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Neuro Red Memorize Material Flashcards

1
Q

CBF normal

A

CBF-50ml/100 gm/ min (750 ml/min)

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2
Q

CBF % of CO

A

15-20% of cardiac output

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3
Q

CBF impaired values

A

CBF <20-25
cerebral impairment/slowing EEG
CBF < 15-20
isoelectric EEG
CBF <10
irreversible brain damage

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4
Q

Cerebral Autoregulation & CBF

A

The brain normally tolerates wide swings in blood pressures with little change in blood flow…like the heart /kidneys
Changes in flow result in vasodilatation & vasoconstriction to maintain flow
*In the normal brain
CBF remains with MAP 50 - 150

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5
Q

CBF & PaCO2 tensions

A

CBF is directly proportionate to PaCO2 between tensions of 20 - 80 mmHg

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6
Q

CBF changes per PaCO2 changes

A

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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7
Q

critical oxygen tension & CBF

A

when O2 falls below 50 mmHg, rapid increase in CBF and arterial blood volume

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8
Q

Brain Tissue Oxygen Monitoring Systems
Critical Thresholds:

A

Goal: above 20-25 mmHg
Brain Oxygen <20 mmHg = cerebral ischemia
Brain Oxygen >50 mmHg = Luxury Perfusion
Local area of cerebral hyperemia or increased cerebral blood flow
Hyperemia may contribute to brain swelling & we can adjust therapies…

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9
Q

CPP and ICP

A

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

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10
Q

CPP low values and EEG

A

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

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11
Q

CPP autoreg

A

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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12
Q

CPP and brain injury

A

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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13
Q

CPP is a…

A

Maintaining CPP is a cornerstone of modern brain injury therapy

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14
Q

CPP and mortality

A

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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15
Q

CPP & MAP

A

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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16
Q

CBF values (again)

A

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

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17
Q

CPP abnormal values

A

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

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18
Q
A

A - ICP
B – PaCO2
C – CPP
D – PaO2

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19
Q

Monro Kellie Hypothesis

A

INCREASE in the volume of any ONE requires a corresponding DECREASE in the other TWO components

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20
Q

Cushings Triad

A
  1. HTN
  2. Bradycardia
  3. Resp disturbances
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21
Q

CSF volume flow and photo

A

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

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22
Q

CSF Dynamics - how much in body, produced amnt, where produced, and eliminated

A

100-160cc in the body
500cc produced q 24 hours
Production: Choroid plexus
**Elimination/Reabsorbed: ** Arachnoid villi
Effects of drugs: Enflurane/Lasix

