Effects Of Anesthetics On Cerebral Blood Flow
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Effects Of Anesthetics On Cerebral Blood Flow

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Enumerates the effect of different anesthetic agents on the CNS and compares their relative efficacy and safety in providing good outcome in neuroanesthesia

Enumerates the effect of different anesthetic agents on the CNS and compares their relative efficacy and safety in providing good outcome in neuroanesthesia

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Effects Of Anesthetics On Cerebral Blood Flow Effects Of Anesthetics On Cerebral Blood Flow Presentation Transcript

  • EFFECTS OF ANESTHETICS ON CEREBRAL BLOOD FLOW & CMRO2 PRESENTER Dr Unnikrishnan P COORDINATOR Dr Linnette Morris MODERATORS Dr Ushakumari Dr Chitra
  • Why this session…?
    • What is the substance of this discussion?
    • How Physiology transforms into Anesthesiology….
    • What should be our ultimate
    • aim in neuroanesthesia?
    • …………… . is to give the patient the best possible brain
  • Keep the terms close to your heart….
    • CMRO2  how fast the brain eats its food
    • Why it eats food?
    • 1. electrical activity(signaling) 2. cellular homeostasis
    • CBF  the amount of the food supply to brain
    • If CBF increase  brain swells  ICP increase
    • What is coupling?
    • Why it is so important in this discussion?
  • CBV-CBF
    • Cerebral perfusion= mean BP - ICP
    • CBF or CBV .. Which is more important in determining ICP?
    • Remember CBF and CBV may not always go parallel..So be cautious
  • CBV AND AUTOREGULATION
    • When MAP rises  autoregulation  CBV decrease
    • When MAP rise  no autoregulation  CBV increase
    • When MAP decreases  vasodilation  CBV increase
    • If intracranial compliance is poor  reduce Cerebral Perfusion Pressure[CPP]
  • Epileptogenesis -concerns
    • Seizure increase CMRO2  go unnoticed in anesthetized  CMRO2 exceed blood supply  neuronal injury
    • Also can persist in post op period….
  • INTRAVENOUS ANESTHETICS
    • r
  • I V ANESTHETICS
    • Generally we suppress brains appetite {CMRO2 decrease}
    • So CBF decrease
    • Hence coupling
    • Ketamine is the rebel among us
    • We also have direct effects
  • BARBITURATES
    • Dose dependent reduction in CBF& CMR
    • Metabolism related with brain’s electrical activity is mainly suppressed
    • CMRO2 decrease  vascular resistance increase  CBF decrease  ICP decrease
    • CBF/CMRO2 ratio unchanged
  • Barbiturates….
    • Cerebral perfusion= mean BP - ICP
    • MAP reduction +
    • ICP reduction +++
    • So cerebral perfusion pressure preserved
    • Thiopentone protect brain from incomplete ischemia:
    Suppression of CMR Free radical scavenging CBF redistribution effects Decrease ATP consumption
  • Barbiturates ….
    • Tolerance…
    • Autoregulation maintained
    • CO2 responsiveness intact
  • ABOUT METHOHEXITAL
    • Myoclonic activity
    • Patients with seizures of temporal lobe origin[psychomotor variety ]are specifically at risk
    • Used to activate seizure foci during cortical mapping
  • PROPOFOL
    • Primarily reduce CMR  vasoconstriction  decrease CBF & ICP
    • In patients with high ICP, significant reduction in CPP
    • Fentanyl + propofol  ablates increase in ICP at intubation
    • CO2 responsiveness preserved
    • Autoregulation preserved
  • Propofol and seizure incidence
    • Though seizures,dystonic & choriform movements,opisthotonus etc have been reported with its use, SYSTEMATIC STUDIES HAVE FAILED TO CONFIRM THE NOTION THAT PROPOFOL IS PROCONVULSANT
    • ECT induced seizures are shorter with Propofol
    • Awake resection of seizure foci with propofol- no seizures
    • Appears to be anticonvulsant in animals
    • [Millers anesthesia,6/e]
  • Propofol & brain protection
  • Etomidate
    • Parallel reductions in CBF and CMR
    • Regionally variable; more in forebrain
    • Reactivity to CO2 preserved
    • Concerns …………
  • ETOMIDATE continued
    • Precipitate generalized epileptic EEG activity in epileptic patients..avoided here
    • Activate seizure foci and low doses used for intra op EEG localization
    • When used in ECT  longer seizures compared to Thiopentone and Propofol
    • But used in refractory status epilepticus
  • NARCOTICS
    • In general, little effects in normal brain
    • When occur, modest reduction in CBF& CMR
    • ?reduction in arousal
    • ?pain relief
  • MORPHINE
    • Modest depressive effect on CMR & CBF
    • Histamine release
    • Autoregulation preserved
  • FENTANYL & ALFENTANYL
    • FENTANYL
    • modest reduction CBF & CMR in quiescent brain
    • Larger reduction during arousal
    • ALFENTANYL
    • No significant changes
  • Fentanyl
    • Grandmal seizures reported
    • No neuro excitatory activity
    • ? exaggerated rigidity phenomenon
    • But alfentanyl augments temporal lobe spike activity
  • SUFENTANYL
    • Either reduction or no change in CMR&CBF
    • But sometimes….
