Cardiac Drugs – First Aid Updates – Flashcards
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Diuretics for HTN
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Thiazide and loop diuretics
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Captopril (capoten)
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ACE inhibitor clin: stage 1/2 HTN, CHF, diabetic renal disease tox: bradykinin cough reflex, hyperkalemia, teratogenic *oral, effective up to 12 hours *others: enalapril, lisinopril, ramipril
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Losartan (cozaar)
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Angiotensin-II type 1 receptor antagonist (ARB) clin: stage 1/2 HTN, CHF tox: hyperkalemia, teratogenic *oral, no cough reflex *others: olmesartan, telmisartan, valsartan
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Aliskiren (tekturna)
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Renin inhibitor clin: HTN 2nd to renal failure or diabetes tox: angioedema, renal impairment *no significant advantage over other RAAS inhibitors for most types of HTN
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Propranolol (inderal)
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non-selective beta-adrenergic receptor agonist clin: HTN, CHF, angina, arrhythmias, atrial ventricular tachy, performance anxiety, migraine tox: bradycardia, AV block, bronchospasm, CNS sedation -Other: contraindicated in asthma, crosses BBB
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Metoprolol (lopressor)
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selective B1-adrenergic receptor antagonist clin: CHF, HTN, atrial tachycardia tox: bradycardia, AV block, CNS sedation *widely used for stage 1/2 HTN, reduces mortality in future heart failure pts
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Labetalol (trandate)
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-mixed α1 and b1-adrenergic receptor antagonist -clin: pregnancy induced HTN, eclampsia, pre-eclampsia, HTN crisis -tox: bradycardia, AV block, CNS sedation, less bronchospasm *composed of 4 stereoisomers: (R,R) isomer: β1-adrenergic receptor antagonist (S,R) isomer: α1-adrenergic receptor antagonist
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Carvedilol (coreg)
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mixed α1 and β1-adrenergic receptor antagonist -clin: CHF, HTN -tox: bradycardia, AV block, CNS sedation, less bronchospasm *4 stereoisomers, reduces mortality in heart failure pts
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Ambrisentan (letairis)
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selective endothelin-A receptor antagonist -clin: pulmonary HTN -tox: hepatic impairment, headache *100x more selective for endothelin A receptor; bosentan antagonises endothelin A and B receptors
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Riociguat (adempas)
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-direct activator of soluble GC -clin: pulmonary HTN, combine with ET antagonist for max effect -tox: headache, hypotension, GI disorders
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Prazosin (minipress)
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selective α1-adrenergic receptor antagonist -clin: HTN, benign prostatic hyperplasia -tox: orthostatic hypotension, reflex tachycardia *used in hypertension patients unresponsive to other therapies
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Clonidine (catapres)
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selective α2-adrenergic receptor agonist -clin: HTN, ADHD -tox: severe withdrawl, sedation *penetrates CNS and inhibits sympathetic nervous system NE release; available as transdermal patch
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Hydralazine (apresoline)
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- decreases afterload - nitric oxide mechanism: increases cGMP --> smooth muscle relaxation - vasodilates arterioles > veins -uses: hypertensive crisis, pregnancy induced htn, heart failure -SE: tachycardia (contraindicated in angina/CAD), Na and H2O retention, headache, angina, Lupus-like syndrome - frequently administered with beta blocker to inhibit reflex tachycardia *mechanism of action not completely understood; can cause lupus-like syndrome
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Targets to treat angina
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1. Decrease venous return/afterload 2. Decrease myocardial O2 demand 3. Treat CAD/atherosclerosis
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Decrease venous return/afterload
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Nitrovasodilators & vascular selective Ca2+ channel blockers
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Decrease myocardial O2 demand
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beta-adrenergic receptor antagonists & cardioselective Ca2+ channel blockers
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Treat CAD/atherosclerosis
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-decrease cholesterol: statins -prevent thrombi/clots: aspirin -surgical procedures: stents/angioplasty -lifestyle changes: exercise, diet, stop smoking
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Nitroglycerin (Nitrostat)
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-mechanism: Nitrovasodilator, nitric oxide donor - effect: decrease preload, increase coronary vasodilation (minor) -clin: angina, acute coronary syndrome -tox: tachycardia, orthostatic hypotension, headache -other: sublingual for acute angina: rapid onset (<1 min) short duration (~10-30 min) oral for prophylactic: slow onset, longer duration (6 - 8 h)
