L11 Flashcards
what is the role of the vascular bed (capillary network) in each organ
perfuses the organ and delivers O2 and removes CO2
what is blood flow regulated by
myogenic, neural and metabolic control
is regulation of blood flow uniform in all of the organs. why?
no because some vascular beds are specialised
what is special about cardiac muscle in terms of it specialised regulation of blood flow
the muscle is completely dependent on aerobic metabolism (compeered to skeltal which can do both)
what is special about the pulmonary blood flow
it is the only organ that receives 100% of the CO as it is the site of gas exchange
describe the locations of the coronary vessels
large coronary arteries are on the epicardial surface
smaller vessels penetrate into the myocardium
how much of the CO do the coronary arteries receive
5%
where do the coronary arteries arise from
just outside of the aortic root by the the SL valve
what helps blood flow into the coronary arteries
recoil
what does the right main coronary artery supply
the right main coronary artery supplies blood to the RA, RV and inferior posterior region of the LV
what does the left main coronary artery split into
the circumflex and left anterior descending arteries
what does the circumflex artery supply
the La and the posterior LV
what does the left anterior descending artery supply
the anterior side of the left ventricle
why does the heart have a dense cappilary network
it ensures that each cardiac muscle cell is closely associated with several capillaries. this is important because cardiac muscle cells can only use aerobic respiration therefore they need to have a good supply of O2 and fast removal of waste
where do all the cardiac veins empty back into
the coronary sinus which empties into the right atrium
when is the myocardium perfused
during diastole
what happens to cardiac circulation during systole
myocardium contraction causes the vessels to become compressed decreasing the radius therefore increasing resistance and decreasing the floow
the opposite happens during diastole
what % od perfusion to the hart happens during diastole
75%
what makes puffusion different in the heart compered to other parts i the body
it is pulsatile
what is the difference between the left and the right sides of the heart in terms of blood flow and puffsion
the right does not experience the pulsatile effects as much as the left side
this is because the right side is not as strong as the left therefore it doesn’t contract as much
what % of O2 does the heart extract from the blood
65-75%
it is always working at maximum which means that increased O2 demand in the heart means that it has a limited ability to extract more O2 from the blood
how does the heart increase its O2 levels when it has higher metabolic demands eg when exercising
the heart has the ability to increase its O2 capacity by 5x
it does this through its vasodilator reserve capacity
increased O2 demand = increased flow to the heart
what are the extrinsic regulator of coronary blood flow
the sympathetic nervous system
how does the sympathetic NS have extrinsic control over coronary blood flow
it releases noradrenaline which binds to alpha adrenergic receptors OR beta adrenergic receptors
what happens when noradrenaline binds to the alpha adrenergic receptors
it causes vasoconstriction which leads to increased resistance
what happens when noradrenaline binds to the beta adrenergic receptors
it leads to increased HR and SV
why is extrinsic regulation of coronary blood flow not suitable
because it only has a transient effect as b increases work but a decreases supply
therefore this is overcome by metabolic autoregulation
what is the primary regulator of coronary blood flow
metabolic autoregulation
aka active hyperemia
what is active hyperemia
metabolic autoregulation
this is when you have increased metabolic activity which leads to less O2 and more waste products. adenosine and hypoxia leads to vasodilation which increases blood flow to the organ
what are some vasodilator messengers that are able to regulate coronary blood flow
increased metabolism (increased AMP) leads to the production of adenosine
endothelium also produce NO
both of these cause vasodilation
these happen in hypoxia (low O2)
how many people in NZ dies of cardiovascular disease
1 in 3
one every 90 min
what is atherolosclerosis
it is the underlying cause of heart disease and is the development of lesions (plaques) in arterial wall of larger arteries
what are some common sites of atherosclerosis
Aortic sinus Aortic arch Brachiocephalic Carotid arteries Large epicardial arteries (LAD, Right coronary, circumflex)
when does atherosclerosis start to cause symptoms of heart disease
when 60 - 70% of the lumen is black which means that distal to where the blockage is wont receive O2
what are some risk factors of heart disease
high cholesterol, smoking and age
