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25. Neurophysiology & Anesthesia. 마취통증의학과 R1 이강우. CEREBRAL PHYSIOLOGY. CEREBRAL METABOLISM Brain - total body oygen 의 20% 를 소비 ( 그중 60% 는 ATP 를 생산하는데 소비 ) Cerebral metabolic rate(CMR) ≒ Oxygen consumption (CMRO2) Interruption of Cerebral perfusion

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25. Neurophysiology & Anesthesia

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25 neurophysiology anesthesia

25. Neurophysiology & Anesthesia

마취통증의학과

R1 이강우


Cerebral physiology

CEREBRAL PHYSIOLOGY

CEREBRAL METABOLISM

Brain - total body oygen의 20%를 소비

(그중 60%는 ATP를 생산하는데 소비)

Cerebral metabolic rate(CMR)

≒ Oxygen consumption (CMRO2)

Interruption of Cerebral perfusion

→unconsciousness within 10s

if reestablished within 3~8min

→irreversible cellular injury

hippocampus와 cerebellum이 hypoxic injury에

가장 민감

Neuronal cells

- primary energy source:  glucose

- acute sustained hypoglycemia ≒ hypoxia

hyperglycemia : cerebral acidosis & cellular injury

--> global & focal hypoxic brain injury 악화시킴


Cerebral physiology1

CEREBRAL PHYSIOLOGY

CEREBRAL BLOOD FLOW

CBF 는 metabolic activity 에 따라 변한다.

total CBF : 약 50ml/100g/min

CBF < 20-25 ml/100g/min : cerebral impairment

15~20 ml/100g/min : flat EEG

< 10 ml/100g/min : irreversible brain damage


Cerebral physiology2

CEREBRAL PHYSIOLOGY

REGULATION OF CEREBRAL BLOOD FLOW

1.Cerebral Perfusion Pressure(CPP)

- CPP = MAP – ICP (or CVP) (단, CVP가 ICP보다 매우 큰 경우 CVP사용)

    - CPP = 80-100mmHg

      (대개 ICP < 10mmHg,  ∴ CPP는 MAP에 의해 좌우됨)

      if, sustained CPP < 25mmHg : irreversible brain damage

2.Autoregulation

   - brain : 혈압의 큰 변화에도 cerebral blood flow는 큰 변화가 없다.

     (ex. CPP ↓ → cerebral vasodilation)

    - CBF : MAP 60~160mmHg사이에서는 일정

      이 범위밖에서 blood flow는 pressure dependent

    - MAP > 150~160mmHg

: BBB disrupted → cerebral edema, hemorrhage


Cerebral physiology3

CEREBRAL PHYSIOLOGY

REGULATION OF CEREBRAL BLOOD FLOW

3.Extrinsic Mechanism

1) Respiratory Gas Tensions

- the most important extrinsic influence, 특히 PaCO2

     - PaCO2 : 20-80mmHg에서 CBF는 PaCO2에 비례

- 이차적으로 CSF 와 뇌  조직의 pH에 영향

2) Temperature

     - CBF 는 온도1도의 변화에 따라 5-7%가 변함

- Hypothermia : CMR와 CBF → 감소

3) Viscosity

- 일반적으로 blood viscosity와 CBF는 큰 연관이 없다

     - viscosity를 결정하는 가장 중요한 요소는 hematocrit

- ↓hematocrit → ↓viscosity → ↑ CBF

4) Autonomic influences

     - brain injury와 stroke시 cerebral vasospasm에 중요한 역할


Cerebral physiology4

CEREBRAL PHYSIOLOGY

BLOOD-BRAIN BARRIER

-cerebral blood vessel

: junctions between vascular endothelial cells are nearly fused

- blood brain barrier

: lipid barrier, lipid soluble substances를 통과시킴

ionizedor large molecular weight 를 갖는 물질 제한

- across the BBB:size, charge, lipid solubility,protein binding의 정도

CO2, O2, lipid soluble substances(대부분의 마취제)water : freely across

  ∴ rapid changes in plasma electrolyte concentration

→ transient osmotic gradient between plasma and the brain

so, marked abnormalities in serum sodium or glucose concentrations should be corrected slowly!

