Neuro Anesthesia Part 1 (VanPelt) Flashcards
Goals for Neuroanesthesia
Anesthesia-Analgesia-Amnesia AKINESIS
Oxygen to the neuron
Surgical exposure
Minimize surgical retraction
+/- Neurophysiological monitoring
Rapid Emergence
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)
The Cranial Vault =
Brain 80%
Blood 12%
CSF 8%
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…
Volume and Flow
volume does not equal flow
What are some elements of flow that impact ICP?
ml/100g/B/min
metabolic demands
chemical elements
local mediators
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
What is the normal or ideal CBF?
CBF = 50ml/100 gm/ min (750 ml/min)
15-20% of cardiac output
CBF < 20-25 ml/100gm/min = _____
cerebral impairment/slowing EEG
CBF < 15-20 ml/100gm/min = _____
isoelectric EEG
CBF < 10 ml/100gm/min = _____
irreversible brain damage
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
CBF and MAP relationship chart
CBF is directly proportionate to PaCO2 between tensions of _____
20-80 mmHg
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
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
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…
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
CPP values
CPP** < 50 mmHg** - Slowing of EEG
CPP **25-40 mmHg **- Flat EEG
CPP < 25 mmHg - Irreversible brain damage
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
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
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
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
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
Graph trends
Cranial Vault %’s
80% Brain
12% Blood
8% CSF
Determinants of ICP - Monro Kellie Hypothesis
Increase in the volume of ONE requires a corresponding decrease in the volume of the other TWO components.
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
Cushing Triad
- Hypertension
- Bradycardia
- Respiratory disturbances
*Late & unreliable sign that usually precedes brain herniation
Cushing Triad
- Hypertension
- Bradycardia
- Respiratory disturbances
*Late & unreliable sign that usually precedes brain herniation
ICP : Skull Contents
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%)
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
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
