treatment of angina Flashcards
what 3 things effect the window for coronary flow?
- increased hr
- increased ventricular pressure (due to volume increase/ can’t fill swell)
- decreased aortic pressure
cause of angina
Chemically, angina is thought to be caused by the build-up of chemical factors (e.g adenosine) due to increased metabolism of the tissue and lack of blood supply to give nutrients and take away waste products produced by this increased metabolism
what are the 3 causes that shrink the coronary window and their examples?
1- shortening diastole (increased hr)
2- increased ventricular end and diastolic pressure (aortic valve stenosis- this will cause incomplete emptying which increases ventricular pressure- you don’t get the same volume of blood pushed out.)
3- reduced diastolic arteriole pressure (mitral or aortic valve incompetence, heart failure- regurgitation of blood, not enough force)
what is demand ischaemic?
specific type of ischamia where the oxygen requirement of the myocardium are not being met due to some increased need
what is coronary ischaemia usually a result of and what may it cause?
- result of atherosclerosis
- cause angina
cause of sudden iscahemia and as a result of what?
- caused by thrombosis
- result in cardiac infarction
during ischaemia, what happens to calcium levels?
(cellular calcium overload) release of a high conc of calcium which will change the excitability in the local region = dysrhythmias or cell death
what do coronary spasms sometimes cause?
angina
what is angina pectoris?
- chest pain due to inadequate supply of oxygen to the heart
- typically severe and crushing
- tight constricting, dull or heavy
what are the characteristic distribution of pain in angina pectoris?
what is it Brought on by?
what is responsible for the pain?
- retrosternal, or left side of chest and can radiate down the left arm, neck, jaw and back
- Brough on by exertion, cold or excitement
- chemical factors that cause pain in skeletal muscle are though to be the cause (K, H and adenosine)
what can angina accompany or be a precursor of?
heart attack
angina?
temporary disturbance in blood flow to the heart that will not cause permenant damage.
unstable anima (if not treated) can lead to a heart attack.
both are caused by coronary heart disease
3 classes of angina?
- printzmetals variant angina
- chronic stable angina
- unstable angina
printzmetal’s angina?
- caused by vasospasm
- supply ischaemia
- uncommon
- caused by coronary artery spams (vasospasm) - random spasms of the vasculature I the heart which can block blood supply
- not completely understood but associated with atherosclerosis
chronic stable angina?
- caused by fixed narrowing of the coronary vessels
- fixed stenosis
- demand ischaemia
- predictable chest pain on exertion
unstable angina?
- supply ischaemia
- occurs at rest with less exertion than stable angina
- associate with a thrombus around a rupturing atherosclerotic plaque but without complete occlusion of the vessel.
treatment to reduce chest pain symptoms?
- beta blockers
- nitrates
- calcium channel antagonists
- nicroandril
- ivabradine
- ranolazine
treatment for prolonged survival of angina?
- beta blockers
- aspirin (blood thinning)
- statins (lipid lowering, reduced atherosclerotic complications)
- angiotensin converting enzyme inhibitor
- angiotensin II receptor blocker
different types of treatment for the symptoms?
1- offer short acting nitrates for preventing and treating episodes of angina
2- offer first line treatment = beta blocker or calcium channel blocker
3- if control by B-blockers isn’t that good, add CCB
4- if both are not working optimally, use other drugs like nicorandril or ivabradine.
how do antianginal drugs work?
- ## mainly work by decreasing the metabolic demand of the muscle
what are the antianginal drugs that are vasodilators?
- organic nitrates
- nicorandril
- calcium antagonists
they will decrease the preload or after load (decrease the force that heart has to exert to move blood out)
how does beta blockers and ivabradine work as antianginal drugs?
- they will slow down the hr
- they decrease the metabolic demand of the muscle
what are the 2 types of organic nitrates?
glyceryl trinitrate (shorter acting)
isosorbide mononitrate
how do the 2 organic nitrates work?