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Sildenafil (Viagra)
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-phosphodiesterase type 5 inhibitor -clin: angina, erectile dysfunction -tox: tachycardia, hypotension, vision disturbances (yellow halos) -other: contraindicated with nitrovasodilators
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Digoxin (lanoxin)
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- inhibit Na/K ATPase --> increased intracellular Na+ --> inhibits Na/Ca antiporter --> increased intracellular Ca2+ --> positive inotropy; stimulates vagus nerve --> decreased HR - effect: increase contractility - uses: CHF, atrial fibrillation (decreased conduction at AV node and depression of SA node) - SE: N/V, diarrhea, blurry yellow vision, arrhythmias, hyperkalemia (poor prognosis) - predispose to toxicity: renal failure, hypokalemia, verapamil, amiodarone, quinidine (decreased clearance) - antidote: slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+ -other: only approved cardiotonic agent for CHF, no net effect on CHF mortality, low therapeutic index (~2)
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Hydrochlorothiazide (microzide)
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-inhibit Na+/Cl- co-transporter (NCC) in distal convoluted tubule -clin: HTN, CHF, idiopathic hypercalciuria -tox: hypokalemic metabolic alkalosis, hyponatremia, hyper-lipidemia, uricemia, calcemia -other: low ceiling diuretic, component of many combo therapies
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Spironolactone (aldactone)
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-competitive antagonist of aldosterone receptor -clin: hyperaldosteronism, CHF, HTN -tox: hyperkalemia, endocrine effects (i.e. gynecomastia) -other: used in combo with loop or thiazide to prevent hypokalemia; epleronone lacks anti-androgen effect
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Amrinone (inocor)
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-Phosphodiesterase-3 inhibitor -clin: acute decompensated heart failure -tox: arrhythmia -other: IV for acute decompensated heart failure; short duration (minutes)
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Dobutamine
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-β1-adrenergic receptor agonist -clin: acute decompensated heart failure -tox: arrhythmia -other: IV for acute decompensated heart failure; short duration (minutes)
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Nitroprusside (Nitropress)
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-mechanism: nitrovasodilator, nitric oxide donor: increases cGMP via direct release of NO. Short acting. - effect: decreases preload and afterload - uses: acute decompensated heart failure, hypertensive emergency - SE: cyanide toxicity -other: IV for acute decompensated heart failure; short duration (minutes)
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Statins
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- HMG-CoA reductase inhibitor - big decrease in LDL, decrease TG, increase HDL - uses: hyperlipidemia, prophylactic for CAD (decrease mortality), acute coronary syndrome - SE: myopathy (especially when used with vibrates or niacin), hepatic dysfunction, teratogen, rhabdomyolysis -other: slow onset, long duration, effective at night (Torvast, Crestor, etc)
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Cholesterol Binding Resins
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- examples: cholestyramine, colestipol, colesevelam - decrease LDL, slightly increase TG and HDL - mechanism: prevent intestinal reabsorption of bile acids --> liver must use cholesterol to make more - SE: GI upset, decreased absorption or other drugs and fat-soluble vitamins
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Evolocumab (Repatha)
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PCSK9 inhibitor -clin: hyperlipidemias, prophylactic for CVS disease -tox: pain related (muscle, back), nausea, neurocognitive events -other: Brand new! IV inj soln, monoclonal anti-PCSK9 antibody, lowers serum LDL levels by ~60% over 12wks
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Gemfibrozil (lopid)
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- huge decrease in TG, decrease LDL, increase HDL - mechanism: PPAR-alpha agonist --> upregulate HDL synthesis. Also upregulate LPL to increase TG clearance. - uses: hypertriglyeridemia, dysbetalipoproteinemia - SE: myopathy (increased risk with statins), cholesterol gallstones -other: used with statins for max efficacy
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Ezetimibe (zetia)
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- decrease LDL, no change in TG or HDL - Cholesterol transporter NPC1L1 inhibitor (intestinal sterol absorption inhibitor) --> prevent absorption of cholesterol - uses: primary hypercholesterolemia, elevated LDL - SE: diarrhea, hepatic dysfunction (rare) -other: use in combo with statin for max efficacy
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Niacin (Niacor)
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- decreased LDL > TG, increase HDL - mechanism: inhibits lipolysis by inhibiting diacylglycerol acyl-transferase 2 (hormone sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis - Uses: primary hyperlipidemias, elevated LDL, VLDL, low HDL - SE: flushing (GPCR 109A agonist, decreased by NSAIDs or long-term use), hyperuricemia, hyperglycemia -other: use in combo with statin or bile-acid binding resin for max efficacy
