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Cerebral blood flow & intracranial pressure
- 1. Cerebral blood flow & Intracranial Pressure DR CARUNYA MANNAN
- 2. Cerebral blood supply Anterior cerebral circulation and posterior cerebral circulation Internal carotid arteries and vertebral arteries The anterior and posterior cerebral circulations are interconnected via bilateral posterior communicating arteries Part of the Circle of Willis Provides backup circulation to the brain
- 3. The Circle of Willis
- 8. Cerebral venous drainage Dural venous sinuses - located on the surface of the cerebrum. The most prominent of these sinuses is the superior sagittal sinus confluence of sinuses sigmoid sinuses which go on to form the two jugular veins In the neck, jugular veins superior vena cava. Deep venous drainage veins inside the deep structures of the brain, which join behind the midbrain to form the vein of Galen merges with the inferior sagittal sinus to form the straight sinus which then joins the superficial venous system mentioned above at the confluence of sinuses
- 10. Regulation of cerebral blood flow
- 11. Cerebral blood flow • Weighs 1400g or 2% of the total body weight • CBF = 50ml/100g/min • CBF is 700ml/min or 15% of the resting cardiac output • High oxygen consumption - 3.3ml/100g/min (50ml/min in total) • 20% of the total body consumption --> cerebral metabolic rate for oxygen or CMRO2 • Higher in the cortical grey matter and generally parallels cortical electrical activity
- 12. Brain Oxygen Requirement 60% Activation metabolism 40% Basal metabolism NEURONAL ACTIVITY CELLULAR INTEGRITY
- 13. Cerebral blood flow 1. Affecting cerebral perfusion pressure 2. Affecting the radius of cerebral blood vessels
- 14. Cerebral Perfusion Pressure Pressure gradient between the arteries and the veins Difference between the mean arterial blood pressure (MAP) and the mean cerebral venous pressure CPP = MAP – ICP MAP - diastolic blood pressure + 1/3 pulse pressure Usually around 90mmHg ICP is much lower and is normally less than 13mmHg CPP is normally about 80mmHg
- 15. Cerebral blood flow 1. Cerebral metabolism 2. Carbon dioxide and oxygen 3. Autoregulation 4. Neurohumeral factors 5. Vasoactive drugs - Anaesthetics,Vasodilators, Vasopressors 6. Blood viscosity 7. Temperature
- 16. Cerebral metabolism Increases in metabolic demand met rapidly by an increase in CBF and substrate delivery and viceversa flow- metabolism coupling Hydrogen ions, potassium, CO2, adenosine, glycolytic intermediates, phospholipid metabolites, nitric oxide
- 17. pCo2 & CBF Increase Cerebral Blood Flow in Response to Excess Carbon Dioxide or Excess Hydrogen Ion Concentration. CO2 H2O HCO3 H+ IONS Vasodilatation Regulated by a complex and interrelated system of mediators Nitric oxide, prostanoids, cyclic nucleotides, potassium channels, Calcium
- 18. pCo2 & CBF Moderate hypotension -- impairs the response of the cerebral circulation to changes in PaCO2 The response of the cerebral vessels to CO2 can be utilised to help manage patients with raised intracranial pressure, for example after traumatic brain injury Hyperventilation reduces the PaCO2 vasoconstriction reduces cerebral blood volume and ICP However if PaCO2 is reduced too much vasoconstriction worsening cerebral ischaemia Hypercapnia and the resulting vasodilatation and increase in ICP must be avoided PaCO2 - best maintained at low-normal levels to prevent raising ICP This reactivity may be lost in areas of the brain that are injured CO2 reactivity is generally preserved during inhalation anaesthesia and can therefore be utilised to help control ICP and brain swelling during surgery
- 19. Oxygen & CBF CBF increases once PaO2 drops below 50mmHg so that cerebral oxygen delivery remains constant Release of adenosine/prostanoids cerebral vasodilatation Cerebrovascular smooth muscle hyperpolarisation and reduce calcium uptake both mechanisms enhancing vasodilatation
- 20. Vasodilatory Cascade CPP Vasodilatation CBV ICP SABP Hypovolemia Cardiogenic Pharmacologic oedema CSF CMR Viscosity Hypoxia Hypercapnia
- 21. Myogenic (autoregulation) Cerebral autoregulation – ability to maintain a relatively constant organ bld flow over a range of perfusion pressure Autoregulation MAP 70 to 150 mmHg Below / above 70 -150 CBF becomes pressure passive
- 22. Mechanism Myogenic Intrinsic response of myogenic smooth muscle in cerebral arterioles to changes in MAP (NO) Autonomic innervation of cerebral blood vessels May also contribute to autoregulation of blood flow Metabolic CMR determines arteriolar tone when tissue demand exceeds blood flow release of tissue metabolites Vasodilatation CBF
- 23. Chronic hypertension - shifts Autoregulation curve to right Protects the brain against “ breakthrough” by surpassing the upper limit of autoregulation, at expense of lower limit Symptoms of cerebral hypoxia do not occur even at MAP 35-40 mmHg in normotensives but can appear at a significantly higher BP in chronic hypertensives Vascular hypertrophy size of intravascular lumen proximal conductance vessel resistance Autoregulation
- 25. Vascular changes & autoregulatory shift induced by chronic HTN is modified by long term anti-HTN therapy, degree of reversal determined by length of t/t Head trauma, brain lactic acidosis, brain injury – abolish autoregulation Tumour brain tissue blood flow is not autoregulated Potent inhaled anaesthetics & hypercarbia abolish autoregulation in a dose dependent manner Autoregulation
