Anesthesia For Neurosurgery Barash 37 Flashcards
Basal Ganglia is made of
1-Caudate Nucleus 2-Substantia Nigeria 3-Red Nucleus 4-Globus Pallidus 5- Putamen
Dysfunction if Extrapyramidal System lead to
Parkinson’s
Essential Tremors
Ataxia
Supratentorium contains
1) Paired Cerebral Hemispheres
2) Diencephalon : Thalamus and Hypothalamus
What makes the extrapyramidal system
Basal Ganglia
Cerebellum
Auditory and Vestibular system
Where the diencephalon located
Cephalad to the midbrain
Thalamus role
Sensory and motor Relay station
Connect the cortex and the rest of the nervous system functionally and physically
Hypothalamus located where? It’s function ? It is connected to ?
Below the thalamus
Autonomic and Endocrine function
Connected to the pituitary glad via the Infundibulum
Limbic play a role in (3)
1) Cognitve
2) Memory
3) Emotional
The limbic system components are :
Amygdala
Hippocampus
Some regions of the Cortex : Insular region example
Part of the hypothalamus
Brain stem has nuclei for CN 3 and 12 . true or False ?
True
Brain receives 70 % blood from and 30 % from
70% from Two internal carotid arteries .
30% from vertebral arteries posteriorly forming the basilar artery , subsequently converge to for circle of willin
Common carotid emerges from the
Aortic arch and divides at the level of the thyroid cartilage in the internal and the external carotid arteries
The internal carotid artery traverse the ____through the ____and subsequently travels through the _____and into the _____
The skull though foreman lace rum
The cavernous sinus and into the carotid groove .
Bil vertebral arteries originate from the_____and converge to form the ____at the _____junction
From the Subclavian arteries
Form the basilar artery
At the pontmedullary junction
Basilar reached midbrain and divides into the
Posterior cerebral arteries and anastomoses with the PCOMs = completes the circle of Willis .
Less than ___% of people demonstrate a complete circle of Willis
50 %
All the sinus Darin into the
Sigmoid sinus and thereafter the internal jugular veins
CSF is produced mostly by choroid Plexus of lateral and third ventricle. True or False ?
True
Average volume of CSF in an adult is
150 ml ( approx)
CSF is created at a rate of ___ and moves from
15- 20 ml .hr
Moves from the ventricles via the aqueduct of sylvius to the fourth ventricle .
CSF flow
Choroid plexus of third and lateral ventricle(aqueduct of Sylvius )»_space;4th ventricle» ( Foramen of Magendie and lateral foramina of Lushka)»_space;Subarachnoid space of the cranium .
Primary sinus where CSF gets reabsorbed
Superior Sagittal Sinus via arachnoid villi and granulations
Some CSF traverses the Foramen Magnum , enters the subarachnoid space of the spinal column . This movement is important how?
Acute and chronic compensation in elevated ICP
How vertebraes
33 vertebrae 7 C 12 T 5L 9 fused sacral (5) And coccygeal (4)
Dorsal Columns containing tracts responsible for :
Proprioception, light touch
Central gray Matter *
Lateral Spinothalamic Tract responsible for
Pain and temperature
Central gray matter *
The outer white mater contains the ______Tract
lateral Corticospinal
Lateral gray column contain the cell bodies of the ______neurons that enter the _____chain , running on either side of the vertebral bodies , arising from
Preganglionic
Sympathetic chain
Arsing from T1 to L2/L3
Spinal cord ends
L1 or L2 in adults
Conus medullaris and film terminale
Spinal cord receives blood from :
1 anterior spinal
2 posterior spinal arteries
The anterior spinal artery originates from
6 - 8 major radicular arteries derived from the aorta.
The largest of the radicular arteries in the anterior spinal artery is the
Artery of Adamkiewicz
Occurs at T11/T12 but supplies T8 to conus medullaris terminus
Artery of Adamkiewicz is responsible for supplying blood to the _______of the spinal cord
Anterior 2/3 of the spinal cord
The posterior Spinal arteries supply the ______and ______and feeds ______of the spinal cord
Dorsal horn and the white matter
Posterior 1/3 of the spinal cord.
Brain is ___% of total body weight and ___% of O2 consumption and ____% of total body glucose consumption
2% Total Body weight
20% O2 consumption
25% total glucose consumption
brain glucose consumption
5mg/100g/min
CMRO2 normal is
3 - 3.8 ml/100g/min
Normal CBF
50ml/100g/min or 750 ml/min .therefore the brain receives 15% of the cardiac output
Irreversible Brain injury will occur how long after lack of O2 supply ?
