What classes of drugs act on the vasculature? (there are more but this lecture focuses on 2 main types)
What are the 4 direct acting vasodilators?
Direct acting vasodilator- arteriole vasodilator
Htn, heart failure (+nitrate)
Decreases resistance to LV doesnt need to pump as hard --> increases CO
Low bioavailability, short half life
SE: HA, palpitations, flushing, nausea, anorexia, lupus like syndrome
Direct vasodilator: arteriolar (increased K channel permeability)
Severe or refractor htn (rarely used!)
SE: reflex tachycardia, fluid retention, hypertrichosis (excessive hair growth--ROGAINE), pericardial effusion
"balanced" vasodilator- acts on arteries and veins; potent/rapid
metabolized to NO and to cyanide
Decrease arterial/systemic resistance, increase venous capacitance -- works best on pt with normal or reduced LV function
Treat hypertensive emergency (with beta blocker) & severe CHF -- IV infusion, 30 seconds to on, minutes off
SE: thiocyanate toxicity --> blurred vision, tinnitus, disorientation, nasuea
Direct acting vasodilator-- arteriolar
dopamine 1 agonist --> vasodilation
Thought to enhance renal perfusion
IV, rapid onset, rapid offset, metabolized in liver, renally excreted
SE: HA, dizzy, tachycardia, increased intraocular pressure (avoid in pt with glaucoma)
What conditions? Mechanism? Contraindications? How administered?
Vascular smooth muscle relaxation --> venodilation --> CO falls secondary to this
Use for angina, acute coronary syndromes, HF
Don't use in preload sensitive patients i.e. RV MI
Fast acting formulas for acute i.e. sublingual
Chronic i.e. oral, transdermal
IV nitroglycerin for unstable angina, pulm edema, HF
Drug tolerance develops with continued use- drug holiday
SE: hypotension, reflex tachycardia, HA, flushing
What is the main 5-phosphodiesterase-5 inhibitor?
PhDiEs-5 inhibitor --> decreases pulm vasc resistance in pt with pulm arterial htn
Don't use with nitrates or viagra!! Severe systemic hypotension
Calcium Channel blockers: how they work and 2 main classes
Decreases intracellular Ca concentrations --> vasodilation in vasc smooth muscles and/or inotropic effect in cardiac cells
Non-dihydropyridines: mainly negative inotrope
Dihydropyridines: mostly vasodilators
When do you use Ca Channel blockers?
2nd line for angina
Coronary artery spasm
Verapamil and Dilitazem: Supraventricular Arrhythmias
What are the SE of Ca Channel blockers?
Verapamil: hypotension, bradycardia, AV block, constipation
Diltiazem: hypotension, peripheral edema, bradycardia
Dihydropyridines: hypotension, HA, flushing, peripheral edema (esp amlodipine)
What are the 4 main anti-adrenergic classes?
CNS alpha 2 agonists
Peripheral alpha antagonists
Reseripine: sym nerve ending antagonist
Alpha and beta receptors location/response
What are the CNS alpha 2-antagonists? What is their effect?
Diminished sympathetic outflow from the medulla --> decreased peripheral vasc resistance, drop in BP and HR
Clonidine, alpha-methyldopa, guanabenz, guanfacine
SE: refractory htn
Symp nerve-ending antagonist
Inhibits NE uptake --> depletion of catecholamines --> decreased TPR
SE: CNS toxicity (sedation, loss of conc, psychotic depression) = rarely used! Reserpine is the serpent for your brain
What are the main peripheral alpha antagonists?
Alpha-1 selective: "-sin": prazosin, terazosin, doxazosin (CHF risk)
** these are great for benign, prostatic hypertrophy; also used for htn but not as much
Non-selective: phentolamine, phenoxybenzamine
*** great for pheochromocytoma