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266 Cards in this Set

  • Front
  • Back
Intracranial Compartment
Brain: ___ of total volume
Blood: ___ of total volume
CSF: ___ of total volume
Brain: 80% of total volume
Blood: 10% of total volume
CSF: 10% of total volume
Brain is a compressible or non-compressible compartment?
↑ ICP can lead to interruption of _______.
cerebral perfusion pressure (CPP)
Brain receives ____ of cardiac output when body is at rest.
CSF volume:
infants = ?

adults = ? (amt in intracranial space?)
infants ~50 ml

adults ~ 150 ml (75 ml in intracranial space)
Body makes _______ of CSF per day.
500-600 ml/day
where is CSF formed and reabsorbed?
formed in choroid plexus in ventricles

reabsorbed by arachnoid villi into dural venous sinuses

Normal = ?
Abnormal: ?
Warrants aggressive tx = ?
Normal ICP: <15 mmHg

Abnormal: exceeds 15 to 20 mmHg

Warrants aggressive treatment: > 20
Monroe-Kellie doctrine
To maintain a normal ICP, a change in volume of 1 compartment must be offset by a reciprocal change in another compartment
in normal brain what is the goal regarding maintaining daily ICP?
rate of absorption of CSF must match rate of production
Two classifications?

what are primary INTRACRANIAL TUMORS?
Arise from the brain and its coverings
Subclasses of primary brain tumors and examples.
a.Histologically benign
-Pituitary adenoma
-Acoustic neuroma

b.Histologically malignant
what are Metastatic INTRACRANIAL TUMORS?
Most often from primary sites in the lungs or breasts; Likely to find presence of more than one lesion
which primary brain tumors are most common in children ?
most common brain tumors in adults?
Pituitary adenomas
Metastatic tumors
most common benign brain tumor?
only unequivocal risk facotr ID'd for glial and meningeal neoplasms?
ionizing radiation
are CTs useful for dxing brain tumors? any disadvantages?
useful but may miss structural lesions
benefit of Cranial MRI for dxing brain tumors? any disadvantages?
Contrast agents enhance the images

Imaging angiography can help distinguish a vascular mass from a brain tumor
diagnostic methods for brain tumors.
3.Positron emission tomography
4.Single photon emission computed tomography
Treatments and when their typically used(3)
1.Surgery - Partial or complete resections

2.Radiation therapy
(malignant brain tumors)

(combination with radiation or as initial tx in children)
increased neurologic deficits during radiation cause & tx?
caused by cerebral edema

tx'd with corticosteriods
why radiation therpy often avoided in children?
potential long-term deterimental effects like developmental delay and panhypopituitarism
early S&S from brain tumors often due to?
intracranial HTN
cause of dull HA during waking hrs in pts w/ brain tumors?
1st - increased PaCO2

2nd - cerebral vasodilation

3rd - increased intracranial contents that exceeds limits of compensation

4th - increased ICP
Intracranial tumors
Progression of Intracranial Hypertension S&S. (10)
1.Papilledema (visual disturbances)
3.Mental status changes
4.Nausea & vomiting
5.↑ systemic blood pressure (to maintain CPP in presence of intracranial hypertension)
6.reflex bradycardia
7.Apnea & unconsciousness (midbrain compression)
8.Hemiplegia (cerebral peduncle compression)
10.decreased pupil rxn
11.midline shift on CT
INTRACRANIAL TUMORS Anesthetic management
Principal objectives. (4)
1.Keep ICP within normal range
2.Hemodynamically stable induction and maintenance of anesthesia
3.Minimal brain swelling to optimize surgical exposure
4.Rapid return to a level of consciousness that permits neurologic assessment
explain Intracranial Pressure-Volume
Compliance Curve Points A-B
compensatory: shows little
change in ICP due to CSF shifting from cranium to spinal subarachnoid space
explain Intracranial Pressure-Volume
Compliance Curve Points C
decompensatory: compensation
for↑in intracranial volume and ICP
2.even small ↑ in ICV
produce marked changes in ICP
3.symptoms of ↑ ICP appear
explain Intracranial Pressure-Volume
Compliance Curve Points D
decompensatory: Additional ↑ in volume at point C can precipitate abrupt increases in ICP.
increased ICP effect on CBF and CPP.
decreased CBF & CPP
what is the compensatory mechanism associated with decreased CPP & CBF? what happens if this mechanism fails?
increased systemic BP

cerebral ischemia
equation and normal range for CPP
Cerebral Perfusion Pressure (CPP) = MAP - ICP

