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Cardiac Output
The amount of blood the heart ejects out in 1 minute.
Preload
How much blood is coming into the heart.
Afterload
The resistance the heart has to overcome which affects stroke volume.
Inotrope
How hard the heart is contracting.
ACE Inhibitor
Blocks conversion of angiotensin I into angiotensin II.
ARB (Angiotensin Receptor Blocker)
Blocks angiotensin II receptors.
Aldosterone Antagonist
Blocks aldosterone receptors.
Direct Renin Inhibitor
Binds to renin, disabling it from activating angiotensin I.
Calcium Channel Blocker
Blocks calcium channels in vascular smooth muscle, causing peripheral vasodilation.
Alpha-1 Blocker
Blocks alpha-1 receptors, causing vasodilation.
Beta Blockers
Blocks beta receptors, resulting in decreased HR, decreased contractility, & slows conduction
Centrally Acting Alpha-2 Agonist
Stimulates alpha2 receptors to reduce sympathetic release of norepinephrine.
Alpha/Beta Blocker
Blocks both alpha & beta receptors, resulting in vasodilation, decreased HR, Na + H2O excretion
Direct Acting Vasodilator
Directly vasodilates arterioles, causing decreased BP.
Thiazide Diuretic
Blocks reabsorption of H2O, Na, & Cl by acting on proximal portion of tubule.
Loop Diuretic
Blocks reabsorption of H2O, Na, & Cl by acting on the loop of Henle.
Potassium Sparing Diuretic
Blocks aldosterone, resulting in Na & H2O excretion, & K retention.
Inotropic Agent/Cardiac Glycoside
Inhibits Na-K ATPase enzyme, causing calcium accumulation.
Inotropic/Sympathomimetic
Stimulates beta1 receptors, resulting in increased contractility & cardiac output.
Inotropic/Phosphodiesterase Inhibitor
Inhibits PDE3, increasing contractility & cardiac output.
HMG CoA Reductase Inhibitor
Inhibits HMG CoA reductase enzyme resulting in lower LDL, lower total cholesterol, higher HDL, and lower VLDL
Nitrate
Causes coronary vasodilation, decreases preload.
Class IA/Sodium Channel Blocker
Blocks Na channels, slows conduction, decreases automaticity, prolongs refractory period.
Class IB/Sodium Channel Blocker
Blocks Na channels, slows conduction, decreases automaticity, prolongs refractory period, treats ventricular dysrhythmias
Class IC/Sodium Channel Blocker
Blocks Na channels, slows conduction, decreases automaticity, prolongs refractory period (>than other Na channel blockers) ,Treats ventricular dysrhythmias & a-fib
Class II/Beta-Blocker
Blocks beta receptors, decreases HR, decreases contractility, slows conduction
Class III/Potassium Channel Blocker
Blocks K channels, decreases automaticity, slows conduction, decreases contractility, & causes vasodilation
Class IV/Calcium Channel Blocker
Blocks Ca channels, decreases automaticity, decreases contractility, slows conduction, Converts SVT into NSR & slows HR in A-fib or A-flutter