CVR Ischaemic heart disease & hypoxia Flashcards
(52 cards)
WHat is IHD?
the term given to heart problems caused by narrowed heart arteries that supply its muscle
signs of IHD
- angina (syncope, aching, radiation in arms, high or low BP)
- Heart rhythm problems (palpitations, heart murmurs, tachycardia, atrial fibrillation, S4, S3 gallop from non-compliant ventricle)
- general important symptoms (nausea, sweating, fatigue, shortness of breath diaphoresis, leg swelling)
what is the leading cause of death in the world?
IHD
where is IHD most prevalent?
eastern europe
who is IHD most prevalent amongst?
older people (65+)
who is IHD most prevalent amongst?
older people (65+)
risk factors types of IHD (2)
modifiable
non modifiable
non-modifiable risk factors types of IHD
age, gender. family history CVD. ethnicity. genetic evidence, previous history of CVD
modifiable risk factors types of IHD
high BP, cholesterol, smoking, blood sugar/diabetes/LVH, BMI, diet, stress, low socioeconomic state, alcohol, income, certain meds, social deprivation environment
causes of IHD
obstruction cause by atheroma. spasms, embolus
what is involved in artherosclerosis? (3)
What is the process called?
lipids,
macrophages
smooth muscle cells
-> process is called artherogenesis
how do smooth muscle cells interact with plaques?
proliferate and cover plaque. Contains the plaque (lumen of blood vessel reduced)
TGF B and T-reg cells and macrophages do what to fibrous cap of stable plaque?
stabilise and protect it
when does a plaque become vulnerable?
when the fibrous cap thins
when does a plaque become vulnerable?
when the fibrous cap thins
presentations of IHD (3)
- asymptomatic
- chronic stable angina (stable fixed plaque)
- unstable angina, non-ST elevation MI, ST elevation MI (unstable plaques)
how does an occlusion occur in IHD?
- direct contact with the flowing blood
- blood platelets adhere to it, fibrin deposited, RBC entrapped to form a clot
- clot grows until artery occlude
- can break away e.g. PE
what happens to collaterals in sudden event?
doubling by the second/third day
- achieve normal flow within 1 month
what happens to collaterals in chronic atherosclerotic patients??
- slow occlusion vessels can develop at the same time while the atherosclerosis become more severe-
- these collaterals can also get damaged
- sometimes hypoxic area is too large
soon stages after MI (2)
- small amount of collaterals open
- local blood vessels dilate and cause overfilling with stagnant blood,
muscle fibres use all remainign O2 -> bloof turns blue brown
later stages after MI
vessel wall permeability increases, fluid leak and local tissue oedematous
- cardiac muscle cells swell and no blood supply means they die within a few hours
causes of death after MI (4)
- decreased CO (systolic stretch from muscle death and cardiac shock)
- damming of blood in body’s venous system
- ventricular fibrillation
- rupture of infarcted area (Early little danger after few days infarcted area begin to degenerate heart walls become very thin stretched until finally rupture)
x
x
recovery after an acute MI
- when large area of ischemia:
- > some of centre dies
- > immediate surrounding can recover