Normal: CPP of 60-80 mmHg
CPP < 60 mmHg will lead to?
↑ risk for ischemic neuronal damage
CPP will be higher in what population of pts?
patient with chronic HTN
When monitoring ICP
Sudden bilateral pupillary dilation is associated with ?
herniation of the brain stem through the foramen magnum
how can ICP be monitored?
1.Epidural transducer
2.subdural transducer
3.intraventricular catheter
what are “plateau waves” ? are they good/bad and why?
Abrupt ↑ to as high as 100 mmHg


could exacerbate symptoms and induce hyperventilation.
Reasons for ↑ ICP before procedure
2.Painful stimulation
3.Induction (sympathetic stimulation)
4.Noxious stimulation
Methods to ↓ ICP
3.CSF drainage
4.Hyperosmotic drugs
when is hyperventilation a good option during ICP mngmt?
rapid ↓ ICP: Maintain PaCO2 near 30 mmHg
what is the time frame for getting benefit from hyperventilation for decreasing ICP?
Duration of hyperventilation may be limited (beneficial effects wanes in 6-12 hours)
disadvantages of hyperventilation for ICP mgmt?
1.excessive (PaCO2)lowering can ↓ CBF to the point of cerebral ischemia

2.Rebound ↑ in ICP is a potential problem
Appropriate to initiate more aggressive hyperventilation in children to maintain PaCO2. Why?
higher CBF than adults
what effect does hyperventilation have on cerebral vasculature?
what patients would hyperventalation not be benefical for controling increased ICP?
If the problem with intracranial hypertension is decreased blood flow, it may not be logical to treat the disorder with vasoconstriction
what head position lowers ICP? why?
Elevate head 30˚ above heart level

encourages venous outflow from brain
what head position elevates ICP?
head down
CSF drainage locations?
Lateral cerebral ventricles or lumbar subarachnoid space
Hyperosmotic drug for lowering ICP? MOA?

produces transient ↑ in osmolarity of plasma, which draws water from tissues including the brain
does of mannitol and infusion rate? what are the typical results?
0.25 to 1.0 g/kg IV over 15 to 30 min

loss of 100 ml of water from brain within 30 min
mannitol cautions? (2)
1.elderly as BBB may not be intact thus causing cerebral edema

2.has direct vascular vasodilating properties→ ↑CBV & ↑ICP
Diuretic for lowering ICP? when is it useful?

Useful with ↑ vascular fluid volume & pulmonary edema
Corticosteroids means of decrasing ICP?
1.Stabilization of membranes
2.reduces cerebral edema
3.reduces CSF production
4.increases seizure threshold
Barbiturates are Helpful for treating ICP after what? MOA
after acute head injury

Potent cerebral vasoconstrictor that ↓ CBV & ↓CBF while ↓CMRO2
determinants of CBF?
3.arterial BP & autoregulation
4.venous BP
5.anesthetic drugs/techniques
Normal CBF:
50 ml/100g/min
CBF increases how much for every 1 mmHg ↑ PaCO2 above 40?
1 ml/100g/min
CBF ↓ how much when PaCO2 is 20 mmHg?
by about 50%
Intracerebral steal syndrome
↑ PaCO2, blood flow is shunted away from tumor
Robin Hood phenomenon
Hypocapnia constricts normal vessels which can shunt blood flow to acidotic areas surrounding tumors
Hypoxemia & hypercarbia exert a additive or synergistic effect with ↑ in CBF?
synergistic effect
_____ is the most important determinant of CBF!
cerebral Autoregulation
Ability of the brain to maintain CBF at constant levels despite changes in MAP
Autoregulation may be lost or impaired in the presence of ? (3)
1.intracranial tumors,
2.head trauma or 3.administration of volatile anesthetics
cerebral autoregulation MAP range
60-150 mmHg
what happens in brain when MAP > 150 mmHg ?
↑ CBF → overdistention of the wall of cerebral blood vessels → cerebral edema
what happens in brain when MAP < 60 mmHg?
may see symptoms of cerebral ischemia (nausea, dizziness, slow cerebration)
presence of chronic hypertension does what to the cerebral autoregualtion curve?
displaced to right, meaning a higher MAP is tolerated before CBF becomes pressure dependent
in what body position is venous pressure Usually low ?
in supine or standing patients
what is predominant determinant of cerebral perfusion pressure?
why Consider avoiding PEEP in patients undergoing intracranial surgery?
b.↑venous pressure (can ↑ bleeding during surgery)
c.↑ CBF
d.↑ ICP
e.↓ CPP
Volatile anesthetics ___ MAC are often potent cerebral vasodilators producing dose-dependent ___ CBF. Is this good or bad?
>0.6; increases

can be bad b/c patients with intracranial tumors may not displace CSF to compensate and end up with an ↑ ICP
is Nitrous oxide bad during brain tumor ICP mgmt?
unlikely to ↑ ICP in patient with intracranial tumors maintained at normocarbia
Drugs that produce cerebral vasoconstriction and predictably ↓ CBF and ICP. (4)
1.barbiturates-thiopental, 2.etomidate,
can Succinylcholine or nondepolarizing neuromuscular blocking drugs be used on patients with brain tumors ?
unlikely to alter ICP; However, drug induced histamine release could theoretically produce cerebral vasodilation with associated ↑ in CBF and ICP
is Ketamine bad during brain tumor ICP mgmt? why?

dilates the cerebral vasculature and ↑ CBF & ICP
↑ ICP, Loss of consciousness, and slow breathing are signs of?
herniation of cerebellar tonsils through foramen magnum
should Avoid what during preop prep of brain tumor pts for surgery?
Medications causing sedation or respiratory depression
should be Cautious with what group of drugs preop and why?

