Neuro Anesthesia Part 1 (VanPelt) Flashcards by Julianne Fitzgerald

Goals for Neuroanesthesia

Anesthesia-Analgesia-Amnesia AKINESIS
Oxygen to the neuron
Surgical exposure
Minimize surgical retraction
+/- Neurophysiological monitoring
Rapid Emergence

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Components of getting oxygen to the neuron

Supply = Deliver oxygenated blood under adequate pressure and cardiac output (CPP)
Demand = Decrease the demand of oxygen (CMO2)
**Protection **= Improve ability to tolerate low oxygen states (Neuroprotection)

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The Cranial Vault =

Brain 80%
Blood 12%
CSF 8%

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What are some anesthesia goals for neurosurgery driven by the surgeon?

Wake up on a dime
Follow commands
They think cough=extubation
They want the SBP greater than 120mmHg
BUT less than 140mmHg…

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Volume and Flow

volume does not equal flow

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What are some elements of flow that impact ICP?

ml/100g/B/min
metabolic demands
chemical elements
local mediators

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What are the determinants of volume?

Arterial blood pressure - ABP
Cerebral blood flow - CBF
Cerebral perfusion pressure - CPP
Cerebral vascular resistance – CVR
Arterial carbon dioxide levels - PaC02
Arterial oxygen Tension – PaO2
Cerebral metabolic rate – CMR

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What is the normal or ideal CBF?

CBF = 50ml/100 gm/ min (750 ml/min)
15-20% of cardiac output

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CBF < 20-25 ml/100gm/min = _____

cerebral impairment/slowing EEG

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CBF < 15-20 ml/100gm/min = _____

isoelectric EEG

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CBF < 10 ml/100gm/min = _____

irreversible brain damage

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In the normal brain, changes in flow result in ____.

Changes in flow result in vasodilatation & vasoconstriction to maintain flow
*In the normal brain
CBF remains with MAP 50 - 150

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CBF and MAP relationship chart

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CBF is directly proportionate to PaCO2 between tensions of _____

20-80 mmHg

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Blood flow changes with PaCO2 changes

Blood flow changes approximately 1-2 ml/100g/min per mm hg change in PaCO2
This effect is immediate & is thought to be secondary to changes in pH of CSF & cerebral tissue

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Arterial Oxygen Tension

Low arterial oxygen tension has profound effects on cerebral blood flow

When it falls below 50 mmHg (6.7 kPa) rapid INCREASE in CBF and arterial blood volume

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Oxygen to the neuron

What is the perfusion pressure under the retractor?
What is going on under the retractor?
In order to know that what do we need to know?
What is the under the retractor…

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Cerebral Perfusion Pressure

CPP normal = 70-100 mmHg
Since ICP is normally <10 mmHg, CPP is largely dependent on MAP
However, moderate to severe increases in ICP** ( > 30 mmHg) **can significantly compromise CPP & CBF even in the presence of normal MAP

CPP = the pressure gradient driving cerebral blood flow (CBF)
hence oxygen and metabolite delivery

The NORMAL brain autoregulates its blood flow to provide a constant flow regardless of blood pressure by altering the resistance of cerebral blood vessels

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CPP values

CPP** < 50 mmHg** - Slowing of EEG
CPP **25-40 mmHg **- Flat EEG
CPP < 25 mmHg - Irreversible brain damage

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CPP & Brain Injury

These homeostatic mechanisms are often lost
CVR is usually increased
The brain becomes susceptible to changes in b/p!
Ischemic brain regions or those at risk of ischemia are critically dependent on adequate cerebral blood flow thus CPP

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Maintaining CPP - mortality

Maintaining CPP is a cornerstone of modern brain injury therapy…

Mortality increases approximately 20% for each 10mmHg loss of CPP
In those studies where CPP is maintained above 70mmHg:
The reduction in mortality is as much as 35% for those with severe head injury

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Maintaining CPP

CPP may be maintained by raising the MAP or by lowering the ICP.
In practice ICP is usually controlled to within normal limits (<20mmHg) and MAP is raised therapeutically
It is unknown whether ICP control is necessary providing CPP is maintained above the critical threshold

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If b/p =96/50 (MAP= 60) CVP = 4 - whats the CPP?