    • Sudden decrease in MAP  decrease in CPP  autoregulation  small increase in ICP
    • So be cautious…..
  • REMIFENTANYL
    • Low sedative doses cause minor increase in CBF
    • Along with other anesthetics / higher doses  modest reduction or no change in CBF
  • Benzodiazepines
    • Modest reduction in CBF
    • The reduction attained is intermediate between that caused by
    •  narcotics(modest)
    •  barbiturates(substantial)
    • Remember they can produce respiratory depression  increase in paCO2
    • If we avoid this… BENZODIAZEPINES appears safe
  • FLUMAZENIL # true or false #
    • It cant reverse the cerebral effects of benzodiazepines
    • Overshoot phenomenon may occur
    • Overshoot may be a part of arousal phenomenon
    • Better avoided or used cautiously to reverse BZD sedation in patients with impaired I.C. compliance
  • DROPERIDOL
    • Tranquillizer[antidopaminergic] used in post operative refractory nausea & vomiting
    • Can cause abrupt fall in MAP  vasodilation  increase in ICP [occasional]
    • No action per se
  • KETAMINE
    • Increases CMR  secondarily increase CBF  increase ICP
    • Effect is regionally variable[limbic system^]
    • Racemic mixture: S increase , R decrease CMR
    • Diazepam , Midazolam ,Isoflurane /N2O, Propofol …. They blunt this effect
    • Better to avoid as sole agent….
    • Reasonable to use it along with the above drugs… cautiously
  • LIDOCAINE
    • Reduce CMRO2
    • Large doses : reduction greater with lignocaine than with high dose barbiturate!
    • How?
    • ? membrane stabilizing effect of lignocaine also reduces energy needs for membrane integrity
    • Rx & prevention of a/c rise in ICP, also during ETT suctioning
    • Trials ..
  • INHALED ANAESTHETICS
  • VOLATILE AGENTS….
  • EFFECTS @ DIFFERENT MACs
  • Beyond 1 MAC what happens?
    • Coupling persists…..(most probably)
    • Dose related increase in CBF/CMR occur
    • Greater luxury perfusion
    • Order of vasodilatory potency:
    • HALOTHANE >> ENFLURANE > DESFLURANE = ISOFLURANE > SEVOFLURANE
  • Volatile agents Also……
    • The vasodilator effect usually appear rapidly than the effects on CMRO2. The CBF falls to near- prevolatile agent levels , 2.5 to 5 hrs later
    • If antecedent lowering of CMR by drugs/disease, then vasodilator effect may predominate
  • Continued (general properties) volatile agents
    • It can also reduce BP
    • CO2 responsiveness preserved
    • Autoregulation :  rising BP(less imp) - impaired
    •  falling BP(important) - preserved
  • HALOTHANE
    • CBF  dramatic increase in CBF with a simultaneous modest reduction in CMR
    • CMR  suppression is less compared to other agents
    • Produces isoelectricity in EEG at MACs >4
    • MACs beyond this what happens?
  • Halothane….. continued
    • Further reduces CMRO2….
    • Surprised or alarmed?
    • Means that these doses interfere with cell metabolism [?oxidative phosphorylation]
    • Means toxicity at higher concentrations [reversible]
  • ENFLURANE
    • CBF  dramatic increase in CBF with a simultaneous modest reduction in CMR
    • Potentially epileptogenic and hypocapnoea potentiates this effect
    • Seizure activity elevate brain metabolism by as much as 400%
    • Will you prefer?
