Vasodilators in Angina Flashcards
Nitrates (i.e. nitroglycerin) and Nifedipine _______ HR.
increase
B-blockers _________ LV volume.
increase
Nitrates and Nifedipine increase what again?
HR
What are the three major types of angina? describe each.
- stable- lumen narrowed by plaque, there is inappropriate vasocontriction
- unstable- The plaque has rupture, there is platelet aggregation and thrombus formation. Vasoconstriction goes unopposed.
- variant- no overt plaques in this case. Angina is caused by intense vasospasms.
How is variant angina different from unstable or stable angina.
no overt plaques in this case. Angina is caused by intense vasospasms.
What is the basic pathophysiology of stable angina?
demand increases (remember angina is just a mismatch in oxygen supply and demand to the heart).
What is the basic pathophysiology of unstable angina?
Thrombus forms and supply decreases.
What is the basic pathophysiology of variant angina?
vasoconstriction-supply decreases
What basic pharmacotherapy principles would you want to invoke in stable angina? What drugs would you use.
decrease demand (or perhaps increase supply)
Drugs- Beta-blockers, Nitrates, Calcium Channel Blockers (these are the three major drugs to remember for any angina. Later notecards will detail exceptions to that rule).
What basic pharmacotherapy principles would you want to invoke in unstable angina? What drugs would you use.
Reduce thrombosis Decrease demand (or perhaps increase supply)
Drugs- 3 major angina drugs (Beta-blockers, Nitrates, Calcium Channel Blockers) as well as ANTITHROMBOTICS for the thrombus.
What basic pharmacotherapy principles would you want to invoke in variant angina? What drugs would you use.
prevent vasospasm
drugs: calcium channel blockers, nitrates (the three major angina drugs minus b-blockers)
When it comes to angina are we better at rectifying by decreasing demand or increasing supply?
decreasing demand.
What are the major nitrate to know?
nitroglycerin, isosorbide mononitrate, isosorbide dinitrate
How do nitrates work?
NO activates guanylate cyclase which increases conversion of GTP to cGMP. This leads to increased levels of cGMP which leads to relaxation of smooth muscle (and decreased levels of myosin phosphate) and vasodilation.
How do calcium channel blockers work?
Normally calcium binds to calmodulin and by other steps leads to muscle contraction. CCBs block Ca entry and lead to relaxation of smooth muscle and vasodilation.
What is the best route of administration to achieve rapid therapeutic levels of nitrates?
sublingual
What are the uses for Nitrates?
treatment for acute angina and prophylaxis for stable angina.
What are important side effects of nitrates?
- orthostatic hypotension (when you stand up), tachycardia and anything else related to vasodilation.
- Also don’t take nitrates with Viagra… this is not a joke. This was mentioned in class… just don’t do it.
What is different about -dipine calcium channel blocking drug side effects (i.e. nifedipine) than other CCBs (i.e. diltiazem, verapamil).
-dipines only have vasodilatory side effects. Whereas diltiazem and verapamil can also cause cardiac depression (i.e. bradycardia, AV block etc).
T or F- B-Blockers are intermediate vasodilators.
F
B-blockers are not vasodilators at all. They just decrease demand by lowering HR, systolic pressure, and contractility which will help the angina.
What does Ranolazine do?
inhibits the late Na+ current and thus prevents Ca2+ overload. Sometimes the late Na current fails to inactivate which messes stuff up and causes intracellular Ca overload (by reversing the Na-Ca exchanger).
Use for stable angina
What is the target of B-Blockers in the heart?
beta-1 adrenergic receptors in the HEART. This leads to reduced rate and contractility and a reduction in myocardial O2 demand (I hope I have drilled home this last point).
Primary target of nitrates?
relaxation of venous capacitance vessels which leads to a reduction in preload and thus a reduction in myocardial demand (heart doesn’t have to work as hard).
Nitrates also can dilate coronary artery vessels to increase myocardial O2 supply but this plays a much bigger role in variant angina than regular anginas.
Primary target of CCBs?
reduce vasoconstriction in BOTH coronary and noncoronary vessels. This increases coronary blood flow and decreases cardiac afterload.
Diltiazem and verapamil also play a second function in the heart only to decrease rate and contractility, reducing myocardial O2 demand.
T or F: Dihydropyridines have a greater ratio of vascular (i.e. relaxation) effects to cardiac (i.e. SA node impulse generation, contractility) effects.
T. nifedipine is the prototype dihydropyridine.
remember diltiazem and verapamil have effects on the heart (phase 0 SA and AV node and phase 2 cardiac muscle).