- mannitol : BBB통과 안됨 → sustained derease in brain water content


Cerebral physiology5

CEREBRAL PHYSIOLOGY

  CEREBROSPINAL FLUID

- 위치 : cerebral ventricle, cisterns,

subarachnoid space

- 기능 : trauma로 부터 CNS보호

- 생산 : choroid plexuses

    성인에서 약 21mL/h 생산

총량은 약150ml정도


Cerebral physiology6

CEREBRAL PHYSIOLOGY

 INTRACRANIAL PRESSURE

- Cranial vault는 rigid structure로서 brain(80%), blood(12%), CSF(8%)로 구성

: 한부분이 증가하면 다른부분이 감소하는 작용에 의해 ICP증가 방지

-ICP: supratentorial CSF pressure 를 의미

lateral ventricleor cerebral cortex에서 측정, 보통 10mmHg이하

- intacranial compliance : determined by measuring the change in ICP

volume증가에 따라 처음에는 compensation이 잘되나 한계점에 이르면 급속한 ICP의 증가를 보임

- major compensatory mechanism

     (1) initial displacement of CSF (from cranial to spinal compartment)

     (2) CSF 의 흡수 증가

(3) CSF 생산 감소

(4) total cerebral blood volume의 감소

- sustained elevations in ICP → catastrophic herniation of the brain


Effect of anesthetic agents on cerebral physiology

EFFECT OF ANESTHETIC AGENTS ON CEREBRAL PHYSIOLOGY

EFFECT OF INHALATION AGENTS (1)

1.Volatile Anesthetics

Cerebral Metabolic Rate(CMR)

- 흡입마취제는 dose-dependent 하게 CMR 감소

- Isoflurane이 가장 많이 감소(50%까지 감소)

Cerebral Blood Flow & Volume

- 흡입마취제는 dilate cerebral vessel, impair autoregulation (dose-dependent)

      - halothane : CBF 에 가장 큰 영향 (200%까지 증가) 

cf. Isoflurane은 20%정도

- time-dependent : 2-5시간동안 지속적으로 투여시 blood flow는 정상치로

돌아오기 시작

- hyperventilation (hypocapnia) 는 흡입마취제가 CBF 에 작용하는것을

         방해하거나 무디게 할수있음

- cerebral blood volume의 증가(10~12%) 는 CBF를 증가시킴


Effect of anesthetic agents on cerebral physiology1

EFFECT OF ANESTHETIC AGENTS ON CEREBRAL PHYSIOLOGY

EFFECT OF INHALATION AGENTS (2)

Cerebrospinal Fluid Dynamics

- 흡입마취제는 CSF의 생산과 흡수에 영향

- Isoflurane : CSF 흡수를 촉진(유일하게 CSF dynamic에 좋은영향)

Intracranial Pressure(ICP)

 -  즉각적인 cerebral blood vol. 변화와 delayed alterations on CSF dynamics, arterial CO2 tension 을 통해 ICP에 effect를 나타냄

- decreased intracranial compliance 시 choice - isofluane

2.Nitrous Oxide

    - N2O의 효과: 대체로 mild하며 다른 약제나 CO2 tension에 의해 쉽게

바뀔수 있다.

