· Intro
· Flow dynamics
· Regulation of vascular resistance
· Regulation of arterial pressure
· Anatomical factors
Physiology |
· Highly active: CMRO2 46mL/min = 3.3mL/min/100g · Highly perfused: CBF 15% cardiac output = 750mL/min = 58mL/min/100g |
Pathology |
· Interruption to flow -> unconsciousness, head injury, ischaemia |
Ohm’s law |
Cerebral blood flow (CBF) = (mAP – ICP or CVP) / cerebral vascular resistance
Hence factors ↓CBF: · ↓ mAP · ↑ ICP / ↑ CVP (Starling resistor – whichever is higher) · ↑ CVR |
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Poiseuille’s law |
Resistance = (8 x length x viscosity) / (π x radius4) – assuming laminar flow
Hence factors ↑resistance: · ↓Radius (note power of 4, most important) · ↑Length (not under control) · ↑Viscosity |
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Autoregulation |
Myogenic: · Global CNS blood flow constant 58mL/min/100g · ↑flow -> ↑stretch -> reflex contraction -> ↓radius -> ↓flow · Effective for perfusion pressure 50-150mmHg
Metabolic: · Regional blood flow ∝ cerebral metabolic rate (CMR) · ↓MR -> ↓H+/K+/adenosine/lactate/pCO2 and ↑pO2 -> local vasoconstriction -> ↓radius -> ↓flow |
Physiological variables |
Oxygen: · ↓PaO2 <50mmHg -> vasodilate -> ↑radius -> ↑CBF · Non-linear response. Doubles at 30mmHg Carbon dioxide: · ↑PaCO2 -> vasodilate · Linear response 20-80mmHg Temperature: · ↓Temp: ↓CMR -> ↓CBF via metabolic autoregulation · Near linear response: ↓7% per 1°C
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Other |
· Neural: noradrenaline at α1 -> vasoconstriction (minor) · Hormonal: adrenaline -> mixed effects at α1, β1 (minor) · Rheologic: ↑Hct -> ↑viscosity -> CVR |
Baroreceptor response |
· Stretch-activated mechanoreceptors in walls of aortic arch and carotid sinuses · ↓mAP -> ↓stretch -> ↓activation -> ↓inhibition of SNS -> o Vasoconstriction -> ↑SVR o Venoconstriction -> ↑preload o ↑HR, ↑contractility -> ↑mAP · Important for maintaining CBF during posture change |
CNS ischaemic response |
· ↓↓CBF -> brainstem ischaemia -> ↑↑SNS activity o ↑BP o ↓HR (reflex) |
Arterial supply |
Circle of Willis:
Supply design: · Chicane-like arteries supply the circle of Willis · Turbulent flow -> ↑pressure drop -> ↓effective arteriolar pressure · Prevents massive rise in cerebral perfusion pressure during SNS activation |
Venous drainage |
Dural venous sinuses:
Drainage design: · No valves: allows equilibration of venous pressure · Elastic and distensible: minimizes resistance to flow |
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