Effect Flashcards
Beta blockers
Decrease CO & BP. -I & -C (reduced workload and oxygen demand of the heart). Decreases renin output which reduces afterload
Alpha 1 blockers (vascular selective) acute effect
reduce arterolar resistance and I erase venous capacitance, may cause reflex increase in HR and plasma renin activity
Alpha 1 blockers (vascular selective) chronic affect
Reduce arterial resistance and hyperplasia
Alpha 2 agonist
Reduces BP by reducing NA release (and sumo output) on heart and peripheral vasculature
Ace inhibitor
Reduce vasoconstriction (arteries) (decreased afterload). Increase venous dilation (reduce preload). Decrease TPR & BP. increase Na & H2O excretion = reduces plasma volume &BP. Reduces aldosterone release
Angiotensin receptor blockers
Prevents vascular sm contraction & vasoconstriction pressor responses, aldosterone activation, profibrotic pathways etc
Statins
Decreases hepatic de bono cholesterol synthesis, increases LDL receptor synthesis which increases LDL clearance from bloodstream also slight increase in plasma HDL.
Activates PPAR which inhibits uptake of LDL by macrophages, and increases endogenous NO (vasodilator) release
Fibrates
Reduces VLDL & TG & LDL by 10%. Increases HDL levels
Low dose aspirin
Inhibits platelet aggregation, reducing risk of thrombus formation
Clopidogrel
Inhibits platelet activation and aggregation, reducing risk of thrombus formation
Enoxaparin
Decreases thrombin formation, ultimately prevents fibrin clot formation
Warfarin
Impacts intrinsic & extrinsic pathways, preventing fibrin formation, ultimately preventing clot formation
Fibrinolytics
Increases plasma levels which breaks down thrombus after formation (thrombolysis)
Amlodipine
Prevent vascular sm contraction = arterial vasodilation = reduced afterload, TPR, BP, cardiac oxygen consumption
Verapamil
-I (reduced force of contraction) -C (reduced rate of contraction) -dromotrope (reduced conduction velocity)
Diltiazem
Vasodilation. Reduced force of contraction, reduced rate of contraction, reduced conduction velocity (-I, -C, -D)
Nitrates and nitrodilators
Venodilation (reduced preload), vasodilation (reduced afterload), reduced workload and O2 demand of heart. Reduces EDP & EDV = lowering intermural pressure
Osmotic diuretic
Decreases Na $ H2P reabsorption in tubules, increasing urinary volume and resulting in decreased BP & BVOL
Loop diuretic
Prevents reabsorption of Na+, K+, Cl- $ H2O. Blocks Na+, Ca2+ & Mg2+ paracellular transport
Thiazide diuretics
Modest increase in Na+ & H2O excretion
Potassium sparing diuretic
Prevent aldosterone from enhancing Na+reabsorption through ENaC and Na+/K+ ATPase. Na+ & H2O loss = decrease BVOL & BP, but K+ retention
Sodium channel antagonist
Decreased rate & magnitude of depol during phase 0, decreases conduction velocity
Potassium channel antagonist
Prolongs atria & ventricular repol, increasing plateau phase & total duration of AP. Contractility is unchanged or increased
Cardiac glycoside
Increase force of contraction, decrease HR