- intravenous agent와 사용시 minimal effect on CBF, CMR, and ICP

- volatile anesthetic와 함께 사용시 CBF를 더 증가

    - 단독 사용시 mild cerebral vasodilation, and ICP증가


Effect of anesthetic agents on cerebral physiology2

EFFECT OF ANESTHETIC AGENTS ON CEREBRAL PHYSIOLOGY

EFFECT OF INTRAVENOUS AGENTS

1.Induction Agents

Ketamine을 제외하고 모든 정맥마취제는 CMR, CBF에 거의 영향을 미치지

         않거나 감소시킴

1) Barbiturates

- major actions on the CNS

(1) hypnosis

         (2) CMR의 저하

(3) cerebral vascular resistance의 증가로 인한 CBF 의 감소

(4) anticonvulsant activity

- 위 이유로 barbiturates (특히, thiopental)는 neuroanestheisa에 가장 흔히 쓰임

     - barbiturate로 인한 CMR, CBF의 감소는 EEG가 isoelectric될때까지 지속

     - reverse steal phenomenon : barbiturate-induced  cerebral vasoconstriction

→normalarea에서 일어남 → blood flow를 ischemic area로 재분배

-CSF의 흡수촉진 → CSF vol. ↓(& CBF↓, cerebral blood vol.↓) → ICP ↓


Effect of anesthetic agents on cerebral physiology3

EFFECT OF ANESTHETIC AGENTS ON CEREBRAL PHYSIOLOGY

EFFECT OF INTRAVENOUS AGENTS

2) Opioids

      - minimal effects on CBF , CMR , ICP

- small doses of alfentanil : activate seizure foci in patients with epilepsy

- morphine : poor lipid solubility로 적합하지 않음

3) Etomidate

      - CMR , CBF , ICP 감소

- induction 시 myoclonic movement , 그러나 이는 seizure와는 관계없음

       - epilepsy Hx 있는 경우에는 avoid ( ∵ activate seizure foci)

  4) Propofol

      - CBF, CMR 감소

- dystonic & choreiform movement와 연관 but, Anticonvulant activity

- short elimination half-life → useful agent for neuroanesthesia

- but, excessive hypotension and cardiac depression → CPP 손상가능


Effect of anesthetic agents on cerebral physiology4

EFFECT OF ANESTHETIC AGENTS ON CEREBRAL PHYSIOLOGY

EFFECT OF INTRAVENOUS AGENTS

5) Benzodiazepines

      - CBF , CMR 감소

-anticonvulsant properties

      - midazolam: choice( ∵ short half-life )

-but, 종종 노인이나 unstable한 환자에서 CPP감소 &emergence가 길어짐

6)Ketamine

      - cerebral vasculature를 확장시키고 CBF 를 증가시킴(50~60%)

- seizure activityinthalamic and limbic areas

- Intracranial compliance가 떨어져있는 환자에서

CBF , cerebral blood volume, CSF volume 증가 → ICP 증가


Effect of anesthetic agents on cerebral physiology5

EFFECT OF ANESTHETIC AGENTS ON CEREBRAL PHYSIOLOGY

EFFECT OF INTRAVENOUS AGENTS

2.Anesthetic Adjuncts

 Iv lidocaine : 다른약제보다 작지만 CMR, CBF, ICP감소

systemic toxicity와 seizures 가능성이 있어 repeat dose제한

3.Vasopressors

 MAP가 50-60mmHg이하 또는 150-160mmHg이상일 경우 CBF 증가

4.Vasodilators

Hypotension이 없을 경우, 대부분의 vasodilators는 cerebral vasodilation을

      일으키며 CBF 를 dose-relate하게 증가 시킴

5.Neuromuscular Blocking Agents

NMBAs 는 brain에 직접적으로 영향을 미치지는 않지만 중요한 secondary

effect 를 가짐

     succinylcholine - ICP 증가

(그러나, induction시 thiopental or propofol, hyperventilation으로 최소화 )


Physiology of brain protection

PHYSIOLOGY OF BRAIN PROTECTION

PATHOPHYSIOLOGY OF CEREBRAL ISCHEMIA

- brain : 상대적으로 높은 산소 소비와 glucose metabolism

→ischemic injury에 취약

(ex. interruption of cerebral perfusion, metabolic substrate, or hypoxemia

→ functional impairment )

- normal oxygen tension, blood flow, and glucose supply가 3~8분내로

공급되지 않으면 ATP가 고갈되고 irreversible neuronal injury 가 시작됨

STRATEGIES FOR BRAIN PROTECTION

1.Hypothermia

- focal and global ischemia시 brain protection에 most effective method

- hypothermia는 basal and electrical metabolic requirements를 감소시킴

- mild hypothermia(33-35도) - some protective effect

fewer adverse effectthan profound hypothermia


Physiology of brain protection1

PHYSIOLOGY OF BRAIN PROTECTION

STRATEGIES  FOR BRAIN PROTECTION

2. Anesthetic Agents

- barbiturates, etomidate, propofol, and isoflurane

    → complete electrical silence of the brain

     - barbiturates : ① produce inverse steal

                   ② reduce cerebral edema and calcium influx

                  ③ inhibit free radical formation

                   ④ blockade of sodium channels

          → effective brain protection in focal ischemia

      - anesthetic agents가 global ischemia에 꾸준한 효과가 있다는 연구결과는 없다.

