * Reflex Tachycardia: Give with a BB to pvt * Edema - Give with a diuretic to pvt. |
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Sodium Nitroprusside
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Direct Venous and Arterial Dilator - Emergency Anti-HTN agent.
MOA * Direct Veno and Arterial Dilator. * Shifts the Frank Starling Curve Up and to the Left by decreasing both afterload and preload. USE * HTN Emergency * CHF * Controlled HOTN in sx, etc SE: * Cyanide Toxicity - NTG is converted to thiocyanate and then to cyanide. Really bad in people with Renal or liver issues. ---> To Tx: Give THIOSULFATE (a cofactor in the conversion of cyanide to thiocyanate) to turn it into thiocyanate and get rid of it. * Reflex Tachycarida - give w/ BB to pvt. * Edema - pvt with a diuretic. |
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Captopril
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ACE Inhibitor
MOA * Inhibit the ACE enzyme and the conversion of ATI to ATII. The prevents the RAAS process of AT VC, Aldosterone production, Na/ H20 retention..increasing preload, etc. * DECR Afterload, Preload, Edema * INCR Cardiac Output. USE * 1st Line Tx of HF. * NOT useful in African Americans, b/c they have no renin production. Use BBs, Hydralazine,and Isosorbide Dinitrate instead. * Essential HTN (Stage 1 and in combo for Stage 2) * Diabetic nephropathy/ neuropathy...minimizes it's progression! SE: * Dry Cough, Angioedema, Asthma Attacks: ......ACE in the lungs causes the breakdown of Bradykinin. ACEIs block it and cause Bradykinin buildup in the lungs. (The bradykinin can also cause some VD). * Hyperkalemia/ metabolic acidosis d/t no Aldosterone. * Tolerance with Chronic use - "Ang II Escape Mechanism...ACE becomes tolerant. Tx..give an ARB. * Lipid Neutral :) Yay! INTERACTIONS: * Potassium Supplements...will exacerbate the hyperkalemia (not aldosterone). * Spironolactone/ Amiloride - will block the effects of aldosterone even more and cause severe hyperkalemia!! * Loop diuretics...will cause severe HOTN, hypovolemia!!!! CONTRAINIDICATION * Bilateral Renal Stenosis....constriction of the efferent arteriole is needed to maintain glomerular capillary pressure and GFR. And ACEI would cause RENAL FAILURE. * Pregnancy: 2nd or 3rd trimester * Hypovolemia and Hyponatremia (caution!). |
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Losartin
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Angiotensinogen -1 Receptor Blocker.
MOA * Blocks the AT-1 receptor for ANG II that is responsible for the VC, Aldosterone production. * Decr Afterload, Preload, Aldosterone synthesis, Edema * Incr CO. * Eliminates the ANGII escape mechanism that occurs w/ chronic ACEI use. (ACE enzyme become tolerant to ACEI...you still have ANG II). USE * 1st line tx of CHF * NOT useful in African Americans, who make no renin. Use Hydralazine, BBs, and Isosoribide Dinitrate instead. SE * Hyperkalemia and metabolic acidosis d/t no Aldosterone INTERACTIONS * Loop Diuretics..will cause hypovolemia, HOTN!! * Spironolactone/ Amiloride - will cause severe hyperkalemia!!! * Potassium Supplements CONTRAINDICATIONS: * Pts with Bilateral Renal Stenosis - ANGII is needed in these pts to constrict the efferent arteriole to maintain glomerular capillary pressure and GFR!!! Blocking the ANG II receptor will cause decrease GFR and RENAL FAILURE!!! |
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Furosemide
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Loop Diuretic - stronger than thiazides
MOA * Blocks the Na/Cl/K transporter in the ascending Loop of Henley. EFFECTS * Reduced ECF volume and Decr Preload * DO NOT reduce CO despite decr preload in CHF pts d/t a plateaued frank starling curve. USE * CHF - decr pulmonary edema and dyspnea. (NO EVIDENCE OF REDUCED MORTALITY like with beta adrenergic drugs). SE * Hypokalemia INTERACTIONS * DIGOXIN: Hypokalemia can cause Digoxin Toxicity..incr Dig binding to Na/K ATPase!!!! |
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Hydrochlorothiazide (HCTZ)
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Thiazide Diuretic.
