L5- Angina Flashcards
(23 cards)
What are the factors affecting the hearts energy status and viability?
- Coronary artery blood flow
- Sympathetic nerves (+/- heart rate)
- Peripheral arterioles (provide vascular resistance known as afterload against which the ventricles pump blood)
- Central venous pressure (preload sets resting ventricular pressure and ionotropic state)
What increases the energy supply to the heart?
Increased coronary blood flow
What decreases the energy demand of the heart and why?
Reduced afterload or preload
Negative ionotropy
What is angina pectoris?
It is a symptom of ischaemic heart disease where chest pain occurs due to reduced blood flow to the heart via the coronary arteries.
What causes angina pectoris?
Due to the effects of reduced coronary flow
Insufficient supply of glucose, O2 and other nutrients
Insufficient removal of metabolic products e.g adenosine (ATP metabolism product) accumulation due to failure of washout
Cause activation of local nerves to generate chest pain
What is the significance of theophylline?
It was used to antagonise the action of adenosine to relieve chest pain. But also causes increases in heart rate and contractility so was stopped.
What are the 3 types of angina?
- Stable- Fixed partial block of coronary artery (atheroma), exercise causes pain and rest alleviates it.
- Unstable- When the atheroma fissures and forms a thrombus which may fully block the coronary artery. Associated with acute MI.
- Inappropriate coronary vasospasm (rare)- coronary arteries appear normal but spontaneously go into spasm.
What is the symptomatic treatment of an acute angina attack?
Sublingual GTN which relieves symptoms via venodilation which reduces central venous pressure (preload)
This reduces the left ventricular diastolic tension and reduces ionotropy and oxygen demand.
What are the clinical features of stable angina?
Coronary supply meets demand at rest.
Coronary response to exercise (and increase in ventricular work) is is vasodilation.
But an atheroma cannot dilate so the diameter of the vessel (where the atheroma is) remains the same in rest and exercise.
Why is coronary dilation not a mechanism for treating stable angina?
Atheroma cannot dilate
Dilating other parts of the diseased artery will not increase blood flow as it is the atheroma that causes the limitation
How is stable angina diagnosed?
Exercise induced chest pain
ST segment elevation in the ECG during exercise which reverses slowly at rest
What are the drugs used for prophylaxis in stable angina?
- Long acting nitrates
- Calcium antagonists
- Beta blockers
- Ivabradine
- Trimetazidine
How are long acting nitrates used for prophylaxis?
Selective reduction of preload by acting on capacitance vessels (veins)
Also act on arterioles but it is a small effect, overcome by sympathetic nerves
Tolerance develops quickly but is overcome by intermittent dosing
What are the long acting nitrates?
Erythrityl tetranitrate
Isosorbide dinitrate
Pentaerythritol tetranitrate
What is the molecular and cellular mechanism of nitrates?
De-nitrated in blood stream to produce NO
NO diffuses into smooth muscle and initiates a cascade involving GMP
End result is smooth muscle relaxation
What are the calcium antagonist drugs?
Verapamil, Diltiazem, Amlodipine, Nifedipine
How do calcium antagonist drugs achieve prophylaxis?
Produce selective reduction of afterload (act on arterioles)
Verapamil and diltiazem may also have negative ionotropic effects
Both effects reduce ventricular work
What is the molecular mechanism of calcium antagonists?
All block Ca2+ entry into cells by blocking L type calcium channels.
Block via slow inward current and cell contraction
In vessels= vasodilation (all)
In heart= negative ionotropy (verapamil and dilitiazem)
How do beta blockers achieve prophylaxis?
Non-selective beta or selective beta-1 adrenoceptor agonists have negative chonotropic (SAN) and ionotropic (ventricular muscle) effects.
Reduce cardiac energy consumption to reduce chest pain.
How does Ivabradine achieve prophylaxis?
Relatively selective for slowing SA node rate
It blocks the funny current (If) which slows down the heart rate
How does Trimetazidine achieve prophylaxis?
Emerging drug
Main form of ATP synthesis in the heart is fatty acid oxidation
The drug blocks the production of fatty acids so ATP production switches to glycolysis which reduces O2 demand.
What are the drugs used in unstable angina?
Nitrates, calcium channel blockers and beta blockers indirectly reduce pain
Aspirin is used as an antithrombotic
How is variant angina treated?
Only form of angina that can be treated using vasodilation due to the angina being caused by a spasm in the artery (otherwise the artery is healthy)