    • So avoid: if seizure predisposition/
    • h/o occlusive cerebrovascular disease/with hypocapnoea/ high doses
  • ISOFLURANE
    • CBF  increases CBF; but to a lesser extent ^
    • CMR  decreases CMRO2 and maximal reduction is attained simultaneously with EEG suppression at clinically relevant concentrations [1.5-2.0 MAC]
    • @ 1 MAC decrease CMRO2 by 25% *
    • ^ Human studies @1.1 MAC halothane 191% isoflurane 19%, Miller 6/e
    • * collation of data p:827 ,Miller 6/e
  • Isoflurane more
    • Distribution of CBF/CMR changes:
    • CBF  CBF increases are greater in subcortical and hindbrain areas than neocortex CMR  CMR suppression is greater in the neocortex than subcortex
    • The institution of hyperventilation , simultaneous with its introduction can prevent increase in ICP [ which may occur with normocarbia]
  • SEVOFLURANE
    • Reduce CBF
    • Reduce CMRO2 by 38% @ 1 MAC
    • Max at EEG suppression
    • At 1.5-2.0 MAC
    • DISTRIBUTION
    • Reduction in CBF within cortex
    • Increase in CBF within cerebellum
    • Has small potential to evoke epileptiform activity ; use with caution in patients with epilepsy ( Miller 6/e)
  • DESFLURANE
    • Reduce CBF
    • Decrease CMRO2 by 22% @ 1 MAC
    • Others = sevoflurane
    • In general, the effect of Isoflurane , Desflurane and Sevoflurane on CBF are modest
  • Summary of volatile agents MAJOR IMPACT ON CBF/CBV & ICP OCCURS WHEN WE EXCEED 1 MAC BECOMES SIGNIFICANT IF INTRACRANIAL COMPLIANCE IS ABNORMAL HERE, IT IS BETTER TO USE A PREDOMINANTLY INTRAVENOUS TECHNIQUE UNTIL THE POINT OF OPENING OF CRANIUM & DURA NET VASODILATORY EFFECT OF ISO/DES & SEVO LESS THAN HALO;SO IF ONE IS TO BE USED, PREFER THE FORMER ONES EFFECT OF HYPOCAPNOEA : HALOTHANE Vs ISO/DES/SEVO ENFLURANE IS EPILEPTOGENIC; SLIGHT RISK WITH SEVOFLURANE CO2 REACTIVITY AND AUTOREGULATION PRESERVED
  • NITROUS OXIDE
    • Can cause significant increase in CBF,CMR & ICP [ sympathoadrenal stimulating effect]
    • Most extensive increase when used
    • alone
    • With IV agents: CBF effect considerably reduced[ thiopentone , Propofol , benzodiazepines , narcotics ]
    • With Volatile Agents: CBF increase is exaggerated
  • Nitrous oxide…
    • Vasodilator effect clinically significant in those with abnormal i.c. compliance  so add IV agents
    • Surgical field persistently “tight”?  N2O may be a culprit
    • It should be avoided in cases, where a closed intracranial gas space may exist , since it can enter and expand it
  • N2O continued
    • CBF response to CO2 preserved
    • No uniform agreement reached on its effect on CMR
  • MUSCLE RELAXANTS
  • NON DEPOLARIZING RELAXANTS
    • Main effect is via Histamine release
    • Cerebral vasodilation  increase ICP
    • Simultaneous decrease in BP
    • Reduction in cerebral perfusion pressure
  • Non depolarizing relaxants- histamine release
  • NDMR continued
    • Pancuronium- large bolus  abrupt increase in BP  if autoregulation defective  increase ICP
    • A metabolite of atracurium, Laudanosine  epileptogenic properties in trials
    • But” it appears highly unlikely that epileptogenesis will occur in humans with atracurium”*
    • * miller 6/e p:831
  • Message…. NDMR use
    • All are reasonable in I.C. hypertension
    • Avoid hypotension… Metocurine/Atracurium/Mivacurium
    • Dose and rate of administration adjusted
    • Curare die-hard fan? Small divided doses
  • SUCCINYL CHOLINE
    • Increase ICP in lightly anaesthetized
    • Prevented by
    • May be an arousal phenomenon , caused by increased afferent signals from muscle spindles
    • Consider rise in ICP Vs rapid attainment of paralysis… in a given case
    • Control of CO2 tension , BP , depth of anesthesia, Defasciculation etc should be taken care of
    Deep anesthesia Defasciculation with metocurine 0.03 mg/kg “ paralysis with Vecuronium”
  • Also know
    • Worried about CSF dynamics?