patients with intracranial pathology may be extremely sensitive to CNS depressant effects; Opioid induced hypoventilation can lead to accumulation of CO2 & resulting ↑ in ICP
Intracranial tumors Anesthetic induction:

what induction drugs produce rapid, reliable onset of unconsciousness with minimal effects on CBF ?
(thiopental, etomidate, propofol)
Intracranial tumors Anesthetic induction:

what other things can you do during induction to Maintain CPP of 60-80 mmHg? (4)
1.followed IV induction drug w/ large doses of a NDMR (ED95)
2.Pretreat: lidocaine, opioids, esmolol can attenuate ↑ in systemic blood pressure and ICP that can accompany tracheal intubation
3.Muscle relaxant
4.Avoid sustained hypotension
Intracranial tumors Anesthetic induction:

perception of noxious stimuli effect on CMRO, CBF & ICP
can abruptly ↑CMRO, CBF & ICP
Intracranial tumors Anesthetic induction:

prevention of perception of noxious stimuli
Adequate depth of anesthesia & skeletal muscle paralysis
when is N2O not good to use in intracranial cases?
sitting position b/c ↑ risk of venous air embolism
what volatile agent is most often used during intracranial cases? at what concentration & why?
Isoflurane 0.6 MAC

high concentrations can ↑ CBF and ICP
why use Caution w/ Peripheral vasodilating drugs (Nitroprusside/ nitroglycerin) in intracranial cases?
may ↑ CBF & ICP
why are glucose replacement solutions not used w/ intracranial cases?
Metabolism of glucose in brain leaves free water in excess
Replace fluid volume depletion with what 3 things and not with what? at what rate?
prbcs, whole blood, or colloid solutions; not with large volumes of balanced salt solutions
Infusion rate should probably not exceed 1 to 3 ml/kg/hr
Can reduce cerebral metabolic rate of oxygen (CMRO2) by approximately __ per __ reduction in body temperature
7%; 1˚ C
what does CMRO2 stand for?
cerebral metabolic rate of oxygen
most common positioning for intracranial cases? why?
Supine with head elevated 10˚-15˚

to facilitate cerebral venous drainage
Sitting position is used for ?
exploration of posterior cranial fossa
disadvantages of sitting position
↓ systemic pressure & CO; potential for venous air embolism
advantages of sitting position
excellent surgical exposure, facilitates cerebral venous & CSF drainage
venous air embolisms are potential hazards when? why additional hazard is noted with craniotomies?
operative site is above the level of the patient’s heart

veins in the skull may not collapse
Pathophysiology of venous air embolisms
Air enters RV→interference of blood flow into pulmonary artery→pulmonary edema & reflex bronchoconstriction may result from movement of air into pulmonary circulation
early signs of venous air embolisms & reason for each. (3)
1.Sudden ↓ ETCO2 (deadspace, continued ventilation of alveoli that are no longer perfused because of obstruction of their vascular supply by air)

2.Increase in RAP and PAP (reflects acute cor pulmonale & correlates with abrupt decreases in ETCO2)

3.During controlled ventilation of lungs, sudden attempts by patients to initiate spontaneous breaths (may be the 1st indication of the occurrence of venous air embolism)
Late signs of venous air embolism. (4)
3.cardiac dysrhythmias, cyanosis,
4.“millwheel” murmur (heard through esophageal stethoscope)
Venous Air Embolism
Treatment (4)
1.If possible- attempt aspiration from right atrial catheter

2.D/C nitrous- need 100% FiO2

3.treat hypotension with sympathomimetic drugs, bronchospasm with β2 agonists

4.Left lateral decubitus position
INTRACRANIAL TUMORS: Postoperative management
GOALs. (3)
1.Keep ICP within normal ranges

2.Prevent reaction to ETT as patient awakens (Lidocaine may attenuate response)

3.If consciousness was depressed preoperatively, may consider not extubating
Stroke is the leading cause of _____ and the 3rd leading cause of ____ in the US
disability; death
ischemic strokes make up _____% and hemorrhagic strokes make up ___% of all strokes
Hemorrhagic stroke 2 classifications?
intracerebral or subarachnoid
Ischemic stroke is described by what 2 ways?
area of brain affected and etiologic mechanisms
Transient Ischemic Attack:
sudden vascular-related focal neurologic deficit that revolves within 24 hours
REVIEW Cerebrovascular Anatomy
REVIEW Cerebrovascular Anatomy
Blood is supplied to the brain via 2 pairs of vessels
1.Internal carotid arteries
2.Vertebral arteries
Internal carotid arteries
Vertebral arteries
Unite to form ?
the basilar artery,
the basilar artery, terminates and splits into what?
two posterior cerebral arteries
the two posterior cerebral arteries supplies blood to what 4 parts?
medial, temporal & occipital lobe, parts of thalamus
the Internal carotid arteries,
Vertebral arteries,
the basilar artery, and the two posterior cerebral arteries join on the surface of the brain to form ?
the intracranial vessels (anterior cerebral artery, middle cerebral artery, posterior cerebral artery) & Circle of Willis
True or False. A stroke represents a medical emergency!
what helps distinguish b/t Hemorrhage or Ischemia stroke?
why is it important to distinguish b/t Hemorrhage or Ischemia stroke?
treatment is substantially different
how can Conventional angiography help in dx and/or tx of strokes?
help detect acute occlusion or a lodge embolus
acute ischemic stroke Most likely reflects what 3 things?

