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)