- 26. Temperature CMR decreases by 6 to 7 % / degree temp reduction Hyperthermia 37 to 42° C CBF & CMR increase >42°C dramatic reduction in cerebral O2consumption (toxic effect of protein enzyme degradation )
- 27. Viscosity Blood vicosity can influence CBF. In healthy subjects variation in hematocrit 33 – 45% caused only modest alteration in CBF Anemia CVR CBF ( viscosity & O2 carrying capacity) Aging from childhood to adulthood progressive reduction in CBF & CMRO2 Age
- 29. Intracranial pressure Intracranial pressure (ICP) is the pressure inside the skull Skull has three essential components: - Brain tissue = 78% - Blood = 12% - Cerebrospinal fluid (CSF) = 10% Any increase in any of these tissues causes increased ICP
- 30. Intracranial pressure Normal value - 7–15 mmHg Factors that influence ICP Arterial pressure Venous pressure Intraabdominal and intrathoracic pressure Posture Temperature Blood gases (CO2 levels)
- 31. Intracranial pressure Normal compensatory adaptations Alteration of CSF absorption or production Displacement of CSF into spinal subarachnoid space Dispensability of the dura
- 32. Causes of raised ICP Mass effect - Brain tumor, infarction with edema, subdural or epidural hematoma Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, hypercarbia, and Reye hepatocerebral syndrome Increase in venous pressure - venous sinus thrombosis, heart failure, obstruction of jugular veins. Obstruction to CSF flow / absorption - hydrocephalus , extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption). Increased CSF production - meningitis, subarachnoid hemorrhage, or choroid plexus tumor. Idiopathic intracranial hypertension Craniosynostosis
- 33. Pathophysiology Increase in any of its contents—brain, blood, or CSF— will tend to increase the ICP Small increases in brain volume do not lead to immediate increase in ICP Because - ability of the CSF to be displaced into the spinal canal & ability to stretch the falx cerebri between the hemispheres and the tentorium between the hemispheres and the cerebellum
- 34. Pathophysiology Injury to the brain occurs both at the time of the initial trauma (the primary injury) and subsequently due to ongoing cerebral ischemia (secondary injury). Cerebral perfusion pressure = CBF – ICP Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls Body’s response to a fall in CPP raise systemic blood pressure and dilate cerebral blood vessels Results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing vicious cycle
- 35. Pathophysiology Severely raised ICP, if caused by a unilateral space- occupying lesion can result in midline shift Midline shift can compress the ventricles and lead to hydrocephalus Prognosis is much worse in patients with midline shift Increased ICP combined with a space-occupying process is brain herniation
- 36. Signs and symptoms of raised ICP Headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain and papilledema If papilledema is protracted visual disturbances, optic atrophy, and blindness Headache - classically a morning headache Worse on coughing / sneezing / bending, and progressively worsens over time If mass effect is present - pupillary dilatation, abducens palsies, and Cushing's triad Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and Cheyne–Stokes respiration
- 37. Signs and symptoms of raised ICP Patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg Only when ICP exceeds 40–50 mmHg, CPP and cerebral perfusion decrease to a level that results in loss of consciousness Any further elevations will lead to brain infarction and brain death
- 38. Investigations CT brain – Haemorrhage, Hydrocephalus, space occupying lesions, midline shift MRI brain – Acute ischemic stroke, central venous sinus thrombosis EEG – Seizures, recurrent status epileptics, severe brain dysfunction LP – Infection , to look for the opening pressure ICP monitoring
- 39. ICP monitoring Ventriculostomy – helps to monitor the ICP & also for drainage of CSF as a treatment
- 40. Treatment for raised ICP Insert ICP monitoring – ventriculostomy or parenchymal device General goals – to maintain ICP < 20mmHg and CPP > 60 mmHg IF ICP > 20 – 25 mmHg for > 5 min Drain CSF via ventriculosotmy
- 41. Treatment for raised ICP Sedation – morphine / propofol / midazolam Neuromuscular paralysis if required Hyperventilation - PaCo2 of 30 – 35 mmHg
- 42. Treatment for raised ICP Elevate head end of bed – 30degree Osmotherapy – Mannitol 25 – 100 g Q4H (Maintain serum osmolality < 320mosmol) or hypertonic saline ( 30ml, 23.4% Nacl bolus) Glucocorticoids – Dexamethasone 4mg Q6H for vasogenic oedema from tumour
- 43. Treatment for raised ICP Pressor therapy – Phenylephrine, dopamine or norepinephrine to maintain adequate MAP to ensure CPP > 60 mmHg Consider second line therapies for refractory elevated ICP High dose barbiturate Aggressive hyperventilation to PaCo2 < 30mmHg Hypothermia Hemicraniectomy
- 45. Thank You!
Editor's Notes
- In case one of the supply arteries is occluded, the Circle of Willis provides interconnections between the anterior and the posterior cerebral circulation along the floor of the cerebral vault, providing blood to tissues that would otherwise become ischemic.