MOA * Blocks the Na/Cl coporter in the distal convoluted tubule of the loop of henley. (Decr ECF and cardiac output). ...causing a diuresis (not as strong as the loops). * Smooth muscle VD action with CHRONIC USE via Increased Renal Prostaglandins. This will decrease TPR and is the MAIN reason Thiazides are prescribed for HTN. ...somehow this also causes a more negative lumen potential in the kidney. . USE * 1st Line Tx in HTN: Esp for African Americans and Geriatric Pts. Used as monotherapy or combined with ACEIs, ARBs, CCBs, etc. * Decr Preload in CHF - will NOT affect the SV/ CO d/t a more plateaued frank starling curve. WILL decr pulmonary edema and dyspnea. (NO EVIDENCE OF INCREASE MORTALITY like with beta adrenergics). SE * Hypokalemia---can offset with an ACEI or an ARB. (Caution when using Digoxin for CHF or when using Sotalol for arrythmias). Combine with an ACEI or ARB to offset the hypokalemia. * Hypercalcemia *Hyperglycemia - Binds to ATP dep K channel on the pancreatic beta cells, leaving it in the open state (activates it). . This suppresss insulin release. (this is the opposite of sulfonureas, which inhibit the K channel and increase insulin release.) * Hyperuricemia - but got uncommon * Hyperlipidemia - incr triglycerides/ LDL cholesterol * Impotence * Photosensitivity INTERACTIONS * DIGOXIN - Hypokalemia can cause incr Dig binding to Na/K ATPase and Dig Toxicity. * Lithium - Thiazides decrease Li clearance * NSAIDS - Decr Prostaglandin formation...this will decr the vasodilation of Thiazides |
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Nesiritide
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Nesiritide - BNP in drug form
MOA: Causes Naturesis and VD. * Nesiritide binds to receptors on the endothelial cells of BV's. Attached to these receptors if the INSOLUBLE (membrane bound) form of Guanylyl Cyclase. Activated rGuanylyl Cyclase then converts GTP into cGMP in the cell. cGMP activates Protein Kinase G. Protein Kinase G DEphosphorrylates the Myosin Light Chains, causing RELAXATION. USE * CHF - Decr preload and pulmonary capillary wedge pressures. * VERY EXPENSIVE SE * HOTN. |
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Reserpine
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Autonomic, Antihypertensive Drugs.
Comes from the plant Rauwolfia Serpentina MOA *Blocks the reuptake of Catcholamines into the vescles - depleted vesicles. * Inhibits the enzyme that allows dopamine and NE to enter the storage vesicles. Therefore, NE can't be synthesized or taken back up, and dopamine can't be secreted. Leads to decreased levels of NE, Dopamine, and Serotonin. . * This causes decr BP, HR. USE: * REFRACTORY HTN: Antihypertensive due to decreased NE. SE: * Severe Depression * Increased HCl Secretion * Increased GI and Urinary motility * Severe Sedation (crosses BBB). Not used alot due to CNS effects. Depression was the cause of the creation of MAOI's. |
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Aliskirin
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Direct Renin Inhibitor for HTN
not very effective. |
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Prazosin
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alpha 1 Blocker
EFFECTS * Decr venous return, decr CO, Decr TPR/SVR USE * 2nd line drug for Essential HTN - used in combo for stage 1 and 2. * Benign Prosthetic Hyperplasia - relaxes urinary sphincter and DECREASES PROSTHETIC TONE. (given in combo with Finasteride, which shrinks the prostate). SE * First dose syncope * Reflex tachycardia * Orthostatic HOTN * Lipid Friendly: Decreases LDLs, increases HDLs |
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Phentolamine
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Competitive alpha 1 Blocker
EFFECTS * Decr venous return, decr CO, Decr TPR/SVR USE * HTN secondary to Pheochromocytoma SE * First dose syncope * Reflex tachycardia * Orthostatic HOTN * Lipid Friendly: Decreases LDLs, increases HDLs |
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Labetalol
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Mixed Alpha1 and Beta 1 Antagonist.
USE * HTN Emergencies - more efficacious than a selective a or B blocker alone. SE * Cardiac Depression * Orthostatic HOTN * No first dose syncope * No reflex tachycardia * No change in Lipids * Upregulation of Beta Adrenergic Receptors...tachycardia w/ abrupt withdrawal. * Exercise Intolerance * masks the signs of hypoglycemia |
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Methyldopa
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Alpha-2 Agonist
Prodrug for a-methylNE MOA: * Activation of a2 receptors decreases NE release and SNS stim. Decr SVR. USE * Refractory Essential HTN * Stage 2 HTN - in combo with other drugs. SE * Sedation * Depression * Edema * Bradycardia * HEMOLYTIC ANEMIA in 20% of pts. Diagnosed with "Coomb's test". |
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Clonidine
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Alpha 2 Agonist
MOA: * Activation of a2 receptors decreases NE release and SNS stim. Decr SVR. USE * Refractory Essential HTN * Stage 2 HTN - in combo with other drugs. SE * Sedation * Depression (d/t decr NE) * Edema * Bradycardia * Rebound HTN with abrupt withdrawal. INTERACTIONS * TCAs (Mertazepine) will decrease NE reuptake...this will incr NE in the synapse and COUNTERACT the effects of a2-Agonists and decr the anti-HTN effect. * Mirtazapine (an anticholinergic that is also an alpha2 antagonist). ...competitive antagonist to clonidine. |
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Guanethidine
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Decreases the release of catecholamines.
