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18 Cards in this Set

  • Front
  • Back
Type of Anginas
Stable Angina: with physical excretion, no myocardial necrosis.

Variant (prinzmetal): secondary to myocardial ischemia, excl at rest, no phys precipitation, assoc w/ ST elevation.

Unstable: at rest last more than 20 min, severe, frank pain, crescendo pattern, ST elevation.

NSTEMI: subtype of unstable, w/o ST elevation
Organic Nitrates: nitroglycerin, isosorbide dinitrate, isosorbide-5-mononitrate
(look for nitro or nitrate in the name). Releax SM in veins at low dose, and arteries at high doses. They release NO to activate gunanylyl cyclase to form cGMP, which then activates light chain phosphatase to dephosphorylate myosin light chain leading to uncouble and vasodilation, particulary in VENULES.
Organic Nitrates: reduction of angina, 3 mechanisms
Dilation of systemic venules decrease PRELOAD and pressure within ventricle >> increase in pressure gradient fro aorta to endocardial surface (so less contraction = more flow into myocardium.

Reduction in PRELOAD > decrease O2 demand (do not directly change contractility of the heart).

Nitrates only dilate large coronary arteries, and the small coronary vessels remain determined by autoregulation (determined by metabolic needs). So, LESS CORONARY steal, unlike vasodilators who vasodiate all vessels.
Organic Nitrates: Application, Contraindications
All anginas, CHF, MI

Contraindications: Pt taking SILDENAFIL, Hypotension, Hypertrophic Obstructive cardiomyopathy, Diastolic heart failure.
Organic Nitrates: Tolerance and Withdrawal Issues
taken at the time of anginal attack or in anticipation of it. Frequent exposure leads to tolerance, so effecitve therapy is to INTERRUPT dosinf for 8-12 hrs each day during the night. Some pt may develop tolerance anyway and will require other drugs.

Withdrawal: Angina intensifies after discontinuation of large dose of long lasting nitrates, with hightened sensitivity to constrictor stimuli.
Organic Nitrates: Rx interactions, side effects, pharmakokinetics
All PDE inhibitors (sildenafil etc)

Side effects: Hypotension, HEADACHE, dizziness, weakness, reflex-tachycardia

Pharmacokinetics: high first pass metabolism, so sublingual or inhaled more effective, short half life of 2-8 Minutes. Isosorbide dinitrate, chewable form w/ 2-3 hrs duratin.
Nitrates Vs. Ca Ch blockers
Nitrates limited to vasculature, but Ca blockers also act on myocardium

Nitrates mainly venodilatory, Ca channel are predominantly arteriolar dilators.
List L-type Ca channel blcokers
verapamil, diltiazem, and the dihydropyridine class called nifedipine.
Ca Ch blocker mech
inhibition of Ca influx evokes relaxation of arteriole, but not venous s.m., thus decreasng coronary resistance and increasing coronary blood flow and reducing angina.

Also, decreases heart contractility of heart to reduce likelihood of ischemia and angina.
List 4 possible mech of action for Ca channel blocker
dilate arteriolar tension, reducing afterload and O2 demand.

reduce contractility and O2 demand.

decrease HR (by slowing AV node conduction)and O2 demand and enhance O2 supply.

Decrease coronary resistance and increase blood flow.
Ca Ch blocker: dihydropyridines Vs. non-dihydropyridines
Nifedipine (a dihydropyridine) relaxes vascular sm at lower conc. than that required for reducing Ca influx in cardiac cells. Thefore, results in reflex increase in carioc output.

The non-dihydropyridine (Verapamil and diltiazem) are less potent and therefore, exert effect on both heart and vascular sm simulataneously, therefore are able to decrease HR, and contractility as well. It is donevia decrease in rate of crecovery of Ca ch after opening and increase delay before Ca ch can reopen, slowing conduction through AV node.

Diltiaem also has nonspec. antagonism of sympath NS, and so non-dihydropyridines are effective treatments for supraventricular reentry tachycardia and beneficial n pts with atrial tachy, flutter and fibrillation.
Ca Ch blocker: Nimodipine
Nimodipine, a dihydropyriine, has high affinity for cerebral vessels and may reduce vasospasm and mortality after subarachnoid hemorrhage.
Ca ch blocker: side effects and contraindications
adv effects: cardiac depression, arrest, bradycardia, AV blocker and CHF.

Non-Dihydropyridines contraindicated in pts with Heart Failure.
Beta-Adr R antagonists: List
Non-selective beta blockers: propranolol, sotalol

beta 1 selective blockers: atenolol
Beta receptors
beta 1: mocardiu, renal JG cells,

beta 2: arteriolar, venous, bronchioles, GI tract, urinary bladder, Uterus.
Mech of Action: Beta blockers
reduce HR, contractility, and arterial BP (afterload) which all reduce O2 consumption
Adverse effects: Beta blockers
erectile dysfunction, depression, insomnia,

Non-sel beta blocker (propranolol) in asthma pt leads to beta 2 block and bronchoconstriction.

non-sel beta blcoker not useful in VASOSPASTIC angina, and may worsen angina if used in Isloation.
4 reasons for contraindications of non-sel beta blockers for variant angina?
beta 2-r blockade causes coronary dilation, allows unopposed alpha-1 receptor mediated coronary vasocontriction to occur.

That causes systemic vascular resistance (increase afterload) and O2 demand.

Also, venoconstriction may result which increases preload and decrease coronary flow.

biochemical mech of focal vasospasm is poorly understood.