4 to 5 minutes of global ischemia
CBF is regulated by …
Flow- metabolism coupling
CPP is the
≠ between MAP and ICO or CVP depends on which is bigger
CBF itself equal to
CPP/CVR
Cerebral auto regulation remain intact between MAP of ___ and it function by ___
*60 -1 60 mmHg ( approx)
Lower limit autoregulation is > 60 mmHg, changes throughout the day , differs per individual.
*Functions by altering CVR on the order of 5 to 60 seconds ( within a minute)
In health brains the LLA may be as high as MAP of
80 mmHg
Altering CVR is accompanied by ( 2 things )
Rapid phase aka dynamic autoregulation (: pulsatile changes link to SBP
Slow phase aka Static autoregulation ( phenomenon that accommodate to changes in MAP over longer time intervals
Above the Upper Limit and Lower to the LLA CBF is
Pressure dependant
Below the LLA what occurs?
Max cerebral vasodilation and Ischemia
Above the autoregulation upper limit , what occurs ?
Max vasoconstriction
Increased perfusion pressure»_space; disrupted BBB» Cerebral edema or cerebral hemorrhage.
Chronic HTN, autoregulatory curve is shifted
Right
Anesthetics do what to your autoregulation ?
Anesthetics, especially the potent ones have a dose dependent DECREASE in autoregulation
What physiologic parameters play important role in regulating CBF ? Which is most important ?
A)MAP
B)PaCO2 : most important **
CBF is linear to PaCO2 ( but the PaCO2 must be between 20 and 80 mmHg )
C) Temp
Hypoventilation does what to the CBF ?
Increase Remember CO2 ( vasodilates you )
What does hyperventilation to your CBF ?
Decrease
Remember low CO2= vasoconstriction
A change in PaCO2 of ___mmHG correlates with changes in ___of _____
PaCO2 change of 1 mmHg = same change in CBF of 1- 2 ml/100g/min
What happens is PaCO2 is lower than 20 mmHG
Max cerebral vasoconstriction»_space; Tissue hypoxia»_space;> reflex vasodilation.
That’s why you start hyperventilating when your ICP is acutely elevated. But that reflex vasodilation can cause ischemia.
The effects of hyperventilation on CBF and ICP only sustainable for how long ?
only 6 hours .
BC Phof CSF will renormalize
When does PaO2 have effect on CBF ?
Marked hypoxia aka PaO2 < 50 mmHg
CBF increases dramatically!
When can PaO2 cause vasoconstriction
When > 350 mmHg Slight vasoconstriction ( to protect itself from O2 toxicity ( O2 free radical formation )
How does Temp affect CBF ?
6- 7% DECREASE in CBF per 1 º C DECREASE in core temp .
Regional CBF is governed by
Humoral and Neurogenic factors
Catecholamines and mediators involved in regional cerebral vasoconstriction are
A1 agonists
Ionic Ca+
Endothelium
Thromboxane A2
Catecholamines and mediators involved in regional cerebral vasodilation are
B2 agonist
Nitric Oxide
Adenosine
PGs
Neurogenic influence over local CBF regulation :
Ach
Dopamine
Serotonin
Substance P
What the effects of Anesthetics on CBF ? ( not autoregulation)
Profound effect !!!
IV anesthetic effects on CBF
Propofol, Etomidate, Benzodiazepines, Thiopental DECREASE CBF bc»_space; decrease in CRMO2»_space; flow-metabolism coupling .
* Autoregulation and PaCO2 remain intact with those !
Ketamine effects on CBF, CMRO2 , Autoregulation, PaCO2 ( 2)
1) Increases CBF and CMRO2
2) Little effect in autoregulation and PaCO2
Volatile anesthesic effects on CBF and autoregulation .
1) Potent volatiles Sevo, ISO and Des = DIRECT cerebral vasodilators ! but»_space; decrease CRMO2»_space; flow-metabolism coupling»_space; offset CBF = none to min. Increase in CBF at lower dose , but at high doses»_space;max suppression of CRMO2» major vasodilation» increased CBF Therefore we say they have **dose- dependent effects of CBF
2) Autoregulation is inhibited : but vessels can still response to PaCO2 changes .
N2O effects on CBF
Direct cerebral vasodilator +
Minimal effect on CRMO2 +
Variable effect on cerebral autoregulation capacity
Propofol + N2O = preserved autoregulation
Sevo+ N2)= impaired autoregulation
Spinal Cord Perfusion Pressure SCPP=
MAP- SSSP ( Spinal subarachnoid Space pressure )
Volume of brain
1400 ml
volume of CSF in cranium
150 ml
CBV ( cerebral volume )
150 ml
Monroe Kellie Doctrine
Increase in the volume of one will lead to a rise in ICP unless it is matched by an equal reduction in the volume of another compartment.
