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36 Cards in this Set

  • Front
  • Back
What are the categories of antianginal drugs?
organic nitrates, beta blockers, CCBs, and ranolazine
What are the most common antianginal drugs prescribed?
organic nitrates/nitrites
How does NO work?
It stimulates cGMP which dephosphorylates myosin light chains.

It is degraded by phosphdiesterase V. Some drugs, like Sildenafil (viagra) blocks PDEV. It should not be taken if pt is on nitric oxide because TOO MUCH vasodiltion would occur.
What does nitric acid increase?
No affect?
Increases stenosis diameter, transmural blood flow, and collateral vessel diameter.

Decreases preload and afterload.

Has no affect on heart rate or contractility.
What is the effect of a beta blocker on angiotensin II?
The amount of Ang. is decreased.
What increases with beta blockers?

What decreases?
No effect?
Nothing is increased.
Afterload, heart rate, tension, and contractility are decreased.

No effects on transmural blood flow, stenosis diameter, collateral vessal diameter, and preload.
What receptors do propanolol and nadolol block?
beta 1 and beta 2 receptors.
What receptors do metaprolol, atenolol, and acebutolol block?
beta 1 receptors.
What are the three major determinants of myocardial oxygen demand?

And what decreases all of these determinants?
HR, contractility, and systolic wall tension.

beta blockers
What are beneficial effects of beta blockers in treating angina?
decreased nitroglycerin consumption and increased exercise tolerance. They are good for angina prophylaxis and pts who have frequent anginal attacks.

They are NOT useful for pts with vasospastic angina.
Which drugs are CCBs?
The "dipines" and verapamil and ditliazem.
How do CCBs work?
They stop calcium from coming in and binding with calmodulin. This prevents phosphorylation of myosin and stops contraction.
At what step does nifedipine bind and what triggers it?
Nifedipine is voltage dependant and thus binds to areas that depolarize more often, such as arterial blood vessels. It binds to channels when they are in the inactive state and impedes transition from closed to open.
At what step do verapamil and diltiazem bind and what triggers them?
They are use/frequency dependent and bind to channels that cycle the most (at any stage). These are located in the myocardium.
Which CCBs have an affect on pacemaker cells and conduction?
Verapamil and diliaztem.
What do CCBs do to preload and afterload?
They decrease afterload by decreasing aortic pressure. They have no affect on preload (and only a little affect on the veins).
What does the reflex stimulation do during the administration of nifedipine and dihydropridine?
Increases contractility and increases heart rate (chronotropic effect).
What hemodynamic effects are specific to verapamil?
Less vasodilation than the other CCBs and direct NEGATIVE effects on chronotropy, inotropy, and dromotropy (conductivity).
Which drug is contraindicated in congestive heart failure patients?
Verapamil because it can decrease the heart's contractlility and left ventricular function.
What effects are specific to diliazem?
It vasodilates the least of all CCBs.
It has direct NEGATIVE effects on chronotropy, dromotropy, and inotropy, but not as negative as verapamil.

It acts as a midpoint between the other families of CCBs, and is often tolerated better.
Which drug vasodilates the periphery the best?
Dihydropyridines (nifedipine).
Which drugs are also indicated in supraventricular arrhythmias?
Verapamil and diltiazem
What are CCBs used for?
angina pectoris, essential hypertension, and cardiac arrhythmias.
What do CCBs increase in the heart?
No effect?
Increases stenosis diameter and collateral vessel diameter.

Decreases contractility, heart rate, wall tension, and oxygen consumption. (Reflexes can oppose these actions). And decreases afterload.

Has no effect on transmural flow or preload.
What drugs are good in treating vasospastic angina?
Verapamil, diltiazem, and dyhydropyridines.
How might CCBs aggrevate myocardial ischemia?
Because of excessive hypotension, there is decreased coronary perfusion or increased sympathetic stimulation that increases oxygen demand.
Which pts should not be treated with diltiazem nor verapamil?
Ones with ventricular dysfunction, SA node or AV node conduction problems.
What is a rare side effect of CCBs?
Gingival hyperplasia.
What is a unique, and the most common effect of verapamil?
What are two most common side effects of nifedipine?
Ankle edema and facial flushing.
Why is amlodipine by itself (Norvasc®) or in combination with ACEI benazepril (Lotreg®) or cholesterol-lowering atorvastatin (Caduet®) the CCB probably now prescribed more than all others combined
Has a long half life (take once per day).
Prevents CV complications better than ACE inhibitors or diuretics do.
It also promotes endothelial NO synthesis, functions as an antioxidant, and interferes with matrix metalloproteinases.
How does Ranolazine work?
Primarily by blocking the stimulation of Na channels that initiate late influx of sodium, and prolongs the QT interval. It has no affect on heart rate or blood pressure.
What are the benefits of Ranolazine?
It can be added to most drug regimens and has smaller side effects--headache and dizziness.
What are the contraindications for Ranolazine?
Using it with another drug that prolongs QT interval or drugs that interfere with CYP3 metabolism.
What drugs need to go with any antianginal regimen?
Aspirin and statins to prevent an MI.
What is used for intermittent exertional relief?
sublingual nitroglycerin.