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Class I Antiarrhythmic Drugs
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- sodium channel blockers - slow or block conduction, especially in depolarized cells (state dependent) - decrease slope of phase 0 depolarization
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Class IA Antiarrhythmic Drugs
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-Reduce Vmax -intermediate rate of binding/unbinding -Prolonged AP and ERP, prolonged QT - uses: atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT -Ex: Procainamide, Quinidine, Disopyramide - "the Queen Proclaims Diso's Pyramid"
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Class IB Antiarrythmic Drugs
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-Less effect on Vmax at therapeutic concentration -Rapid rate of binding/unbinding -Shorten AP duration and ERP in conduction system - preferentially affect ischemic or depolarized Purkinje and ventricular tissue - uses: acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias -Ex: lidocaine, mexiletine (and tocainide) - "I'd Buy Liddy's Mexican Tacos"
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Class IC Antiarrythmic Drugs
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-More strongly reduced Vmax -Slow rate of binding/unbinding -Smaller effect on AP and ERP than Class IA - uses: SVTs including atrial fibrillation, last resort in refractory VT -Ex: Flecainide, propafenone - "Can I have Fries, Please"
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Procainamide
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-Class IA Antiarrhythmic drug -Clin: Broad spectrum for atrial & ventricular arrhythmias; a. flutter, a. fib, v. tachy, v.fib - SE: Cardiac toxicity (slowed conduction/wide QRS >50%--> ventricular arrhythmias), Hypersensitivity (SLE like syndrome)
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Quinidine
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-Class IA Antiarrhythmic drugs, inhibit muscarinic and K+ channels -Clin: broad spect. supraventricular arrhythmias (chronic a.flutter, a.fib, PSVT), ventricular arrhythmias (tachyarrhythmias) - SE: cinchonism (headache/tinnitus), thrombocytopenia, torsades - Low TI due to cardiac effects (wide QRS/v. arrhythmias) -Other: not commonly used anymore; given with digoxin to prevent anti-muscarinic activity
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Disopyramide
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- Class IA Antiarrhythmic - SE: heart failure, thrombocytopenia, torsades de pointes
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Lidocaine
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-Class IB Antiarrhythmic -PK: IV, tissue distribution 8 min, short t1/2 (2 hrs) -Clin: Ventricular arrhythmias in surgery, & ICU, digitalis induced arrhythmias -Tox: High TI, CNS (drowsiness, irritability, convulsions), CV depression -Other: not used in endogenous supraventricular arrhythmias
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Mexiletine & Tocainide
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- Class IB antiarrhythmics - Stable lidocaine analogs (t1/2=10-15hrs) -Clin: oral administration for ventr. arrhythmias, digoxin induced arrhythmias - SE: CNS depression, CV depression
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Flecainide
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-Class IC Antiarrhythmic Drug, inhibit Na channels -Clin: Oral admin for supraventricular tachyarrhythmias -Tox: Increased risk of sudden cardiac death in pts with ventricular damage due to MIs --> contraindicated
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Class III antiarrhythmic drugs
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-K+ channel blockers - increase AP duration, increase ERP, increase QT interval - uses: a. fib, a. flutter, ventricular tachycardia - "AIDS": Amiodarone, Ibutilide, Dofetilide, Sotalol
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Amiodarone
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-Classes 1 - 4 antiarrhythmic hybrid -Mech: high affinity K+ channel & Na+ channel block / low affinity Ca2+ block & beta-R -Clin: recurrent ven. tachy or ven. fib; atrial tachy in pts resistant to other drugs (lower dose) -Tox: pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (40% iodine by weight), acts as happen (corneal deposits, blue/gray skin deposits resulting in photo dermatitis), neuro effects, constipation, bradycardia, heart block, HF - Check PFTs, LFTs, and TFTs when using -Other: increasing use due to reduced mortality, complex PK, hydrophobic drug due to Iodine
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Dofetilide
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-Class III antiarrhythmic, specific K channel (IKr) blocker -Clin: maintains sinus rhythm in pts with a.fib -Tox: prolonged QT & vent. arrhythmia -Other: no increase in mortality with CHF or previous MIs
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Ibutilide
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-Class III antiarrhythmic, specific K channel (IKr) blocker -Clin: immediate conversion of a.flutter of a.fib to sinus rhythm -Tox: prolonged QT and vent. arrhythmia --> torsades -other: not used orally due to 1st pass met.
