Central Nervous System

Zalak Patel, MBBS

Anesthesiology and Perioperative Medicine
Medical College of Georgia
Augusta University
2016
Cerebral Blood Flow
• Cerebral blood flow is 20% of the cardiac output and
averages 50 mL/100 g/min (gray matter 80%, white
matter 10-20%)
• Brain is normally responsible for 20% of total body O2
consumption CMRO2 = 3-3.5 m/100 g/min (50 mL/min)
in adults
• Interruption of CBF causes unconsciousness in 10 sec.
If blood flow is not restored within 3-8 min, irreversible
damage will occur
Cerebral Perfusion Pressure
• CPP = (MAP – RAP or ICP) = 100 mmHg
• Autoregulation serves to achieve constant CBF independent
of MAP over a range of 50-150 mmHg
• CBF < 20-25 mL/100 g/min (CPP <50 mmHg) –cerebral
impairment, as evidenced by slowing on EEG
• CBF 15-20 mL/100 g/min (25-40 mmHg) – flat (isoelectric)
EEG
• CBF <10 mL/100 g/min (sustained CPP <25 mmHg) –
irreversible brain damage
• Normal ICP = 8-12 mmHg; >30 mmHg will compromise CPP
• CSF production = 21 mL/hr (500 mL/day), yet total volume of
CSF = 150 mL
Effect of Temperature, Glucose
• Temperature increases CBF and CMR at 7%/°C
• At 20 °C, EEG becomes isoelectric, but further
decrease continues to reduce CMR throughout brain
• Acute sustained hypoglycemia is equally as
devastating as hypoxia
• Paradoxically, hyperglycemia can exacerbate global
hypoxic brain injury by accelerating cerebral acidosis
and cellular injury
Carbon Dioxide
• Most potent regulator of CBF
• Hyperventilation remains one of the fastest therapeutic
maneuvers to decrease cerebral blood volume (CBV)
• At PaCO2 of 25-65 mmHg, for each 1 mmHg increase
of CO2, there is an increase of 1-2 mL/100 g/min of
CBF (3% of baseline change)
Carbon Dioxide
• PaO2 less than 50 mmHg will increase the CBF
profoundly
• At PaO2 >300 mmHg, vasoconstriction occurs
• Optimal O2 delivery appears to occur at hematocrit of
30-34% range
• Anemia increases CBF via high CO, CPP, and low
viscosity, as well as induced cerebral vasodilation
Anesthetics and Cerebral Function
• Suppression of CMR (exceptions: ketamine and
nitrous oxide [N2O])
• Increasing plasma concentrations of Inhaled
anesthetics (sevoflurane, desflurane, isoflurane), IV
agents (barbiturates, propofol, etomidate) cause
progressive suppression of EEG activity and reduction
in CMR of O2 (CMRO2)
• Maximum reduction (50-60%) occurs with isoelectric
EEG. However EEG suppression produced by the
anesthetic is influenced by agent used
Anesthetics and Cerebral Function
• Barbiturates – at isoelectric EEG there is a uniform
depression in CBF and CMR throughout the brain
• With isoflurane, the relative reduction in CBF and CMR are
greater in the neocortex than in other portions of cerebrum
• All inhaled drugs including N2O have intrinsic cerebral
vasodilatory activity due to direct effect on vascular smooth
muscle
• Net effect on CBF is a balance between augmentation of
CBF due to vasodilatory effect and reduction in CBF due to
suppression of CMR
Effect of Inhaled Anesthetic Drugs
on CBF
• At 0.5 MAC, CMR suppression predominates and CBF
decreases compared to awake state
• At 1 MAC, CBF remains unchanged; suppression and
vasodilatory effects are balanced
• At >1 MAC, vasodilatory effect predominates and CBF
increases significantly even though CMR is suppressed
largely as well (uncoupling of flow and metabolism)
Inhalation Agents and CMR
• All of the volatile agents depress CMR to varying
degrees in a nonlinear fashion
• For most agents, after an isoelectric EEG, no further
decrease in CMR occurs
• Isoflurane abolishes EEG activity at clinically tolerated
doses (around 2 MAC); sevoflurane and desflurane are
similar to isoflurane
Inhalation Agents and CMR
• Critical CBF – blood flow at which EEG evidence of
cerebral ischemia develops – is significantly lower with
isoflurane than halothane (10 mL/100 g/min vs 18-20
mL/100 g/min)
Nitrous Oxide
• Increase in CBF, CMR (partly due to increased
sympathetic activity) and ICP
• N2O administered alone – substantial increase in CBF
and ICP can occur
• N2O + IV anesthetics – vasodilating effect is attenuated
or abolished
• N2O + volatile agents – moderate increase in CBF
• CO2 responsiveness is preserved during N2O
administration
Xenon
• Administration of 1 MAC of xenon – decrease in CBF
(15% reduction in cortex and 35% in cerebellum)
• Parallel reduction in CMR
• Cerebral autoregulation and CO2 reactivity are
preserved
• Xenon expands air-containing spaces, however,
magnitude of expansion is considerably less than with
N 2O
Intravenous Agents
• Barbiturate – decreases CMR and CBF until isoelectric
EEG appears (= maximum of 50-60% reduction in CMR at
this point) and additional doses of barbituate do not further
reduce CMR
• Propofol – similar to barbiturate; reduces CBF more than
reduction in CMRO2
• Etomidate – similar effect; CMR suppression in forebrain
• Methohexital – small doses may activate seizure; large
doses have anticonvulsant properties
• Benzodiazepine – reduces CMR and CBF (not as
pronounced as with barbiturate). Amount of reduction is
probably intermediate between narcotics and barbiturates
Intravenous Agents
• Flumazenil – reverses the CMR, CBF, and ICP lowering
effect of midazolam; use cautiously with high ICP
• Opioids – may cause minor reduction in or no effect on
CBF and CMR
• Morphine – may release significant amount of histamine –
can cause increase in CBV, CBF (depending on blood
pressure effect) because histamine is a cerebral
vasodilator
• Dexmedetomidine – appears to preserve flow-metabolism
coupling in healthy volunteers
Intravenous Agents
• Ketamine – increases CBF and CMR. However, other
anesthetic drugs (midazolam, propofol, isoflurane) appear
to blunt the increase in ICP or CBF associated with
ketamine
• Lidocaine – a bolus dose (1.5 mg/kg) helps to prevent and
treat increase in ICP with endotracheal suctioning
– Larger doses (>2 mg/kg) can cause seizures; therefore,
restrict dose
– Lidocaine produces dose-related reduction in CMRO2
Blood Brain Barrier
• Impedes flow of ions such as K, Ca, Mg, Na; polar
substances such as glucose, amino acids, mannitol;
and macromolecules like proteins
• Uses active or passive (facilitated diffusion-
concentration dependent) transport
• Lipid-soluble substances, i.e., CO2, O2, volatile
anesthetics and water pass rapidly
Pathway for CSF Circulation
Lateral ventricles

