Pathophysiology Of Nervous System

Front 1

Intracranial Compartment
Brain: ___ of total volume
Blood: ___ of total volume
CSF: ___ of total volume

Back 1

Brain: 80% of total volume
Blood: 10% of total volume
CSF: 10% of total volume

Front 2

Brain is a compressible or non-compressible compartment?

Back 2

non-compressible

Front 3

↑ ICP can lead to interruption of _______.

Back 3

cerebral perfusion pressure (CPP)

Front 4

Brain receives ____ of cardiac output when body is at rest.

Back 4

20%

Front 5

CSF volume:
infants = ?

adults = ? (amt in intracranial space?)

Back 5

infants ~50 ml

adults ~ 150 ml (75 ml in intracranial space)

Front 6

Body makes _______ of CSF per day.

Back 6

500-600 ml/day

Front 7

where is CSF formed and reabsorbed?

Back 7

formed in choroid plexus in ventricles

reabsorbed by arachnoid villi into dural venous sinuses

Front 8

ICP:

Normal = ?
Abnormal: ?
Warrants aggressive tx = ?

Back 8

Normal ICP: <15 mmHg

Abnormal: exceeds 15 to 20 mmHg

Warrants aggressive treatment: > 20

Front 9

Monroe-Kellie doctrine

Back 9

To maintain a normal ICP, a change in volume of 1 compartment must be offset by a reciprocal change in another compartment

Front 10

in normal brain what is the goal regarding maintaining daily ICP?

Back 10

rate of absorption of CSF must match rate of production

Front 11

INTRACRANIAL TUMORS
Two classifications?

Back 11

1.Primary

2.Metastatic

Front 12

what are primary INTRACRANIAL TUMORS?

Back 12

Arise from the brain and its coverings

Front 13

Subclasses of primary brain tumors and examples.

Back 13

a.Histologically benign
-Meningioma
-Pituitary adenoma
-Astrocytoma
-Acoustic neuroma

b.Histologically malignant
-Glioblastoma
-Medulloblastoma

Front 14

what are Metastatic INTRACRANIAL TUMORS?

Back 14

Most often from primary sites in the lungs or breasts; Likely to find presence of more than one lesion

Front 15

which primary brain tumors are most common in children ?

Back 15

Astrocytomas
Medulloblastomas

Front 16

most common brain tumors in adults?

Back 16

Meningiomas
Glioblastomas
Pituitary adenomas
Metastatic tumors

Front 17

most common benign brain tumor?

Back 17

Meningiomas

Front 18

only unequivocal risk facotr ID'd for glial and meningeal neoplasms?

Back 18

ionizing radiation

Front 19

are CTs useful for dxing brain tumors? any disadvantages?

Back 19

useful but may miss structural lesions

Front 20

benefit of Cranial MRI for dxing brain tumors? any disadvantages?

Back 20

Contrast agents enhance the images

Imaging angiography can help distinguish a vascular mass from a brain tumor

Front 21

diagnostic methods for brain tumors.

Back 21

1.CT
2.MRI/angiography
3.Positron emission tomography
4.Single photon emission computed tomography

Front 22

INTRACRANIAL TUMORS
Treatments and when their typically used(3)

Back 22

1.Surgery - Partial or complete resections

2.Radiation therapy
(malignant brain tumors)

3.Chemotherapy
(combination with radiation or as initial tx in children)

Front 23

increased neurologic deficits during radiation cause & tx?

Back 23

caused by cerebral edema

tx'd with corticosteriods

Front 24

why radiation therpy often avoided in children?

Back 24

potential long-term deterimental effects like developmental delay and panhypopituitarism

Front 25

early S&S from brain tumors often due to?

Back 25

intracranial HTN

Front 26

cause of dull HA during waking hrs in pts w/ brain tumors?

Back 26

1st - increased PaCO2

2nd - cerebral vasodilation

3rd - increased intracranial contents that exceeds limits of compensation

4th - increased ICP

Front 27

Intracranial tumors
Progression of Intracranial Hypertension S&S. (10)

Back 27

1.Papilledema (visual disturbances)
2.Seizures
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)
9.mydriasis
10.decreased pupil rxn
11.midline shift on CT

Front 28

INTRACRANIAL TUMORS Anesthetic management
Principal objectives. (4)

Back 28

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

Front 29

explain Intracranial Pressure-Volume
Compliance Curve Points A-B

Back 29

compensatory: shows little
change in ICP due to CSF shifting from cranium to spinal subarachnoid space

Front 30

explain Intracranial Pressure-Volume
Compliance Curve Points C

Back 30

decompensatory:
1.no compensation
for↑in intracranial volume and ICP
2.even small ↑ in ICV
produce marked changes in ICP
3.symptoms of ↑ ICP appear

Front 31

explain Intracranial Pressure-Volume
Compliance Curve Points D

Back 31

decompensatory: Additional ↑ in volume at point C can precipitate abrupt increases in ICP.

