pharm detailed antiangina
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metabolic change in the heart caused by imbalance of O2 supply and demand
accumulation of lactic acid, which causes pain
3 electrophysiologic change caused by decreased O2 in heart
- ST segment changes
- T changes
contractile changes caused by decreased O2 in the heart
wall motion abnormalities
the bottom-line role of drugs used to treat angina pectoris
restore balance between myocardial O2 supply and demand
organic nitrates -- treat what? how?
beta blockers treat angina how?
decrease O2 demand
best for treating stable angina than the other types
Ca++ channel blockers
treat what? how?
- increase O2 supply -- do it by reducing contractability of muscles --> dilation ---> increased blood supply
3 primary drug categories to treat angina, and their basic roles
- organic nitrates: decrease O2 demand
- beta blockers: decrease O2 demand
- Ca++ channel blockers: increase O2 supply
brought on by what?
primary characteristic of it?
- O2 demand greatly exceeds supply
treatment of stable angina -- which types of meds?
- mainly organic nitrates and beta blockers
- but Ca++ channel blockers can be used (due to their effect on myocardium and peripheral vasculature rather than their ability to dilate coronary arteries)
- usually treated with a combo of antianginal drugs
variant angina - primary problem? his description of this type?
- O2 supply to myocardium decreases bc of coronary artery vasospasm
- happens when you find out your wife is cheating
first choice drug for variant angina
- Ca++ channel blockers
- long lasting nitrates can be added for management of severe forms
what can trigger variant angina
- endogenous vasoconstrictive agents
- emotional and environmental stim (cheating wife) can also cause the coronary arteries to constrict
- * can occur when pt is at rest
several serious and potentially life-threatening forms of myocardial ischemia associated with thrombosis in the coronary arteries MI
it's a combo of stable and variant - increased myocardial O2 demands at the same time as coronary vasoconstriction
can begin with activity or happen when at rest
- aka variant angina
- it's called spontaneous, but really it's just that something other than exercise, such as stress, is triggering the angina
organic nitrates - basic role?
dilate vascular smooth muscle to produce vasodilation throughout body (not just coronary vessels)
how do organic nitrates impact the heart? 2 ways
- dilation in systemic venous system --> decreased amount of blood returning to heart (cardiac preload)
- dilation of systemic peripheral arterioles --> decreased pressure against which the heart must pump (cardiac afterload)
2 organic nitrate drugs
- isosorbide dinitrate
nitrates are drug precursors. They become active when converted to __ within __
- nitrous oxide
- vascular smooth muscle
nitrous oxide (nitrates turn into this) do what?
how do nitrous oxides cause vasodilation? (remember, organic nitrates become nitrous oxides)
increase the production of cyclic guanosine monophosphate (c-GMP) in muscle cells, --> cGMP acts as a second messenger that initiates phosphorylation of specific contractile proteins --> inhibition of smooth muscle contraction
nitroglycerin -- type of drug? role? ways to take it, in order from fastest to slowest acting?
- organic nitrate
- antianginal - treatment and prevention
sublingual (1-3), buccal (2-3), oral (20-45), transdermal (30 min)
type of drug?
how it differs from the other drug of this class?
- organic nitrate -- treatment and prevention of angina
- antianginal and hemodynamic effects last longer than nitorgylcerine
isosorbide dinitrate - given how for acute vs prevention
- acute - sublingually, buccally, or chewable tablets
- prevention - oral tablets
beta-adrenergic blockers -- basic role? how?
- decrease HR and force of myocardial contractions
- by antagonizing beta-1 receptors on myocardium --> decrease in work the heart must perform & decrease in myocardial O2 demand
can beta-adrenergic blockers be given prophylactically?
yes - can prevent onset of angina by balancing myocardial O2 supply and demand
atenolol and metoprolol are what kind of drug?
cardioselective beta-1 antagonists
blockers that bind to both beta-1 and 2 receptors may induce what side effect in who? so they should be given what?
- bronchoconstriction in pts w asthma
- cardioselective beta-1 antagonists (atenolol or metoprolol)
how do Ca++ channel blockers work?
block entry of calcium into vascular smooth muscle --> less actin-myosin interactions --> relaxation & dilation of blood vessels
the impact of Ca++ blockers?
coronary dilation --> more O2 in myocardium
can Ca++ blockers do systemic vasodilation?
yes, although their primary role is to dilate coronary arteries, they do some systemic vasodilation, so some of their antianginal effects may be due to how they decrease myocardial work load by reducin cardiac pre and afterload
how do Ca++ blockers impact cardiac striated cells?
- by reducing the amount of calcium in them, they decrease their contractility and O2 demand
- by altering conduction of electrical activity can treat cardiac arrhythmia
type of drug?
- Ca++ channel blocker
- vasodilate coronary arteries and peripheral vasculature
- some depression of electrical conduction in SA and AV nodes
- may --> slight bradycardia
type of drug
- it's a Ca++ channel blocker,
- it's of dihydropyridine class of drugs
nifedipine -- Ca++ channel blocker and of diydropyridine class -- does what?
- selectively blocks Ca++ channels in vascular smooth muscle rather than cardiac striated muscles
- dilate coronary arteries and periph vasc w/o affecting heart excitability and contractility
side effects of nitrates and Ca++ channel blockers that may be an issue during a PT session
peripheral vasodilation that can lead to HoTN, orthostatic hotn, dizziness, syncope
nitrous oxide increases production of what?
c-GMP (cyclic guanosine monophosphate)
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