2.large vessel atherothrombolembolism,

3.small vessel occlusive disease
what population of patients are most likely to experience acute ischemic stroke due to small-vessel occlusive disease?
Patients with diabetes mellitus or systemic hypertension
Risk factors for acute ischemic stroke. (5)
1.Systemic hypertension- most significant risk factor
4.Diabetes mellitus
5.Excessive alcohol consumption
Carotid Endarterectomy.

what population has the greatest benefit?
Procedure to ↓ risk of stroke
by surgically treating symptomatic carotid artery stenosis

men with a stenosis diameter >70%
2 alternatives to CEA
Angioplasty and stenting
Carotid Endarterectomy Preoperative Evaluation objectives (4)
1.Examine for cardiovascular, renal, and neurological function

2.Chronic essential hypertension is a common finding (Establish the range of normal arterial blood pressures for patients preoperatively to provide guidelines for acceptable perfusion pressure)

3.Do not palpate carotid artery – could displace fragments of the occlusive intravascular lesion, causing cerebral embolism
Carotid Endarterectomy Management Options:
general or regional anesthesia
Carotid Endarterectomy Management Goals:
1.Maintain hemodynamic stability
2.prompt emergence, allowing rapid assessment of neurologic status
Carotid Endarterectomy Management Monitoring:
1.arterial line,

2.pulmonary artery catheter in patients with poor LV function (CAD or recent MI),

3.brain function during cross clamping of carotid artery
Carotid Endarterectomy Postoperative management:

After extubation, observe patient for the following complications
1.cardiac (BP changes, MI),

2.airway obstruction (hematoma formation)

3.neurologic complications (thrombosis, intracerebral hemorrhage)
Carotid Endarterectomy Postoperative management:

treatment of persisting HTN
hydralazine or labetalol
Medical management of acute ischemic stroke:

Respiratory function objectives
1.Ventilatory drive is usually intact except after medullary or massive hemispheric infarction

2.Ability to protect lungs against aspiration may be impaired

3.Supplemental O2 is usually sufficient
Medical management of acute ischemic stroke:

why is systemic BP so critically important?
Critically important as blood flow to ischemic regions is dependent on cerebral perfusion pressure
Medical management of acute ischemic stroke:

Blood glucose concentration importance?
Hyperglycemia→ poor outcomes (glucose may be metabolized into lactic acid, resulting in acidosis and ↑ tissue injury)
Medical management of acute ischemic stroke:

Hypothermia importance
Body Temperature
may help ↓neuronal oxygen demands, cerebral edema, and neurotransmitter toxicity
Pharmacologic treatment of acute ischemic stroke

Heparin Prophylaxis
for DVT is common

5000 units SQ every 12 hours

Patients with acute hemmorhage are treated with pneumatic compression stockings
Pharmacologic treatment of acute ischemic stroke

Aspirin use recommendations?
initial therapy for acute stroke patients and for prevention of recurrent strokes
Pharmacologic treatment of acute ischemic stroke

Intravenous recombinant tissue plasminogen activator use recommendations?
patients who meet specific eligibility requirements and if patient can be initiated within 3 hours of the onset of acute symptoms
Acute Hemorrhagic Stroke 2 most reliable predictors of outcome:
Estimated volume of blood & LOC
Acute Hemorrhagic Stroke management (4)
2.prompt ventricular drainage,
3.ICP monitoring,
4.tracheal intubation if needed
Subarachnoid Hemorrhage common location
a.Commonly results from aneurysms of the circle of Willis
Subarachnoid Hemorrhage
common S&S (3)
1.terrible headaches

2.inversion of T waves and ST segment depression

3.catecholamine release
Acute Hemorrhagic Stroke
management Goals? (2)
1.prevent increases in transmural pressure of the aneurysmal sac, MAP-ICP, (could increase the risk of aneurysmal rupture)


2.maintaining an adequate CPP to prevent cerebral ischemia
Subarachnoid hemorrhage Treatment
localizing the aneurysm
Acute Hemorrhagic Stroke
Anesthetic management:
1.Limit risks of aneurysm rupture,

2.prevent cerebral ischemia,
3.facilitate surgical exposure

4.“Triple H” therapy can help avoid vasospasm: hypertension, hypervolemia, hemodilution
Acute Hemorrhagic Stroke: Induction goals (4)
1.Limit systemic hypertension during DVL (Nitroprusside before initiating DVL, Lidocaine, short acting opioids)

