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28 Cards in this Set
- Front
- Back
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Cardiac Output = ?
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HR x SV
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What kind of receptors are activated by sympathetic inputs on the heart? parasympathetic?
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-beta-1 receptors - increase HR
-muscarinic receptors - decrease HR |
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Heart failure is...
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the inability of the heart to pump sufficient blood to meet the metabolic demands of the body (reduced efficiency of the heart as a pump)
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What are the two main compensatory changes to the heart muscle that occur in heart failure?
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to compensate for reduced stroke volume -- ventricular dilation (increased volume) and hypertrophy (increased mass)
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an endogenous catecholamine that increases heart rate; the synthetic version
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epinephrine; isoproterenol
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Mechanism/selectivity of Dopamine
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agonist of D1 (dopamine) > Beta > alpha receptors
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Effects of Dopamine
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-increased contractility --> increased SV (beta receptor)
-increased HR (but less than epi or isoproterenol) -increased renal blood flow (D1 receptor) |
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Limitations of Dopamine
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-IV only
-short half-life -risk of tachycardia -tolerance (only for acute treatment) -no mortality benefit |
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Mechanism/selectivity of dobutamine
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agonist of beta > alpha receptors (no dopamine receptor effect)
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Effects of Dobutamine
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-increased contractility --> increased SV
-increased HR (less than iso or dopamine) |
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Limitations of Dobutamine
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-IV only
-proarrythmic (because a beta agonist) -tolerance risk (only short term use) -no mortality benefit |
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Phosphodiesterase is an enzyme that degrades __________ to _______.
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cAMP to AMP
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cAMP is activated by what receptors?
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beta receptor --> cAMP --PDE--> AMP
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Mechanism of Milrinone
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phosphodiesterase inhibitor
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Effects of Milrinone
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-increased cAMP --> phosphorylation of calcium channels --> more calcium available --> increased contractility, SV
-increased cAMP --> smooth muscle relaxation --> decreased afterload (vasodilation) (note different effects in heart vs. smooth muscle) |
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Limitations of Milrinone
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-can cause hypotension
-proarrhythmic -no mortality benefit |
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Class of drugs that Digoxin belongs to
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Cardiac glycosides
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Elimination of Digoxin is carried out by the ___________.
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kidneys (caution with patients with renal problems)
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What is notable about the pharmacodynamics of digoxin
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it has a very narrow therapeutic index
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Describe the mechanism of action of digoxin
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-competes with K+ to inhibit the Na+/K+ ATPase - direct inhibition (K+ in, Na+ out)
-this increases amount of Na+ inside the cell -disrupts the gradient for passive diffusion of the Na+ in and Ca+ out through the Na+/Ca+ exchange (indirect inhibition) -Ca+ builds up intracellularly and more is stored in the SR |
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What is the direct action of digoxin?
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increased contractility
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Why would hypokalemia cause digitoxicity?
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-K+ competes with digoxin for in the Na+/K+ ATPase - if no K+ then digoxin actions are greater
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Describe the effects of digoxin on SV, ventricular size, and blood flow to the kidneys
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-increased SV (more Ca+ so more contractility)
-decreased ventricular size (don't need hypertrophy) -increased blood flow to kidneys |
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What is the sympathetic effect of digoxin on HR?
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-increasing SV increases blood pressure
-decreases the reflex sympathetic stimulation -get a decrease in HR |
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What is the vagal effect of digoxin?
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it slows the rate of electrical conduction through the AV node (via stimulating the parasympathetic nerves)
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What is delayed after depolarization? What causes it?
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-a form of arrhythmia - when the resting potential has a depolarization out of sequence
-occurs from the build up of Ca+ associated with digitoxin (a toxic effect of the drug) |
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Symptoms of digoxin toxicity
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-N/V, diarrhea, vision changes, arrythmias
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How is it treated? (5)
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-decrease or stop drug
-administer K+ if hypokalemic -Atropine to block vagal effects -lidocaine - for ventricular arrhythmias -glycoside antibodies - digibind |