Uses the reuptake system to get into the cell. Blocks release of NE from neurons and depletes NE stores (cell won't make more if it's not being released/ used, causing a decreased SNS tone. USE * Severe refractory HTN. SE * Orthostatic HOTN * Fluid Retention Contraindication: Pheochromocytoma: Competes with epi and NE reuptake at the reuptake site. Tumor to adrenal glands will flood system with cats...if they can't be taken back up will cause a crisis. (it's not a reuptake inhibitor because it doesn't completely block reuptake.) |
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Minoxidil
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Anti-hypertensive
Sulfonurea Agonist MOA * BInds to the sulfonylurea receptor on VASCULAR smooth muscles, activating a K channel on the membrane. K efflux hyperpolarizes the cell. This causes a relaxation of vascular smooth muscle (d/t incr firing threshold of the cells). * Frank Starling curve will shift UPWARD d/t decr afterload. * Also causes "Hypertrichosis" of the face, back, and arms (hairiness). USE * Severe HTN (> 180/110) * Male Pattern Baldness SE * Reflex Tachycardia: give w/ BB to pvt * Edema - give w/ diuretic to pvt. * Hypertrichosis of the face, back, and arms. |
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Lovastatin (Mevacor )
Atorvastatin (Lipotor) Fluvasatin (Lescol) Pravastatin (Pravachol) Simvastatin (Zocor) Rosuvastatin (Crestor) |
Cholesterol Synthesis Inhibitor
DECREASES LDL CHOLESTEROL LEVELS!!!! MOA * HMG CoA Reductase Inhibitior - Inhibits the enzyme in the hepatocytes that converts Acetyl CoA to Cholesterol. This is the RATE-LIMITING STEP in cholesterol synthesis. EFFECTS * Reduced Cholesterol synthesis * Increased expression of LDL receptors (gets rid of LDL into tissues). * Decreased plasma LDL levels 20-25%!! :) - Main effect. * Decreased hepatic VLDL * Decreased Triglyceride levels (amt depends on baseline levels). * Not sure if it decreases HDL levels..uncertain. * CARDIOPROTECTIVE EFFECTS: ---> Improved endothelial function: pvts BV remodelling. ---> Increased plaque stability - hardens the plaque, pvting rupture. ----> Decreased inflammation. ----> Antioxidant Effects ----> Reduced plt aggregation. SE: MORE COMMON WITH COMBO TX * Hepatoxicity: Incr serum aminotransferase activity. (mainly in pts w/ other liver comorbidities). ----> Determine baseline measures, monitor after initiating tx. ----> If levels increase, d/c the Statin. Start a new statin once levels are normal. * Rhabdomyolosis - leading to acute renal failure. ----> Myalgia will be the first sign..flu-like soreness. VERY COMMON. Muscle weakness, fatigue, INCR SERUM CREATININE KINASE LEVELS. ----> Stop the statin, start a new statin once levels are normal. CONTRAINDICATIONS * Pts with liver disease (alcoholics)...can cause hepatotoxicity * Pregnancy - teratogenic |
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Cholestyramine (Questran)
Colestipol (Colestid) Colesevelam (Welchol) |
Bile Acid Binding Resins/ Sequestrants
--> Reduces Cholesterol Levels. --> First drugs used in dyslipidemias...proved that there is a direct correllation b/n cholesterol/LDL and CAD. MOA * Retained in the GI tract. Is not systemically absorbed. Positively charged BADRs bind to neg charged bile acids, which blocks them from entering/ sequestering in the hepatocyte. This will decr the conc there and incr the conversion of cholesterol to bile acids (decr-ing cholesterol levels.). EFFECTS * Stimulates conversion of cholesterol to bile acids in the liver. (decr cholesterol levels) * Increases LDL receptor expression in the liver (more LDL is taken out of bloodstream). SAFE TO USE IN CHILDREN B/N THE AGES OF 11 & 20! :) SE * Liver increases HMG CoA Reductase expression...making more cholesterol...so you have to give it in COMBO with a STATIN. * CONSTIPATION AND BLOATING: decr compliance ----> Mix with a noncarbonated, pulpy juice to prevent. Take in the morning instead of at night. Drink with a straw to decr air entrainment. -----> Hard tablet formulations create a gelatinous mass with GI secretions...pvts bloating. INTERACTIONS * Decreased absorption of other drugs: ---> HCTZ, Furosemide, Propanolol, Warfarin ----> Can be minimized BY TIMING THE DOSES. Take these drugs four hours away from BABRs |
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Niacin
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Anti-cholesterol med
