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27 Cards in this Set
- Front
- Back
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Furosemide (Lasix)
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Loop diuretic
Relieves fluid retention, congestion and preload Side effects: Ion wasting (hypochloremia leads to metabolic alkalosis) |
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Spironolactone
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K sparing diuretic
Weak diuretic- use in combo with ACE/Beta/Loop *Aldo antagonist so blocks negative remodeling |
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Eplerenone
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K sparing diuretic
Give to pts with normal renal function and LOW K Similar to spironolactone but fewer adverse effects |
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Angiotensin II
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Formation is blocked by ACE Inhib
Vasoconstrictor Potentiates NE release Na/H2O retention Negative remodeling |
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Bradykinin
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Metabolism blocked by ACE Inhib.
Vasodilator *causes dry cough |
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ACE Inhibitor
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Mainstay CHF drug
Give low dose initially and gradually titrate up |
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AT1 Receptor
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Bound by AngII
Vasoconstriction Aldosterone secretion SNS activation Na and H2O retention Cardiac remodeling *ARBs (-sartans) block |
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AT2 Receptor
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Vasodilation
Renal NO and PGI2 Na Excretion |
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Nitrates
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Relax vascular SM by NO/Guanylyl Cyclase mechanism
Decrease LV filling pressure Dilate coronary vessels Limited systemic vascular effects Relieve ischemia in emergencies Use in pts who can't tolerate standard ACE or ARB |
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Isosorbide dinitrate/ Hydralazine
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Better than nitrates alone but < ACE I
Hydralazine is a vasodilator Increases renal blood flow Use in ACE resistance pts with renal failure |
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BNP
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Released from stretched ventricular myocytes
Marker of HF Binds to receptor that activates cGMP Nesiritide is drug prep: vasodilates and induces natriuresis and diuresis |
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BNP MOA
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Elevation of cGMP leads to vasorelaxation
Promotes natriuresis and diuresis Blocks fibrosis cardiac remodeling |
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BNP- kinetics and averse effects
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IV infusion with loading dose
Hypotension Don't give if systolic bp<90 |
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Beta Blockers
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Blocks formation of PKA which increases cardiac remodeling, CO, apoptosis and cell damage
*Start patient on ACE first, then start low with BBlock and titrate up |
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Carvedilol
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Use in <35% (ClassII/III)
Hepatic metabolism with the P450 2D6 effect (genetic variation) 2D6 inhibited by Quinidine, Fluoxetine |
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Carvedilol
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Blocks B1/B2
Improves EF and decreases LV mass Antioxidant properties Blocks A in vasculature (dilates) Inhibits SM mitogenesis (restenosis) Decreased SNS activation (lower renin) SEs: CNS, B2 (Reactive airways, vasospasm) |
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B Blocker Drug Interactions
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Increase B Blocker effects: cimetidine, fluoxetine
Decreased B Blocker effects: Barbituates, Phenytoin, Rifampin |
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Metoprolol succinate
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B1 Selective antagonist
Extended release formula Cheaper than carvedilol |
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Bisoprolol
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B1 selective antagonist
Long T1/2 |
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Glycosides (Digoxin)
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Use in CHF with AFib
CHF refractory to ACE/BBlocker No mortality effect: lacks neurohormonal blockade effect Only ORAL + ionotrope Targets systolic dysfunction |
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Glycosides MOA and Kinetics
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Blocks Na/K atpase
Stimulates vagal nucleus Enhance contraction and increase vagal tone to decrease HR Increase CO/ decrease O2 consumption Resevoir in skeletal muscle Excreted by kidney Reverse toxicity by elevating EC K |
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Glycosides and the SA/AV Node
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Increased vagal tone slows conduction by increased ACh release at cardiac nerve ending
*Opposite effects in artrial tissue |
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Glycoside Toxicity
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Increase SNS activity
Catecholamines are released and affect atria and ventricles: beat faster now than SA/AV node and become ectopic pacemakers Cause arrhythmias due to simultaneous stimulation of vagal tone to slow SA/AV and random catecholamine release to atria/vent. fibers |
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Digoxin drug interactions
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Potassium wasting increases effectiveness
Propafenone, Quinidine, Verapamil, Amiodarone decrease renal clearance Erythromycin doubles digoxin absorption rate Hypothyroidism/renal failure increases digoxin blood levels |
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Reversal of Digoxin toxicity
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Atropine- sinus bradycardia and sinoatrial arrest
K+- binds Na/K Atpase to cause drug to fall off Lidocaine or phenytoin-ventricular arrhythmia Digibind- Ab to drug |
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Dobutamine
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Racemic mixture but + does the beneficial work
Stimulates B1 and B2= Increase CO Antagonizes A= Vasodilation Given IV *If vasodilators, ACE-I, BBlock, Diuretics and Digoxin fail |
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PDE Inhibitors
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Type 3 PDE: Milrinone
Elevates cAMP by blocking metabolizer Short term because no remodeling benefit LAST RESORT- intolerable SEs, decreased platelets, increased mortality Combo with other drugs Loading dose required, IV infusion |
