Treatment of angina Flashcards
What are the factors affecting the heart’s energy status and viability?
Coronary artery blood flow, sympathetic nerves (increases rate and force of pumping), peripheral arterioles (provides vascular resistance), and central venous pressure (preload, which sets resting ventricular pressure and hence inotropic state).
What are the factors improving energy status of the ventricles?
Energy supply increased by increased coronary blood flow; energy demand reduced by: reduced afterload, reduced preload, negative inotropy.
What is the cause of angina pectoris (chest pain)?
Adenosine, a product of ATP metabolism accumulates due to failure of washout (reduced coronary flow).
What is stable angina?
With a stable atheroma (fixed partial block of coronary), exercise causes pain and rest alleviates pain.
What is unstable angina?
When the atheroma fissures, a thrombus may form and fully block the coronary artery.
What is Printmetal’s variant?
Inappropriate coronary vasospasm.
What is the symptomatic treatment of an acute angina attack?
Sublingual nitroglycerin provides rapid relief as if is absorbed rapidly. It’s mechanism involves ventilation which reduces central venous pressure (preload), thus reducing left ventricular diastolic tension and via the Starling mechanism, reduces inotropy and energy (oxygen) demand.
What is the prophylaxis in angina?
Stable- Ivabradine
Unstable- aspirin
both- long acting nitrates, calcium antagonists and beta-blockers
Variant- nothing or GTN
What are clinical features of stable angina?
At rest, coronary supply meets demand; coronary response to exercise and increase in ventricular work is vasodilation; maximum flow in a vessel is limited by minimum vessel diameter.
Why is coronary dilation not a mechanism used for treating stable angina?
Normal parts of coronary dilate in exercise however the atheroma part (stenosis) cannot so flow does not increase.
How is stable angina diagnosed?
Stable angina is exercise induced chest pain, this can be reflected in a ECG where there is a ST elevation during exercise and reverses slowly on rest.
Why are long-acting nitrates used for prophylaxis in stable angina?
They achieve benefit by selective preload reduction. They have rapid onset and their site of action is capacitance veins and are functionally selective on vascular smooth muscle. Venodilation reduces left ventricular pressure and hence, inotropic state.
What is the mechanism of long-acting nitrates?
Nitrates are de-nitrated in blood stream, producing NO which diffuses into smooth muscle and initiates a cascade involving cGMP which causes smooth muscle relaxation.
Why are calcium antagonists used as prophylaxis in stable angina?
They produce relatively selective afterload reduction; verapamil and diltiazem may have negative inotropic effects which both reduce ventricular work.
What is the molecular mechanism of calcium antagonists?
They block L type calcium channels which block entry of calcium ions into cells via slow inward current and cell contraction. Therefore, in vessels, they cause vasodilation and in the heart (verapamil and diltiazem) cause negative inotropy.