intraventricular foramen of Monro

Third ventricle
aqueduct of Sylvius

Fourth ventricle (foramen of Luschka)
and lateral aperture (foramen of Magendie)

Cerebral medullary cisterns (cisterna magna
Determinants of ICP
• CSF primarily formed by transport of Na, Cl, HCO3 +
osmotic movement of water
• Furosemide (inhibits Na/Cl transport), acetazolamide
(reduces HCO3 by inhibiting carbonic anhydrase) 
reduce CSF formation
• CSF absorption – Arachnoid villi  venous system
(one-way flow)
• Brain is enclosed in cranium, a bony structure which
has a fixed volume. Therefore, increase in volume of
any of its contents will increase ICP
Changes in PaCO2, CBF, and CSF pH with prolonged
hyperventilation
• Decreased PaCO2 and systemic alkalosis persist for the
duration of hyperventilation
• pH of the brain and CBF return to normal over 8-12 hr
• Vessel caliber returns to baseline
Neuromonitoring by EEG
Neuromonitoring by EEG
Neuromonitoring by EEG
Neuromonitoring by EEG
Other physiologic variables can alter SSEPs
• Hypothermia – increases latency
• Hypotension – MAP <40 decreases amplitude
• Hypoxia – decreases amplitude
• Hypocarbia – end-tidal CO2 <25 increases latency
• Isovolemic hemodilution – Hct <15% increases latency

When body temperature falls to <35 °C, there is progressive

slowly of EEG activity – complete electrical silence at 15-20°C