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Cerebral blood flow
Cerebral blood flow is tightly regulated to meet the high metabolic demands of the brain. Blood circulates to the brain through the carotid and vertebral arteries which connect at the circle of Willis. Factors like blood pressure, carbon dioxide levels, oxygen, temperature and various chemicals regulate blood flow. The brain has autoregulatory mechanisms to maintain constant blood flow over a range of pressures. Failure of autoregulation can lead to ischemia or hyperperfusion. Clinical considerations include risks for hypertensive or elderly patients and treatments focus on preventing hypotension and ischemia.
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Cerebral blood flow
- 1. Cerebral blood flowand regulation Tushar Kumar
- 2. INTRODUCTION Brain is aclosed structure Most of it is brain tissue while some of it is blood and CSF Brain comprises 80% Cerebral blood volume: 12% CSF contribute to 8% of the space inside the skull vault Monro – Kellie doctrine
- 3. Anatomy : • Circulationof brain was first described by WILLIS in 1664 1. Anterior circulation and Posterior circulation via circle of Willis 2. Collateral arterial inflow channels 3. Leptomeningial collaterals- pial to pial anastomoses
- 4. Anatomy Circulation via circleof Willis: anterior circulation: via 2 carotid arteries and their derivations Posterior circulations: via 2 vertebral arteries joining to form basilar artery It lies in subarachnoid space and encircles pituitary gland Willisian channels: anterior communicating artery, posterior communicating artery and ophthalmic artery via external carotid artery
- 5. Circle of williswith its collaterals
- 6. Collateral circulation In anormal individuals there is no net flow of blood across these communicating arteries But to maintain patency and prevent thrombosis there is to an fro flow of blood Their importance appears when a pressure gradient develops Second collateral flow appears in surface connections that bridge pial arteries. They bridge major arterial territories ( ACA – PCA, ACA- MCA, MCA – PCA) They are called leptomeningial pathways or equal pressure path ways.
- 7. Cerebral microcirculation Capillary densityin grey matter is 3 times higher than white matter Pre capillary vessels divide and reunite to form anastomotic circle called as circle of Duret They are highly tortuous and irregular Velocity of RBC’s is higher in these capillaries To facilitate transfer of substrate and nutrients RBC’s have to traverse longer distance via these capillaries
- 8. Cerebral microcirculation Fast capillaries:These are the ones who do not take part in transfer of substrate BUT During cerebral hypoperfusion they have a decrease in blood velocity , diverting blood to slower functional capillaries.
- 9. Venous drainage 3 setof veins drain from brain 1. Superficial cortical vein 2. Deep cortical veins 3. Dural sinuses All ultimately drain into right and left IJV
- 10. Cerebral blood supply: Physiologicalconsiderations: Brain accounts for 2% of body weight yet requires 20% of resting oxygen consumption O2 requirement of brain is 3 – 3.5 ml/100gm/min And in children it goes higher up to 5 ml/100gm/min Brain has high metabolic rate That’s why brain requires higher blood supply 55ml/100gm/min is the rate of blood supply requires more requires more substratete substrate requires mlacks of storage of energy substrate
- 11. Cerebral blood supply Corticalgrey matter 75 – 80 ml/100gm/min Subcortical white matter 20ml/100gm/min CMRO2 : 5.5 ml/100gm/min Functional requirement is 3.3 ml/100gm/min Integrity required 02 is 2.2 ml/100gm/min 60% functional 40 % integrity
- 12. Factors regulating cerebralblood flow • Hemodynamic autoregulation • Metabolic mediators and chemoregulation • Neural control • Circulatory peptides
- 13. Cerebral blood flowregulation 1. Flow metabolism coupling: Hemodynamic regulation Cerebral blood flow (CBF) closely follows cerebral perfusion pressure (CPP) Within the range of 50 to 150 mm Hg of CPP , blood flow remains constant. Where CPP = MAP – ICP MAP :Mean arterial pressure and ICP : Intracranial pressure. Pure changes in perfusion pressure involve myogenic response in vascular smooth muscles (Bayliss effect)
- 14. Flow metabolism coupling: Mechanismthat CPP responds to: mean BP pulsatile pressure Mediators involved are: H+, K+, adenosine, glycolytic intermediate and phospholipid metabolites Nitric oxide controls the smooth muscles tone
- 15. Cerebral blood flowregulation a. Pressure regulation: Ohm’s law: flow = Pi – Pf R Hagen poiseuille relation : R = 8L μ r⁴ where Pi – Pf is change in pressure, R is resistance , L is the length of the tube , μ is coefficient of viscosity and r is radius of the tube. So we derive that: R = Pi – Pf = 8L μ flow r⁴
- 16. Cerebral blood flowregulation Arteriolar diameter as well as cerebral vascular resistance both vary with CPP but CBF remains constant in this range.