MOA * Decr VLDL secretion from hepatocytes (so can't make LDL). * Incr LipProtein Lipase enzyme activity (means more TGs are removed from VLDL...gets rid of TGs. * Decr transport of free fatty acids to the liver: Reduces liver TG synthesis EFFECTS * Reduced TG levels!!! (no VLDL synthesis). * Reduced plasma LDL Levels (20-30 %) * Increased HDL levels (reduced degradation) 30-40%. FORMULATIONS: * CRYSTALLINE NIACIN ---> Immediate Release Formula. ---> Metabolized by the Nictinomide Pathway (low capacity system). Quickly becomes saturated. ---> After saturation, Conjugation Pathway is used for metabolism. Toxic intermediate metabolites are formed which can cause FLUSHED, ITCHY SKIN d/t incr prostaglandins. Tx is ASA 30-60 min prior to Niacin. * SUSTAINED RELEASE NIACIN ---> Metabolized by conjugation pathway. High doses will lead to the formation of toxic metabolites HEPATOXICITY. Must monitor liver function while pt is taking. * NIASPAN ---> Balanced metabolism b/n nictinamide and conjugation pathways...NOT assoc with SE. CONTRAINIDICATION * Pregnancy. |
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Clofibrate (Atromid)
Gemfibrozil (Lopid) |
Fibrates
Anti-lipid, Anti-cholesterol med. MOA * Ligands for transcriptional regulators (PPAR-a) * Causes increase gene expression of LDL receptors and Lipo-Protein Lipase (LPL) enzyme. * This will cause incr removal of LDL from plasma. AND incr removal of TGs from VLDL. EFFECTS * Decreased liver secretion of VLDL * Modest decr in LDL * LARGE decr in TGs * Mildly incr HDL USE * Pts with HIGH TRIGLYCERIDES. SE * Increased risk of Rhabdomyolysis (esp when given with STATINS) |
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Ezetimibe
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Anti-cholesterol Med
MOA * Inhibits intestinal absorption of cholesterol. EFFECTS * Reduced LDL 15-20% * Increased hepatic LDL receptors * Additive effects when combined with statins (30-40% decr in LDLs) - Vytorin. SE * Well tolerated ! :) * No increased risk of hepatotoxicity with statins! :) |
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Vytorin
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Ezeimide + Simvastatin
Allows for a 30-40% decr in plasma LDL levels. |
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Clopidogrel
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Ati-plt Drug
Prodrug - Activated by CYP2C19 MOA * ADP receptor inhibitor. Pvts plt aggregation...they cannot connect via GP IIb, IIIa and fibrin. Cannot form the plt plug. * 5-9% of the pop has reduced CYPC19 acivity...cannot activate all of the clopidogrel. These individuals should receive an increased dose of clopidogrel or the newer ADP receptor blocker PRASUGREL...which is activated by another enzyme. USE * Prophylaxis of MI (for pior MI) * Mandatory after a coronary stent * Prophylaxis of Thrombotic Stroke * ACUTE CORONARY SYNDROME - DOC |
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ASPIRIN
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Cox-1 Inhibitor - Irreversible.
MOA * Inhibits Cox and the formation of Thromboxane, which causes plt aggregation. USE * DOC for TIA Prophylaxis * MI prophylaxis * Mandatory after a coronary stent * Prophylaxis of a Thrombotic Stroke. SE * Inhibits Renal Prostaglandins |
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Streptokinase
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Fibrinolytic
MOA * Binds to Plasminogen activates it into plasmin. USE * Fibrinolytic of Choice for DVTs. SE * Allergic rxns - because it comes from a bacteria. |
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Alteplase...tPA
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Fibrinolytic
MOA * Converts Plasminogen to Plasmin, which dissolves the clot. Pvts formation of the plt plug. USE * Acute Ischemic Stroke (DOC). * Pulmonary Embolism * Acute MI CONTRAINDICATION * Cerebral Hemmorhage * DP > 110 * active bleeding * serious GI bleeding in prior 3 mths. |
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Dipyridamole
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Anti-plt agent
MOA * Inhibits PDE in plts, increasing cAMP, which disaggregates plts. (Mimics the action of Prostacyclin). USE * Pvtion of recurrent stroke and MI (with ASA). |
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Acixamab
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Antiplt Drug
* Hybrid monoclonal antibody to GP Ib/ IIIa (Fibrinogen Receptor). Fibrin can't bind and attach the plts to each other. MOA * Inhibits GP IIa, IIIb receptors. Plts cannot attach to each other. |
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Eptifibatide and Tirofaban
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Selective GP IIa/ IIIb Antagonists. Fibrin can't bind and attach the plts to each other.
Small Molecular Weight. |
