0728 - Special Circulations Flashcards
Which mechanisms do the brain and cardiac circulations use to regulate blood flow?
Brain - CO2 controlled
Cardiac - Metabolic
Why is coronary flow largely during diastole?
Phasic flow - varies with cardiac cycle. LCA is largely diastolic (mostly isovolumetric relaxation), RCA much more stable - maintained throughout with a slight peak at end of fast ejection.
LCA is diastolic due to mechanical compression ‘extravascular compression’ of the muscles in systole (bigger issue internally - subendocardially - makes sense). As RV has less systolic pressure, there is less ‘squeeze’ on the vessels so systolic perfusion is possible.
Consequence - when HR goes up, diastole is shortened, less LCA perfusion.
What are the mechanisms resulting in coronary vasodilation as a consequence of increased cardiac work?
Predominantly metabolic. Increased cardiac work causes increased metabolism. Heart likes to use FAs, so increased metabolism causes a drop in ATP. This is picked up by K(ATP) channel, which disinhibits and releases K+, hyperpolarising the membrane and relaxing the vessel. NO, adenosine, and O2 also very important.
Adenosine->α2 (VSMC). Activates G protein, increases cAMP and activates PKA, which opens KATP. Adenosine also enhances release of NO from endothelium.
Why are subendocardial vessels are prone to ischaemic damage
‘Intensely’ compressed by myocardium on its way through - therefore usually the first area to suffer ischaemic damage.
What factors regulate cerebral blood flow?
Autoregulation very important
PCO2 most important determinant (vasodilation with +CO2, constriction with - CO2)
Sympathetic - Constriction via α1
Para - Dilation via CN7 - dense net of smooth muscle around cerebral arteries.
Neuronal - very small impact.
Metabolic demand/severe hypoxia causes hyperaemia - unknown primary mediators, CO2, O2 are secondary mediators.
What is the role of autoregulation in cerebral blood flow?
Autoregulation - CBF more or less constant under MAP 60-160. Prevents syncope (low) and cerebral oedema (high). Comes partially through a myogenic response (slides don’t elaborate). In hypertension, R shift of curve, risk of syncope with antihypertensives if body not adjusting in time (start them slowly). Increase in intracranial pressure will raise blood pressure via ischaemia in vasomotor centre (flow maintenance - not getting enough so raise BP to get more in - counteract intracranial resistance).
Why are cerebral vessels different to many other vessels?
Very sensitive to PCO2 levels with very rapid response.
CO2 changes perivascular pH - acidosis doesn’t cross the BBB
How does this mechanism for CO2 and BBB compare to respiratory lecture?