**CPP = MAP - CVP OR MAP-ICP depends on which # is higher

60 - 4 = 56

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CBF & CPP values

Normal CBF = 50 ml/100g/min
CBF <20-25: Cerebral Impairment/Slowing of EEG
CBF < 20: Isoelectric EEG/Irreversible brain damage

**Normal CPP: 70-100 **
CPP < 50 mmHg: Slowing of EEG
CPP <25-40 mmHg: Flat EEG
CPP < 25 mmHg: Irreversible

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Graph trends

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Cranial Vault %’s

80% Brain
12% Blood
8% CSF

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Determinants of ICP - Monro Kellie Hypothesis

Increase in the volume of ONE requires a corresponding decrease in the volume of the other TWO components.

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Dr. Cushing & Anesthesia

Largely responsible for the development of the anesthesia record (1905)
Out of concern for the safety of his patients, he emphasized the need to record the surgical patient’s pulse, RR, temp, & B/P

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Cushing Triad

Hypertension
Bradycardia
Respiratory disturbances

*Late & unreliable sign that usually precedes brain herniation

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Cushing Triad

Hypertension
Bradycardia
Respiratory disturbances

*Late & unreliable sign that usually precedes brain herniation

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ICP : Skull Contents

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Brain Shrinkage (3 ways)

Decrease CSF Volume: with lumbar drain, shunt, or loop diuretics
Decrease Intracranial blood volume: hyperventilation, IV agents (mannitol) burst suppression, hypothermia
Decrease brain cell volume: osmotic duretics, and dehydration/avoid free water

**CSF Flow

Lateral Ventricle
Foramina of Monro
Third Ventricle
Cerebral aqueduct of Sylvius
Fourth Ventricle –>
Foramen of Magendie (medial)
Foramen of Luschka (lateral)
Cisterna Magna
SA Circulation
Absorbed in the arachnoid granulations over the cerebral hemispheres

memorize

The mnemonic is

Lady Monroe’s Three Siblings Fought, for Magical Lights Seeing Arrogant Seniors

CSF Dynamics - how much, made, etc.

100-160cc in the body
500cc produced q 24 hours
Production: Choroid plexus
Elimination/Reabsorbed: Arachnoid villi
Effects of drugs: Enflurane/Lasix: decreases reabsorption, therefore, is avoided

CSF Drain

ensure its at proper level, open vs. closed, and NOT on a pressure bag

Diuretics & CSF

Complete inhibition of carbonic anhydrase maximally reduces CSF flow 40-60%
Acetazolamide 30 mg/kg IV (Diamox)
They have found only ~ 20% reduction from control after furosemide at 50 mg/kg
- partial inhibition of carbonic anhydrase of choroid plexus (and perhaps other sites of CSF secretion) based on the affinity of furosemide for carbonic anhydrase

Diamox MOA

Reversible inhibition of the enzyme carbonic anhydrase resulting in reduction of hydrogen ion secretion at renal tubule and an increased renal excretion of sodium, potassium, bicarbonate, and water to decrease production of aqueous humor

Also inhibits carbonic anhydrase in central nervous system to retard abnormal and excessive discharge from CNS neurons

Perioperative Concerns

Neurosurgical patients may be on Acetazolamide preoperatively…
Side effect: Metabolic Acidosis
Duration of the drug: 4-5 hours
Typically corrects itself…

Blood Volume (12%)

Hyperventilation
CMO2 rate in relation to CBF –how we effect the “coupling” of the two
How does temperature effect blood volume?…

Hyperventilation

It has long been known that hyperventilation will decrease intracranial pressure (ICP)

At the beginning of the 1990s, it was widely held that this provided universal therapeutic value

The advent of the oximetric pulmonary artery catheter:
- Allowed investigators to retrogradely cannulate the jugular vein in head trauma patients
- examine venous hemoglobin oxygen saturation in response to therapeutic intervention.

Hyperventilation cont.

In some patients, hyperventilation actually increased brain oxygen deficit.

Presumably was a result of vasoconstriction, which augmented ischemic states

Jugular venous hemoglobin oxygen saturation monitoring has become widely applied in the intensive care unit
***Remains impractical in most operative settings

Perioperatively - Hyperventilation

Without such monitoring, it is impossible to predict in which patients hyperventilation may be detrimental or beneficial
Owing to the observations made in head trauma patients, the use of hyperventilation in the OR has been largely abandoned unless surgical conditions directly dictate additional brain relaxation

Goals with hyperventilation

We do hyperventilate (“mild”)
Goal: Between 30-35
Reasons:
Surgical Exposure (Inverse Steal)
Use of VA
AND Robin Hood effect

Inverse Steal or Robin Hood Phenomenon

Back to hyperventilation:
Decreased PCO2 constricts normal vessels but not the ischemic areas (d/t vasomotor paralysis).

