Cerebral-physiology-and-the-effects-of-Anesthetic-drugs (3).pptx

ppt made for education purpose for anaesthesia residents

1. Cerebral physiology and the effects of Anesthetic drugs Presented by: Dr. Priya Jain Moderator: Dr. Pa v an Gupta

2. Introduction to Cerebral Circulation 1 Overview of Cerebral Blood Supply The brain receives about 15-20% of cardiac output, making it highly dependent on an uninterrupted supply of blood. 2 Importance of Constant Perfusion Neurons are highly sensitive to ischemia, making cerebral perfusion crucial for maintaining brain function. 3 Main Blood Vessels Involved The internal carotid and vertebral arteries are the primary sources of cerebral blood supply.

3. The Arterial System Internal Carotid Arteries Arise from the common carotid arteries and supply the anterior circulation. Vertebral Arteries Arise from the subclavian arteries and merge to form the basilar artery, contributing to the posterior circulation. Cerebral Arteries The anterior, middle, and posterior cerebral arteries supply distinct regions of the brain.

4. Circle of Willis Location and Structure Located at the base of the brain, the Circle of Willis is a vascular structure providing collateral circulation. It connects the anterior and posterior cerebral circulation Components Consists of the internal carotid, anterior and posterior cerebral arteries, and communicating arteries. Function Maintains perfusion even if one part of the system is occluded.

5. Major Arteries of the Brain Anterior Cerebral Artery (ACA) Supplies the medial portions of the frontal and parietal lobes, including the motor cortex. Middle Cerebral Artery (MCA) Supplies the lateral cerebral cortex, including areas important for language and movement. Posterior Cerebral Artery (PCA) Supplies the occipital lobe and visual cortex.

6. Venous Drainage of the Brain 1 Superficial and Deep Venous Systems Drain blood from the cortex and deeper brain structures. 2 Dural Venous Sinuses Large venous channels located between the layers of the dura mater that collect blood from the brain. 3 Drainage into the Internal Jugular Veins Final pathway for cerebral venous return to the heart.

7. CSF formation and circulation Provides mechanical protection for the brain and the spinal cord. produced primarily by ependymal cells in choroid plexus in lateral ,third and 4th ventricles Normal CSF production-21 ml/hr There is about 125 ml of CSF at a time and total daily CSF production averages 450 ml occupies the subarachnoid space and the ventricular system around and inside the brain and spinal cord

8. Cerebral Metabolism / weight of the brain-1400gm- 2% of total weight of body Blood flow to the brain-12-15% of the resting cardiac output Brain normally consumes 20% of total body oxygen. Normal cerebral blood flow= 45-55 ml/100gm tissue /min CMRO2(cerebral metabolic rate of oxygen consumption)-rate at which brain utilizes oxygen= 3-3.5ml/100gm/minute Neuronal cells normally utilise glucose as their primary energy source.

9. Cerebral Blood Flow (CBF) Definition CBF refers to the amount of blood flowing through 100 grams of brain tissue per minute. Normal Values Typically, CBF is around 50 ml/100g brain tissue/min, representing 15-20% of the body’s total cardiac output. Oxygen Delivery The brain, despite its relatively small size, utilizes a significant portion (around 20%) of the body’s total oxygen supply. Anesthetic Significance Maintaining adequate CBF is crucial during anesthesia to prevent brain ischemia, a condition characterized by insufficient blood flow to the brain.

10. Cerebral Perfusion Pressure (CPP) 1 Formula CPP = MAP (mean arterial pressure) - ICP. 2 Normal Values Optimal CPP is 60-80 mmHg. Too low, and ischemia can occur; too high, and there is risk of elevated ICP. 3 Factors Influencing CPP Anesthesia, systemic blood pressure, and intracranial pathology all play a role.