Front 32

increased ICP effect on CBF and CPP.

Back 32

decreased CBF & CPP

Front 33

what is the compensatory mechanism associated with decreased CPP & CBF? what happens if this mechanism fails?

Back 33

increased systemic BP

cerebral ischemia

Front 34

equation and normal range for CPP

Back 34

Cerebral Perfusion Pressure (CPP) = MAP - ICP

Normal: CPP of 60-80 mmHg

Front 35

CPP < 60 mmHg will lead to?

Back 35

↑ risk for ischemic neuronal damage

Front 36

CPP will be higher in what population of pts?

Back 36

patient with chronic HTN

Front 37

When monitoring ICP
Sudden bilateral pupillary dilation is associated with ?

Back 37

herniation of the brain stem through the foramen magnum

Front 38

how can ICP be monitored?

Back 38

1.Epidural transducer
2.subdural transducer
3.intraventricular catheter

Front 39

what are “plateau waves” ? are they good/bad and why?

Back 39

Abrupt ↑ to as high as 100 mmHg

bad

could exacerbate symptoms and induce hyperventilation.

Front 40

Reasons for ↑ ICP before procedure

Back 40

1.Anxiety
2.Painful stimulation
3.Induction (sympathetic stimulation)
4.Noxious stimulation

Front 41

Methods to ↓ ICP

Back 41

1.Hyperventilation
2.Posture
3.CSF drainage
4.Hyperosmotic drugs
5.Diuretics
6.Corticosteroids
7.Barbiturates

Front 42

when is hyperventilation a good option during ICP mngmt?

Back 42

rapid ↓ ICP: Maintain PaCO2 near 30 mmHg

Front 43

what is the time frame for getting benefit from hyperventilation for decreasing ICP?

Back 43

Duration of hyperventilation may be limited (beneficial effects wanes in 6-12 hours)

Front 44

disadvantages of hyperventilation for ICP mgmt?

Back 44

1.excessive (PaCO2)lowering can ↓ CBF to the point of cerebral ischemia

2.Rebound ↑ in ICP is a potential problem

Front 45

Appropriate to initiate more aggressive hyperventilation in children to maintain PaCO2. Why?

Back 45

higher CBF than adults

Front 46

what effect does hyperventilation have on cerebral vasculature?

Back 46

vasoconstriction

Front 47

what patients would hyperventalation not be benefical for controling increased ICP?

Back 47

If the problem with intracranial hypertension is decreased blood flow, it may not be logical to treat the disorder with vasoconstriction

Front 48

what head position lowers ICP? why?

Back 48

Elevate head 30˚ above heart level

encourages venous outflow from brain

Front 49

what head position elevates ICP?

Back 49

head down

Front 50

CSF drainage locations?

Back 50

Lateral cerebral ventricles or lumbar subarachnoid space

Front 51

Hyperosmotic drug for lowering ICP? MOA?

Back 51

Mannitol

produces transient ↑ in osmolarity of plasma, which draws water from tissues including the brain

Front 52

does of mannitol and infusion rate? what are the typical results?

Back 52

0.25 to 1.0 g/kg IV over 15 to 30 min

loss of 100 ml of water from brain within 30 min

Front 53

mannitol cautions? (2)

Back 53

1.elderly as BBB may not be intact thus causing cerebral edema

2.has direct vascular vasodilating properties→ ↑CBV & ↑ICP

Front 54

Diuretic for lowering ICP? when is it useful?

Back 54

Lasix

Useful with ↑ vascular fluid volume & pulmonary edema

Front 55

Corticosteroids means of decrasing ICP?

Back 55

1.Stabilization of membranes
2.reduces cerebral edema
3.reduces CSF production
4.increases seizure threshold

Front 56

Barbiturates are Helpful for treating ICP after what? MOA

Back 56

after acute head injury

Potent cerebral vasoconstrictor that ↓ CBV & ↓CBF while ↓CMRO2

Front 57

determinants of CBF?

Back 57

1.PaCO2
2.PaO2
3.arterial BP & autoregulation
4.venous BP
5.anesthetic drugs/techniques

Front 58

Normal CBF:

Back 58

50 ml/100g/min

Front 59

CBF increases how much for every 1 mmHg ↑ PaCO2 above 40?

Back 59

1 ml/100g/min

Front 60

CBF ↓ how much when PaCO2 is 20 mmHg?

Back 60

by about 50%

Front 61

Intracerebral steal syndrome

Back 61

↑ PaCO2, blood flow is shunted away from tumor

Front 62

Robin Hood phenomenon

Back 62

Hypocapnia constricts normal vessels which can shunt blood flow to acidotic areas surrounding tumors

Front 63

Hypoxemia & hypercarbia exert a additive or synergistic effect with ↑ in CBF?

