Cerebral circulation and anaesthetic implications

1. Cerebral circulationand anaesthetic implications Modreator-Dr Manoj Bharadwaj Speaker-Dr Amlan Swain www.anaesthesia.co.inanaesthesia.co.in@gmail.com

2. Overview of cerebral circulation

3. Overview of cerebral circulation Arterial supply Posterior Cerebral artery Anterior Cerebral artery Basilar artery 30% of CBF Vertebral artery Middle Cerebral artery Internal Carotid artery (70% of CBF)

4. Overview of cerebral circulation Circle of Willis Anterior CA Internal CA Middle CA Posterior CA Basilar A Vertebral A

5. Overview of cerebral circulation Venous drainage

6. 1 2 3 5 4 5 Cerebral Artery Areas 1. anterior cerebral 2. Middle cerebral 3. Penetrating branches of middle cerebral 4. anterior choroidal 5. Posterior cerebral

7. Cerebral physiology • 2% of BW • 20% of Total body oxy consumption • (60% used for ATP formation) • CMR O2 3-3.8mL /100 gm/min • (50 ml /min in Adult) • 15% 0f CO • Glucose consumption 5 mg/100gm/min • (25% of total body consumption/min)

8. ….contd • High oxygen consumption but no reserve • Grey matter of cerebral cortex consumes more • Directly proportional to electrical activity • (Hippocampus & cerebellum most sensitive to hypoxic injury)

9. NORMAL PHYSIOLOGIC VALUES

10. Approximately 60 % of the brain's energy consumption is used to support electrophysiological function. • Remaining 40%-?

11. Local CBF (l-CBF) and local CMR (l-CMR) within the brain are very heterogeneous, and both are approximately four times greater in gray matter than in white matter.

12. The brain's substantial demand for substrate must be met by adequate delivery of O2 and glucose. • However, the space constraints imposed by the noncompliant cranium and meninges require that blood flow not be excessive. • Not surprisingly, there are elaborate mechanisms for the regulation of CBF.

13. Cerebral perfusion pressure • MAP—ICP( or CVP whichever is greater) • Normally 80 to 100mm Hg • ICP is <10 mmHg so CPP primarily dependent on MAP • Increase in ICP>30 =CPP & CBF compromise • CPP<50 slowing of EEG • 25-40 Flat EEG • CPP <25 result in Irreversible brain death

15. Factors influencing CBF • CHEMICAL/METABOLIC • MYOGENIC • RHEOLOGIC • NEUROLOGIC • CHEMICAL/METABOLIC • MYOGENIC • RHEOLOGIC • NEUROLOGIC

16. CHEMICAL/METABOLIC

17. Cerebral Metabolic Rate • Increased neuronal activity results in increased local brain metabolism • Although it is clear that local metabolic factors play a major role in these adjustments in CBF, the complete mechanism of flowmetabolism coupling remains undefined.

18. CMR is influenced by several phenomena in the neurosurgical environment • functional state of the nervous system • anesthetic agents, and • temperature

19. Functional State. • CMR decreases during sleep and increases during sensory stimulation, mental tasks, or arousal of any cause. • During epileptoid activity, CMR increases may be extreme, whereas CMR may be substantially reduced in coma.

20. Anesthetics. • In general, anesthetic agents suppress CMR • Ketamine and nitrous oxide the notable exceptions. • It appears that the component of CMR on which they act is that associated with electrophysiologic function. • However, increasing the plasma level beyond that required first to achieve suppression of the EEG results in no further depression of CMR..

21. The interdependencyof cerebral electrophysiologic function and CMR

22. Temperature. • CMR decreases by 6 to 7 percent per Celsius degree of temperature reduction. • However, in contrast to anesthetic agents, temperature reduction beyond that at which EEG suppression first occurs does produce a further decrease in CMR

23. The effect of temperature reduction on the cerebral metabolic rate of oxygen

24. Temperature on CBF • 6-7 % decrease /0C FALL IN TEMP. • 37-42 0C - CBF & CMRO2 • >42 0C - CMRO2 • 20 0C - ISOELECTRICITY

25. Partial Pressure of Carbon Dioxide • CBF varies directly with PaCO2 • The effect is greatest within the range of physiologic PaCO2 variation. • CBF changes 1 to 2 mL/100 g/min for each 1 mm Hg of change in PaCO2around normal PaCO2 values. • This response is attenuated below a Pa CO2 of 25 mm Hg.

26. The changes in CBF caused by PaCO2 are apparently dependent on pH alterations in the extra cellular fluid of the brain • Note that in contrast to respiratory acidosis, acute systemic metabolic acidosis has little immediate effect on CBF because the blood-brain barrier (BBB) excludes the hydrogen ion from the perivascular space.

