Neuroanesthesia
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Questions and Answers

What is the primary mechanism by which autoregulation maintains a constant Cerebral Blood Flow?

  • Neurogenic responses to adrenergic and cholinergic nerve fibers
  • Metabolic responses to CO2 and O2
  • Myogenic response to changes in vascular transmural pressures (correct)
  • Cerebral vasculature's response to changes in venous pressure

    • What is the approximate percentage of cerebral metabolism that supports ionic gradients?

  • 80%
  • 60% (correct)
  • 40%
  • 20%

    • What is the effect of increased PaCO2 on Cerebral Blood Flow?

  • A biphasic response, with initial increase followed by a decrease
  • A decrease in CBF of 1mL/100g/min for every 1mmHg increase in PaCO2
  • An increase in CBF of 1mL/100g/min for every 1mmHg increase in PaCO2 (correct)
  • No effect on CBF

    • What is the primary mechanism by which hypoxia leads to vasodilation?

    <p>Activation of ATP-dependent K+ channels</p> Signup and view all the answers

    What is the normal range of Intracranial Pressure?

    <p>5-15mmHg</p> Signup and view all the answers

    What is the primary function of the rostral ventrolateral medulla in regulating Cerebral Blood Flow?

    <p>Monitoring oxygen levels in the brain</p> Signup and view all the answers

    What is the gold standard for measuring Intracranial Pressure?

    <p>Intraventricular catheter</p> Signup and view all the answers

    What is the primary goal of autoregulation in maintaining Cerebral Blood Flow?

    <p>Maintaining a constant CBF despite changes in CPP</p> Signup and view all the answers

    What is the effect of increased venous pressure on Intracranial Volume?

    <p>An increase in Intracranial Volume</p> Signup and view all the answers

    What is the primary mechanism by which CO2 affects Cerebral Blood Flow?

    <p>Undergoes carbonic anhydrase reaction to form H+ ions</p> Signup and view all the answers

    Which cranial nerve arises from the superior part of the spinal cord?

    <p>CN XI</p> Signup and view all the answers

    What is the primary function of the Vagus Nerve (X)?

    <p>75% of all parasympathetic activity</p> Signup and view all the answers

    Which of the following glial cell subtypes is responsible for repairing neurons?

    <p>Microglia</p> Signup and view all the answers

    What is the primary function of the Blood-Brain Barrier?

    <p>Keeping the brain environment in homeostasis</p> Signup and view all the answers

    Which cranial nerves are responsible for parasympathetic output?

    <p>CN III, CN VII, CN IX, and CN X</p> Signup and view all the answers

    What is the approximate ratio of glial cells to neurons in the CNS?

    <p>5:1</p> Signup and view all the answers

    What is the effect of volatile anesthetics on cerebral blood flow in normal tissue?

    <p>Increase</p> Signup and view all the answers

    Which volatile anesthetic agent is classically considered to be the agent of choice in neuroanesthesia?

    <p>Isoflurane</p> Signup and view all the answers

    What is the effect of nitrous oxide on cerebral blood flow and cerebral metabolic rate?

    <p>Increase CBF, increase CMR</p> Signup and view all the answers

    What is the concern when using nitrous oxide in neuroanesthesia?

    <p>Closed intracranial gas space</p> Signup and view all the answers

    What is the beneficial effect of benzodiazepines in neuroanesthesia?

    <p>Anxiolytic, anticonvulsant, and amnestic effects</p> Signup and view all the answers

    What is the advantage of opioid-based anesthetic techniques in neuroanesthesia?

    <p>Hemodynamic stability and predictable emergence</p> Signup and view all the answers

    What is the effect of volatile anesthetics on cerebrovascular resistance?

    <p>Decrease</p> Signup and view all the answers

    What is the effect of isoflurane on cerebral metabolic rate?

    <p>Decrease</p> Signup and view all the answers

    What is the central concept of ischemic damage?

    <p>Reduced energy necessary to produce adequate amounts of ATP</p> Signup and view all the answers

    What is the result of ischemia on ATPase ion pumps?

    <p>They begin to fail</p> Signup and view all the answers

    What is the primary effect of increased Ca++ in ischemic neurons?

    <p>Structural damage to neuronal membranes</p> Signup and view all the answers

    What is the result of neuronal membrane destabilization?

    <p>Release of fatty acids</p> Signup and view all the answers

    What is the effect of increased prostaglandins and leukotrienes on neuronal membranes?

