Angina and Vasodilators Flashcards
What is angina?
Pain in the chest of cardiac origin
If often referred to the left shoulder/upper arm
Caused by inadequate blood supply to the myocardium
What the different methods by which blood flow to the myocardium can become reduced?
Occlusion of coronary arteries - atheroma normally, This tends to be asymptomatic, the development from atheromatous deposit, plaques to atherosclerosis tend to align with stable, unstable angina and thrombosis/MI
Vasospasm of coronary arteries - rarers and is referred to as Prinzmetals angina.
What pathologies beside angina have a similar cause?
Cerebral circulation -stroke
Peripheral vascular disease
What is the difference between stable and unstable angina?
Stable is more common - attacks have a trigger such as exercise and stop with rest
Unstable - attacks have no trigger and no continue even with rest. This is a medical emergency
What is the typicall progression of pathology from chest pain?
May be from a non-cardiac cause
May be stable angina
Or be be an acute coronary syndrome - this could be a STEMI, unstable angina (normal troponin) or a NSTEMI (raised troponin)
What drugs tend to be used for acute episodes of stable angina?
Short acting nitrates
What drugs tend to be used for chronic prevention of stable angina?
Beta blockers
Calcium Channel blockers
Long-acting nitrates
Nicorandil
Ivabradine
What is the basic aim of all drugs used to treat stable angina?
Cause coronary artery vasodilation (increase oxygen supply)
And decrease myocardial effort decreasing oxygen demand
This should prevent the mismatch between oxygen supply and oxygen demand.
Why are the after affects of an MI or angina attack different between people/event?
Highly dependent on the vessel effect and what anatomical region of the heart this vessel supplies.
What is the basic physiology underpinning how angina episodes normally occur during stress or exercise?
Coronary arteries only fill with blood duing diastole
The pressure created by systole occludes the coronary arteries
Therefore increased cardiac work (increase contractility and diastole ends prematurely) resulting in reduced time for coronary artery filling.
Tend to have increased sympathetic activity - increased HR, less time in diastole, inc contraction force - incr vessel closure
This decreases cardiac efficiency and perfusion to the myocardium
This explain why stable angina episodes normally happen during exercise or psychological stress.
Explain how changes in the diameter of coronary vessels contributes to angina pathophysiology?
Norm - artery dilated, arteriole constricted at rest, arteriole can dilate during exercise to inc blood flow to the heart
Angina - artery is chronically occluded by an atheroma, arterioles are dilated at rest in order to constantly inc blood flow to the myocardium, therefore at exercise the arterioles have no remaining vasodilation so blood flow can not increase further
This results in a mismatch between O2 demand and blood flow
Resulting in pain from ischemia.
How does the idea of collateral blood vessels contribute to a safety mechanismin angina?
If one branch of an artery is occluded
A collateral vessel can develop to redirect some flow to the ischaemic area (delaying damage) - note this flow as not a sufficient as original
This is aided by dilating ischemic area arterioles and constricting normal area arterioles in order to direct blood flow
Drugs must dilate certain blood vessels in order to maintain this safety mechanism.
Where is the ideal area for nitrovasodilators to act?
Dilation of collateral blood vessels would increase flow to ischemic area - nitrous oxide does preferentially dilate this area
Dilation of the normal area would reduce blood flow to the collaterals - potentially making damage worse than before drug treatment.
What are the different nitrovasodilators and what do they tend to be used for?
Sodium nitroprusside - hypertensive emergency/heart failure normally given by IV infusion - systemic effect
Isosorbide dinitrate - angina, LV failure, prophylaxis
Isosorbide mononitrate - angina, congestive heart failure
Glyceryl trinitrate - angina, sublingual use for rapid onset treatment of acute episodes
What is basic pharmacology of all nitrates?
Pro-drug, is broken down or metabolised to release nitric oxide
NO actives NO-sensitive soluble guanylyl cyclase, this increases cGMP levels, activates PKG, this causes vasodilation by activating myosin phosphatase and other responses (platelet inhibition)
This mainly effects capitance veins decreasing filling pressure reducing preload so reducing cardiac effort.