11. Factors influencing cerebral blood flow 1 MYOGENIC Autoregulation;MAP 2 NEUROGENIC Extracranial sympathetic and parasympathetic pathways 3 CHEMICAL Paco2 Pao2 Temperature anesthetics vasopressors vasodilators

12. Autoregulation of Cerebral Blood Flow Mechanism The brain exhibits autoregulation, which maintains a consistent CBF within a specific range of mean arterial pressure (MAP). This is achieved through the dilation or constriction of cerebral blood vessels in response to changes in MAP. MAP Range Autoregulation generally functions effectively within a MAP of 60-160 mmHg. Loss of Autoregulation Various factors, including trauma, stroke, or anesthesia, can impair autoregulation, leading to fluctuations in CBF.

13. Autoregulation (myogenic) Autoregulation curve is shifted to the right in chronic hypertensive patients and to left in neonates and younger children,gradually moving to adult values as they get older At the lower limit of autoregulation,cerebral vasodilation is maximal,and below this level the vessels collapse and CBF falls passively with falls in MAP At the upper limit,vasoconstriction is maximal and beyond this the elevated intraluminal pressure may force the vessels to dilate,leading to an increase in CBF and damage to the blood-brain barrier Pressure autoregulation can be impaired in many pathological conditions like brain tumor,SAH,stroke etc

14. Failure of autoregulation may occur in- hypoxemia, hypercapnia High dose volatile anesthetics ischemic cerebrovascular disease SAH,traumatic brain injury tumours DM,chronic hypertension

15. Chemical regulation of C BF 1 CEREBRAL METABOLIC RATE Increase neuronal activity →increase local brain metabolism→increase in CMR Increase in CMR related with proportional changes in CBF is known as : FLOW METABOLISM COUPLING Increase activity→ increases metabolites( K+,H+ , lactate , adenosine)→vasodilatation ,pivotal role in increasing CBF Increase synaptic activity→increases glutamate→generation of downstream mediators like increase NO→Vasodilatation

16. Chemical regulation of C BF 2 PaCO2 CBF is directly proportionate to Paco2 between tensions of 20 and 80 mm hg Blood flow changes approx 1 to 2 ml/100 g/min per milimeter of mercury change in Paco2. This effect is secondary to changes in ph of CSF and cerebral tissue Hypercapnia (elevated CO2 levels) triggers vasodilation, increasing CBF. Conversely, hypocapnia (low CO2 levels) causes vasoconstriction, reducing CBF.

17. Chemical regulation of C BF 3 PaO2 CBF increases once Pao2 drops below 50 mm hg so that cerebral oxygen delivery remains constant hypoxia acts directly on cerebral tissue to promote the release of adenosine that contributes to cerebral vasodilation. hypoxia acts directly on cerebrovascular smooth muscle to produce hyperpolarisation and reduce calcium uptake,both mechanism enhancing vasodilatation

18. 4 Temperature and CBF CMRO2 decreases by 7% for each 1 degree celsius fall in body temperature and is paralleled by a similar reduction in CBF The reduction in CMRO2 is the factor that allows cold patients to withstand prolonged periods of reduced CBF without ischaemic damage Hyperthermia (above 42 degreeC) may result in neuronal cell injury 5 Blood Viscosity and CBF hematocrit is the single most important determinant . Increased blood viscosity (thickness) can impede CBF Optimal haematocrit where there is balance between flow and capacity,usually about 30%

19. Hyperventilation and Its Impact on CBF Role in Decreasing CBF Hyperventilation reduces PaCO2, leading to vasoconstriction and decreased ICP. CO2 Reduction Used in acute situations to lower ICP, but long-term hyperventilation risks ischemia. Use in Neurosurgery Common practice in managing patients with elevated ICP.

20. Neural Regulation of Cerebral Blood Flow Sympathetic Nervous System Sympathetic stimulation leads to vasoconstriction, reducing CBF. Parasympathetic Nervous System Parasympathetic stimulation promotes vasodilation, increasing CBF. May play a part in hypotension and reperfusion injury Baroreceptor Reflex This reflex adjusts CBF based on changes in systemic blood pressure, helping to maintain brain perfusion.