    <p>Increased permeability</p> Signup and view all the answers

    What is the effect of a preexisting high serum glucose on ischemia?

    <p>It accelerates the process</p> Signup and view all the answers

    What is the innermost region of ischemia characterized by?

    <p>Membrane destruction and neuronal death</p> Signup and view all the answers

    What is the CBF threshold for functional impairment in the penumbra region?

    <p>Less than 20ml/100g/min</p> Signup and view all the answers

    What is the mechanism by which barbiturates decrease CMR?

    <p>Potentiating GABA activity</p> Signup and view all the answers

    What is the effect of barbiturates on ischemic areas of the brain?

    <p>Redirecting blood flow to the area</p> Signup and view all the answers

    What is the primary mechanism by which propofol decreases CBF and CMR?

    <p>Preserving cerebral autoregulation</p> Signup and view all the answers

    What is the effect of etomidate on CBF and CMR?

    <p>Decreases CBF and CMR</p> Signup and view all the answers

    Which volatile anesthetic produces the greatest decrease in CMR?

    <p>Isoflurane</p> Signup and view all the answers

    What is the effect of volatile anesthetic agents on CBF?

    <p>Increase CBF in a dose-related manner</p> Signup and view all the answers

    Which barbiturate is known to produce excitatory phenomena?

    <p>Methohexital</p> Signup and view all the answers

    What is the effect of propofol on ICP?

    <p>Decreases ICP</p> Signup and view all the answers

    Meperidine is commonly used in neuroanesthesia because of its minimal effects on CBF and CMR.

    <p>False</p> Signup and view all the answers

    Ketamine is known to decrease CBF and CMR.

    <p>False</p> Signup and view all the answers

    Atracurium has minimal histamine release compared to other nondepolarizing muscle relaxants.

    <p>False</p> Signup and view all the answers

    Vasodilators can decrease ICP by reducing CBF.

    <p>False</p> Signup and view all the answers

    Succinylcholine is commonly used in neuroanesthesia without any precautions.

    <p>False</p> Signup and view all the answers

    Study Notes

    Autoregulation

    • Autoregulation keeps CBF constant despite changes in CPP
    • There are three mechanisms:
      • Myogenic: local effect, intrinsic vascular smooth muscle response to changes in vascular transmural pressures (e.g. increased pressure → constriction)
      • Metabolic: moderate effect, local responses to CO2, O2, H+, and metabolic by-products (e.g. adenosine, lactate, prostaglandins, thromboxane)
      • Neurogenic: larger vessels, cerebral vasculature is innervated by adrenergic, cholinergic, serotonergic, and gabaminergic nerve fibers, with astrocytes playing a role in regulating ion and metabolite concentrations

    Cerebral Metabolism

    • Aerobic metabolism: sufficient O2, oxidative phosphorylation occurs, 1 glucose = 36 ATP
    • Anaerobic metabolism: glycolysis produces only 2 ATP, pyruvate → lactic acid
    • Brain has low levels of glycogen stores
    • ~60% of metabolism supports ionic gradients, primarily through Na-K pumps
    • ~40% supports homeostasis of neurons and glial cells, maintaining membranes and protein synthesis

    Neurovascular Coupling

    • CBF changes proportional to CMR changes
    • CBF can parallel metabolic needs from 20-300ml/100g tissue/min
    • Examples:
      • Increased neuronal activity → glutamate release → synthesis and release of NO (vasodilator)
      • CMR increased by: hyperthermia, seizures, ketamine, N2O
      • CMR decreased by: hypothermia (~6%/°C), anesthetics

    CO2

    • PaCO2 rapidly affects CBF in a directly proportional manner (every 1mmHg of PaCO2 affects CBF by 1mL/100g/min)
    • CO2 readily crosses the blood-brain barrier, but not H+ (which causes vasodilation)
    • CO2 undergoes carbonic anhydrase reaction with water in CSF and cerebral tissues to form H+ ions
    • PaCO2 range of adaptation of CBF is 25-75mmHg
    • PaCO2 effects on CBF are time-limited: CSF adapts to pH changes within 6-8 hours

    O2

    • Changes in PaO2 have minimal effect on CBF at 60-300 mmHg
    • Rapid changes in CBF are seen at PaO2 < 60mmHg
    • Hypoxia → ATP-dependent K+ channel activation → vasodilation
    • The rostral ventrolateral medulla monitors oxygen levels in the brain and responds via neurogenic and local humoral mechanisms to affect CBF