2.Loss of consciousness: thiopental, propofol, etomidate

3.NDNBA: to facilitate tracheal intubation

4.Monitoring: arterial line, central venous pressure line (useful with fluid shifts), pulmonary artery catheter (helpful in patients with CAD)
Acute Hemorrhagic Stroke: Maintenance Goals (5)
1.Provide a depth of anesthesia appropriate to the level of surgical stimulation,
2.facilitating surgical exposure through optimal brain relaxation, 3.maintaining CPP,
4.reducing transmural pressure in the aneurysm during clipping of the aneurysm,
5.prompt awakening to permit neurologic assessment
Acute Hemorrhagic Stroke: Maintenance options (2)
1.volatile agents and supplemented with opioids

2.TIVA (Propofol & fentanyl)
why should nitrous be avoided in acute hemorrhagic stroke anesthesia maintenance?
potent cerebral vasodilator
ways to achieve optimization of brain relaxation during acute hemorrhagic stroke anesthesia. (3)
1.Loop and/or osmotic diuretics

2.Proper positioning to facilitate cerebral venous drainage

3.Normovolemia or modest hypervolemia (avoid glucose containing solutions)
Controlled Hypotension
induction of a MAP < 50 mmHg for the short period of time needed to clip an intracranial aneurysm
Guideline for safe levels of controlled hypotension:
decrease MAP no more than 30 to 40 mmHg below the patient’s normal awake level (assuming a CVP of 10 mmHg or less and PaCO2 near 35 mmHg)
during controlled hypotension consider the possibility of ?
a rightward shift of the curve for autoregulation of CBF
Acute Hemorrhagic Stroke: Emergence goals? (4)
1.immediate neurologic evaluation of the patient

2.Incremental doses of antihypertensive drugs (labetalol or esmolol) as patient emerges

3.Lidocaine may help facilitate less stimulating extubation

4.Evaluate pupils (unequal pupils not present preop reflect a surgical event)
who should you suspect in?
in patients who complain of visual loss during 1st postoperative week
Ischemic Optic Neuropathy (Progressive blindness) aka?
stroke of the optic nerve
2 classifications of Ischemic Optic Neuropathy (Progressive blindness)
Anterior ION & Posterior ION
after suspecting Ischemic Optic Neuropathy (Progressive blindness)what should be obtained urgently?
opthalmologic consultation for diagnosis and treatment
Anterior Ischemic Optic Neuropathy
infarction at watershed zones between areas of distribution of posterior ciliary arteries
Anterior Ischemic Optic Neuropathy S & S?
1.sudden, painless, monocular visual deficits

2.varing in severity from slight visual acuity to blindness
Anterior Ischemic Optic Neuropathy
2 forms
nonarteric & arteric
Nonarteric AION
a.period of manifestation
a.more likely to manifest during the postoperative period

b.attributed to decreased oxygen delivery to optic disc in association with hypotension and/or anemia

c.hemorrhagic hypotension, anemia, cardiac surgery, head & neck surgery, cardiac arrest, hemodialysis
Arteritic AION
c.treatment (rationale)
a.less common

b.associated with thrombosis of the short posterior ciliary arteries

c.high-dose steroids (to prevent progression and protect the contralateral eye)
Posterior Ischemic Optic Neuropathy
Acute loss of vision and visual fields
Posterior Ischemic Optic Neuropathy patho
↓ oxygen delivery to posterior portion of optic nerve between optic foramen and central retinal artery’s point of entry
Posterior Ischemic Optic Neuropathy Etiology. (6)
3.air embolism,
4.venous obstruction, 5.infection
6.altered anatomy
what is interesting about Posterior Ischemic Optic Neuropathy S & S?
Symptom free period precedes loss of vision
Posterior Ischemic Optic Neuropathy assoicated with what surgeries? (4)
1.prolonged spine surgery in prone position,
2.cardiac surgery,
3.radical neck dissection, 4.hip arthroplasty
Man-in-the-Barrel Syndrome
a.BUE paresis w/ intact motor fxn in BLE; cortical blindness possible

b.watershed ischemia or infarction of border zone b/t anterior cerebral artery & posterior cerebral artery following period of global hypoperfusion