This is one reason we do hyperventilate patients with intracranial tumors and ICP

Cerebral Metabolic Rate

an increase in CMRO2 would be accompanied by an increase in CBF
- CBF is COUPLED to CMRO2
- some drugs and processes cause an UNCOUPLING of CBF and CMRO2 – such as hyperventilation
- INCREASES in metabolism result in DECREASES in vascular resistance, increasing CBF

Effects of anesthetic agents on CMRO2 and CBF

Altered Coupling of CBF & CMO2 - VA

VA alter the normal coupling of CBF & CMR
The combination of a DECREASE in neuronal metabolic demand with an increase in cerebral blood flow (metabolic supply) is termed** luxury perfusion**
May only be desirable during induced hypotension & it supports the use of a VA, particularly Iso, during this technique

Altered coupling - VA w/ ischemia

In contrast to this potentially beneficial effect during global ischemia:
- a detrimental circulatory steal phenomenon is possible with VA in the setting of focal ischemia

VA INCREASES CBF in normal areas of the brain but not in ischemic are, where arterioles are already maximally dilated AKA: Vasomotor paralysis

Circulatory Steal

End result: redistribution of blood flow away from ischemic to normal areas

Volatile Agents that increase CBF

conflicting evidence …
Increases in CBF (from most to least)
- Halothane
- Enflurane
- Isoflurane
- Desflurane

VAgents that decrease CMRO2

decreases in CMRO2
- isoflurane
- halothane
- enflurane

*enflurane at high concentrations cause SZ like activity

VA’s & CBF

VA dilate cerebral vasculature & impair autoregulation in a dose dependent manner
At equivalent MAC & MAC
- Halo increases CBF up to 200%, ENFL up to 40%, Iso (& Des & Sevo) up to 20%
Dose-dependent impairment of autoregulation
- Halo > 1 MAC - cerebral autoregulation abolished

VA and CBF - PCO2 and when does CBF normalize?

Cerebrovascular response to PCO2 is generally preserved
Hyperventilation with use of VA counteracts the increase in CBF
After 2-5 hours of administration of VA (NOT over MAC), CBF begins to normalize

Volatile Anesthetics & CMO2

Reduction in CMR is maximal when EEG becomes isoelectric, unlike hypothermia
Barbiturates produce a dose dependent decrease in CMR & CBF until EEG becomes isoelectric
Iso & Enfl (& Des & Sevo?) reduce CMR by up to 50%
Halothane reduces CMR by less than 25%

CBF & Temperature

Hypothermia - decreases CBF & CMR
Decreases CMR by 6-7% per degree Celsius w/proportional decrease in CBF
CBF changes 5-7% per C
At 20 degrees C - EEG = isoelectric
Hyperthermia - increases CBF & CMR
At 42 degrees C - O2 activity begins to decrease & may reflect cell dam

Unintentional hypothermia

A multinational consortium of investigators was formed to examine the risks and benefits of mild hypothermia in patients undergoing aneurysm surgery.

The International Hypothermia Aneurysm Surgery Trial (IHAST2) was performed over five years

IHAST2

This was believed to be the first prospective, randomized, double-blinded outcome trial with sufficient statistical power to define whether an intervention made by neuroanesthesiologists benefits long-term postoperative outcome.
Until this study is completed, the use of mild hypothermia remains of speculative benefit …

IHAST 2 results & conc.

There were no significant differences between the group assigned to intraoperative hypothermia & the group assigned to normothermia in the duration of stay in the intensive care unit, the total length of hospitalization, the rates of death at follow-up or the destination at discharge.

Conclusions: Intraoperative hypothermia did not improve the neurologic outcome after craniotomy among good-grade patients with aneurysmal subarachnoid hemorrhage.

Determinants of ICP - Parenchymal Volume

Cerebral Edema:
- Cytoxic: bad NA/K pump
- Vasogenic: leaky capillaries
- Osmotic

Shrinking of brain cell:
- mannitol
- lasix

avoid iatrogenic increase in brain volume d/t hypotonic crystalloids

Mannitol - mechanisms

Mechanisms:
- intravascular compartment hypertonic relative to intracelebral fluid
- requires intact cell membranes*
- Osmotically active diuretic
Major effect is to increase water excretion, in large doses, osmotically active diuretics also increase NA & K excretion
100ml of H2o is expected to be removed from the brain

Mannitol - doses

Dose:
- Initial: 0.25-1 gram/kg over 30 min
- repeat: serum osmolality of 320 mOsm/L
- 20% Mannitol: Know How To Calculate Dose!!!

