0729- Special circulations: coronary and cerebral- CG Flashcards
Coronary artery supply to heart in general- which part does right and left coronary arteries supply .
Right- right ventricle and atrium, posterior wall Left- left ventricle and atrium, septum wall, anterior High density of capillaries Vein drain into coronary sinus, then directly to right atrium
How does blood flow in the left and right coronary arteries? Why are subendocardial vessels more susceptible to damage?
LCA- no flow at start of isovolumetric contraction phase, maximal flow at early diastole (perfused only during diastole). X8 higher than RCA, so more critical than RCA. Drops to 0 during systole because of high pressure in ventricle- translates to -120mmhg pericardial pressure (transmural) NB- subepicardial vessels not compressed, hence not prone to hypoxia compared to subendocardial vessels RCA- variable and maintained during systole and diastole, but maximal at diastole. Doesn’t drop to 0 during systole because pressure in ventricles lower (cavity pressure)
How is perfusion regulated
Auto regulation- immediate and renders flow independent of aortic pressure! within 60 to 180mmhg autoregulation maintains constantish blood flow Regulation determined by change in arteriolar resistance (pre capillary Sphincters), mostly likely due to myogenic effect
How is regulation controlled by neural mechanisms?
Not neural controlled! blood flow is metabolic controlled. Increased cardiac work with increased flow, even if transplanted (no neural innervation) in ventricular fibrillation, removal of transmural tension result in increased perfusion of coronary vessels and increase O2. Over time, auto regulation vasoconstricts and restrict flow (myogenic) Via stellate ganglion and a1 to vasoconstrict
How is coronary resistance modulated? What chemicals and mechanisms cause change to vascular resistance?
Increased myocardial contractile activity Increased metabolism and decreased O2 Mostly via drop in ATP activating Katp channels (Gated by ATP), no, adenosine 1. activated Katp result in hyper polarised vsmc, drop in ca, vasodilation. Katp in cardiac myocytes reduces ap width and ca entry 2. Adenosine released from myocardial cells (transient effect), activate Katp 3. No relaxes vsmc
Compare substrate utilisation at rest and exercise
At rest, glucose, lactate and fatty acids equal. During exercise, lactate most important- (Demand mostly met via perfusion↑. But O2 consumption↑ slightly more than perfusion↑: slight O2 extraction↑ -extraction ratio already high, can’t increase much further)
Cerebral circulation characteristics
Relatively high, largest flow via carotid art Collateral paths via circle of willis- pathological conditions can change direction Fixed volume (cranium)- hence need tight volume control
How is flow affected in coronary stenosis?
O2 extraction in heart is nearly maximal- flow limited Narrowing >80% only cause significant flow decreases at rest However, exercise accentuates this (exercise stress test) Atherosclerotic plaque hinder vasomotion- Stenosis causes pressure drop and auto regulation mechanisms, resulting in reduced flow. Compensatory vasodilation in post stenotic bed- however, healthy vascular beds also dilated, hemodynamic stealing from atherosclerotic vessel because lowered resistance means blood will take the easy oath (may precipitate heart attack- danger in exercise testing) Actuate- hypoxia or ischaemia Chronic- build up of collateral vessels
Neural control of cbf
Sympathetic constriction- Parasympathetic dilation (unique, not found in other places) Neuronal impact small, fibre accompany. vessels into cranium Auto regulation Constant cbf between 60-160, myogenic response can partially compensate Lower- dangerous drop- syncope Higher- dangerous rise- risk of oedema due to filtration, intracranial pressure rise In hypertension, curve right shifted curve (map to cbf graph), risk of syncope at start of htn therapy Increased intracranial pressure also increase (see later)
Explain in greater detail local control of cbf
Regional neural activity increase metabolism, also increase blood flow (fMRI basis) Ultimately due to LOCAL co2 pressure (peri vascular ph change)- acidosis in rest of body doesn’t effect brain- bbb Vasodilation with increase, vasoconstriction with decrease Affected by bp (change co2 pressure independent of concentration) and hypercapnia (long term co2 retention ) What about po2? Little effect under normal conditions, but mild and severe hypoxia cause massive vasodilation (high altitude oedema). However, hyperbaric hypoxia little effect
Stricker summary
Coronary perfusion is largest during diastole. • Autoregulation renders flow independent of aortic pressure. • Metabolic effect more powerful than neuronal. • ATP, NO and adenosine play a crucial role in metabolically regulating cardiac perfusion. • Only large stenosis (>80%) causes a significant flow limitation at rest. • Cerebral vascular bed is special because it has a parasympathetic innervation. • Metabolism is the most important determinant of resistance. • Regulation happens at local level to limit volume changes. • PCO2 is the most important determinant of CBF.