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d,l-Sotalol
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-Class II/III antiarrhythmic hybrid -Mech: beta-adrenergic blocker (low/high dose), K channel blocker (high dose) -Clin: Ventricular tachyarrhythmias, supraventricular tachyarrhythmias (including a.fib) -Tox: excessive beta blockade, arrhythmogenic, long QT --> torsades -Other: only racemic mixture used
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Class II Antiarrhythmic Drugs
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-Beta-adrenergic receptor blockers - mechanism: decrease sympathetic tone --> decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents. Increase PR interval. reduce Vmax - effect: decrease HR - Uses: SVT, ventricular rate control for a fib and a flutter - SE: impotence, exacerbation of COPD and asthma, bradycardia, AV block, HF, sedation, sleep alterations, dislipidemia (metoprolol), exacerbate vasospasm in prinzmetal angina (propranolol) - may mask signs of hypoglycemia - treat overdose with saline, atropine, glucagon -Ex: propranolol, carvedilol, esmolol (very short acting)
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Class IV antiarrhythmic drugs
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-Calcium Channel blockers -3 structural classes: 1. Dihydropyridines: nifedipine and many others 2. Phenylalkylamines: verapamil 3. Benzothiazepines: diltiazem - Mechanism: Block phase 2 calcium current --> decrease conduction elocity, increase ERP and PR interval - effect: non-dihydropyridines increase coronary vasodilation and decrease HR, dihydropyridines decrease afterload - Frequency dependent (verapamil>diltiazem>>nifedipine) - Voltage-dependent (nifedipine>diltiazem=verapamil) -Other: dihydropyridines not useful in tx of arrhythmias
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Verapamil, Diltiazem
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- Class IV antiarrhythmic - mechanism: cardiac selective Ca2+ channel blockers (voltage-gated L-type Ca2+ channels)--> decreased CO - effects: increase coronary vasodilation, decrease HR -uses: hypertension, angina, atrial fibrillation/flutter - SE: cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia, AV block, hyperprolactinemia (verapamil) - verapamil>diltiazem
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Dihydropyridines (nifedipine, amlodipine)
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- mechanism: vascular selective Ca2+ channel blocker --> decreased arterial and venous contraction (decrease TPR) - effect: decrease after load - uses: HTN, angina, Raynauds, subarachnoid hemorrhage (nimodipine --> prevents cerebral vasospasm) - SE: cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia, - amlodipine = nifedipine
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Adenosine
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-Antiarrhythmic, physiological antagonist of sympathetic tone -Mechanism: activates outward K+ current in atria --> hyper polarizes cell and decreases Ca2+ current --> antagonizes HCN channels - Uses: acute re-entrant supra ventricular tachycardias - Very short acting (15 seconds) - Effects blunted by theophylline and caffeine (adenosine receptor antagonists) - SE: flushing, hypotension, chest pain, sense of impending doom, bronchospasm
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Fenoldopam
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- Dopamine D1 agonist --> coronary, peripheral, renal, and splanchnic vasodilation - decreases BP, increases natriuresis - uses: hypertensive emergency
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Nitrates
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- nitroglycerin, isosorbide dinitrate, isosorbide mononitrate - mechanism: vasodilator by increasing NO in vascular smooth muscle --> increase cGMP --> decrease intracellular calcium --> decrease activity of myosin light chain kinase --> myosin light chain dephosphorylation and smooth muscle relaxation - dilate veins >> arteries - effect: decreases preload --> decreases SV --> decreases systemic BP --> decreases afterload. also increases coronary vasodilation (minor) - uses: angina, acute coronary syndrome, pulmonary edema - SE: reflex tachycardia (treat with beta blockers), hypotension, flushing, headache, "Monday disease" in industrial exposure (development of tolerance for vasodilation during the work week and loss of tolerance over the weekend --> tachycardia, dizziness, headache on reentrance)