21. Metabolic Regulation of Cerebral Blood Flow Metabolic Demand Brain areas with higher metabolic activity require more blood due to increased oxygen consumption. Astrocytes Astrocytes play a crucial role in neurovascular coupling, regulating CBF in response to neuronal activity. Blood Flow Adjustment Astrocytes release signaling molecules that induce vasodilation in active areas, delivering more oxygen and nutrients.

22. Monitoring Cerebral Blood Flow Techniques : T rans-cranial Doppler (measures blood velocity) - an ultrasound probe (2 Mhz ,pulse wave doppler) is placed in the temporal area above zygomatic arch .velocities greater than 120 cm/s can indicate cerebral artery vasospasm. Near infrared spectroscopy -primarily reflects cerebral venous oxygen saturation Brain tissue oximetry measures the oxygen tension in brain tissue through placement of a bolt with a clark electrode oxygen sensor

23. CBF Management in the Elderly Aging and Cerebral Autoregulation Autoregulation may be impaired in elderly patients, increasing the risk of ischemia. Anesthetic Considerations Lower doses of anesthetics are often required due to reduced cerebral reserve. Postoperative Cognitive Dysfunction (POCD) More common in elderly patients, with careful management required to prevent long-term cognitive decline.

24. Intracranial Pressure (ICP) 1 Definition and Normal Range ICP is the pressure within the skull, normally between 5-15 mmHg in supine position 2 Factors Affecting ICP Blood volume, cerebrospinal fluid (CSF), and brain tissue volume all contribute to ICP. 3 Monro-Kellie Doctrine The principle that the sum of brain, blood, and CSF volumes must remain constant.

25. Causes of raised ICP Physiological - Fever,seizures,hypothermia,hypoventilation Hypoxia,hypercarbia,excess fluids,hypertension intubation Pathological - increased brain tissue( tumour, abscess,hematoma) Increased CSF volume(hydrocephalus,blocked shunt) Increased blood volume

26. Effect of Intracranial Pressure (ICP) on Cerebral Blood Flow Increased ICP Reduced Cerebral Perfusion Pressure (CPP) Potential for Brain Ischemia Herniation High ICP can cause brain tissue to shift, compressing vital structures Life-Threatening Consequences Treatment Strategies Medications like mannitol to reduce ICP Surgical interventions like decompressive craniectomy to restore CBF

27. Management of Patients with Elevated ICP Anesthetic Strategies Use of propofol, hyperventilation, and mannitol to reduce ICP. Avoiding Increases in Cerebral Blood Volume Minimizing hypercarbia, which leads to vasodilation. Controlled Ventilation Key to maintaining PaCO2 in a safe range.

28. Effect of IV anaesthetic drugs The action of most iv anaesthetics leads to parallel reduction in CMR and CBF except ketamine which causes increase in CMR and CBF. BARBITURATES - dose dependent reduction in CBF and CMR anticonvulsant property Both CBF and CMRO2 decrease by 30% large doses causes complete EEG suppression,CBF and CMR are reduced by approximately 50 to 60% barbiturates also facilitate absorption of CSF. The resultant reduction in CSF volume,combined with decrease in CBF makes barbiturates highly effective in lowering ICP

29. Effect of IV anaesthetic drugs BARBITURATE COMA - Temporary coma(a deep state of unconsciousness) brought on by a controlled dose of a barbiturate drug,usually thiopental Barbiturate comas are used to protect the brain during major neurosurgery,and as a last line of treatment in certain cases of status epilepticus Barbiturates reduce the metabolic rate of brain tissue,as well as the CBF.With these reductions,the blood vessels in the brain narrow,decreasing the amount of volume occupied by the brain and hence intracranial pressure.

30. Effect of IV anaesthetic drugs PROPOFOL - Both CBF and CMR decreases after administration of propofol In healthy volunteers, surgical level of propofol reduces regional CBF by 53 to 79% in comparison with awake state Both CO2 responsiveness and autoregulation are preserved during administration Its short elimination half life makes it a useful agent for neuroanesthesia. ETOMIDATE - Similar to barbiturates Parallel reduction in CBF and CMR ,accompanied by progressive suppression of EEG Both CBF and CMRO2 decrease by 30% additional concern is occurrence of adrenocortical suppression caused by enzyme inhibition.

