2021B07 Describe the normal regulation of cerebral blood flow and outline physiological factors which may alter it. DO NOT discuss the effect of medications or pathology.

 

List:

·        Intro

·        Flow dynamics

·        Regulation of vascular resistance

·        Regulation of arterial pressure

·        Anatomical factors

 

Intro: the brain

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

 

Cerebral blood flow dynamics:

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

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

 

 

Regulation of cerebral vascular resistance:

Autoregulation

Myogenic:

·     Global CNS blood flow constant 58mL/min/100g

·     ↑flow -> ↑stretch -> reflex contraction -> ↓radius -> ↓flow

·     Effective for perfusion pressure 50-150mmHg

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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

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

 

Regulation of arterial pressure:

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)

 

Anatomical factors:

Arterial supply

Circle of Willis:

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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:

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Drainage design:

·     No valves: allows equilibration of venous pressure

·     Elastic and distensible: minimizes resistance to flow

 

 

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