    Integrated Contemporary Model

    • Not specified in the provided text

    Venous Pressure

    • Increases in venous pressure result in decreased venous drainage
    • This increases intracranial volume → increases intracranial pressure (ICP)
    • Two clinically important related concepts:
      • Highlights importance of proper positioning
      • Intrathoracic pressure (cough/PEEP) = ↑ venous pressure

    Intracranial Pressure

    • Intracranial contents contained within the cranial vault (~1500ml)
    • Components:
      • Brain tissue (85%)
      • CSF (10%)
      • Cerebral blood volume (5%)
    • Normal ICP: 5-15mmHg
    • Intracranial hypertension: >20mmHg
    • Crucial in calculating cerebral perfusion pressure (CPP): CPP = [MAP-CVR] - ICP
    • Gold standard measurement is with intraventricular catheter
    • Also measurable via subdural bolt and catheter

    External Ventricular Drain

    • Indications:
      • Acute symptomatic hydrocephalus
      • ICP monitoring
      • Bridge for malfunctioning/infected VP shunts
      • Cerebral "relaxation"
      • Targeted therapies (antibiotics)
    • Sterile management techniques
    • Flushless transducer systems, primed with preservative-free saline, gravity drain
    • Leveled to external auditory meatus
    • Recommendations:
      • Clamp for transport
      • Coordinate with surgeon for intraoperative management
      • Label ports and lines
      • Report and note changes in CSF color, drainage >20mL or 0/hr, line disconnections, or loss of waveform

    Glial Cells

    • Besides neurons, the other primary CNS cell type is glial cells
    • Glial cells are more abundant (5x) and supportive in nature
    • Functions:
      • Maintain ionic environment
      • Modulate action potential conduction
      • Control reuptake of neurotransmitters
      • Repair neurons
    • Glial cell subtypes:
      • Astrocytes
      • Ependymal cells
      • Oligodendrocytes
      • Microglia

    Blood-Brain Barrier

    • The environment of the brain is kept in homeostasis via the blood-brain barrier
    • Central concept of ischemic damage is the reduced energy necessary to produce adequate amounts of ATP
    • Ischemia results in inefficient glycolysis rather than oxidative phosphorylation
    • ATPase ion pumps begin to fail, increasing intracellular Na+, a decrease in K+, and especially Ca++ increases
    • Causes neurons to depolarize and release excitatory neurotransmitters (glutamate) causing further depolarization and allowing more Ca++ to enter via NMDA receptor channels
    • Calcium is the dominant factor in the ischemic damage process

    Pharmacology

    • Barbiturates:
      • Decrease CMR (up to 60%) and CBF in a dose-dependent fashion
      • Decrease CMR by:
        • Reducing Ca++ influx
        • Na+ channel blockade
        • Inhibiting free radical formation
        • Potentiating GABA activity
        • Inhibiting glucose transfer across the blood-brain barrier
      • Facilitate CSF absorption, thus reducing ICP
      • Have anticonvulsant properties, reducing the potential of seizure activity
      • May have free radical scavenging properties
    • Propofol:
      • Similar to barbiturates in producing a dose-dependent reduction in CBF and CMR
      • Decreases CBF and CMR up to ~50%
      • Preserves cerebral autoregulation
      • Decreases ICP > volatile anesthetics
      • Significant anticonvulsant activity
    • Etomidate:
      • Near parallel CBF and CMR changes
      • ~40% reductions with CBF
      • CMR suppression is preferentially focused to the cerebral cortex
      • Myoclonic movements are not epileptic activity, but etomidate does precipitate seizure activity at lower doses
    • Inhalation anesthetics:
      • Decrease CMR in a concentration-dependent manner (up to 50%)
      • Isoflurane produces the greatest decrease in CMR
      • Volatile anesthetic agents are potent cerebrovascular dilators, and increase CBF in a dose-related manner
      • Increases in CBF are greatest with halothane, and least with isoflurane and sevoflurane
      • Appears to be time-limited: 3-6 hours
    • Nitrous oxide:
      • Increases CBF, CMR, and ICP
      • Increases in CBF are also noted when used in combination with volatile agents
      • Additive vasodilating effect of N2O in the presence of a volatile agent
      • Should be avoided when a closed intracranial gas space exists or intravascular air entrainment is a concern

    Blood-Brain Barrier

    • The blood-brain barrier consists of capillary endothelial cells connected by tight junctions and a lipid bilayer membrane that prevents the passage of polar molecules.
    • Astrocytes interpose between capillaries and neurons to aid in maintenance.
    • Lipid-soluble substances pass easily through the blood-brain barrier, while polar molecules require active transport.