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23
Q

Hyperventilation

A

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

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24
Q

Inverse Steal or Robin Hood Phenomenon

A

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

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25
VA and Coupling
VA **alter** the normal coupling of CBF & CMR The combination of a 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
26
VA and coupling - blood flow changes
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 CBF in normal areas of the brain but not in ischemic are, where arterioles are already maximally dilated AKA: **Vasomotor paralysis**
27
cbf change per temp change
**CBF changes 5-7% per C**
28
cbf changes with hyperthermia
Hyperthermia - increases CBF & CMR At 42 degrees C - O2 activity begins to decrease & may reflect cell dam
29
CBF changes with hypothermia
Hypothermia - decreases CBF & CMR Decreases CMR by 6-7% per degree Celsius w/proportional decrease in CBF At 20 degrees C - EEG = isoelectric
30
hypothermia and normo
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.
31
IHAST2 trial conc.
**Conclusions**: Intraoperative hypothermia did not improve the neurologic outcome after craniotomy among good-grade patients with aneurysmal subarachnoid hemorrhage.
32
Mannitol Dose
Initial: 0.25 - 1 g/kg over 30 min Repeat: serum osmolality of 320mOsm/L 20% mannitol
33
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)
34
Factors that may predict a higher postoperative morbidity rate:
patient-related factors advanced age comorbid states: DM/CAD/Altered LOC Tumor factors location / size / vascularity of tumor neural involvement prior surgery &/or radiotherapy
35
midline shift
Midline shift** > 5 mm and/or encroachment on CSF cisterns** suggest intracranial hypertension Avoid preop pharmacologic sedation and ventilatory depression
36
inverse steal
Inverse Steal/Robin Hood Phenomenon- Vasoconstriction of normal vessels but not in ischemic areas (d/t vaso motor paralysis). This is one reason we hyperventilate pts. w/ tumors and increased ICP.
37
luxury perfusion
Luxury perfusion- **BAD**-Perfusion in excess of metabolic needs. Vasodilatation to surrounding tissues. AKA Circulatory/Cerebral Steal phenomenon- localized ischemic areas are already maximally dilated . It you further dilate surrounding vessels, you "steal" blood flow to other areas of the brain away from the ischemic area...
38
N2O
Effects are generally mild & easily overcome by other agents or changes in CO2 tension… Combined with other IV agents: N2O has minimal effects on CBF, metabolic rate, & ICP **Controversial**... **Adding** Nitrous Oxide to a VA, can further increase CBF When given **alone**, mild cerebral vasodilatation with the potential to increase ICP
39
Ketamine
Generally **increases** CMRO2 & CBF **If **PaCO2 maintained normal in presence of elevated ICP or cerebral trauma, then ketamine does not adversely alter CBF or ICP
40
Post crani emesis
Occurs in approximately **50%** of patients Appears to be largely prevented by ondansetron 4mg administered near the time of dural closure…
41
induction
STP, propofol, or etomidate **Prompt induction **without ICP elevation Muscle relaxant to facilitate endotracheal intubation & mechanical hyperventilation (BEWARE: coughing causes marked increases in ICP) Succinylcholine does not significantly alter CBF or ICP in patients with neurological injury…
42
Mayfield Pin Placement BP increase
Goal: Not to have large hemodynamic swings in blood pressure. with insertion & then after due to the fact you administered a longer acting agent and now there is “down time”… No one way is “perfect” Know that your SBP will predictably **rise** ~40mmhg
43
pin placement timing
Therefore need to lower b/p… Do **NOT** let them start until you do this… AND do **NOT** lower the b/p **UNTIL they have pins in hand ready to go…** What does the evidence reveal & what do I do…
44
research and pin placement
“The effect of skull-**pin** insertion on cerebros**pin**al fluid pressure and cerebral perfusion pressure: influence of sufentanil and fentanyl” Conclusion: In anesthetized patients, an intravenous bolus of fentanyl(4.5 mcg/kg) or sufentanil (0.8mcg/kg) prior to skull-**pin** insertion results in stable values of CSFP, CPP, BP, and HR... The b/p was modified with phenylephrine / atropine were indicated
45
pin placement and meds
Minimum of 4 mcg/kg Fentanyl Titrate Iso to **NO** more than 1.0 MAC Propofol 1mg/kg, titrated to response Esmolol/Ntg – Only if necessary Lower SBP by ~40mmg Consider Lidocaine* **PIN Placement** Lower Iso, Propofol, NTG effects gone… B/P Normalizes
46
neuro positioning
Positioning…100% fio2 Ett/IV can dislodge monitor vitals closely can take longer than you think... Position depends on tumor location Supratentorial: supine Infratentorial: prone or **sitting** (BEWARE: greatly increases risk of **venous air embolism**)
47
Reasons for Mannitol & Importance of **“Perfect Timing”**
Mannitol reduces brain bulk by creating an osmotic gradient across the “intact”blood brain barrier causing water to flux from the extracellular extravascular to intravascular compartments. There also is evidence that mannitol improves deformability of red blood cells, thereby reducing viscosity promoting increased blood flow.
48
mannitol timing
Mannitol is best given **PRIOR** to the time of skin incision (typically 0.5 mg/kg) so the peak effect becomes available upon dural opening. Additional mannitol may be of value if the brain is still "tight".
49
what is common with mannitol if __ and __ are not repleted?
If F & E are not repleted with diuresis **Hypokalemia** ensues…VERY COMMON in neurosurgery… 5.Transient Hyponatremia & decrease in hgb concentration (acute hemodilution) VERY COMMON Refer to Handout related to Mannitol
50
Posterior Fossa Crani
51
VAE best non-invasive detection?
Precordial Doppler ultrasound near right upper sternal border is **most sensitive non-invasive monitor (**detects 0.25 ml)
52
VAE - invasive and most sensitive?
trans-esophageal echocardiography is most **sensitive**, but more **invasive** and cumbersome then doppler, "mill-wheel" murmur
53
VAE S&S
sudden decrease in ETCO2, increase in ETN2 , increase in PAP’s hypoxemia, hypotension, dysrhythmias
54
where is the pituitary gland located?
These benign lesions originate from the cells of the pituitary gland, which is located in the **Sella turcica **- behind nose and ethmoid
55
most common secreting tumor
The most common type of secreting tumor is the **prolactin** tumor
56
pituitary tumor resection
**DO NOT** treat like other tumors (space occupying lesions) Normovolemic, normotensive, normocapnic Do not shrink brain. A full brain will push tumor down to surgeon-GOOD
57
circle of willis
58
cerebral aneurysm size and occurance
Cerebral aneurysms can by classified according to size in: Small. If less than 12 mm in diameter** (78 %) ** Large. From 12 to 24 mm in diameter **(20 %) ** GIANT. If more than 24 mm in diameter** (2 %) **
59
cerebral vasospasm
occurs generally 3-4 days after bleed **major cause of morbidity **
60
Cerebral Vasospasm symptoms
diagnosis transcranial Doppler positive before symptoms: worsening headache hypertension
61
aneurysm coiling anesthesia plan
**A-line PRE- INDUCTION** CVP as indicated Triple H therapy may be used postop Neurologic Monitoring SSEP’s & BAER’s are useful for posterior circulation aneurysm
62
aneurysm coiling induction plan
REBLEEDING IS LETHAL Careful B/P control Weigh risk of full stomach vs adequate depth of anesthesia & relaxation Titrate induction agent Blunt response to intubation Fentanyl LTA
63
giant aneurysm considerations - size and hypothermia levels
GIANT = > 24mm Hypothermic Circulatory Arrest Mild Hypothermia: Core Temp down to 33C Moderate Hypothermia: 32.5-33C Deep Hypothermia: to 18C-Permits the brain to tolerate up to 1 hour of circulatory arrest Profound hypothermia:<10C-Allows several hours of complete ischemia Review article: “Anesthetic Management of Deep Hypothermic Circulatory Arrest for Cerebral Aneurysm Clipping” Anesthesiology: Volume 96(2) February 2002 pp 497-503
64
AVM's
Arteriovenous malformations (AVMs) complex tangles of dilated, thin-walled blood vessels. O2-ated blood is pumped by the heart to arteries to capillaries = nourished tissues De-O2ated blood passes back via veins AVM’s **LACK** the tiny capillaries

Concepts 3 (12 decks)

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