- 17. Cerebral blood flowregulation 2. Venous physiology: Venous system contains most of the cerebral blood volume Slight change in vessel diameter has profound effect on intracranial blood volume But evidence of their role is less Less smooth muscle content Less innervations than arterial system
- 18. Cerebral blood flowregulation Pulsatile perfusion: Fast and slow components of myogenic response bring a change in perfusion pressure Cardiac output: Cardiac output may be responsible for improved cerebral blood flow They are indirectly related via central venous pressure and large cerebral vessel tone.
- 19. Cerebral blood flowregulation Rheological factors: Related with blood viscosity. Hematocrit has main influence on blood viscosity. Flow is inversely related with hematocrit. In small vessels cells move faster than plasma. This reduces microvascular hematocrit and viscosity FAHRAEUS LINDQVIST EFFECT
- 20. Metabolic and chemicalregulation 1. Carbon dioxide coupler between flow and metabolism At normal conditions CBF has linear relationship with CO2 between 20 – 80 mm Hg For every mm Hg change of PaCO2 CBF changes by 2 – 4 %
- 21. CO2 induced vasodilatation Mechanismby which CO2 produces vasodilatation
- 22. CARBON DIOXIDE :How it works ADULT ↑CO2 ↑H+ ions NO ↑nNOS C GMP K+ Channel Ca2+ Channel ↓Ca2+ ↓Ca2+ Smooth Ms Relaxation ↑K+
- 23. CARBON DIOXIDE :How it works Neonates ↑CO2 ↑H+ ions PG ↑COX endothelium C AMP K+ Channel Ca 2+ Channel ↓Ca2+ ↓Ca2+ Smooth Ms Relaxation ↑K+
- 24. Metabolic and chemicalregulation Oxygen: Within physiological range PaO2 has no effect on CBF Hypoxia is a potent stimulus for arteriolar dilatation At PaO2 50 mmHg CBF starts to increase and at PaO2 30 mm Hg it doubles
- 25.
- 26. Metabolic and chemicalregulation Temperature: Like other organs cerebral metabolism decreases with temperature For every 1˚C fall in core body temperature CMRO2 decreases by 7 % At temperature < 18 ˚C EEG activity ceases
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- 28. Pharmacology and autoregulation Anaestheticdrugs can alter autoregulatory responses as seen with blood pressure and CO2 drug CBF CMR Preserve response to CO2 Preserve autoregulation barbiturates ↓ ↓ yes yes propofol ↓ ↓ yes yes etomidate ↓ ↓ yes …. morphine ± ↓ …. yes fentanyl ± ± yes yes benzodiazepines ↓ ↓ yes … ketamine ↑ ↑ yes yes lignocaine ↓ ↓ … … response
- 29. Pharmacology and autoregulation Inhalationalagents affecting CBF volatile anaesthetic CBF CMR Preserve response to CO2 Preserve autoragulation Xenon ↓ ↓ yes yes desflurane ↑ ↓ yes yes sevoflurane ↑ ↓ yes yes isoflurane ↑ ↓ yes yes enflurane ↑ ↓ yes yes halothane ↑↑↑ ↓ yes yes nitrous oxide ↑ ↑ … …
- 30. Pharmacology and autoregulation Vasoactiveagents: Drugs that do not cross blood brain barrier do not affect CBF
- 31. Pharmacology and autoregulation Dexmedetomidine: Causes25% reduction in CBF primarily by reducing CMR ACE inhibitors, Angiotensin receptor antagonists, β blockers…….. Do not reduce CBF or alter autoregulation
- 32. Metabolic mediators and chemoregulation ControlCBF by acting as local vasodilators Ions and chemicals H+, K+, adenosine and phospholipid metabolites Final common pathway is via NO
- 33. Neurogenic effects Neurogenic effects:sympathetic tone shift the curve to right
