logging in or signing up Cerebral circulation aSGuest51334 Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 2781 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: June 26, 2010 This Presentation is Public Favorites: 1 Presentation Description Cerebral circulation - Effect of anaesthetic drugs Comments Posting comment... Premium member Presentation Transcript Cerebral circulation Effect of anesthetic drugs : Cerebral circulation Effect of anesthetic drugs Dept. of Anaesthesiology Osmania Medical College Hyderabad India Peculiarities of brain : Peculiarities of brain Has a high metabolic rate Has no oxygen stores Unable to maintain its integrity through anaerobic metabolism Neurons don’t require insulin for transport of glucose across cell membrane Neurophysiology : Neurophysiology 2% of body weight 17% of Cardiac output consumption at rest 20% of inspired oxygen 60% - for neuronal activity 40% - to maintain cellular integrity CMR / CMRO2 - 3-3.8ml/100g/min 50ml/min Cerebral glucose consumption - 5mg/100g/min cerebral blood flow : cerebral blood flow 80% - Internal carotid arteries 20% - Vertebral arteries Anterior n posterior communicating arteries Circle of Willis Communication between exl & int carotids – opthalmic arteries Circle of willis : Circle of willis Physiology of CBF : Physiology of CBF Parallels with metabolic activity Can vary from 10 – 300 ml/100g/min Average – 50ml/100g/min Gray matter – 80ml/100g/min White matter- 20ml/100g/min Total CBF- averages 750ml/min < 20-25ml/100g/min- ischemia FACTORS CONTROLLING CBF : FACTORS CONTROLLING CBF Intrinsic factors Myogenic Regulation Metabolic Regulation Neuronal Regulation Hormonal Regulation FACTORS CONTROLLING CBF : FACTORS CONTROLLING CBF Extrinsic factors Respiratory gas Arterial BP Hematocrit Temperature SAFETY FACTOR : SAFETY FACTOR Normal brain receives 3x required oxygen 7x required glucose Safety factor for oxygen < glucose Anoxia is the initial component of ischemia. Cerebral perfusion pressure : Cerebral perfusion pressure CPP is the difference between Mean arterial pressure and intracranial pressure (or cerebral venous pressure, which ever is greater) CPP = MAP – ICP CPP = MAP - ICP : CPP = MAP - ICP Normal CPP – 80 to 100mmHg More dependent on MAP ICP > 30mmHg compromise CPP CPP < 50mmHg – slowing of EEG 25 – 40 mmHg – flat EEG < 25 mmHg – irreversible brain damage Cerebral auto regulation : Cerebral auto regulation Ability of the cerebral blood vessels to alter their caliber in order to maintain a constant flow in face of variations in blood pressure Cerebral auto regulation : Cerebral auto regulation CBF is kept constant over a wide range of MAP ( 50 – 160 mm Hg ) CPP = MAP – Ven Press = MAP - ICP ↑ MAP Cerebral vasoconstriction ↓ MAP Cerebral vasodilatation Constant CBF is maintained Cerebral auto regulation : Cerebral auto regulation graph Pressures above 160mmHg Disrupts BBB Cerebral edema Haemorrhage Auto regulation…… : Auto regulation…… Autoregulatory changes take time up to 60 sec Large MAP changes may cause increased CBF even in presence of intact autoregulation In Hypertensive persons autoregulatory range shifts to higher pressure levels : 180 – 200mm Hg Dynamic vs Static : Dynamic vs Static Dynamic auto regulation describes the CBF response that takes place over seconds in response to a sudden drop in CPP. Static / slower auto regulation is the steady state achieved over 1 – 5 min Changes in autoregulation : Changes in autoregulation Absent ( Vasomotor paralysis ) brain trauma surgical retraction high ICP brain tumor seizures Shift to right Systemic hypertension States of sympathetic activation Shift to left Volatile anesthetic agents FACTORS CONTROLLING CBF : FACTORS CONTROLLING CBF Intrinsic factors Myogenic Regulation Metabolic Regulation Neuronal Regulation Hormonal Regulation Extrinsic factors Respiratory gas Arterial BP Hematocrit Temperature Myogenic factors : Myogenic factors Is the intrinsic response of smooth muscle cells in cerebral arterioles to changes in MAP Protective mechanism against excessive pressure fluctuation at capillary level Metabolic regulation : Metabolic regulation NO Hydrogen ions potassium adenosine prostanoids ↑ CO2 ↑ H+ ↓ O2 ↑ K+ ↑ Adenosine EDRF / Nitric Oxide Innervation : Innervation The sympathetic fibers arise mainly from the superior cervical ganglion The parasympathetic from the sphenopalatine and otic ganglia Sensory fibers from the trigeminal ganglion The functional significance of neural innervations has yet to be elucidated. Neuronal regulation : Neuronal regulation α-Adrenergic receptors in arterial smooth muscle Postganglionic sympathetic fibers release noradrenaline Causes smooth muscle contraction and arterial constriction Sympathetic innervation is responsible for vascular tone Sympathetic : Sympathetic Large & Medium sized arteries normally overridden by autoregulation Historically thought to have no role in cerebral circulation Comes into play in states of excessive circulatory activity / pathologic states Role in prevention of cerebral h’ge – cerebral vasospasm Hormonal regulation : Hormonal regulation Adrenaline Vasopressin Angiotensin II Effect of CO2 on CBF : Effect of CO2 on CBF CBF œ PaCO2 