Neuroanesthesia and cardiac toxicity

From WikiCNS
Jump to: navigation, search
Checkmark.gif This article has been reviewed by the NeuroWiki Editorial Board


  1. Intravenous anesthetics
    1. all anesthetics except ketamine decrease cerebral blood flow (CBF); ketamine is also the only one that does not increase cerebrovascular resistance
    2. barbiturates
      1. barbiturates produce the greatest reduction in the cerebral metabolic rate of oxygen consumption (CMRO2) and CBF
      2. also associated with hypotension from venodilation, myocardial depression, and decreased cardiac output
      3. NOTE: low-dose barbiturates cause bursts of 20-24 Hz activity on EEG in the central and frontal regions
    3. propofol
      1. causes 15-30% increase in systemic vascular resistance and decreases cardiac output
      2. produces dose dependent reduction in CBF and 40-60% decrease in CMRO2
    4. narcotics (fentanyl, morphine)
      1. decrease in CBF and CMRO2
    5. benzodiazepines (diazepam, midazolam, lorazepam)
      1. modest decrease in CBF and CMRO2
      2. mild cardiovascular effects; usually good for hypovolemic patients
      3. flumazenil can reverse but can cause dramatic rebound increase in CBF and ICP
    6. etomidate
      1. decreases CBF and CMRO2 and may cause cerebral vasoconstriction
      2. minimal cardiovascular effects
      3. suppresses adrenocortical response to stress
    7. ketamine
      1. large increase in CBF and no change to small increase in CMRO2
      2. interferes with autoregulation
      3. dissociative anesthetic
  2. inhalation anesthetics
    1. cause cerebrovascular dilation and an increase in CBF, with increase of ICP, but reduces CMRO2; not recommended in patients with intracranial pathology
    2. halothane
      1. increases CBF (cortical) and ICP but decreases CMRO2
      2. interferes with autoregulation
      3. causes myocardial depression and sensitizes the myocardium to catecholamines and may cause ventricular arrhythmias
    3. enflurane
      1. weaker cerebrovasodilator than halothane but more potent depressant of cerebral metabolism
      2. induces seizure discharges
    4. isoflurane
      1. increases CBF (global) and decreases CMRO2
      2. of the volatile anesthetics, increases CBF the least
    5. desflurane
      1. more pronounced suppression of brain electrical activity compared to isoflurane; still causes increase in CBF
      2. ICP does not change
    6. nitrous oxide
      1. dramatically increases CBF and ICP when intracranial compliance is compromised; potent vasodilator
      2. may cause air embolus because nitrous oxide diffuses into an air space faster than environmental air
      3. nitrous oxide abuse interferes with cobalamin dependent enzyme reactions and causes inactivation of methionine synthesis resulting in peripheral neuropathy and low hematocrit
  3. muscle relaxants
    1. succinylcholine
      1. increase ICP and CBF (increase in ICP may be blocked by prior administration of a nondepolarizing muscle relaxant)
      2. also associated with hyperkalemia
  4. monitoring of BAERs may be affected by inhalation drugs but tend to be fairly resistant to this effect however SSEPs are not and the dose of inhalation agent must be reduced
    1. nitrous oxide is controversial in posterior fossa surgery due to the risk of venous air embolism with nitrous oxide
    2. succinylcholine should not be used in paraplegics more than 24 hours after injury because of the hypersensitivity of the motor endplates
Personal tools