College aantekeningen
Unit 3 Summary
- Vak
- Instelling
Includes lecture notes, workbooks, and associated videos in one summary
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Part 1: Acute Coronary SyndromeBackground
Atheroma formation- atherogenesis
o Intima: inner layer of vessel is composed of single layer of endothelial cells and
endothelium provides physical barrier between internal vessel wall and circulating
blood. Endothelium is more than passive structural barrier, highly interactive
interface. Its two main functions are:
Secrete vasoactive substances- NO and prostacyclin for vasodilation and
endothelin for vasoconstriction
Secrete many anticoagulants including prostacyclin which physically
repels platelet cells and prevents them from attaching to endothelial wall.
If platelets find attachment, formation of thrombus would occur.
Endothelial functions become impaired during plaque formation and lose
vasodilation. Damage to intima/ endothelium is first step in atheroma
development
o Media or tunica media is thickest layer of arterial wall, between intima and
adventitia, separated from them by thin layer of collagenous tissue known as
internal and external elastic laminae. Media mostly made of smooth muscle
o Adventitia or tunica externa- external wrapping, made of densely packed collagen
fibres and collagen secreting fibroblasts. Small BV, lymphatic capillaries and
nerve fibres also travel along arteries by passing through adventitia.
*arteriosclerosis= hardering of arteries
The process of plaque formation- certain conditions for plaque formation
High levels of LDL
Damage to or irritation of; endothelium: could be from high levels of frictional or
shearing forces (usually secondary to high BP), blood glucose or insulin, micro-
organisms (e.g. viral or bacterial illness), inflammatory mediators and toxins or irritants.
Damaged endothelial cells (can be from smoking, hypertension, etc.) release substance
that attract monocytes and platelets which bind to endothelium and enter intima.
Monocytes can change to macrophages and release free radicals and reactive oxygen
species. LDLs can also enter and can become oxidized by ROS. Macrophages can ingest
oxidized LDLs (called foam cells) and release more ROS that attract more monocytes
and LDLs, continue to increase over time. (positive feedback situation)
Platelets and foam cells release growth factors, which cause smooth muscle cells to
migrate from tunica media to intima via gaps in to internal elastic lamina, this blurs the
, intimal and medial components. The SMCs proliferate and collagen and elastin fibres
secreted and this forms the plaque/atheroma. LDLs and salts continue to accumulate and
plaque gets larger and matures (called fibrous cap).
As atheroma develops and increases in size, it impacts degree of obstruction to blood
flow and degree of turbulence it produces in blood flow
Ageing and Degeneration of Atheroma:
Plaque ages and fibrous cap plaque degenerates and starts to fissure prior to plaque
rupture. When rupture occurs, haemostatic response triggered (haemostasis) whereby
blood clot formation occurs and a thrombus can form at top which can cause total or near
total vessel occlusion. Thrombus embolization associated with PE, stroke, MI. Embolus
is when plaque moves. Heart attack if it affects coronary arteries
o Blood clot: thromboplastic released, forms thrombin fibrin mesh is formed and
blood clot (thrombus is form)
Also, growth of atheroma over time will cause clinically silent narrowing of artery,
compromising blood flow until ischemia occurs. The point where blood flow and demand
become uncoupled is known as ischaemic threshold. Might become symptomatic when:
o Atheroma grows large enough to occlude vessel lumen lowering the ischaemic
threshold so it impacts activity
o When increase activity levels (climbing stairs or running for bus) and tissues
supplied by affected artery increase demand for blood flow (O2)
Coronary Arteries- Anatomy and Physiology
Coronary arteries supply essential nutrients and oxygen to the highly aerobic cardiac
muscle fibres (cardiomyocytes)
, Heart needs its own supply because even though 5-6 L of blood passes though cardiac
chambers per minutes, very little can get through the thick cardiac muscle wall and
diffusion is not efficient.