    •  Prolonged closed cranial procedure
    •  ?enflurane: increase secretion,
    • decrease absorption
    • Blood Brain Barrier
    •  acute hypertension can breach BBB; certain anesthetics may facilitate this
  • Textbook of neuroanesthesia & criticalcare/Basil F Matta SURGERY INDUCTION RELAXANT MAINTENANCE SUPRATENTORIAL ICSOL TPS/P’FOL ATRA/VEC/MIVA/ROC P’FOL-FENT / FENT- LD ISO / N2O- HD ISO VASCULAR Sx TPS/ETO/P’FOL VEC/ATRAC/PAN/? SCOLINE* P’FOL-OPIOID +/- VOL AGENT* ?N2O CAROTID Sx FENT/ETO/TPS/ P’FOL VEC FENT/ISO/N2O POST FOSSA OPIOID/TPS/ P’FOL NDMR VARIES ?N2O-PC/VAE ?VOL-TRANS PUL,SSEP NSx WITHOUT CRANIOTOMY FENT/TPS/P’FOL NDMR ISO WITH HYPOCAPNOEA Cx SPINE RSI-SCOLINE PED TPS/P’FOL/SEVO SUXA/NDMR N2O+LD ISO/SEV OR P’FOL i/FEN OR AIR+HD VA
  • .
    • Great Brain , Great anesthesia First surgical operation carried out with a general anaesthetic at the Massachusetts Hospital in Boston on 16 October 1846. Dr Thomas Morton (1819-1868), administered the anaesthetic - sulphuric ether - and can be seen at the far end of the table holding a flask near the patient's face. Dr John Collins Warren successfully removed a tumour from the neck of the patient, Gilbert Abbot. A diorama, based on an original daguerreotype of the scene
    • THANK YOU
  • REFERENCES
    • MILLER’S ANESTHESIA,6/e
    • ANESTHESIA &COEXISTING DISEASE,4e
    • WYLIE & CHURCHILL DAVIDSONS’ APRACTICE OF ANESTHESIA
    • TEXTBOOK OF NEUROANESTHESIA AND CRITICAL CARE Basil F. Matta, David K. Menon, John M. Turner
  • BRAIN PROTECTION
    • .
  • COMPLETE GLOBAL ISCHEMIA
    • CULPRITS: Hypotension and late phase intracranial hypertension
    INDUCTION OF MILD HYPOTHERMIA IN THE RANGE OF 32-32 ^C X 24 HRS  PASSIVE REWARMING OVER 8 HRS CALCIUM CHANNEL BLOCKER NIMODIPINE NORMALIZATION OF pH Rx OF SEIZURES NORMOTENSION
  • FOCAL [INCOMPLETE] ISCHEMIA
    • Anesthesia per se is protective
  • Thiopentone
    • Decrease ATP consumption
    • Suppress CMR
    • Free radical scavenging
    • CBF redistribution effects
    • Potentiate GABAergic action
    • Inhibit glucose transfer across BBB
    • Also shown by Methohexital
  • Propofol
    • Attenuate changes in ATP,Ca++,Na & K caused by hypoxic injury
    • Antioxidant action by inhibiting lipid per oxidation
    • Used in aneurysm Sx & Carotid endarterectomy
  • ISOFLURANE/VOLATILE AGENTS
    • Potent suppressant of CMR in cortex
    • Similar among the group
    • Isoflurane’s effect not sustained
  • ETOMIDATE
    • Was proposed to have neuroprotection
    • NO synthase inhibition/ NO binding
    • ?worsening of hypoxia,acidosis
    • Not used now
  • Others
    • Nimodipine
    • Nicardipine
    • Tissue plasminogen activator for thrombolysis
  • .
    • Great Brain , Great anesthesia First surgical operation carried out with a general anaesthetic at the Massachusetts Hospital in Boston on 16 October 1846. Dr Thomas Morton (1819-1868), administered the anaesthetic - sulphuric ether - and can be seen at the far end of the table holding a flask near the patient's face. Dr John Collins Warren successfully removed a tumour from the neck of the patient, Gilbert Abbot. A diorama, based on an original daguerreotype of the scene
    • THANK YOU
  • REFERENCES
    • MILLER’S ANESTHESIA,6/e
    • ANESTHESIA &COEXISTING DISEASE,4e
    • WYLIE & CHURCHILL DAVIDSONS’ APRACTICE OF ANESTHESIA
    • TEXTBOOK OF NEUROANESTHESIA AND CRITICAL CARE Basil F. Matta, David K. Menon, John M. Turner
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