A site for medical students - Practical,Theory,Osce Notes

Physiology and autoregulation of cerebral circulation

Cerebral circulation  is very important and essential circulation
Why because if there is arrest of cerebral circulation
for more than 5 seconds it  causes loss of consciousness
Arrest for more than 3 min causes irreversible damage of the grey mater of the cortex of brain
 Cerebral Blood Vessels
2 internal carotid arteries (major source)
2 vertebral arteries join to form basilar artery
These arteries unit together forming the circle of Willis from which 6 cerebral arteries arise to supply the brain
There is no crossing of circulation from one side to the other as pressure is equal on both sides
functionally  these vessels are called end arteries .The cerebral arteries are connected together by pre-capillary anastomosis, but can't prevent cerebral infarction
Normal values
In normal adult the brain weights 1400 gm.
It receives 750 ml blood/min (14%of COP).             
In children CBF is double the adult value and it falls to the adult level at puberty.
Factors involved in regulation of CBF
Intrinsic and  extrinsic mechanism is involvedin  cerebral autoregulation
Intrinsic mechanisms 
Change in arterial blood pressure  ( Autoregulation of CBF)
Extrinsic mechanisms are the following
  • Nervous regulation
  • Chemical regulation
  • Mechanical regulation
Autoregulation of CBF
This  is the ability of brain to maintain its flow constant despite of changes in ABP.
Range of cerebral blood flow
Range of cerebral blood flow varies  from 70 to 150 mmHg.
In hypertensive patient this mechanism operates up to a blood pressure level of 180 mmHg
 Time :
It operates and restores the CBF to its normal basal level within 1-2 minutes of derangement
Mechanism of autoregulation of cerebral blood flow
1.Myogenic response
It is produced by the smooth musles response to stretch by contraction
Myogenic Mechanism
  • With increased ABP  stretch of the vascular wall  result in smooth musles contraction  vasoconstriction and decrease of  CBF  back to its normal  level.
  • With reduction in ABP the opposite occurs.
2. Metabolic response is the local changes in brain metabolites
  •  Increased ABP leads to:Local   increase in O2 tension  and  reduction of CO2 and  H+(hydrogen ion) will lead to cerebral vasoconstriction   and CBF back to its normal level.
  • On the other hand decreased ABP leads to: Local  decrease in O2 tension  and  increase in CO2 and  H+ (hydrogen) will result in  vasodilatation   of  cerebral vessels and  bring the CBF back to its normal level
3. Nervous Regulation of cerebral blood
It include both sympathetic and parasympathetic regulation
a) Sympathetic regulation:
The cerebral blood vessels receive sympathetic supply from the superior cervical ganglia
 i) Mild to moderate sympathetic stimulation results in cerebral vasoconstriction and  has little effect on the CBF as it is overcomed by the autoregulation mechanism
ii) In severe sympathetic stimulation (as in moderat to severe  exercise) there is strong vasoconstriction of large and medium sized arteries and  is very important to prevent the high pressure to reach the small cerebral vessels and  protect them from rupture (cerebral hemorrhage)
 b. Parasympathetic stimulation 
It has  no role in regulation of CBF
 4.Chemical Factors for cerebral autoregulation
Hypercapnia (↑CO2) and acidosis (↑H)  result in marked vasodilatation of the cerebral vessels and ↑ the CBF.
When the CO2 tension increase in the blood, it crosses the blood-brain barrier and combines with H2O to form H2CO3 which dissociates to HCO3 & H → H causes dilatation of the cerebral vessels (CO2 has no direct VD effect).
 5.Mechanical Factors of cerebral autoregulation
Blood viscosity-  when there is a reduction in  blood viscosity it increase  the CBF and vice versa.
The mean cerebral arterial and venous blood pressures:The CBF depends mainly on the difference between the arterial and venous pressures at the brain level, which is called the effective perfusion pressure.This means that, the CBF increaseses when the arterial pressure is ↑ed or venous pressures ↓ed, and vice versa. 
The intracranial pressure (ICT):The ICT is produced mainly by the cerebrospinal fluid (CSF) and normally this is about 11 mmHg.The effect starts to occur when the ICT rises to about 33 mmHg.Slight rise of ICT results in compression of cerebral  vessels slightly with slight reduction  of CBF.Marked rise of ICT (more than 33 mmHg), compresses the cerebral vessels with marked reduction of CBF
The intracranial pressure (ICT):In forced expiration with straining as in cough, defecation and labour, the mean venous pressure increases which increased ICT and the CBF  is decreased markedly  by,decrease in effective perfusion pressure.Compression on vesselsThis  protect the cerebral vessels from rupture (cerebral haemorrhage).
 (The cerebrospinal fluid (CSF) is the fluid which fills the ventricles of the brain and the subarachnoid space. Its volume is about 150 ml. CSF has almost the same constituents as the brain interstitial fluid)
Cushing Reflex
Cushing reflex is a physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia
Acceleration forces:
During acceleration of the body upwards against  gravity blood moves towards the feet and the ABP at the level of the head falls.  The venous pressure also decreases, consequently the ICT drops to maintain the CBF.
During acceleration downwards (-ve gravity)  Opposite occurs  

The key characteristics of cerebral circulation
  • Cerebral circulation is enclosed in a solid skull, so the brain tissue, blood and CSF volumes are kept constant at any time.
  • Brain tissue and CSF are incompressible while the blood vessels are compressible.So ↑ ICT affects mainly blood vessels and ↓CBF
  • Glucose is the major source of energy in the brain and sometimes amino acids during starvation.
  • Brain is very sensitive to hypoxia and hypoglycemia however, hypoxia is more serious:
  • Loss of consciousness if hypoxia is more than 5 sec.
  • Irreversible tissue damage if hypoxia is more than 3 min.