Back 63

synergistic effect

Front 64

_____ is the most important determinant of CBF!

Back 64

PaCO2

Front 65

cerebral Autoregulation

Back 65

Ability of the brain to maintain CBF at constant levels despite changes in MAP

Front 66

Autoregulation may be lost or impaired in the presence of ? (3)

Back 66

1.intracranial tumors,
2.head trauma or 3.administration of volatile anesthetics

Front 67

cerebral autoregulation MAP range

Back 67

60-150 mmHg

Front 68

what happens in brain when MAP > 150 mmHg ?

Back 68

↑ CBF → overdistention of the wall of cerebral blood vessels → cerebral edema

Front 69

what happens in brain when MAP < 60 mmHg?

Back 69

may see symptoms of cerebral ischemia (nausea, dizziness, slow cerebration)

Front 70

presence of chronic hypertension does what to the cerebral autoregualtion curve?

Back 70

displaced to right, meaning a higher MAP is tolerated before CBF becomes pressure dependent

Front 71

in what body position is venous pressure Usually low ?

Back 71

in supine or standing patients

Front 72

what is predominant determinant of cerebral perfusion pressure?

Back 72

MAP

Front 73

why Consider avoiding PEEP in patients undergoing intracranial surgery?

Back 73

sequence
a.PEEP
b.↑venous pressure (can ↑ bleeding during surgery)
c.↑ CBF
d.↑ ICP
e.↓ CPP

Front 74

Volatile anesthetics ___ MAC are often potent cerebral vasodilators producing dose-dependent ___ CBF. Is this good or bad?

Back 74

>0.6; increases

can be bad b/c patients with intracranial tumors may not displace CSF to compensate and end up with an ↑ ICP

Front 75

is Nitrous oxide bad during brain tumor ICP mgmt?

Back 75

unlikely to ↑ ICP in patient with intracranial tumors maintained at normocarbia

Front 76

Drugs that produce cerebral vasoconstriction and predictably ↓ CBF and ICP. (4)

Back 76

1.barbiturates-thiopental, 2.etomidate,
3.propofol,
4.opioids

Front 77

can Succinylcholine or nondepolarizing neuromuscular blocking drugs be used on patients with brain tumors ?

Back 77

unlikely to alter ICP; However, drug induced histamine release could theoretically produce cerebral vasodilation with associated ↑ in CBF and ICP

Front 78

is Ketamine bad during brain tumor ICP mgmt? why?

Back 78

yes

dilates the cerebral vasculature and ↑ CBF & ICP

Front 79

↑ ICP, Loss of consciousness, and slow breathing are signs of?

Back 79

herniation of cerebellar tonsils through foramen magnum

Front 80

should Avoid what during preop prep of brain tumor pts for surgery?

Back 80

Medications causing sedation or respiratory depression

Front 81

should be Cautious with what group of drugs preop and why?

Back 81

Opioids-

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

Front 82

Intracranial tumors Anesthetic induction:

what induction drugs produce rapid, reliable onset of unconsciousness with minimal effects on CBF ?

Back 82

(thiopental, etomidate, propofol)

Front 83

Intracranial tumors Anesthetic induction:

what other things can you do during induction to Maintain CPP of 60-80 mmHg? (4)

Back 83

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

Front 84

Intracranial tumors Anesthetic induction:

perception of noxious stimuli effect on CMRO, CBF & ICP

Back 84

can abruptly ↑CMRO, CBF & ICP

Front 85

Intracranial tumors Anesthetic induction:

prevention of perception of noxious stimuli

Back 85

Adequate depth of anesthesia & skeletal muscle paralysis

Front 86

when is N2O not good to use in intracranial cases?

Back 86

sitting position b/c ↑ risk of venous air embolism

Front 87

what volatile agent is most often used during intracranial cases? at what concentration & why?

Back 87

Isoflurane 0.6 MAC

high concentrations can ↑ CBF and ICP

Front 88

why use Caution w/ Peripheral vasodilating drugs (Nitroprusside/ nitroglycerin) in intracranial cases?

Back 88

may ↑ CBF & ICP

Front 89

why are glucose replacement solutions not used w/ intracranial cases?

Back 89

Metabolism of glucose in brain leaves free water in excess

Front 90

Replace fluid volume depletion with what 3 things and not with what? at what rate?

Back 90

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

Front 91

Can reduce cerebral metabolic rate of oxygen (CMRO2) by approximately __ per __ reduction in body temperature

Back 91

7%; 1˚ C

Front 92

what does CMRO2 stand for?

Back 92

cerebral metabolic rate of oxygen

Front 93

most common positioning for intracranial cases? why?

Back 93

Supine with head elevated 10˚-15˚

to facilitate cerebral venous drainage

Front 94

Sitting position is used for ?

Back 94

exploration of posterior cranial fossa

Front 95

disadvantages of sitting position

Back 95

↓ systemic pressure & CO; potential for venous air embolism

Front 96

advantages of sitting position

Back 96

excellent surgical exposure, facilitates cerebral venous & CSF drainage

Front 97

venous air embolisms are potential hazards when? why additional hazard is noted with craniotomies?

