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Flashcards in special circulations (CVS13) Deck (26):

physiology of coronary circulation (blood supply to myocardium)

-right and left coronary arteries arise from the base of the aorta
-most coronary venous blood drain via the coronary sinus into the right atrium
-oxygen demand of cardiac muscle is high especially during exercise
-coronary circulation requires special adaptations


coronary heart disease

-if left coronary artery is blocked at the beginning of the artery before any branches, then the full left ventricle will be deprived of blood supply
-if left coronary artery is blocked at one of its terminal branches, then only the area surrounding that branch will be deprived of blood supply


special adaptations of coronary circulation

-high capillary density
-high basal blood flow
-high oxygen extraction (~75% compared to 25% whole body average) under resting conditions
-this means that extra O2 (when required) cannot be supplied by increase O2 extraction
-> can only be supplied by increasing coronary blood flow
-coronary blood flow is controlled by intrinsic and extrinsic mechanisms


control of coronary blood flow (intrinsic mechanisms)

-decreased PO2 causes vasodilation of the coronary arterioles
-metabolic hyperaemia matches flow to demand
-adenosine (from ATP) is a potent vasodilator



hyperemia is the increase of blood flow to different tissues in the body. It can have medical implications, but is also a regulatory response, allowing change in blood supply to different tissues through vasodilation


control of coronary blood flow (extrinsic mechanisms)

-coronary arterioles supplied by sympathetic vasoconstrictor nerves BUT
-over ridden by metabolic hyperanaemia as a result of increased heart rate and stroke volume
-so sympathetic stimulation of the heart results in coronary vasodilation despite direct vasoconstrictor effect (functional sympatholysis)
-circulating adrenaline activates beta2 adrenergic receptors, which causes vasodilation



tending to oppose the physiological results of sympathetic nervous activity


control of coronary blood flow

-sympathetic stimulation:
->increases circulating adrenaline (which activates beta2 adrenergic receptors, causing vasodilation which increases coronary blood flow)
->has a negative effect itself on coronary blood flow as it causes vasoconstriction (however this is over ridden by the metabolic hyperanaemia which causes vasodilation)
->increases SV and HR (causing an increase in CO which increases coronary blood flow)
->the increase in SV also increases cardiac work (which increases metabolism)
-the increase in metabolism:
->decreases PO2 (which causes vasodilation and increases adenosine which is a potent dilator to achieve this, therefore increases coronary blood flow)
->increases adenosine which causes vasodilation and increases coronary blood flow
->produces metabolites (eg. K+, PCO2 and H+) which increase coronary blood flow



a substance formed in or necessary for metabolism


coronary flow during the cardiac cycle (graph)

-the peak of the left coronary flow occurs during diastole
-diastole is shortened eg. by a very fast heart rate which decreases coronary flow


physiology of cerebral circulation (blood supply to the brain)

-the brain is supplied by the internal carotids and vertebral arteries
-the brain needs a secure supply of oxygen
-the grey matter is very sensitive to hypoxia (deficiency in the amount of oxygen reaching the tissues) therefore consciousness is lost after a few seconds of ischaemia (an inadequate blood supply to an organ or part of the body) and irreversible cell damage occurs within ~3 minutes of it
-> as a result of this, special adaptations of the cerebral circulation is needed to ensure the brain always has secure supply of O2


special adaptations of cerebral circulation (circle of willis)

-basilar artery (formed by two vertebral arteries) and carotid arteries anastomose to form circle of willis
-major cerebral arteries arise from circle of willis
-cerebral perfusion (process of a body delivering blood to a capillary bed in its biological tissue) should be maintained even if one carotid artery gets obstructed
-nevertheless, obstruction of a small branch of a main artery would deprive a region of the brain of its blood supply



-stroke is caused by interruption/cut-off blood supply to a region of the brain
-main types of stroke:
->haemorrhagic (bleeding) stroke (blood leaks out of artery wall which is damaged) - happens to branch of vertebral artery
->ischaemic stroke (formed due to a blood clot which forms on atheroma/the fatty material which forms deposits in the arteries, on the artery wall or comes from another part of the body and gets stuck, blood cannot flow past the clot) - occurs in internal carotid branches


special adaptations of the cerebral circulation (regulation)