L and R coronary arteries arise from root of aorta and encircle the ehart travelling in to
the AV groove
Left coronary artery goes towards left side of heart and divides in toL
o Anterior descending branch (anterior interventricular artery)_ supplying the inter-
ventricular septum and anterior walls of both ventricles
o Circumflex artery which supplies left atrium and posterior aspect of left ventricle
Right coronary artery supplies blood to walls of RV and part of posterior LV. Also
supples SAN, AVN, and Bundle of His
There are many small anastomoses (small interconnecting vessels) between coronary
arteries that can provide collateral routes for circulation with repeated episodes of
ischemia (e.g. angina). This collateral circulation would allow blood to flow even if an
artery is completed occluded with an atheroma
Anatomic Region of the Heart Coronary Artery (most likely affected)
Inferior Right coronary
Anteroseptal Left anterior descending
anteroapical Left anterior descending (distal)
anterolateral circumflex
posterior Right coronary artery
The cardiac regions can be assessed by 12 lead ECG to localize ischemic or infarctic regions.
But because of vessel heterogeneity between individuals, actual vessel involvement needs to be
verified by coronary angiograms or other types of imaging.
All major vessels in epicardium give off smaller branches that travel towards endocardium.
Coronary arteries divide in to arterioles+ capillaries and lateral reassemble in to venules and
veins. High capillary to cardiomyocytes ratio and short diffusion distances ensure efficiency
oxygen delivery to myocytes and removal of waste but this is poorer with greater diffusion
distances in less healthy
After passing through myocardium, the now venous blood if transported via coronary veins,
most join to form coronary sinus that empties directly into RA.
Coronary artery blood flow is intermittent or pulsatile because:
, Intermittent contraction of heart, where systole is contraction phase and increases
myocardial intra-muscular pressure which compromises coronary vessels and temporarily
stops blood flow. Most coronary blood flow occurs during diastole.
When aortic valve is opened (as on ejection- culmination of systole), its flap partially
obstructs entrance to coronary arteries further impeding blood flow in coronary arteries.
** aortic valve opens when pressure in LV greater than pressure in aorta, blood in to aorta
But myocardium makes up for this with efficient extraction of O2 from coronary blood supply,
which is measured by a-VO2 difference of coronary blood and comparing it to a-VO2 difference
of skeletal muscle blood
(a-vO2 difference is difference in O2 content in arterial blood compared to venous, when arterial
O2 content supplying a tissue is compared to venous, difference corresponds to amount of O2
extracted and utilised by the tissue)
The a-VO2 difference in skeletal muscle at rest is 25% ( only 25% of O2 content of arteriak
blood passing through is used, so venous blood still very oxygenated (~75%)
The a-vO2 difference is 65-70% at rest for coronary artery blood flow, this shows heart is
extremely efficient at extracting and utilising O2 but this means that there isn’t more O2 to tap in
to and the blood flow has to be increased via vasodilation of coronary artery. Vasodilation occurs
due to low O2, high CO2, and release of vasodilator substances (NO, H, K, adenosine).
Temporary inadequacy of O2 can result in loss of cardiac muscle function and dysfunction
within intrinsic conducting system but if sustained, can cause permanent damage
Regulation of coronary artery diameter:
Calibre of coronary arteries regulated by local factors and ANS (weak effect), main
determinant of calibre are environmental factors. Lumen of artery changes from slightly
VC at rest to dilated during exercise.
During physical activity, HR and SV increase, fibres need more O2 and produce more
metabolic waste like H, K, adenosine which cause VD (VC to other blood vessels around
body) via B2 receptors. Local endothelial cells secrete NO, prostacyclin, and bradykinin
which also cause VD
PNS also thought to have VD effect on coronary circulation
Unhealthy coronary arteries: can’t full vasodilate due to loss of endothelia VD including nO an d
due to obstructive atheroma. Leads to reduced aerobic capacity and ability to extract and utilise
O2, and myocardium of unfit heart will need higher blood flow as well
Unhealthy coronary arteries and unhealthy body: inadequate physical activity can lead to
atheromas, reduced CO2 through type 1 skeletal muscle atrophy and reduced aerobic efficiency.
Deconditioned skeletal muscles increased demand on heart for blood flow and heart has to work
harder.
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