what is angina
Angina is a type of chest pain caused by reduced blood flow to the heart
what is a myocardial infarction
it is a heart attack
occurs when blood flow to the heart muscle is abruptly cut off
what is stenosis
90% blockage
how does atherosclearosis affect the production of nitric oxide
it changes supply and demand which impacts NO production
because NO is a mechanism for increasing flow as metabolic autoregulation. less metabolism = less NO
how does coronary atherosclerosis effect the myocardial supply and demand ratio
it means that increased demand does not = increased supply as more blood cant get there
therefore coronary disease causes a decrease in maximal coronary blood flow
what happens when NO production decreases
increased resistance –> decreases flow decreased vasodilatory reserve capacity –> exercise induced angina (chest pain)
why is the pulmonary circuit highly branches
You can get up to 20 different branches in the pulmonary circulation
You need a haigh surface area as this is where diffusion takes place
In the lungs it is a range of parallel circuits
describe the characteristics of the pulmonary circulation
it is a high flow, low pressure, low resistance, high compliance system
compare the pressure between the pulmonary and systemic circuits
pulmonary = 25/10mmHg
systemic = 120/80mmHg
how many more x lower is the resistance in the pulmonary circuit compeered to the systemic circuit
10 to 15x lower
this is because of shorter vessels (therefore lower resistance). the veins and arteries also have a large radius
what happens in the lungs when CO increases
the lungs receive 100% of the cardiac output therefore they need to have high compliance for when the CO increases as they need to be able to keep the pressure the same for perfusion
what is different about starling’s forces in the pulmonary circuit
because of the low pressure in the pulmonary circuit water is more likely to go back into the circulation then it is to go out.
this is good because you don’t want water in the lungs as it would affect gas diffusion
what is postures effect on the lungs
when you are standing up there is a difference in pressure between the upper and the lower lung
what is the difference between hypER and hypOfussion
hypO is in the upper lung and hypER is in the lower lung
what is postors effect on the upper lung
a decrease in hydrostatic pressure and vessels partially collapse. this causes an increase in resistance and a decrease in blood flow
hypofussion
what is postures effect on the lower lung
increase in hydrostatic pressure therefore vessels become distended. this decreases resistance and increases blood flow
hyperfusion
what is the importance of hyper and hypofusion
With excursive you have a increase in CO and the hypoperfusion gives us the capacity to be able to dilate and spread the blood flow around all of the lung
it allows for extra space for the extra blood to go
what does a reduction in pulmonary O2 lead to
constriction
If there is no fresh air going into the avioli then the blood will be redirected. Eg if there is no O2 at a specific alvioli then the arteries supplying at avoli will constrict and the blood will be redirected
Therefore you are matching ventilation and perfusion and by doing this we are optimising the gas exchange in the P circuit
what are the 2 ways on intrinsic control of pulmonary blood flow
NO and endothelin 1 from the endothelium
NO causes the smooth muscle to relax –> vasodilation –> decreased resistance and increases flow
ET1 contracts smooth muscles therefore it is the opposite
what does imbalance of the intrinsic control mechanisms in the pulmonary circuit lead to
pulmonary hypertension
what is the extrinsic control over the P circuit
the SNS
alpha adrenoreceptors are mainly found in the large conduit vessels (right and left pulmonary artery) whereas beta adrenoreceptors are in the smaller resistance vessels
a causes vasoconstriction
b cause vasodilation
normally these will balance eachother out
why do we have extrinsic controls if they cancel each other out
We have this because we need to be able to adapt to changes
Eg when you go up altitude there is less O2 therefore it will cause vasoconstriction in the alveoli because none of them will have good O2 levels.
This causes the SNS to kick in and overcome this to cause vasodilation to overrule generalised hypoxia
In the pulmonary circulation, hypoxia will cause the vasculature to:
A: Dilate to increase flow to under ventilated regions
B: Constrict to redirect blood flow to well ventilated regions
C: Dilate to remove excess waste products
D: Constrict to reduce flow to increase the time available for gas exchange
B
Coronary blood flow increases during diastole
BECAUSE
the elastic recoil of the
aorta produces the pressure required to provide flow in the coronary system during diastole
both statements are true and causal