c.hypotension that causes global cerebral hypoperfusion
Arnold-Chiari Malformation
Downward displacement (herniation) of cerebellum and portion of medulla through foramen magnum into upper cervical spinal canal
what pathophysiology results from Arnold-Chiari Malformation? (6)
1.Arachnoidal adhesions 2.obstruction of CSF flow from 4th ventricle 3.hydrocephalus,
4.↑ ICP,
5.compression of cranial nerves,
6.torsion of brain stem
Arnold-Chiari Malformation S/S:
1.occipital HA and down shoulders and arms; worsens with cough and head movement;
2.visual disturbances; 3.intermittent vertigo, 4.ataxia
Arnold-Chiari Malformation Treatment:
surgical decompression by freeing adhesions and enlarging foramen magnum
Arnold-Chiari Malformation Anesthesia implications:
associated ↑ ICP
the formation of cavities in an organ, especially in lung tissue as a result of diseases like tuberculosis
Slow progressive degeneration of spinal cord → cavitation → syringobulbia
extension of cavitation process cephalad into medulla
what pathophysiology results from Syringomyelia? (3)
Obstructed outflow of CSF from 4th ventricle in embryo development → pressure to canal of spinal cord → cyst formation
Syringomyelia S/S: (5)
1.Begin in 40’s;
2.sensory impairment of UE (pain and temperature)
3.skeletal muscle weakness and wasting with areflexia (from destruction of lower motor neurons)
4.thoracic scoliosis (from weakness of paravertebral muscles)
5.paralysis of palate, tongue, vocal cords and loss of sensation over face (from syringobulbia)
Syringomyelia Treatment:
no know effective tx
Anesthetic management of syringomyelia or syringobulbia. (5)
1.scoliosis → VQ mismatch
2.skeletal muscle wasting → hyperkalemia w/Sux
3.exaggerated response to nondepolarizers
4.Impaired thermoregulation (mentioned in class!!)
5.Decreased protection of airway → be careful during extubation
Amyotrophic Lateral Sclerosis
Degenerative disease of motor ganglia in anterior horn of spinal cord and pyramidal tracts
Amyotrophic Lateral Sclerosis
common age & population
men 40-60yrs
Amyotrophic Lateral Sclerosis Etiology
Viral, genetic
Amyotrophic Lateral Sclerosis
1.upper and lower motor neuron dysfunction;
2.skeletal muscle atrophy, weakness, fasciculations (beginning in hands → skeletal muscles;
3.tongue, pharynx, larynx, and chest);
4.ANS dysfunction (orthostatic hypotension & resting tachycardia); 5.uncontrolled emotions; 6.lung carcinoma;
7.dysphagia leading to pulmonary aspiration; 8.cramping and aching muscles (esp legs)
Amyotrophic Lateral Sclerosis
death within 6 yrs from resp failure
Amyotrophic Lateral Sclerosis
anesthesia management
1.General anesthesia → exaggerated ventilatory depression possible

2.Regional anesthesia likely avoided → exacerbation possible
Friedreich’s Ataxia
Autosomal recessive disorder causing degeneration of spinocerebellar and pyramidal tracts
Friedreich’s Ataxia
Fatal by early adulthood from cardiac failure
Friedreich’s Ataxia
1.Cardiomyopathy in 10-50% of pts
2.Kyphoscoliosis → steady deterioration of pulmonary function in 80% of pts
3.Ataxia- primary presenting symptom
4.Dysarthria, nystagmus, skeletal muscle weakness and spasticity, DM may be present
Friedreich’s Ataxia
Anesthetic Implications:
1.Same as ALS
2.neg inotropic effects of anesthetic drugs w/cardiomyopathy
3.Epidural placement difficult w/kyphoscoliosis
4.Chance of postop ventilatory failure increased (especially w/kyphoscoliosis)
Parkinson’s Disease etiology
Unknown cause
Parkinson’s Disease
neurodegenerative → Loss of dopaminergic fibers in basal ganglia
Parkinson’s Disease pathological effects
Dopamine mediates or decreases firing rate of extrapyramidal movement → unopposed action of Ach
Parkinson’s Disease classic triad of major signs
tremors, rigidity, akinesia
Parkinson’s Disease: where skeletal muscle rigidity first appears?
proximal muscles of neck
Parkinson’s Disease: manifestations
1.loss of associated arm swings when walking
2.absence of head rotation when turning body
3.facial immobility
4."pill-rolling tremor"
5.resting tremors
7.oily skin,
8.pupillary abnormalities, 9.diaphragmatic spasms, 10.oculogyric crises
Parkinson’s Disease: Levadopa side effects
1.Orthostatic hypotension
2.↑ myocardial contractility
3.N/V from stim of CTZ area in brain
Parkinson’s Disease: Surgical Tx:
1.Thalamic nucleus interventions (transient), 2.Pallidotomy,
3.Fetal tissue transplant
Anesthetic implicattions os levadopa
1.No interruption more than 6-12 hours → skeletal muscle rigidity → problems with ventilation
2.Give am dose 20 min prior to induction (can given intra and post op)
3.Causes orthostatic hypotension, cardiac dysrhythmias, and HTN
Questionable drugs for parkinson's dz
1.Butorphenones (droperidol) – antagonizes dopamine in basal ganglia
2.Alfentanil- opioid-induced decreases in central dopaminergic transmission
3.Ketamine- exaggerated SNS responses (has been safely given)
Huntington’s Chorea
Autosomal dominant trait Premature degenerative disease of CNS
Huntington’s Chorea patho effects
1.Marked atrophy of caudate nucleus (mostly), putamen, and globus pallidus
2.Deficiency of Ach in basal ganglia, its synthesizing enzyme choline acetyltransferase, and GABA
Huntington’s Chorea age & duration
appears at 35-40 yrs old