-autoregulation of cerebral blood flow guards against changes in cerebral blood flow if mean arterial blood pressure changes within a range (~60-160mmHg)
-direct sympathetic stimulation has little effect on overall cerebral blood flow (therefore only decreases cerebral blood flow slightly)
-participation of the brain in baroreceptors reflex is negligible, which is just as well!
-increased PCO2 causes cerebral vasodilation increasing cerebral blood flow (cause of hypercapnia), decreased PCO2 causes vasoconstriction (this is why hyperventilation could lead to fainting, because when you hyperventilate you are trying to get more O2 into the body, therefore CO2 decreases causing vasoconstriction, so the lack of CO2 causes the vessels to constrict and less O2 reaches the brain as a result)
-blood flow increases to active parts of the brain (regional hyperaemia), mechanism is unknown, may be due to rise in [K+]o as a result of K+ efflux from repetitively active neurones?


autoregulation of the cerebral blood flow

-autoregulation of cerebral blood flow guards against changes in cerebral blood flow if mean arterial blood pressure changes within a range (~60-160mmHg)
-if MABP rises, resistance vessels automatically contstrict to limit blood flow
-if MABP falls, resistance vessels automatically dilate to maintain blood flow
->autoregulation fails if MABP falls below ~60mmHg (cerebral blood flow falls), or rises above ~160mmHg (cerebral blood flow rises)



is a condition in which you suddenly start to breathe very quickly. Healthy breathing occurs with a healthy balance between breathing in oxygen and breathing out carbon dioxide


effect of PaCO2 in cerebral blood flow

-increase in PCO2 causes vasodilation in order to allow diffusion of CO2 across capillary therefore increases cerebral blood flow



-Hypercapnia, also known as CO2 retention, hypercapnea, and hypercarbia, is a condition of abnormally elevated carbon dioxide (CO2) levels in the blood
-causes an increase in cerebral blood flow


effect of intracranial pressure (ICP) on cerebral blood flow

-skull is a rigid box filled with approximately : 80% brain, 12% blood and 8% cerebrospinal fluid/CSF
-normal intracranial pressure (ICP) within the skull is about 8-13mmHg
-cerebral perfusion pressure (CPP)= MAP (mean arterial pressure - ICP
-increasing ICP (eg.due to a head injury or brain tumour) decreases CPP and cerebral blood flow
-some conditions which increase ICP can lead to failure of autoregulation of cerebral blood flow


the blood brain barrier (BBB)

-cerebral capillaries have very tight intercellular junctions (the blood brain barrier)
-cerebral capillaries are highly permeable to O2 and CO2
-glucose crosses the BBB by facilitated diffusion using specific carrier molecules
-brain has obligatory/compulsory requirement for glucose
-the BBB is exceptionally impermeable to hydrophillic substances such as ions, catecholamines, proteins etc
->this helps protect the brain neurones from fluctuating levels of ions etc in blood


physiology of pulmonary circulation

-entire cardiac output flows from right ventricle into pulmonary circulation
-metabolic needs of airways met by systematic bronchial contraction
-pulmonary resistance is only ~10% of that of the systemic circulation
-pulmonary artery BP is typically (20-25) divided by (6-12) mmHg


special adaptations of pulmonary circulation

-pulmonary capillary pressure is low (~8-11mmHg) compared to systemic capillary pressure (~17-25mmHg)
-absorptive forces exceed filtration forces (protects against pulmonary oedema)
-hypoxia causes vasoconstriction of pulmonary arterioles (completely opposite to effect of hypoxia on systemic arterioles, why?)
->purpose of this is to help divert blood from poorly ventilated areas of lung


physiology of skeletal muscle circulation

-skeletal muscle ~40% of adult body mass
-resistance of skeletal muscle vascular bed has large impact on blood pressure
-resting blood flow is low because of sympathetic vasoconstrictor tone


skeletal muscle circulation during exercise

-skeletal muscle blood flow increases during exercise
-during exercise, local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
-circulating adrenaline causes vasodilation (beta2 adrenergic receptors)
-plus cardiac output (CO) increases during exercise
->these 2 factors could increase skeletal muscle flow many folds


the skeletal muscle pump

-large veins in limbs lie between skeletal muscles
-contraction of muscles aids venous return
-one way venous valves allow blood to move forward towards the heart
-skeletal muscle pump reduces the chance of postural hypotension and fainting
-blood pools in the lower limb veins if venous valves become incompetent (varicose veins)
-varicose veins usually don't lead to reduction of cardiac output -> because of chronic compensatory increase in blood volume


varicose veins

-blood pools in the lower limb veins if venous valves become incompetent (varicose veins)
-varicose veins usually don't lead to reduction of cardiac output -> because of chronic compensatory increase in blood volume