Back 97

operative site is above the level of the patient’s heart

veins in the skull may not collapse

Front 98

Pathophysiology of venous air embolisms

Back 98

Air enters RV→interference of blood flow into pulmonary artery→pulmonary edema & reflex bronchoconstriction may result from movement of air into pulmonary circulation

Front 99

early signs of venous air embolisms & reason for each. (3)

Back 99

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)

Front 100

Late signs of venous air embolism. (4)

Back 100

1.hypotension,
2.tachycardia,
3.cardiac dysrhythmias, cyanosis,
4.“millwheel” murmur (heard through esophageal stethoscope)

Front 101

Venous Air Embolism
Treatment (4)

Back 101

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

Front 102

INTRACRANIAL TUMORS: Postoperative management
GOALs. (3)

Back 102

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

Front 103

Stroke is the leading cause of _____ and the 3rd leading cause of ____ in the US

Back 103

disability; death

Front 104

ischemic strokes make up _____% and hemorrhagic strokes make up ___% of all strokes

Back 104

(80%)(20%)

Front 105

Hemorrhagic stroke 2 classifications?

Back 105

intracerebral or subarachnoid

Front 106

Ischemic stroke is described by what 2 ways?

Back 106

area of brain affected and etiologic mechanisms

Front 107

Transient Ischemic Attack:

Back 107

sudden vascular-related focal neurologic deficit that revolves within 24 hours

Front 108

REVIEW Cerebrovascular Anatomy

Back 108

REVIEW Cerebrovascular Anatomy

Front 109

Blood is supplied to the brain via 2 pairs of vessels

Back 109

1.Internal carotid arteries
2.Vertebral arteries

Front 110

Internal carotid arteries
Vertebral arteries
Unite to form ?

Back 110

the basilar artery,

Front 111

the basilar artery, terminates and splits into what?

Back 111

two posterior cerebral arteries

Front 112

the two posterior cerebral arteries supplies blood to what 4 parts?

Back 112

medial, temporal & occipital lobe, parts of thalamus

Front 113

the Internal carotid arteries,
Vertebral arteries,
the basilar artery, and the two posterior cerebral arteries join on the surface of the brain to form ?

Back 113

the intracranial vessels (anterior cerebral artery, middle cerebral artery, posterior cerebral artery) & Circle of Willis

Front 114

True or False. A stroke represents a medical emergency!

Back 114

true

Front 115

what helps distinguish b/t Hemorrhage or Ischemia stroke?

Back 115

CT

Front 116

why is it important to distinguish b/t Hemorrhage or Ischemia stroke?

Back 116

treatment is substantially different

Front 117

how can Conventional angiography help in dx and/or tx of strokes?

Back 117

help detect acute occlusion or a lodge embolus

Front 118

acute ischemic stroke Most likely reflects what 3 things?

Back 118

1.cardioembolism,

2.large vessel atherothrombolembolism,

3.small vessel occlusive disease

Front 119

what population of patients are most likely to experience acute ischemic stroke due to small-vessel occlusive disease?

Back 119

Patients with diabetes mellitus or systemic hypertension

Front 120

Risk factors for acute ischemic stroke. (5)

Back 120

1.Systemic hypertension- most significant risk factor
2.Smoking
3.Hyperlipidemia
4.Diabetes mellitus
5.Excessive alcohol consumption

Front 121

Carotid Endarterectomy.

what population has the greatest benefit?

Back 121

Procedure to ↓ risk of stroke
by surgically treating symptomatic carotid artery stenosis

men with a stenosis diameter >70%

Front 122

2 alternatives to CEA

Back 122

Angioplasty and stenting

Front 123

Carotid Endarterectomy Preoperative Evaluation objectives (4)

Back 123

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

Front 124

Carotid Endarterectomy Management Options:

Back 124

general or regional anesthesia

Front 125

Carotid Endarterectomy Management Goals:

Back 125

1.Maintain hemodynamic stability
2.prompt emergence, allowing rapid assessment of neurologic status

Front 126

Carotid Endarterectomy Management Monitoring:

Back 126

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

Front 127

Carotid Endarterectomy Postoperative management:

After extubation, observe patient for the following complications

Back 127

1.cardiac (BP changes, MI),

2.airway obstruction (hematoma formation)

3.neurologic complications (thrombosis, intracerebral hemorrhage)

Front 128

Carotid Endarterectomy Postoperative management:

treatment of persisting HTN

Back 128

hydralazine or labetalol

Front 129

Medical management of acute ischemic stroke:

Respiratory function objectives

Back 129

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

Front 130

Medical management of acute ischemic stroke:

why is systemic BP so critically important?

Back 130

Critically important as blood flow to ischemic regions is dependent on cerebral perfusion pressure

Front 131

Medical management of acute ischemic stroke:

Blood glucose concentration importance?

