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Flashcards in Angina Deck (10):

What is angina pectoris?

A symptom of IHD. Chest pain due to reduced coronary blood flow.


Stable angina?

Partial blockage of the coronary. Exercise causes pain but rest alleviates it. Flow in vessels is limited by the minimum vessel diameter...and the atheroma part can't dilate (therefore cant treat with coronary dilation)
Elevated/supressed ST segment (dependant on lead) during exercise but is reversed slow on rest.


Unstable angina?

Progression of stable angina, atheroma fissures...exposes thrombogenic core (lipids and Ca++) thrombus forms, and causes a full block of the coronary. If sustained may cause an infarction.


Variant angina?

INAPPROPRIATE Coronary vasospasm not usually due to an atheroma. Aka, prinzmetal's variant.


Symptomatic treatment of an acute angina attack?

Regardless of cause; sub-lingual GTN (nitroglyceride). Provides rapid relief by reudcing neodilation (decrease CVP and preload). THerefore LV diastolic tension decreases and via starling's law, decreased inotropy and energy (O2) demand.


Outline the prophylaxis of angina?

Stable: long acting nitrates, calcium antagonists and beta blockers
Unstable; as for stable and aspirin
Variant; nothing or GTN (nitroglycerin)


Long acting nitrates?

Erythrityl tetranitrate, given po (orally) or transdermally.
Acts on capacitance veins (functional selective effects on venous system). There is a brieif afterload reduction but this is surmounted by sympathetic reflexes.

mechanism: venodilation, decrease LV pressure and therefore decrease inotropic state.

Tolerance builds quickly, therefore use intermittent dosage.

Nitrates de-nitrated in the blood stream to NO. Diffuse into SM where it initiates a cascade involving cGMP which results in SM relaxation and in BV = vasodilation.


Calcium antagonists?

verapamil or nifedipine.

relatively secletive decrease in afterload.
Verapamil is selective as it acts on heart l-type calcium channels to block inward current and therefore Ca++ entry and block contractions = vasodilation


Beta Blockers?

Non selective B or B1 (atenolol) antagonists have negative inotropic and chronotropic effects. Decrease cardiac energy consumption.
Okay to use even if heart failure is present.
However they cause bronchospasm is asthmatic so use a selective B1 in that case.



Irreversibly (cpavalently) block COX - block TxA2 (platelet aggregation and vasoconstriction) and PGI2 (antiaggregatory, prevent vasospasm). Endothelial cells can resynthesis COX and therefore PGI2, but platelets cannot. Therefore aggregatory effects of PGI2 dominate.