Kaplan Section 3 Chapter 5 Anti-Anginal Drugs
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| Why does a pt get chest pain in ischemic heart disease? | Anginal pain happens when O2 delivery to the heart is inadequate for myocardial requirement.
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| What is classic angina? | angina of effort or exercise
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| What is classic angina due to? | coronary atherosclerotic occlusion
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| What is Prinzmetal angina? | vasospastic
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| What is Prinzmetal angina due to? | reversible decrease in coronary blood flow
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| What is unstable/crescendo angina? | Acute coronary syndrome with platelet aggregation
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| What are the two drug strategies to treat classic and vasospastic angina? | 1. inc O2 delivery by dec vasospasm (use nitrates and CCB's); 2. dec O2 requirement by dec TPR, dec CO, or dec both (use nitrates, CCB's, and B blockers)
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| Name 4 endogenous compounds that can activate the NO pathway | Ach, Bradykinin, Serotonin, Histamine ==> vasodilation!
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| Name 2 nitrates. | Nitroglycerin, isosorbide
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| What is the mechanism of nitrates? | NO --> activate guanylyl cyclase --> inc cGMP --> dephosphorylate myosin light chain --> myosin can't interact with actin --> relaxation of vascular sm musc --> venule dilation --> dec preload --> dec cardiac work --> dec O2 requirement
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| What happens with hi-dose nitrates? | In addition to what happens normally, you also get arteriolar dilation --> dec afterload --> dec O2 requirement
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| What makes using nitrates especially promising for pts? | decreases infart size and decreases post-MI mortality
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| What drugs should be used to treat cyanide poisoning? What is the mechanism? | Na-nitrite or Amyl-nitrite --> forms metHb --> MetHB binds CN- ions (prevents CN- from binding to and inhibiting complex IV on the ETC) --> forms cyanometHb ---(add Na-thiosulfate)--->becomes metHb & SCN- (less toxic)
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| Adverse effects of nitrates | 1. MetHbnemia, (more likely with nitrites than with nitrates), 2. tachyphylaxis (require > 12 hr period of "rest"), 3. reflex tachy and fluid retention, 4. effects of vasodilation: flushing, headache, orthostatic hypotension (syncope)
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| Why shouldn't you use Sildenafil with? | Nitrates or other potent vasodilators. Sildenafil causes vasodilation, so combined with another vasodilator --> severe decrease in BP --> can lead to death!
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| What is the mechanism of CaCB's? | block vascular L-type Ca channels --> myosin can't be phosphorylated to interact with actin --> prevention of smooth muscle contraction --> vasodilation --> dec afterload (arterioles most sensitive) --> dec cardiac work
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| Nifedipine | CaCB - vascular selective --> vasodilation in arterioles --> dec afterload --> dec cardiac work. Use for angina or HTN.
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| Bepridil | CaCB - dilates coronary vessels. Also blocks Na and K channels (--> implicated in torsades). Used for angina.
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| Why would you use B blockers to treat angina? | No actions on vascular smooth muscle. With B blockers, you are directly targeting the heart --> dec HR, dec contractility (inotropy), dec CO --> dec O2 requirement.
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| For what type of angina would B blockers be most effective? | Classic (angina of effort) -- not vasospastic. Can also use to offset the reflex tachy caused by use of nitrates (vasodilators).
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| Compare Carvedilol and Isosorbide | Both have been shown to be equally effective vasodilators. (Carvedilol has both a and B blocking actions.)
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| What is the drug strategy for unstable angina? | Nitrates + B blockers + supplemental O2. Prevent thrombosis (and MI) with heparin, warfarin, and antiplatelets (ASA, ticlopidine)
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| What drugs should you consider for acute coronary syndromes (including unstable angina)? | Glycoprotein IIb/IIIa receptor inhibitors (abciximab, eptifibatide, tirofiban)
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