Lasts for about 17 yrs
Huntington’s Chorea S/S: (5) dementia 2.choreoathetosis
3.pharyngeal muscle inbolvement → pulmonary aspiration;
proximal jerky involuntary movements → hypotonia/hypertonia
Huntington’s Chorea Tx:
2.Butyrophenones (interfere w/NT effects of dopamine)
Huntington’s Chorea Anesthesia management:
1.preop meds
3.intraop meds
1.Preop sedation w/droperidol
2.Aspiration precaution if pharyngeal muscle involved
3.Opioid, droperidol, N2O, and Sevo
Huntington’s Chorea drug caution/contraindications (2)
1.Decreased plasma cholinesterase! Prolongs Sux (can still give, just know its prolonged)
2.Sensitive to effects of nondepolarizing muscle relaxants
Shy-Drager Syndrome
-ANS dysfunction
-parenchymatous degeneration in CNS and spinal cord → neuronal cells
-depletion of NE from peripheral efferent nerve endings
Shy-Drager Syndrome S/S: (7)
1.orthostatic hypotension → syncope,
2.urinary retention,
3.bowel dysfunction,
5.sexual impotence,
6.↓pupil reflexes,
7.abnormal control of breathing
Shy-Drager Syndrome
1.what happens to NE w/ standing or exercise?

2.what happens w/ baroreceptors w/ hypotension
1.NE concentrations fail to show normal ↑ after standing or exercise

2.Failure of baroreceptor reflexes to ↑ HR or vasoconstriction in response to hypotension
Shy-Drager Syndrome: Often develops s/s of of what toher neurologic disorder?
Shy-Drager Syndrome Tx: (5)
1.head-up tilt at night, 2.elastic stockings,
3.↑ Na intake (vol expansion),
4.alpha antagonists (ie, yohimbine—release of NE from post gang nerve endings), 5.Levodopa- for Parkinson’s symptoms
Shy-Drager Syndrome: drugs that have exaggerated effects w/ this disorder?
1.neg inotropic drugs (extreme bradycardia)
2.Vasopressors (extreme HTN)
3.volatile anesthetics (extreme brady & hypotension)
Shy-Drager Syndrome: relationship of heart beat & respirations?
absent beat-to-beat variability in HR when deep breathing
Shy-Drager Syndrome: vasopressor that's best to use?
low dose Phenylephrine
Shy-Drager Syndrome: why is it hard to tell if they have adequate depth of anesthesia?
↓ SNS response to noxious stimulation
Shy-Drager Syndrome Drugs of caution:
1.Thiopental (if hypovolemic or with rapid administration → exaggerated hypotension);

2.Ketamine → increased HTN
Leber’s Optic Atrophy
• Degeneration of retina and atrophy of optic nerves → blindness
• Sex-linked autosomal recessive trait
• Abnormality of cyanide metabolism
Leber’s Optic Atrophy
what drug to avoid?
Creutzfeldt-Jakob Disease
Transmissible spongiform encephalopathy w/ 10-15% family history of autosomal dominant inheritance
Creutzfeldt-Jakob Disease
incubation period
months to years
Creutzfeldt-Jakob Disease
pathologic effects
Abnormal prion protein which acts as a neurotransmitter that accumulates in the CNS
Creutzfeldt-Jakob Disease
S&S (4)
1.Rapid progressive dementia 2.ataxia
3.myoclonus (rare at the onset)
4.Seizures (late onset)
Creutzfeldt-Jakob Disease
• Dx confirmation
• Differential diagnosis:
w/brain biopsy

Creutzfeldt-Jakob Disease
Anesthesia and other Implications
• Universal precautions
• Handling CSF--double glove, protective eyeware, and label “infectious”
• For brain biopsy use disposable instruments or soak in Na hypochlorite or autoclave
Creutzfeldt-Jakob Disease: only body fluid resulting in transmission
Creutzfeldt-Jakob Disease
• Transmission has been attributed to
tx w/growth hormone and gonadotropic hormones
Multiple Sclerosis
Autoimmune disorder affecting CNS; occurs in genetically susceptible persons after environmental exposure
Multiple Sclerosis
• Causes:
predisposition (twins) environmental
infectious exposures
Multiple Sclerosis
- population
• Twice as common in women than men
Multiple Sclerosis
• Pregnancy
rate of relapse ↓ in 3rd trimester of pregnancy and ↑ during first 3 months postpartum
Multiple Sclerosis
- relapse causes
-Viral illness and infections
-first 3 months postpartum
Multiple Sclerosis
• patho Characteristics
1.inflammation, demyelination of CNS and spinal cord,
2.axonal damage in CNS; 3.loss of myelin followed by formation of demyelinative plaques;
Multiple Sclerosis:
are Peripheral nerves affected?
Multiple Sclerosis:
• S/S (8)
1.Optic neuritis → diminished visual acuity and defective pupil reaction
2.Cerebellum involvement → gate disturbances
3.Spinal cord lesions → limb paresthesias and weakness, urine incontinence, and 4.sexual impotence
5.Brain stem pathways for eye coordination involvement → paresis of medial rectus muscle on lateral conjugate gaze, nystagmus seen in abducted eye
6.Ascending spastic paresis of skeletal muscles
7.Cervical intramedullary disease → electrical sensation that runs down back into legs in response to flexion of neck (Lhermitte’s sign)
8.Increased seizure occurance in MS
Multiple Sclerosis:
what is Subacute?
relapses and remissions vs. Chronic and progressive
Multiple Sclerosis
• Remissions result from?
correction of transient chemical and physiologic disturbances that have interfered with nerve conduction in the absence of demyelination
Multiple Sclerosis
• after 35 yrs
Multiple Sclerosis
• Diagnosis: (4)
1.clinical features; 2.immunoglobulines in CSF; 3.prolonged latency of evoked potentials;
4.changes in white matter seen on cranial MRI (sensitive marker-demyelinative plaques)
Multiple Sclerosis
• Treatment: (5)
1.Corticosteroids 2.Interferon-beta 3.Glatiramer acetate
4.Azathioprine 5.Methotrexate
Multiple Sclerosis:
(shortens duration of relapses)
Devic’s disease-
variant of MS affecting optic nerves and cervical spinal cord
Multiple Sclerosis: Corticosteroids action
(shortens duration of relapses)
Interferon-beta indication for MS & side effects
—for relapsing-remitting MS