Back 131

Hyperglycemia→ poor outcomes (glucose may be metabolized into lactic acid, resulting in acidosis and ↑ tissue injury)

Front 132

Medical management of acute ischemic stroke:

Hypothermia importance

Back 132

Body Temperature
may help ↓neuronal oxygen demands, cerebral edema, and neurotransmitter toxicity

Front 133

Pharmacologic treatment of acute ischemic stroke

Heparin Prophylaxis
a.indication
b.dose
c.exception

Back 133

for DVT is common

5000 units SQ every 12 hours

Patients with acute hemmorhage are treated with pneumatic compression stockings

Front 134

Pharmacologic treatment of acute ischemic stroke

Aspirin use recommendations?

Back 134

initial therapy for acute stroke patients and for prevention of recurrent strokes

Front 135

Pharmacologic treatment of acute ischemic stroke

Intravenous recombinant tissue plasminogen activator use recommendations?

Back 135

patients who meet specific eligibility requirements and if patient can be initiated within 3 hours of the onset of acute symptoms

Front 136

Acute Hemorrhagic Stroke 2 most reliable predictors of outcome:

Back 136

Estimated volume of blood & LOC

Front 137

Acute Hemorrhagic Stroke management (4)

Back 137

1.sedation,
2.prompt ventricular drainage,
3.ICP monitoring,
4.tracheal intubation if needed

Front 138

Subarachnoid Hemorrhage common location

Back 138

a.Commonly results from aneurysms of the circle of Willis

Front 139

Subarachnoid Hemorrhage
common S&S (3)

Back 139

1.terrible headaches

2.inversion of T waves and ST segment depression

3.catecholamine release

Front 140

Acute Hemorrhagic Stroke
management Goals? (2)

Back 140

1.prevent increases in transmural pressure of the aneurysmal sac, MAP-ICP, (could increase the risk of aneurysmal rupture)

WHILE

2.maintaining an adequate CPP to prevent cerebral ischemia

Front 141

Subarachnoid hemorrhage Treatment

Back 141

localizing the aneurysm

Front 142

Acute Hemorrhagic Stroke
Anesthetic management:

Back 142

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

Front 143

Acute Hemorrhagic Stroke: Induction goals (4)

Back 143

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)

Front 144

Acute Hemorrhagic Stroke: Maintenance Goals (5)

Back 144

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

Front 145

Acute Hemorrhagic Stroke: Maintenance options (2)

Back 145

1.volatile agents and supplemented with opioids

2.TIVA (Propofol & fentanyl)

Front 146

why should nitrous be avoided in acute hemorrhagic stroke anesthesia maintenance?

Back 146

potent cerebral vasodilator

Front 147

ways to achieve optimization of brain relaxation during acute hemorrhagic stroke anesthesia. (3)

Back 147

1.Loop and/or osmotic diuretics

2.Proper positioning to facilitate cerebral venous drainage

3.Normovolemia or modest hypervolemia (avoid glucose containing solutions)

Front 148

Controlled Hypotension

Back 148

induction of a MAP < 50 mmHg for the short period of time needed to clip an intracranial aneurysm

Front 149

Guideline for safe levels of controlled hypotension:

Back 149

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)

Front 150

during controlled hypotension consider the possibility of ?

Back 150

a rightward shift of the curve for autoregulation of CBF

Front 151

Acute Hemorrhagic Stroke: Emergence goals? (4)

Back 151

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)

Front 152

who should you suspect in?

Back 152

in patients who complain of visual loss during 1st postoperative week

Front 153

Ischemic Optic Neuropathy (Progressive blindness) aka?

Back 153

stroke of the optic nerve

Front 154

2 classifications of Ischemic Optic Neuropathy (Progressive blindness)

Back 154

Anterior ION & Posterior ION

Front 155

after suspecting Ischemic Optic Neuropathy (Progressive blindness)what should be obtained urgently?

Back 155

opthalmologic consultation for diagnosis and treatment

Front 156

Anterior Ischemic Optic Neuropathy
Cause?

Back 156

infarction at watershed zones between areas of distribution of posterior ciliary arteries

Front 157

Anterior Ischemic Optic Neuropathy S & S?

Back 157

1.sudden, painless, monocular visual deficits

2.varing in severity from slight visual acuity to blindness

Front 158

Anterior Ischemic Optic Neuropathy
2 forms

Back 158

nonarteric & arteric

Front 159

Nonarteric AION
a.period of manifestation
b.patho
c.causes

Back 159

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

Front 160

Arteritic AION
a.frequency
b.location
c.treatment (rationale)

Back 160

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)

Front 161

Posterior Ischemic Optic Neuropathy

Back 161

Acute loss of vision and visual fields

Front 162

Posterior Ischemic Optic Neuropathy patho

Back 162

↓ oxygen delivery to posterior portion of optic nerve between optic foramen and central retinal artery’s point of entry

Front 163

Posterior Ischemic Optic Neuropathy Etiology. (6)

Back 163

1.hypotension,
2.anemia,
3.air embolism,
4.venous obstruction, 5.infection
6.altered anatomy

Front 164

what is interesting about Posterior Ischemic Optic Neuropathy S & S?