27. Although the CBF changes in response to Pa CO2 alteration occur rapidly, they are not sustained. • In spite of the maintenance of an elevated arterial pH, CBF returns to normal over 6 to 8 hours because cerebrospinal fluid (CSF) pH gradually normalizes as a result of the extrusion of bicarbonate.

28. Although the CBF changes in response to Pa CO2 alteration occur rapidly, they are not sustained. • In spite of the maintenance of an elevated arterial pH, CBF returns to normal over 6 to 8 hours because cerebrospinal fluid (CSF) pH gradually normalizes as a result of the extrusion of bicarbonate.

29. . Acute normalization of PaCO2 results in a significant CSF acidosis (after hypocapnia) or alkalosis (after hypercapnia). • The former results in increased CBF with a concomitant intracranial pressure (ICP) increase that will depend on the prevailing intracranial compliance. The latter conveys the theoretic risk of ischemia.

30. Steal Phenomenon • If local autoregulation is impaired and PaCO2 increases, vessels in surrounding normal brain will dilate. • Vessels in the abnormal area are already maximally dilated due to loss of autoregulation.

31. Vascular resistance will be decreased in surrounding normal brain; blood will be shunted away from abnormal areas, resulting in further hypoxia

32. Inverse Steal or Robin Hood Phenomenon • Opposite may occur as PaCO2 is decreased by hyperventilation. • Vessels in surrounding normal brain will vasoconstrict; vessels in the damaged or abnormal area of brain are already maximally dilated and are unable to constrict.

33. Because of the vasoconstriction in normal brain, vascular resistance increases, shunting blood into the abnormal area

34. Partial Pressure of Oxygen • Changes in PaO2from 60 to more than 300 mm Hg have little influence on CBF. • When the PaO2is less than 60 mm Hg, CBF increases rapidly . • At high PaO2values, CBF decreases modestly.

35. The mechanisms mediating the cerebral vasodilation during hypoxia are not fully understood, but they may include neurogenic effects initiated by peripheral and/or neuraxial chemoreceptors as well as local humoral influences • At 1 atm O2,CBF is reduced by 12 percent.

37. Myogenic Regulation (Autoregulation) • Autoregulation refers to the capacity of the cerebral circulation to adjust its resistance in order to maintain CBF constant over a wide range of mean arterial pressure (MAP).

38. In normal human subjects, the limits of autoregulation occur at MAPs of approximately 70 and 150 mm Hg • Above and below the autoregulatory plateau, CBF is pressure dependent (pressure passive) and varies linearly with CPP.

40. Autoregulation Curve shift to Rt in Chronic hypertensive • Decreased CPP Leads to vasodilation • Increased CPP leads to vasoconstriction

41. The precise mechanism by which autoregulation is accomplished is not known. • NO may participate in the vasodilation associated with hypotension in some species, but not, according to a single study, in primates

42. Neurogenic Regulation • There is considerable evidence of extensive innervation of the cerebral vasculature. • The density of innervation declines with vessel size, and the greatest neurogenic influence appears to be exerted on larger cerebral arteries.

43. This innervation includes autonomic, serotonergic, and vasoactive intestinal peptide-ergic (VIPergic) systems of extra-axial and intra-axial origin.

44. Viscosity Effects • Blood viscosity can influence CBF. • Hematocrit is the single most important determinant of blood viscosity. • In healthy subjects, hematocrit variation within the normal range (33-45%) probably results in only trivial alteration of CBF. • Beyond this range, changes are more substantial.

45. EFFECTS OF ANESTHETIC AGENTS ON CBF AND CEREBRAL METABOLIC RATE • In neuroanesthesia, considerable emphasis is placed on the manner in which anesthetic agents and techniques influence CBF. • The rationale is 2-fold.

46. First, the delivery of energy substrates is dependent on CBF, and, in the setting of ischemia, modest alterations in CBF can substantially influence neuronal outcome.

47. Second, the control and manipulation of CBF are central to the management of ICP because, as CBF varies in response to vasoconstrictor-vasodilator influences, such as Pa CO2 and volatile anesthetics, CBV varies linearly with it • Autoregulation normally serves to prevent MAP-related increases in CBV

48. In healthy subjects, the initial increases in CBV do not result in significant ICP elevation because there is latitude for compensatory adjustments by other intracranial compartments • When intracranial compliance is reduced, a CBV increase can cause herniation or may reduce CPP sufficiently to cause ischemia.

49. There have been several investigations of the effects of anesthetic agents on CBV in normal brain. • In general, the observed effects confirm a parallel relationship between CBF and CBV. • However, the relationship is not consistently one to one, and CBF-independent influences on CBV may occur.

50. Anesthetic agents may influence the venous side of the cerebral circulation. • At present, there is no evidence that these direct effects have clinical significance.