- decrease preload by dilation of the venous system
- vasodilators
- work by being metabolised to NO and relax smooth muscle (in particular vascular smooth muscle)
- act on veins to decrease cardiac preload
- decrease in cardiac workload is helped by dilation of collateral coronary vessels
what will have to happen for organic nitrates to work on arteries swell?
higher concentration can effect arteries and therefore decreasing the after load
the decrease in cardiac workload from organic nitrates will cause what?
- it will improve the distrubution of coronary blood flow towards ischaemic areas
- dilation of constricted vessels is particularly beneficial in variant angina.
describe the clinical use of organic nitrates for stable angina?
prevention by sublingual glyceryl trinatrate shortly before exertion or isosorbide mononitrate long before
describe the clinical use of organic nitrates in unstable angina?
intravenous glyceryl trinitrate
what are the side effect of organic nitrates
- headache (decreased venous return and cardiac output)
- postural hypotension
what are the 2 other clinical uses of organic nitrates?
- acute heart failure = give intravenous gyleryl trinatrate
- chronic heart failure = give isosorbide mononitrate with hydralazine in patients of African American background.
what is different about African American patients and why they get slightly different treatment?
because they are subject to epithelial sodium channel differences
beta blockers?
- important in the first line treatment
- important in the prophylaxis and treatment of stable and unstable angina
- bisoprolol, atenolol
hw to BB work?
decrease cardiac oxygen consumption by slowing the heart rate
- they also have an antidysryhtmic action which reduced cell death/death after MI
how do calcium channel blockers work?
- they prevent the opening of voltage gated L-type calcium channels
- blocking the entry of calcium
- this mainly effects the heart and smooth muscle to inhibit calcium entry upon muscle cell depolarisation
what are the 2 main types of calcium channel blockers?
- dihydropyridine derivatives (eg amlodipine and lercanidipine)
- rate limiting (eg verapamil and diltiazem)
describe the vasodilator effect of calcium channel blockers?
- it is mainly on resistance vessels
- reduces the after load
- also dilates coronary vessels (important in variant angina)
what can verapamil and diltiazem be used for?
it can reduce and impair AV conduction and myocardial contractility
what are the clinical uses of CCB in angina:
when would you use amlodipine or lercandipine?
the choice between any of the 4 drugs will depend on combirbidity and drug interactions:
- it is safe in patients with heart failure, it will be used instead of beta blockers in prinzmetal angina or alongside beta blockers in most angina.
what are the clinical uses of CCB in angina:
when would you use diltiazem or verapamil?
the choice between any of the 4 drugs will depend on combirbidity and drug interactions:
- they can be used but are contraindicated in her failure, bradycardia, AV block or in the presence of Beta blockers.
side effects of CCB
headache
constipation
ankle oedema (decreasing resistance, increasing flow down to ankle, change in frank starling forces)
2 other clinical uses of CCB?
1- antidysrhymias (mainly verapamil)
- slows ventricular rate in rapid atrial fibrillation
- prevents recurrence of supra ventricular tachycardia (SVT)
- no effect on ventricular arrhythmias
2- hypertension (elevated after load)
- mainly amlodipine or lercanidpine
what drug is a potassium channel activator and how does it work?
nicroandril
- combines activation of potassium ATP channel with nitrovasodilator actions
- causes hyperpolarisation of vascular smooth muscle (decreases the likelihood of vascular contraction, moves towards resting membrane potential)
- both an arterial and venous dilator
nicorandril side effects?
headaches
flushing
dizziness
when would nicorandril be used?
in patients who remain symptomatic despite optimal management with other drugs
2 other anti-anginals?
1- ivabradine
2- ranolazine
ivabradine
= inhibits funny ‘f’type channel in heart
reduces cardiac pace maker activity
therefore inhibits heart rate
ranolazine?
unique anti-anginal used as a last resort
influences Na
- decreases calcium in cells
- decreases contractility
- decrease hr
preload?
the force that stretches the cardiac muscle prior to contraction., with greater volumes of blood providing greater stretch
afterload?
the pressure of systemic vascular resistance in the aorta that the left ventricle has to pump against in order to push blood into systemic circulation