Back 164

Symptom free period precedes loss of vision

Front 165

Posterior Ischemic Optic Neuropathy assoicated with what surgeries? (4)

Back 165

1.prolonged spine surgery in prone position,
2.cardiac surgery,
3.radical neck dissection, 4.hip arthroplasty

Front 166

Man-in-the-Barrel Syndrome
a.S&S
b.patho
c.etiology

Back 166

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

Front 167

Arnold-Chiari Malformation

Back 167

Downward displacement (herniation) of cerebellum and portion of medulla through foramen magnum into upper cervical spinal canal

Front 168

what pathophysiology results from Arnold-Chiari Malformation? (6)

Back 168

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

Front 169

Arnold-Chiari Malformation S/S:

Back 169

1.occipital HA and down shoulders and arms; worsens with cough and head movement;
2.visual disturbances; 3.intermittent vertigo, 4.ataxia

Front 170

Arnold-Chiari Malformation Treatment:

Back 170

surgical decompression by freeing adhesions and enlarging foramen magnum

Front 171

Arnold-Chiari Malformation Anesthesia implications:

Back 171

associated ↑ ICP

Front 172

cavitation

Back 172

the formation of cavities in an organ, especially in lung tissue as a result of diseases like tuberculosis

Front 173

Syringomyelia

Back 173

Slow progressive degeneration of spinal cord → cavitation → syringobulbia

Front 174

syringobulbia

Back 174

extension of cavitation process cephalad into medulla

Front 175

what pathophysiology results from Syringomyelia? (3)

Back 175

Obstructed outflow of CSF from 4th ventricle in embryo development → pressure to canal of spinal cord → cyst formation

Front 176

Syringomyelia S/S: (5)

Back 176

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)

Front 177

Syringomyelia Treatment:

Back 177

no know effective tx

Front 178

Anesthetic management of syringomyelia or syringobulbia. (5)

Back 178

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

Front 179

Amyotrophic Lateral Sclerosis

Back 179

Degenerative disease of motor ganglia in anterior horn of spinal cord and pyramidal tracts

Front 180

Amyotrophic Lateral Sclerosis
common age & population

Back 180

men 40-60yrs

Front 181

Amyotrophic Lateral Sclerosis Etiology

Back 181

Viral, genetic

Front 182

Amyotrophic Lateral Sclerosis
S/S

Back 182

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)

Front 183

Amyotrophic Lateral Sclerosis
prognosis

Back 183

death within 6 yrs from resp failure

Front 184

Amyotrophic Lateral Sclerosis
anesthesia management

Back 184

1.General anesthesia → exaggerated ventilatory depression possible

2.Regional anesthesia likely avoided → exacerbation possible

Front 185

Friedreich’s Ataxia

Back 185

Autosomal recessive disorder causing degeneration of spinocerebellar and pyramidal tracts

Front 186

Friedreich’s Ataxia
prognosis

Back 186

Fatal by early adulthood from cardiac failure

Front 187

Friedreich’s Ataxia
S/S:

Back 187

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

Front 188

Friedreich’s Ataxia
Anesthetic Implications:

Back 188

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)

Front 189

Parkinson’s Disease etiology

Back 189

Unknown cause

Front 190

Parkinson’s Disease

Back 190

neurodegenerative → Loss of dopaminergic fibers in basal ganglia

Front 191

Parkinson’s Disease pathological effects

Back 191

Dopamine mediates or decreases firing rate of extrapyramidal movement → unopposed action of Ach

Front 192

Parkinson’s Disease classic triad of major signs

Back 192

tremors, rigidity, akinesia

Front 193

Parkinson’s Disease: where skeletal muscle rigidity first appears?

Back 193

proximal muscles of neck

Front 194

Parkinson’s Disease: manifestations

Back 194

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
6.seborhea,
7.oily skin,
8.pupillary abnormalities, 9.diaphragmatic spasms, 10.oculogyric crises

Front 195

Parkinson’s Disease: Levadopa side effects

Back 195

1.Orthostatic hypotension
2.↑ myocardial contractility
3.N/V from stim of CTZ area in brain

Front 196

Parkinson’s Disease: Surgical Tx:

Back 196

1.Thalamic nucleus interventions (transient), 2.Pallidotomy,
3.Fetal tissue transplant

Front 197

Anesthetic implicattions os levadopa

Back 197

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

Front 198

Questionable drugs for parkinson's dz

Back 198

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)

Front 199

Huntington’s Chorea

Back 199

Autosomal dominant trait Premature degenerative disease of CNS

Front 200

Huntington’s Chorea patho effects

Back 200

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

Front 201

Huntington’s Chorea age & duration

Back 201

appears at 35-40 yrs old

Lasts for about 17 yrs

Front 202

Huntington’s Chorea S/S: (5)

Back 202

1.progressive dementia 2.choreoathetosis
3.pharyngeal muscle inbolvement → pulmonary aspiration;
4.depression
5.suicide