-SE influenza s/s for 24-48 hours, Leucopenia, anemia, Co-existing depression
Glatiramer acetate
-Multiple Sclerosis-good for interferon resistant patients

—mimics myelin basic protein;
-Multiple Sclerosis

—depresses cell-mediated and humoral immunity; ↓ rate of relapses;
-used for secondary progressive MS patients

—inhibits cell-mediated and humoral immunity;
sign of exacerbations during postop period and cause?
-ANY increase in body temp (even 1 degree celcius)

-caused from complete block of conduction in demyelinated nerves
Spinal anesthesia → postop exacerbations. why?
local anesthetic neurotoxicity due to lack of protective sheath around spinal cord (↑ susceptibility to neurotoxicity of locals in white matter)
effects of sux on MS
-Sux → exaggerated release of K+
2 effects of nondep agents on MS
1.Prolonged effects w/co-existing skeletal muscle weakness (“myasthenia-like”); decreased skeletal muscle mass

2.Upregulation of extrajunctional cholinergic receptors cause resistance in upper motor neuron lesions
number 1 perioperative drug for MS
Corticosteroid supplementation if chronic tx
Guillain-Barre Syndrome:
another name for it?
(Acute Idiopathic Polyneuritis)
Guillain-Barre Syndrome:
Sudden of skeletal muscle weakness or paralysis
Guillain-Barre Syndrome
-Initially in legs and spreads cephalad over the next few days → arms, trunk, face

-Bulbar involvement → bilateral facial paralysis
Guillain-Barre Syndrome Serious S/S: (2)
1.difficulty swallowing d/t pharyngeal muscle weakness

2.impaired ventilation d/t intercostal muscle paralysis
Guillain-Barre Syndrome
other symptoms (10)
1.Pain in form of HA, backache, or tenderness of skeletal muscles to deep pressure

ANS dysfunction and other s/s:
2.Wide fluctuations in BP
3..Sudden profuse diaphoresis
4..Peripheral vasocon
5.Resting tachycardia
6.Cardiac conduction abnormalities on EKG
7.Severe orthostatic hypotension (elevation on pillow → syncope)
8.Theomboemobolism more frequent in GBS
9.Sudden death
10.Increased ICP (rare symptom)
Guillain-Barre Syndrome:
-Complete recovery from acute episode in a few weeks with segmental demyelination

-If axonal degeneration, slower recovery with some permanent weakness
Guillain-Barre Syndrome:
sepsis, acute respiratory failure, pulmonary embolism, and cardiac arrest
Guillain-Barre Syndrome:
clinical s/s
Guillain-Barre Syndrome:
when do s/s typically appear?
Occurs after respiratory or GI infection in about ½ of pts
Guillain-Barre Syndrome:
tx (6)
1.VC < 15ml/kg → requires ventilator support
2.Pharyngeal muscle weakness (cuff ETT) predispose to aspiration
3.Treat hyper or hypotension
4.Plasma exchange
5.Gamma globulin infusion
6.No corticosteroids - not helpful
Guillain-Barre Syndrome:
two anesthesia considerations
Two considerations:
1.Altered function of ANS
2.Lower motor neuron lesions
Guillain-Barre Syndrome:
Lower motor neuron lesions anesthetic considerations?
6.mechanical ventilation
1.Absent compensatory CV responses → profound hypotension (posture change, blood loss, and PEEP)
2.Laryngoscopy → exaggerated increased BP
3.Exaggerated responses to indirect-acting vasopressors (IVF may be best to tx hypotension if possible)
4.No Sux! (K+ release from denervated skeletal muscles)
5.Nondepolarizing muscle relaxant w/minimal circulatory effects best choice (rather than pancuronium)
6.Mechanical ventilation during surgery w/likely continued support postop
what arteries make up the Circle of Willis?
1.Internal carotids
2.Anterior cerebral arteries
3.Anterior communicating artery
4.Posterior communicating arteries
5.Posterior cerebral arteries
6.Basilar artery
what is the Circle of Willis
point where blood carried by the two
internal carotids and the basilar system
comes together and then is redistributed
by the anterior, middle, and posterior
cerebral arteries
Which aretery in the Cirlce of Willis is Common for formation of aneurysms
Anterior communicating artery