Special Circulations Flashcards
outline the physiology of coronary circulation and its clinical relevance
right and left coronary arteries - arise from base of aorta
most coronary venous blood drains via coronary sinus to right atrium
oxygen demand of cardiac muscle is high especially during exercise
coronary circulation requires special adaptions
describe how coronary blood flow is regulate by intrinsic mechanisms
decreased PO2 causes vasodilation of coronary arterioles
metabolic hyperaemia matches flow to demand
adenosine (from ATP) is potent vasodilator
describe how coronary blood flow is regulate by extrinsic mechanisms
coronary arterioles supplied by sympathetic vasoconstrictor nerves but;
over-ridden by metabolic hyperaemia 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 cause vasodilation
when does left coronary blood flow occcur
during diastole
shortening diastole (e.g. very fast heart rate) will decreases coronary flow myocardial perfusion also occurs during diastole when the subendocardial vessels from left coronary artery are not compressed
outline the physiology of cerebral circulation and its clinical relevance
brain supplied by internal carotids and vertebral arteries
brain needs secure supply of oxygen
grey matter is very sensitive to hypoxia - consciousness lost after few seconds of ischemia, irreversible cell damage within ~ 3 minutes
special adaptions of cerebral circulation needed
explain how cerebral blood flow is auto-regulated
auto-regulation of cerebral blood flow guards against changes in cerebral blood flow if MAP changes within a range (~60 - 160 mmHg)
direct sympathetic stimulation has little effect in overall cerebral blood flow
participation of the brain in baroreceptor reflexes is negligible
if MABP rises - resistance vessels automatically constrict to limit blood flow
if MABP falls - resistance vessels automatically dilate to maintain blood flow
auto-regulation fails if MABP falls below 60mmHg or rises above 160 mmHg
MABP below 50mmHg 50mmHg results in confusion, fainting, brain damage
increased PCO2 causes cerebral vasodilation
decreased PCO2 causes vasoconstriction => hyperventilation leads to fainting
blood flow increases to active parts of the brain (regional hyperaemia)
mechanism unknown - may be due to rise in [K+}o as a result of K+ efflux from repetitively active neurones
outline the effects of raised intracranial pressure in the cerebral blood flow
skull filled with - brain (80%), blood (12%) and cerebrospinal fluid (8%)
normal intracranial pressure = 8-13 mmHg
cerebral perfusion pressure = MAP - intracranial pressure
increasing intracranial pressure (e.g. head injury, brain tumour) decreases cerebral perfusion pressure and cerebral blood flow
some conditions which increase intracranial pressure can lead to failure of auto-regulation of cerebral blood flow
describe blood brain barrier
cerebral capillaries have very tight intercellular junctions - blood brain barrier
cerebral capillaries high permeable to oxygen and carbon dioxide
glucose crosses blood brain barrier by facilitated diffusion using specific carrier molecules
brain has obligatory requirement for glucose
exceptionally impermeable to hydrophilic substances (e.g. ions, catecholamines, proteins) - helps protect brain neurones from fluctuating levels of ions in blood
describe physiology of pulmonary circulation
entire cardiac output flows from right ventricle into pulmonary circulation
metabolic needs of airways met by systemic bronchial circulation
pulmonary resistance is only ~10% of that of systemic circulation
pulmonary artery BP = 20-25/6-12 mmHg
describe how hypoxia affects pulmonary circulaiton
hypoxia causes vasoconstriction
helps divert blood from poorly ventilated areas of lung
outline physiology of skeletal muscle circulation
skeletal muscle ~40% body mass
resistance of skeletal muscle vascular bed has large impact on BP
resting blood flow is low due to sympathetic vasoconstrictor tone
describe the effect of exercise in muscle blood flow
during exercise, local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
circulating adrenaline causes vasodilation (beta 2 adrenergic receptors)
increased cardiac output during exercise, these could increase skeletal muscle blood flow many folds
describe skeletal muscle pump and its role in venous return
large veins in limbs lie between skeletal muscles
contraction of muscle aids venous return
one way venous valves allow blood to move towards heart
skeletal muscle pump reduces change for postural hypotension and fainting
blood pools in lower limb veins if venous valves become incompetent - varicose veins
varicose veins don’t lead to reduction of cardiac output because of chronic compensatory increase in blood volume
describe special adaptions of pulmonary circulation
pulmonary capillary pressure is low (~8-11 mmHg) compared to systemic capillary pressure (~17-25 mmHg
absorptive forces exceed filtration forces - protects against pulmonary oedema
special adaptions 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 extra O2 (when required) cannot be supplied by increasing O2 extraction
Can only be supplied by increasing coronary blood flow
Coronary Blood Flow is controlled by Intrinsic & Extrinsic Mechanisms