    Circumventricular Organs

    • Certain areas of the blood-brain barrier are compromised by the presence of fenestrated capillaries, allowing for increased permeability.
    • These areas, known as circumventricular organs, serve as points of neuroendocrine control.
    • Examples of circumventricular organs include the subfornical organ, subcommissural organ, area postrema, neurohypophysis, and organum vasculosum of the lamina terminalis.

    Cerebrospinal Fluid (CSF)

    • CSF provides cushioning, buoyancy, and an excretory pathway for the CNS.
    • CSF is found in the ventricles, cisterns, and subarachnoid space of the brain and spinal cord.
    • The total volume of CSF is approximately 150ml, with a production rate of 500ml/day.
    • CSF is formed primarily by active transport of Na+ by ependymal cells in the choroid plexus.

    CSF Circulation

    • CSF is ultimately absorbed by the arachnoid villi of the superior sagittal sinus and drains into the venous circulation.
    • The complete turnover of CSF volume occurs approximately 3 times a day.

    Blood-CSF Barrier

    • The blood-CSF barrier is similar to the blood-brain barrier, with endothelial cells connected by tight junctions.
    • Free movement of water and lipid-soluble substances occurs across the blood-CSF barrier.
    • Carrier-mediated active transport is required for glucose, amino acids, and ions.

    Venous Drainage

    • Veins traverse the arachnoid and meningeal layers of the dura mater to flow into the nearest sinuses.
    • Cerebral venous circulation is divided into 2 functional components: the superior sagittal sinus and the inferior sagittal sinus/vein of Galen.

    Arterial Circulation

    • The blood supply to the brain is fed by an anterior and posterior circulation.
    • The anterior circulation arises from the aorta and is fed by internal carotid arteries.
    • The posterior circulation arises from the subclavian artery and is fed by vertebral arteries.

    Circle of Willis

    • The circle of Willis is a critical structure that allows for redundancy in cerebral blood flow.
    • The circle of Willis is formed by the convergence of the anterior and posterior circulations.

    Neurophysiology

    • The brain relies on a steady supply of oxygen and glucose, with a disproportionately high degree of blood flow.
    • Gray matter has a greater requirement of blood flow than white matter.
    • Cerebral blood flow is adaptive to avoid fluctuations and pauses in supply.

    Regulation of Cerebral Blood Flow

    • Regulation of cerebral blood flow is managed by several determinants of flow-metabolism coupling.
    • These determinants include cerebral perfusion pressure, autoregulation, venous pressure, and extrinsic mechanisms such as gas tensions and temperature.

    Cerebral Metabolism

    • Aerobic metabolism is the primary source of energy for the brain, with anaerobic metabolism occurring in times of insufficient oxygen.
    • The brain has low levels of glycogen stores and relies on a constant supply of glucose.
    • Neurovascular coupling ensures that changes in cerebral metabolism are accompanied by proportional changes in cerebral blood flow.

    CO2 and O2

    • PaCO2 rapidly affects cerebral blood flow in a directly proportional manner.
    • CO2 readily crosses the blood-brain barrier, but not H+ ions.
    • Changes in PaO2 have a minimal effect on cerebral blood flow at 60-300 mmHg.

    Intracranial Pressure

    • Intracranial pressure is determined by the volume of intracranial contents, including brain tissue, CSF, and cerebral blood volume.
    • Normal intracranial pressure is 5-15 mmHg.
    • Increased intracranial pressure can result in decreased cerebral perfusion pressure.

    External Ventricular Drain

    • External ventricular drains are used to monitor intracranial pressure and drain CSF.
    • Indications for external ventricular drains include acute symptomatic hydrocephalus, ICP monitoring, and bridge for malfunctioning/infected VP shunts.
    • Sterile management techniques and flushless transducer systems are used to minimize the risk of infection.

    Pharmacology

    • Barbiturates decrease cerebral metabolism and cerebral blood flow in a dose-dependent fashion.
    • Barbiturates may have free radical scavenging properties.
    • Propofol, etomidate, and inhalation anesthetics also decrease cerebral metabolism and cerebral blood flow.
    • Ketamine has a unique effect on cerebral physiology, increasing cerebral blood flow and metabolism.

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