Effects Of Anesthetics On Cerebral Blood Flow

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Information about Effects Of Anesthetics On Cerebral Blood Flow
Health & Medicine

Published on October 9, 2009

Author: drunnikrishnanz

Source: slideshare.net

Description

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

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

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?

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

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]

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….

Seizure increase CMRO2  go unnoticed in anesthetized  CMRO2 exceed blood supply  neuronal injury

Also can persist in post op period….

INTRAVENOUS ANESTHETICS r

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

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

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

Cerebral perfusion= mean BP - ICP

MAP reduction +

ICP reduction +++

So cerebral perfusion pressure preserved

Thiopentone protect brain from incomplete ischemia:

Barbiturates …. Tolerance… Autoregulation maintained CO2 responsiveness intact

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

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

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]

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 …………

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

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

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

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

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

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…..

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

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

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

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

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

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 ..

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

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

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

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?

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]

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

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

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]

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)

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

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

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

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

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

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

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

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”

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

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

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

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

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

CULPRITS: Hypotension and late phase intracranial hypertension

FOCAL [INCOMPLETE] ISCHEMIA Anesthesia per se is protective

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

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

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

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

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

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

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

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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