Front 203

choreoathetosis

Back 203

proximal jerky involuntary movements → hypotonia/hypertonia

Front 204

Huntington’s Chorea Tx:

Back 204

1.Haldol;
2.Butyrophenones (interfere w/NT effects of dopamine)

Front 205

Huntington’s Chorea Anesthesia management:
1.preop meds
2.precautions
3.intraop meds

Back 205

1.Preop sedation w/droperidol
2.Aspiration precaution if pharyngeal muscle involved
3.Opioid, droperidol, N2O, and Sevo
•

Front 206

Huntington’s Chorea drug caution/contraindications (2)

Back 206

1.Decreased plasma cholinesterase! Prolongs Sux (can still give, just know its prolonged)
2.Sensitive to effects of nondepolarizing muscle relaxants

Front 207

Shy-Drager Syndrome

Back 207

-ANS dysfunction
-parenchymatous degeneration in CNS and spinal cord → neuronal cells
-depletion of NE from peripheral efferent nerve endings

Front 208

Shy-Drager Syndrome S/S: (7)

Back 208

1.orthostatic hypotension → syncope,
2.urinary retention,
3.bowel dysfunction,
4.↓sweating,
5.sexual impotence,
6.↓pupil reflexes,
7.abnormal control of breathing

Front 209

Shy-Drager Syndrome
1.what happens to NE w/ standing or exercise?

2.what happens w/ baroreceptors w/ hypotension

Back 209

1.NE concentrations fail to show normal ↑ after standing or exercise

2.Failure of baroreceptor reflexes to ↑ HR or vasoconstriction in response to hypotension

Front 210

Shy-Drager Syndrome: Often develops s/s of of what toher neurologic disorder?

Back 210

Parkinson’s

Front 211

Shy-Drager Syndrome Tx: (5)

Back 211

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

Front 212

Shy-Drager Syndrome: drugs that have exaggerated effects w/ this disorder?

Back 212

1.neg inotropic drugs (extreme bradycardia)
2.Vasopressors (extreme HTN)
3.volatile anesthetics (extreme brady & hypotension)

Front 213

Shy-Drager Syndrome: relationship of heart beat & respirations?

Back 213

absent beat-to-beat variability in HR when deep breathing

Front 214

Shy-Drager Syndrome: vasopressor that's best to use?

Back 214

low dose Phenylephrine

Front 215

Shy-Drager Syndrome: why is it hard to tell if they have adequate depth of anesthesia?

Back 215

↓ SNS response to noxious stimulation

Front 216

Shy-Drager Syndrome Drugs of caution:

Back 216

1.Thiopental (if hypovolemic or with rapid administration → exaggerated hypotension);

2.Ketamine → increased HTN

Front 217

Leber’s Optic Atrophy
(3)

Back 217

• Degeneration of retina and atrophy of optic nerves → blindness
• Sex-linked autosomal recessive trait
• Abnormality of cyanide metabolism

Front 218

Leber’s Optic Atrophy
what drug to avoid?

Back 218

Nitroprusside

Front 219

Creutzfeldt-Jakob Disease

Back 219

Transmissible spongiform encephalopathy w/ 10-15% family history of autosomal dominant inheritance

Front 220

Creutzfeldt-Jakob Disease
incubation period

Back 220

months to years

Front 221

Creutzfeldt-Jakob Disease
pathologic effects

Back 221

Abnormal prion protein which acts as a neurotransmitter that accumulates in the CNS

Front 222

Creutzfeldt-Jakob Disease
S&S (4)

Back 222

1.Rapid progressive dementia 2.ataxia
3.myoclonus (rare at the onset)
4.Seizures (late onset)

Front 223

Creutzfeldt-Jakob Disease
• Dx confirmation
• Differential diagnosis:

Back 223

w/brain biopsy

Alzheimer’s

Front 224

Creutzfeldt-Jakob Disease
Anesthesia and other Implications

Back 224

• Universal precautions
• Handling CSF--double glove, protective eyeware, and label “infectious”
• For brain biopsy use disposable instruments or soak in Na hypochlorite or autoclave

Front 225

Creutzfeldt-Jakob Disease: only body fluid resulting in transmission

Back 225

• CSF

Front 226

Creutzfeldt-Jakob Disease
• Transmission has been attributed to

Back 226

tx w/growth hormone and gonadotropic hormones

Front 227

Multiple Sclerosis

Back 227

Autoimmune disorder affecting CNS; occurs in genetically susceptible persons after environmental exposure

Front 228

Multiple Sclerosis
• Causes:

Back 228

predisposition (twins) environmental
infectious exposures

Front 229

Multiple Sclerosis
- population

Back 229

• Twice as common in women than men

Front 230

Multiple Sclerosis
• Pregnancy

Back 230

rate of relapse ↓ in 3rd trimester of pregnancy and ↑ during first 3 months postpartum

Front 231

Multiple Sclerosis
- relapse causes

Back 231

-Viral illness and infections
-first 3 months postpartum

Front 232

Multiple Sclerosis
• patho Characteristics

Back 232

1.inflammation, demyelination of CNS and spinal cord,
2.axonal damage in CNS; 3.loss of myelin followed by formation of demyelinative plaques;

Front 233

Multiple Sclerosis:
are Peripheral nerves affected?

