see also:

• cerebrospinal fluid (CSF)
• glymphatic system of the brain

• control of arterial and venous blood flows to the brain are important for supply of nutrients including oxygen and glucose or neurologic function and removal of waste including that from CSF

• arterial blood flow is dependent upon:
  • cerebral perfusion pressure
    • Mean Arterial Pressure (MAP)
    • Intracranial Pressure (ICP)
      • the cranial vault is a fixed volume which consists of:
        • 80% is brain parenchyma
        • 10% is CSF
        • 5% is intracranial blood
      • compensatory mechanisms to reduce high ICP:
        • cerebral venous system can collapse and vasoconstrict, forcing blood out of the intracranial vault to make room for expanding tissues.
        • CSF is immediately displaced from the cranial vault down into the compliant lumbar thecal sac in the spinal column.
        • increase in the rate of CSF absorption
      • physiologic states can increase ICP:
        • head down posture, etc
      • pathologic states can increase ICP:
        • space occupying lesions (tumours, cysts, abscesses, intracranial haemorrhage)
        • cerebral oedema - infarcts, tumours, encephalitis, etc
        • impaired CSF outflows causing hydrocephalus or benign raised idiopathic intracranial hypertension
  • cerebral arterial vasodilatation:
    • autoregulation:
      • to protect the brain, cerebral vessels naturally constrict in a myogenic response to rising blood pressure and dilate in response to falling pressure.
      • this keeps blood flow remarkably constant as long as the MAP stays within the normal physiological range of approximately 60 to 160mmHg.
    • metabolic factors which alter the degree of cerebral vasodilation:
      • hypercapnia increases cerebral vasodilation and increases blood flow
      • low carbon dioxide levels cause cerebral vasoconstriction and reduce blood flow
      • hypoxia acts as a strong vasodilator to increase blood delivery
      • substances released by active neurons and astrocytes, such as adenosine, potassium ions, and hydrogen ions (acidic pH), trigger local vasodilation
    • other blood vessel mediated responses:
      • endothelial factors:
        • the endothelium of cerebral arteries releases vasoactive chemicals such as nitric oxide (NO) which is a profound vasodilator that increases flow
    • body temperature:
      • cerebral blood flow increases by about 5% to 7% for every 1 degree C rise in body temperature, while hypothermia decreases flow by reducing the brain's metabolic demand
    • autonomic nervous system:
      • while less influential than chemical and metabolic controls, the sympathetic nervous system provides baseline constriction to protect the cerebral vasculature during sudden, extreme spikes in systemic blood pressure
  • cerebral venous pressure
    • see below
  • blood viscosity:
    • thicker blood (high haematocrit) creates more resistance, which can slow down flow.
    • very low viscosity (severe anaemia) increases flow because of reduced resistance, but limits oxygen-carrying capacity

cerebral perfusion pressure (CPP) = Mean Arterial Pressure (MAP) - Intracranial Pressure (ICP)

Poiseuille’s Law: laminar flow is proportional to blood vessel radius⁴ x (perfusion pressure - cerebral venous pressure) / viscosity

thus blood vessel radius is the most powerful determinant of blood flow

cerebral venous flow = cerebral arterial flow (what goes in must come out)

cerebral venous flow (Q) is governed by the difference between cerebral venous pressure (P_v) and the right atrial pressure (P_RA), divided by venous resistance (R)

• unlike arteries, veins have minimal ability to alter their diameter via changes in smooth muscle tone and can collapse if external pressures are high such as high ICP
• while veins are passive, they are indirectly controlled by systemic arterial and metabolic factors that alter upstream blood volume and flows
• if ICP rises above cerebral venous pressure, veins collapse to create a “waterfall” or Starling resistor effect, meaning flow becomes dependent on the difference between arterial pressure and ICP rather than just downstream venous pressure
• gravity and posture
  • hydrostatic forces heavily influence venous return.
  • in an upright posture, the hydrostatic column creates a negative pressure in the cranial veins, causing collapse in the jugular veins and shunting flow through the vertebral venous plexus
• venous compliance:
  • the large dural venous sinuses are distensible and can buffer fluctuations in cerebral blood volume, acting as capacitance vessels
• extracranial and mechanical controls:
  • intrathoracic and abdominal pressure:
    • intrathoracic pressure directly dictates right atrial pressure.
    • breathing, coughing, or the Valsalva maneuver increases intrathoracic pressure, impeding cerebral venous outflow and transiently elevating ICP
  • respiration (The Thoracic Pump):
    • during inspiration, the drop in intrathoracic pressure creates a vacuum effect, actively drawing blood from the cranial vault into the central veins and increasing venous outflow.
  • body position:
    • head positioning (e.g., flexion or rotation) can mechanically compress the jugular veins, forcing cerebral blood to find alternative collateral pathways like the deep vertebral and epidural venous plexuses.
    • elevating the head of the bed to 30 to 45 degrees facilitates gravity-driven cerebral venous drainage
  • physiological and biochemical influences
    • cerebral arterial blood flow (CBF):
      • because venous flow is a direct consequence of arterial inflow, any factor that increases CBF (see above) will passively increase cerebral venous volume and flow velocity
      • what goes in must come out!
    • pulsatility:
      • the compliance of the cerebral veins dampens the pulsatile wave generated by cardiac contractions.
      • conditions that alter vascular tone can disrupt this, increasing cerebral venous pulsatility and placing strain on delicate microvascular beds and the glymphatic system of the brain.