Week 3/4 - B - Special Circulations - Coronary (R./L.C.A, hyperaemia, Cerebral (willis/autoreg), Pulmonary, Skeletal (varicose) Flashcards
CORONARY CIRCULATION Where do the right and left coronary arteries arise? What arteries do they give off? Where does most coronary venous blood drain?
The coronary arteries arise from the base of the aorta RCA gives off the RMA and travels posteriorly to become the PIA (inferior) LCA divides to become the LCA (lateral) and LAD artery (anterior) The coronary venous blood drains via the coronary sinus into the right atrium
The coronary circulation has some special adaptions to adequately perfuse the heart What are these?
The coronary circulation has some special adaptations * It has a high capillary density * High basal blood flow * High oxygen extraction under resting conditions
Normally the body on average will use approx 25% of the oxygen supplied to a specific area under resting conditions, however under resting conditions, the heart extracts 75% of the oxygen supplied to it Due to the heart’s already high oxygen extraction, when extra O2 is required, how can this be supplied?
When extra O2 is supplied by the heart, the O2 extraction cannot be further increased and can only be supplied by increasing coronary blood flow
Coronary Blood Flow is controlled by Intrinsic & Extrinsic Mechanisms What are the intrinsic mechanisms that can increase coronary blood flow? * 2 cause vasodilation * One increases the flow
The intrinsic mechanisms that increase blood flow are * A decreased O2 will cause vasodilation of the coronary and systemic arteries (remember it causes vasoconstriction of pulmonary arteries to correct V?Q mismatch) * Metabolic hyperaemia matches flow to demand * Adenosine is a potent vasodilator
What is metabolic hyperaemia?
Hyperaemia is an increase in the blood flow - Metabolic hyperaemia is where an increases in the metabolic activity of eg cardiac muscle or skeletal muscle leads to an increase in different metabolites such as lactic acid, CO2 or adenosine. These cause vasodilation
As already stated, there are also extrinsic mechanisms controlling coronary blood flow Coronary arterioles are supplied by sympathetic vasoconstrictor nerves. What can override this control
The vasoconstrictor function of coronary arterioles can be overridden by metabolic hyperaemia as a result of increased heart rate and stroke volume This therefore causes the sympathetic stimulation of the heart to result in coronary vasodilation via B2-adrenergic receptors The B2-adrenergic receptors normally cause vasodilation
How does sympathetic stimulation affect coronary blood flow?
Sympathetic stimulation decreases coronary blood flow via a1 ADR receptors (causes vasoconstiction) - which increases SVR/MAP * also increases heart rate and contraction force via B1 ADR also increases coronary vasoconstriction via B2 ADR which cause coronary vasodilation due to metabolic hyperaemia
When does most of the coronary blood flow take place? How does this happen?
Most of the coronary blood flow takes place in diastole. When the ventricles relax, there is a slight backflow of blood that will close the semilunar valves of the aorta. As the coronary arteries are located adjacent to the valves at the aorta base, this blood filling here will spill into the coronary arteries
What can a decrease in diastole therefore result in?
A decrease in diastole can therefore result in a decrease in coronary blood flow which can result in chest pain or tachycardia
CEREBRAL CIRCULATION What are the arteries which supply blood to the brain? What is the special adaptation of the cebral artery supply that should maintain blood supply to the brain even if eg the ICA becomes obstructed?
It is the internal carotid arteries and the vertebral arteries which supply the blood to the brain The two vertebral arteries join to form the basilar artery. The basilar artery anastamoses with the two ICAs to form the Circle of Willis Major cerebral arteries arise from the circle of willis
The circle of willis is one special adaption for the cerebral circulation What is the special adaptation that protects the brain against changes in cerebral blood flow if the MABP changes? What MABP will cause this adaptation to fail?
This would be AUTOREGULATION This guards the cerebral blood flow against changes even if the MAP increases or decreases AUTOREGULATION is only able to work however as long as the MABP stays within 60-160mmHG (normal is 70-105mmHg)
Other important regulators of cerebral blood flow (aside from circle of willis and autoregulation) are carbon dioixde levels What does an increase or decrease in CO2 cause?
An increase in CO2 levels causes cerebral vasodilation - to try and increase )2 supply to the brain A decrease in CO2 levels causes cerebral vasoconstriction - this is why hyperventilation can lead to fainting
Skull rigid box filled with approximately: brain 80%, blood 12%, and cerebrospinal fluid (CSF) 8% What is the normal intracranial pressure within the skull How is the cerebral perfusion pressure calculated?
Normal intracranial pressure = 8-13mmHG Cerebral perfusion pressure is the mean arterial pressure minus the intracranial pressure CPP = MAP - ICP
What does an increased ICP (eg due to head injury or brain tumour) cause?
Increased ICP causes a decrease in the CPP and cerebral blood flow
Cerebral capillaries have very tight intercellular junctions - THE BLOOD BRAIN BARRIER How can O2 and CO2 cross this barrier? How does CO2 affct respiration?
Cerebral capillaries are highly permeable to O2 and CO2 (remember from resp CO2 crosses the BBB and then generates H+ ions which are sensed by central chemoreceptors near surface of the medulla which alter ventilation in accordance)
What ensures that blood flow in the veins goes back to the heart during contraction?
The skeletal muscle pump Contraction of muscles aids venous return One way venous valves allow blood to move forwards towards the heart during muscle contraction
What are the different complications that can arise due to long standing chronic venous insufficiency? Usually signs that there has been disease for a long time
Skin changes — look for hyperpigmentation (brown-red discolouration - haemosiderin deposition), venous eczema (itchy, red, scaly, and/or flaky skin which may have blisters and crusts on the surface), lipodermatosclerosis (painful, hardened, tight skin), atrophie blanche (white scarring)