between 20 – 80 mmHg 1mmHg ↑↓ PaCO2-↑↓ CBF by 1-2ml/100g/min After 24 – 48 hrs CSF HCO3- compensation limits the effects of hypocapnia/ hypercapnia Persistent hyperventilation L/ODC cerebral impairment Hypercarbia - CBF : Hypercarbia - CBF The relationship between PaCO2 and CBF is sigmoid with plateaus below 25 mmHg and above 75 mmHg. The slope is approximately linear Mechanism of CO2 on CBF : Mechanism of CO2 on CBF The mechanism of CO2 induced changes in vessel caliber An increase in perivascular H+ concentration Associated NOS activation An increase in intracellular cGMP K+ efflux A reduction in intracellular Ca + + resulting in dilation NOS inhibition attenuates the Cyclooxygenase inhibition CBF response to CO2 Effect of oxygen : Effect of oxygen Hyperoxia – minimal decrease in CBF 10% Severe hypoxia – PaO2 < 50mmHg Increases CBF Haematocrit : Haematocrit in haematocrit viscosity CBF O2 carrying capacity haematocrit viscosity CBF Optimal haematocrit – 30% to 34% Temperature : Temperature CBF changes 5- 7% per OC Hypothermia CBF & CMR Pyrexia has reverse effect Slide 33: Clinical application Applied aspects : Applied aspects Effects of anesthetic drugs on CBF Volatile anesthetics Induction agents Anesthetic adjuncts Vasopressors Vasodilators Neuromuscular blocking agents Volatile agents : Volatile agents Volatile agents – dose dependent dilatation of cerebral vessels Impair auto regulation Response to CO2 retained May increase cerebral blood volume May result in elevated ICP Slide 36: Halothane Has greatest effect on CBF Con.> 1% - abolishes auto regulation Generalized increase in CBF At equivalent MAC CBF up to 200% Prior hyperventilation to be initiated Isoflurane CBF Auto regulation maintained up to 1 MAC is > in sub cortical than neocortical areas At equivalent MAC CBF up to 20% Simultaneous hyperventilation can prevent in ICP Slide 37: Sevoflurane: CBF effects similar to isoflurane Produce slightly less vasodilation Auto regulation maintained up to 1.5 MAC Desflurane: CBF similar to isoflurane but at >1 MAC > sevoflurane. Autoregulation progressively abolished as dose increases Slide 38: Nitrous Oxide: When administered on its own- increases both CBF and metabolism. when added to a background of another anesthetic, it increases CBF without changing metabolism It is a direct acting and potent cerebral vasodilator IV induction agents : IV induction agents Intravenous anesthetics reduce CBF in a dose dependent fashion coupled to the reduction in metabolism Once maximal suppression of metabolism occurs, no further reduction in CBF occurs Barbiturates : Barbiturates Barbiturates maximal 50% reduction in CBF and metabolism CO2 reactivity is maintained but is quantitatively reduced compared to the awake response Cerebral auto regulation maintained intact Propofol : Propofol Propofol produces a coupled dose dependent reduction in CMRO2 and CBF High doses vasodilator effect overcomes the coupling & CBF increases Both CO2 responses and auto regulation are maintained intact in the normal brain In head injured patients static auto regulation may be impaired by high propofol infusion rates Ketamine : Ketamine Dilates the cerebral vasculature and increases CBF ( 50 – 60%) Increases in CBF, CBV, CSF volume can increase ICP markedly in patients with decreased IC compliance Opioids : Opioids Opioids at low doses produce very little effect on CBF (provided CO2 is not allowed to rise) Auto regulation remains intact BP vasodilatation to maintain CBF cerebral blood volume increase intracranial pressure. Vasopressors : Vasopressors With intact auto regulation & BBB in CBF occurs when MAP<50 -60mmHg MAP>150 – 160mmHg In the absence of auto regulation, vasopressors CBF Vasodilators : Vasodilators In the absence of hypotension Cerebral vasodilatation CBF With Hypotension CBF is maintained CBV & ICP in patients with IC compliance NMBD : NMBD No direct effect on CBF Histamine releasing agents can cause hypotension , CPP Slide 47: What is Luxury perfusion ? Intra cerebral steal ? Reverse steal phenomenon ? Luxury perfusion : Luxury perfusion The combination of a decrease in CMRO2 and increase in CBF has been termed luxury perfusion met. Demand met. Supply Luxury perfusion… : Luxury perfusion… Seen in Acute cerebral infarction Vessels – max. dilated Less response to PCO2 Changes Induced hypotension with isoflurane Intracerebral Steal : Intracerebral Steal In a setting of focal ischemia , vasodilatation in a normal area would shunt blood away from the diseased area. ischemic normal Steal : Steal Seen in in PaCO2 in cerebral ischemia Volatile anesthetic agents Results in vasodilatation in normal areas not in ischemic areas Reverse Steal phenomenon : Reverse Steal phenomenon Diversion or redistribution of blood flow from normal to ischemic areas in the brain is termed Reverse Steal / Robin Hood phenomenon ischemic normal CBF / ICP : Better Anesthetic choice for neuro-anesthesia Monitoring for major intracranial procedures Approaches to emergence from anesthesia after craniotomy Understanding treatment options for increased intracranial pressure Hypotensive anesthesia CBF / ICP Slide 55: Thank you You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.