3. Specific Adjuncts

- calcium channel blockers : cerebral vasodilation, CBF 증가

→ neurologic outcome을 향상 시키지는 않는다

- nimodipine : subarachnoid hemorrhage pt. manage

- methylprednisolone : reduce neurological deficits following spinal cord injury


Physiology of brain protection2

PHYSIOLOGY OF BRAIN PROTECTION

STRATEGIES  FOR BRAIN PROTECTION

  4.General Measures

     - 적절한 CPP 유지는 중요

        ∴ 1) arterial blood pressure : normal or slightly elevated

        2) venous and ICP 증가는 피해야 한다.

3) oxygen carrying capacity 는 적절히 유지되어야 함

: normal arterial oxygen tension & 30% hematocrit

- Hyperglycemia : neurologic injury 악화 ( focal or global ischemia후 )

- normocarbia 유지 :① hypocarbia– induced cerebral vasoconstriction

→ ischemia 악화

                       ②hypercarbia:steal phenomena 야기 & acidosis 악화


Physiology of brain protection3

PHYSIOLOGY OF BRAIN PROTECTION

EFFECT OF ANESTHESIA

ON ELECTROPHYSIOLOGICAL MONITORING

: CNS 의 기능정도를 평가

- 주로 EEG 와 Evoked potentials사용

- 정확한 이해는 anesthetic depth- & dose- related change 와 blood

pressure, body temperature, respiratory gas tension 영향을

고려해야함

- recording은 bilateral하여야 하며( 비교하기 위해) , 술중 event와

연관하여 모니터링 하여야 함


Physiology of brain protection4

PHYSIOLOGY OF BRAIN PROTECTION

ELECTROENCEPHALOGRAPHY

- EEG : cerebral perfusion의 적정성을 평가하는데 가장 유용

carotid endarterectomy(CEA), controlled hypotension 시 사용

- activation : light anesthesia, surgical stimulation

- depression : deep anesthesia, cerebral compromise

- 대부분의 마취약제들은 biphasic pattern을 나타냄

: initial activation 후 dose-dependent depression

1. Inhalation Anesthetics

- Isoflurane : high dose(1-2 MAC)하에서 isoelectric EEG를 나타내는 유일한 약제

- Sevo and Des : burst suppression pattern at high dose (>1.2 &1.5 MAC)

2. Intravenous Agents

- Benzodiazepines : typical biphasic pattern on EEG

     - Barbiturates, etomidate, and propofol : typical biphasic pattern

                           high dose시에는 burst suppression and electrical silence

- opioid : produce only a monophasic, & dose dependent depression of EEG


Physiology of brain protection5

PHYSIOLOGY OF BRAIN PROTECTION

EVOKED POTENTIALS

1. Somatosensory evoked potentials (SSEPs)

: dorsal spinal columns과 sensory cortex의 상태를 평가

spinal tumor의 resection 과 spine, CEA, aortic surgery시 사용

2. Motor evoked potentials

: aortic surgery시 spinal cord perfusion을 평가함

3.Brain stem auditory evoked potentials

: 8th cranial nerve and auditory pathways above pons를 monitor 함

4. Visual evoked potentials : monitor optic nerve and upper brain stem

during resections of largre pituitary tumor  

- EEG 보다 more complicated

- poststimulus latencies를 갖는다. ( short, intermediate, and long)

- short-latency evoked potentials : 자극받은 nerve나 brain stem

- long-latency evoked potentials : primarily of cortical origin

- 수술중 단지 short and intermediate potentials만 모니터링 할 수 있다.


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