Back 233

no

Front 234

Multiple Sclerosis:
• S/S (8)

Back 234

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

Front 235

Multiple Sclerosis:
what is Subacute?

Back 235

relapses and remissions vs. Chronic and progressive

Front 236

Multiple Sclerosis
• Remissions result from?

Back 236

correction of transient chemical and physiologic disturbances that have interfered with nerve conduction in the absence of demyelination

Front 237

Multiple Sclerosis
Onset

Back 237

• after 35 yrs

Front 238

Multiple Sclerosis
• Diagnosis: (4)

Back 238

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)

Front 239

Multiple Sclerosis
• Treatment: (5)

Back 239

1.Corticosteroids 2.Interferon-beta 3.Glatiramer acetate
4.Azathioprine 5.Methotrexate

Front 240

Multiple Sclerosis:
Corticosteroids

Back 240

(shortens duration of relapses)

Front 241

Devic’s disease-

Back 241

variant of MS affecting optic nerves and cervical spinal cord

Front 242

Multiple Sclerosis: Corticosteroids action

Back 242

(shortens duration of relapses)

Front 243

Interferon-beta indication for MS & side effects

Back 243

—for relapsing-remitting MS

-SE influenza s/s for 24-48 hours, Leucopenia, anemia, Co-existing depression

Front 244

Glatiramer acetate
-indication
-action

Back 244

-Multiple Sclerosis-good for interferon resistant patients

—mimics myelin basic protein;

Front 245

Azathioprine
-indication
-action

Back 245

-Multiple Sclerosis

—depresses cell-mediated and humoral immunity; ↓ rate of relapses;

Front 246

Methotrexate
-indiction
-action

Back 246

-used for secondary progressive MS patients

—inhibits cell-mediated and humoral immunity;

Front 247

MS:
sign of exacerbations during postop period and cause?

Back 247

-ANY increase in body temp (even 1 degree celcius)

-caused from complete block of conduction in demyelinated nerves

Front 248

MS:
Spinal anesthesia → postop exacerbations. why?

Back 248

local anesthetic neurotoxicity due to lack of protective sheath around spinal cord (↑ susceptibility to neurotoxicity of locals in white matter)

Front 249

effects of sux on MS

Back 249

-Sux → exaggerated release of K+

Front 250

2 effects of nondep agents on MS

Back 250

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

Front 251

number 1 perioperative drug for MS

Back 251

Corticosteroid supplementation if chronic tx

Front 252

Guillain-Barre Syndrome:
another name for it?

Back 252

(Acute Idiopathic Polyneuritis)

Front 253

Guillain-Barre Syndrome:

Back 253

Sudden of skeletal muscle weakness or paralysis

Front 254

Guillain-Barre Syndrome
course

Back 254

-Initially in legs and spreads cephalad over the next few days → arms, trunk, face

-Bulbar involvement → bilateral facial paralysis

Front 255

Guillain-Barre Syndrome Serious S/S: (2)

Back 255

1.difficulty swallowing d/t pharyngeal muscle weakness

2.impaired ventilation d/t intercostal muscle paralysis

Front 256

Guillain-Barre Syndrome
other symptoms (10)

Back 256

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)

Front 257

Guillain-Barre Syndrome:
recovery

Back 257

-Complete recovery from acute episode in a few weeks with segmental demyelination

-If axonal degeneration, slower recovery with some permanent weakness

Front 258

Guillain-Barre Syndrome:
Death

Back 258

sepsis, acute respiratory failure, pulmonary embolism, and cardiac arrest

Front 259

Guillain-Barre Syndrome:
Dx

Back 259

clinical s/s

Front 260

Guillain-Barre Syndrome:
when do s/s typically appear?

Back 260

Occurs after respiratory or GI infection in about ½ of pts

Front 261

Guillain-Barre Syndrome:
tx (6)

Back 261

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

Front 262

Guillain-Barre Syndrome:
two anesthesia considerations

Back 262

Two considerations:
1.Altered function of ANS
2.Lower motor neuron lesions

Front 263

Guillain-Barre Syndrome:
Lower motor neuron lesions anesthetic considerations?
1.CV
2.laryngoscopy
3.vasopressors
4.sux
5.nondepo
6.mechanical ventilation

Back 263

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

Front 264

what arteries make up the Circle of Willis?

Back 264

1.Internal carotids
2.Anterior cerebral arteries
3.Anterior communicating artery
4.Posterior communicating arteries
5.Posterior cerebral arteries
6.Basilar artery

Front 265

what is the Circle of Willis

Back 265

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

Front 266

Which aretery in the Cirlce of Willis is Common for formation of aneurysms

Back 266

Anterior communicating artery