Brain can’t compress so CSF and CBV adjust to maintain ICP
CBV decrease how ?
Reflex arterial vasoconstriction + increase venous Efflux from brain and venous sinuses .
Care of elevated ICP patients
1) Avoid Hypoventilation
2) Maintain CPP
3) Reduce intracranial volume : Mannitol, CSF 4)diversion, Cerebral vasoconstricting anesthetics ????
5) Consider decompression craniectomy
Normal ICP is
7 - 15 mmHg ( 5-15 mmHg PP)
Poor neurological outcome is from ICP above
20 - 25 mmHg
High ICP does what to CBF ?
Decrease
Intracranial elastance curve
Visualizing the ICP -Volume relationship
Cerebral elastance formula
E= dP/dV
Lumbardrain, extraventricular drain.
“Flat of the curve “( intracranial elastance curve means :
Elastance is low
In normal brain , changes in volume compensated for easily by CSF and CBV
Elbow of the curve ( intracranial elastance curve )means :
Elastance increases
Small increase in volume = rapid rise in ICP
Most common cause of elevated ICP is
**Cerebral edema **
Cytotoxic : increase intracellular water i.e Post ischemia.
Vasogenic: loss of integrity of BBB. Happens in tissue around tumors, abcess, contusion. Dexamethasone*
Interstitial : increase extrecellular fluids + intact BBB i.e hydrocephalus
Why dexamethasion only can treat vasogenic edema ?
BC it upregulates the proteins responsible for the integrity of the tight junctions
How can increase CBV increase ICP ?
Increase arterial inflow plus decreased venous efflux = rise in ICP
What can increase arterial inflow ?
Vasodilators
Hypercapnia
Severe hypoxemia/ Acidosis
What can cause decreased Venous efflux ? Thus increasing ICP
Jugular vein obstruction
Elevated pressure within the airways
Clinical symptoms of elevated Intracranial Hypertension.
Headache
N/V
Papilledema
As ICP continues to increase you will see what ?
Cushing Triad
1 HTN
2 Bradycardia
3 Irregular respiration
Signs of herniation
Depends on structures herniating Pupillary Dilation Oculomotor weakness Absent light reflex Cardiorespirations
CT results of elevated ICP
Effacement of Sulci
Compression of ventricles
Midline shift
Even possible ventriculomegaly
In acute phase of spinal cord injury , what are the s/s ?
Flaccid paralysis and hypotension
Flaccid paralysis and Hypotension are seen in which phase of spinal injury ?
Acute
Spastic , Pain and risk for autonomic hyperreflexia are seen in which phase spinal cord injury ?
Chronic
Both chronic and acute spinal injury may have what s/s ?
Loss of sensory, motor, autonomic function below the level of injury.
Most important monitor of CNS function is
Neuro exam of an an awake and responsive patient.
BAEP and VEPs are less commonly used. True or False ?
True
Amplitude is measured in ____ for SSEP and BAEP and measured in _____for MEPs
Microvolts
Millivots
Latency is measured in ___ refers to the _____
Milliseconds
Refers to The delay in peak signal following stimulation and reflects transit time along the neural pathway.
SSEP elicited from ____and is measured at the level of ______
A peripheral nerve
Subcortex : upper cervical spine , inion and cortex : scalp.
SSEP stimuli travel through
Posterior Column/ Medial Lemnicus pathway in the CNS
SSEP is useful for monitoring integrity of
Peripheral Nerves Dorsal Column Brainstem Subcortex ( upper cervical spine, inion) Sensory cortex of the brain
SSEP stimuli are recorded in the contralateral side scalp because
Sensory tracts crosses at the brainstem before getting through the thalamus and up the sensory Cortex
SSEP are used during
Spine Surgery
Neurovascular brain surgery : cerebral aneurysm clipping.
Significant changes in SSEP means
Decrease amplitude by 50%
Increase Latency by 50%
MEPs are produced at the level of the
Cortex by direct stimulation of the cerebral cortex or by
Indirect stimulation of the scalp
Lower extremity SSEP which artery ?
ACA
Upper extremity SSEP which artery ?
MCA
MEPs for assessing what ?
Motor cortex and anterolateral spinal cord ( containing the corticospinal tracts )
MEPs how is stimulation produced ?
Indirect electrical stimulation of motor cortex via scalp electrodes»_space;pulses travel caudad» depolarization of upper motor neurons in spinal cord» accumulating in the ventral horn»_space; alpha motor neurons»_space;motor endplates» muscle movement