- 34. Circulatory peptides: Vasoactive peptideslike angiotensin II do affect CBF. Reactive oxygen molecules Alteration to vasomotor function Vascular remodeling De silva et al: effects of angiotensin II on cerebral circulation: role of oxidative stress; review article – front physiology ; jan 2013
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- 36. Clinical considerations Hypertensive patients: Autoregulatorycurve shifts to right Protection from breakthrough but at the cost of risk of ischemia May suffer cerebral ischaemia during hemorrhage, shock or hypotension
- 37. Clinical considerations Elderly patients: Withage CBF decreases Younger people have increased blood flow in frontal areas…. Frontal hyperaemia But with age this increased flow reduces Flow in other areas are well maintained hence blood is more uniformly distributed Autoregulatory failure occurs in morel elderly
- 38. Auto regulatory failure Forauto regulatory failure to occur vasomotor paralysis is the end point • Acute ischemia • Mass lesions all lead to • Inflammation vasomotor • Prematurity paralysis • Neonatal asphyxia • Diabetes mellitus
- 39. Autoregulatory failure Right sidedfailure Hyperperfusion leads to circulatory breakthrough Fluid from capillaries seep into the extracellular space leading to edema e.g. AVM Left sided failure Hypoperfusion Ischemia Na˖ and Ca 2˖ influx with water and K+ efflux leads to cytotoxic edema and infarction e.g. ischemic stroke
- 40. Autoregulatory failure Two stagesbefore infarction: a. Penlucida at flow 18 – 23 ml/100gm/min brain becomes inactive but function can be restored at any time by reperfusion b. Penumbra at lower flow rates brain function can be restored by reperfusion but only within a time limit
- 41. Hemodynamic considerations Cerebral steal:it means blood is diverted from one area to another if pressure gradient exists between the two circulatory beds Vasodilatation in ischemic brain takes blood from ischemic areas to normal areas causing more ischemia Vasoconstriction results in redistribution of blood from normal to ischemic areas leading to inverse steal or ROBIN HOOD EFFECT
- 42. Hemodynamic considerations Vessel lengthand viscosity At breakthrough point flow depends on vessel length and viscosity Autoregulation has failed and it behaves like fluid in a rigid tube Pressure gradient across the ends are now same so distal area have the lowest flow This makes watershed areas more vulnerable to ischemic changes
- 43. Considerations for ischemia Considerationrelevant to global ischemia Prevent and treat hypotension as well as vasogenic & cytotoxic edema Induction of mild hypothermia for 24 hrs Consideration relevant to focal ischemia Barbiturate coma, volatile anesthetics (xenon), calcium channel antagonists PaCO2 and temperature
- 44. Therapies for enhancingperfusion • Induced hypertension • Inverse steal • Hypocapnea • Hemodilution • Pharmacological agents • Barbiturates, propofol • Intra arterial delivery of drugs. Like mannitol and vasodilators
- 45. References: 1. Mishra LD; cerebral blood flow and anaesthesia; Indian J. Anaesth. 2002; 46 (2) : 87-95 2. Joshi et al; cerebral and spinal cord blood flow; Cottrell and Young’s Neuroanesthesia; 5th ed, 2010: 17 – 59 3. Patel et at; Cerebral physiology and effect of anesthetic drugs; Miller’s anesthesia 8th ed : 387 – 423 4. De silva et al: Effects of angiotensin II on cerebral circulation: role of oxidative stress; review article – front physiology ; jan 2013
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