31. NARCOTICS Likely have relatively less effect on CBF and CMR in the normal,unstimulated nervous system If changes do occur,modest reduction in both CBF and CMR MORPHINE - No effect on global CBF and a 41% decrease in the CMRO2 histamine release ,causes vasodilation resulting in increased CBV and CBF. FENTANYL - moderate global reduction in CBF and CMR in normal quiescent brain similar to morphine,causes larger reductions when administered during arousal

32. BENZODIAZEPINES - Cause parallel reduction in CBF and CMR Moderate reduction in CBF Safe to administer in patients with intracranial hypertension provided that respiratory depression and an associated increase in Paco2 do not occur KETAMINE - Unique ability to cause increase in both CBF and CMR The (s)-ketamine enantiomer increases CMR substantially,whereas the (R) enantiomer tends to decrease CMR. CO2 responsiveness is preserved can elicit seizures in patients with epilepsy

33. VOLATILE ANESTHETICS All volatile anesthetics suppress cerebral metabolism in a dose related manner possess intrinsic cerebral vasodilatory activity as a result of direct effects on vascular smooth muscle the net effect on CBF is therefore a balance between a reduction in CBF caused by CMR suppression and an augmentation of CBF caused by direct cerebral vasodilation At 0.5 MAC- CMR suppression -reduction in CBF At 1 MAC -CBF remains unchanged, CMR suppression and vasodilatory effect are in balance Beyond 1 MAC ,the vasodilatory activity predominates. and CBF significantly increases,even though CMR is substantially reduced.

34. NITROUS OXIDE Causes increase in CBF, CMR & ICP -sympathoadrenal stimulating effect Nitrous oxide alone - dramatic increase in ICP & CBF This effect is attenuated by using other drugs-barbiturates,narcotics,propofol In circumstances where ICP is persistently raised ,N20 should be viewed as a potential contributing factor N2O should be avoided when a closed intracranial gas space may exist

35. MUSCLE RELAXANTS NON DEPOLARISING RELAXANTS - Effect is mediated by histamine Histamine results in reduction in CPP because of increase in ICP( cerebral vasodilation) and decrease in MAP A metabolite of atracurium, laudanosine may be epileptogenic cis-atracurium has the least histamine releasing effect amino steroids like vecuronium,rocuronium does not have significant effect on cerebral physiology in patients with brain tumors. SUCCINYLCHOLINE - Can produce modest increase in ICP in lightly anesthetised humans deep anesthesia prevents succinylcholine induced increase in ICP.

36. Cerebral Protection and Anesthetic Techniques Hypothermia Reduces metabolic rate and provides cerebral protection during prolonged surgeries. Barbiturate Coma Induced to protect the brain in cases of severe injury or ischemia. Advanced Strategies Tailoring anesthetic depth to prevent ischemic damage.

37. Special Considerations in Pediatrics Pediatric CBF Higher metabolic rate compared to adults, making them more sensitive to changes in CBF. Anesthetic Implications Careful control of ventilation and ICP is critical in children with neurosurgical conditions. Vulnerability to Ischemia Pediatric patients are more vulnerable to ischemic brain injury during anesthesia.

38. Neuromonitoring during Anesthesia BIS (Bispectral Index) Measures brain activity and anesthetic depth . Cerebral Oximetry Monitors oxygen saturation in brain tissue . EEG (Electroencephalogram Records electrical activity in the brain. summation of excitatory and inhibitory post synaptic potentials generated by pyramidal cells

39. Postoperative Considerations 1 Postoperative Cerebral Hemodynamics Changes in ICP and CBF continue after surgery, necessitating careful monitoring. 2 Risk of Cognitive Decline and Stroke Managing blood pressure and avoiding hypoxia/hypercapnia can minimize these risks. 3 Anesthetic Agent Selection Postoperative care depends on agents used during surgery to prevent complications.