Mannitol - timing

admin with skin incision or dural opening, depending on hospital
- theoretical risk of aneurysm rupture

mannitol - complications

Raises CVP
dehydration
brain swelling
rebound
aneurysm rupture

Shrink the brain cell

mannitol
lasix

avoid iatrogenic increase in cell size:
hypotonic crystalloids
large, sudden bolus’ of fluids

Brain capillary

Peripheral Capillary

Osmolarity of 0.9% NS and LR

0.9% NS: osmolarity 308 mOsmol/L
LR: 273 mOsmol/L

Choice of crystalloid & why

Most of the formal logic for prohibiting the use of glucose-containing solutions still depends on studies performed in animals

The near universal observation that hyperglycemia worsens outcome in models of ischemia and trauma has been supported by a large number of correlative human studies that indirectly provided similar conclusions

In the Neurosurgery patient there may be a rise in blood glucose for various reasons… As in any illness or injury, a relative resistance to insulin effect with a decrease in glucose consumption in brain and muscle that can occur.

High glucose levels together with the failure of oxidative glucose metabolism combine to produce excess lactate, which may account for poor neurological outcome…

Glucose containing solutions

Plasma glucose threshold values of greater than 180 mg/dL are consistent in both animal and human studies for predicting worsened outcome

Remember, these patients may be on steroids preoperatively and have an elevated glucose to begin with

Check glucose routinely

Tonicity of Dextrose Solutions

D5W = 253 = Hypo
D5 1/4NS = 355 = Iso
D51/2NS = 432 = Hyper
D5NS = 586 = Hyper
D5LR = 525 = Hyper

Lactate containing solutions

Tonicity = 273 = Iso

Actually can be considered slightly hypotonic because it provides approximately 100ml of free water per liter

The lactate in this solution is converted by the liver into bicarbonate

In the event of ischemia, lactate is readily available for anaerobic metabolism & will worsen ischemic event
No more than 1L

Excess NSS solution

Dilutional hypercholemic acidosis
High chloride content (154 meq/L) & HCO3 free
Presentation: Metabolic acidosis

Hyperchoremic Metabolic Acidosis

Need to determine the Anion gap
Anion gap = Major plasma cations - Major plasma anions
Anion Gap = NA - Cl + HCO3
Normal 140 - (104 + 24) =12 ( 9-15 meq/L)

Causes of Metabolic Acidosis - increased anion gap

Renal failure
Ketoacidosis
Lactic acidosis
Ingestion of toxins
Rhabdomyolysis

causes of metabolic acidosis - normal anion gap

Normal Anion Gap (Hyperchoremic)
Increased GI losses of HCO3
Increased renal losses of HCO3
TPN
Increased intake of Cl containing solutions
Dilutional
Lg. Amounts of bicarb free fluids

treatment for metabolic acidosis

Depends on the severity
Change IVF
Respiratory component corrected
If pH remains below 7.20, alkali therapy, usually in the form of NaHCO3 (7.5% solution)

Treating base deficit

Dose = 1meq/kg or derived from the base excess
- NaHCO3 = BE x 30% x body weight
- NaHCO3 = -10meq/L x .30 x 70 = 210 meq
- In practice, only 50% of the calculated dose (105) would be given , then perform ABG

Fluid restriction

In the 1980s, it remained standard practice to dehydrate patients with intracranial pathology under the assumption that brain volume would be decreased

This was often performed at the expense of stable hemodynamics and cerebral perfusion pressure.

A large body of laboratory evidence was accumulated that contradicted the logic for fluid restriction.
Accordingly, many practitioners have substantially increased the volume of crystalloid administered during neurosurgical procedures.
Recognition that plasma osmolality should be maintained.

standard practice - fluids

Minimize post-op cerebral edema
Minimal, 1-3 ml/kg/hr
Limit crystalloid to <10 cc/kg + replacement of urine output
Colloid of Choice = Albumin
Hetastarch “OK” but be careful
Blood

Autonomic Influences

Innervated by:
- Sympathetic (Vasoconstrictive)
- Parasympathetic (Vasodilatory)
- Noncholinergic nonadrenergic fibers: serotonin & vasoactive intestinal peptide

The normal physiologic function of this innervation is uncertain but it may play a role in pathologic states…cerebral vasospasm/vasomotor paralysis

so what have we learned?

Maintenance of optimal CPP is critical
ABP should be normal or slightly elevated & increases in ICP or CVP should be avoided
O2 carrying capacity should be maintained…There is always exceptions to the rule
“10/30” rule: UPENN research r/t this concept SAH undergoing an AVM resection

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Neuro Anesthesia Part 1 (VanPelt) Flashcards

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