Neuro

Front 1

During posterior fossa surgery, bradycardia and hypertension suddenly occur. Why?

Back 1

Stimulation of the trigeminal nerve due to pressure on by brainstem.

Front 2

During posterior fossa surgery, bradycardia and hypotension suddenly develop. Why?

Back 2

Either the glossopharyngeal or vagus nerve has been stimulated.

Front 3

What is the concern if the pt is to undergo resection of a posterior fossa tumor that is located around the glosspharyngeal and vagus nerves?

Back 3

The gag reflex may be impaired, increasing the risk of aspiration.

Front 4

What is the concern if the pt is to undergo resection of a posterior fossa tumor located at the floor of the fourth ventricle?

Back 4

Damage to the respiratory centers, leading to postop mechanical ventilation.

Front 5

Your pt had a posterior fossa neurosurgical procedure. Why might awakening from general anesthesia be slow?

Back 5

They may be slow in regaining respirations due to intraoperative trauma to the respirtory centers, impairing ventilation. The swallow and gag mechanisms may also be involved.

Front 6

Name a common postoperative complication following transphenoidal or transcranial procedures for tumor removal.

Back 6

Diabetes insipidus.

Front 7

What is the incidence of cerebral aneurysms in North America? Subarachnoid hemorrhage?

Back 7

1. Cerebral aneurysm - 1 in 50
2. Subarachnoid hemorrhage - 1 in 8,000

Front 8

The pt who is recovering from subarachnoid hemorrhage develops cerebral vasospasm. What is the incidence of cerebral vasospasm after subarachnoid hemorrhage, and when does cerebral vasospasm generally occur after subarachnoid hemorrhage

Back 8

Cerebral vasospasm develops in 30% of pts 4-12 days after subarachnoid hemorrhage.

Front 9

What are three signs and symptoms of vasospasm in pts with subarachnoid hemorrhage? What can be done to prevent/counteract cerebral vasospasm in the postop period after surgery for subarachnoid hemorrhage?

Back 9

Signs and symptoms:
1. Worsening headache
2. Hypertension
3. Confusion

Prevention can be accomplished by maintaining a greater than normal intravascular fluid volume.

Front 10

What are the three most serious complications of subarachnoid hemorrhage?

Back 10

1. Hydrocephalus
2. Increased intracranial pressure
3. Vasospasm

Front 11

Your pt is having a cerebral vasospasm. What should be done first? What additional actions may be necessary?

Back 11

The initial approach involves fluid and blood pressure management. Other actions may include expansion of intravascular volume and increasing blood pressure to the upper extreme of the pt's blood pressure.

Front 12

If the pt with a cerebral vasospasm develops neurologic deficits, what additional two therapies may be instituted?

Back 12

1. Hypertensive-hypervolemic- hemodilution therapy
2. Use of drugs aimed at lessening brain ischemia (Nimodipine)

Front 13

What is the standard regimen for treating cerebral vasospasm?

Back 13

1. Calcium channel blocker (Nimodipine)
2. Hypertensive-hypervolemic-hemodilutional therapy

Front 14

Describe how triple H therapy is used for the treatment of vasospasm.

Back 14

1. Hypertensive therapy is achieved with dopamine, dobutamine or phenylephrine to maintain SBP at 160-200 mmHg.
2. Hypervolemia is achieved by aggressive IV infusion of colloid and crystalloid solution to maintain CVP >10 mmHg or PCWP at 12-20 mmHg without placing the pt in CHF.
3. Hemodilution to target hematocrit of 33% provides balance between oxygen-carrying capacity and viscosity.

Front 15

What is the rationale for triple H therapy?

Back 15

It is intended to increase cerebral blood flow in brain areas that are ischemic due to intense vascular narrowing.

Front 16

The pt who is recovering from subarachnoid hemorrhage develops cerebral vasospasm. What drug could be selected to treat cerebral vasospasm?

Back 16

Nimodipine.

Front 17

What is the goal during induction for the pt who has an intracranial aneurysm?

Back 17

To prevent excessive, prolonged elevation in blood pressure the predictably occurs in response to direct laryngoscopy and tracheal intubation.

Front 18

Which agents are BEST for inducing a pt with an intracranial aneurysm?

Back 18

1. Barbituates
2. Benzos
3. Etomidate
4. Propofol
-followed by a NMDA.

Front 19

What is the primary reason narcotics are used for neurosurgery?

Back 19

To diminish the intubation-induced increase in blood pressure.

Front 20

What are three goals for intracranial aneurysm surgery?

Back 20

1. Avoid aneurysm rupture
2. Maintain cerebral perfusion pressure and transmural pressure
3. Provide a "slack" brain

Front 21

What is the main anesthetic goal for a pt with a cerebral aneurysm?

Back 21

Maintain or decrease cerebral perfusion pressure and transmural aneurysm pressure.

Front 22

What should be done prior to incision for opening the dura during intracranial aneurysm surgery to provide a "slack" brain?

Back 22

Reduce intracranial pressure slowly to relax the brain. Diuretics and head-up position may be helpful.

Front 23

What techniques are instituted during aneurysm surgery to "slack" the brain and facilitate dissection?

Back 23

1. CSF drainage
2. Hyperventilation
3. Osmotic diuretics
4. Barbituates

Front 24

What fluids should be administered prior to and after the clipping of the intracranial aneurysm?

Back 24

1. Before clipping, isotonic crystalloid solutions without glucose are administered to replace npo volume and maintenance only.
2. After the aneurysm is secured, intraoperative fluid deficits are replaced and additional volume is administered.

Front 25

What IV solutions should not be used for a craniotomy pt? Why?

Back 25

Dextrose containing solutions should be avoided. Hypertonic glucose in plasma initially decreases intracranial pressure by exerting an osmotic force and pulling water into the vasculature, but there will be a rebound increase in intracranial pressure as glucose is metabolized in brain cells, thereby decreasing osmotic pressure and pulling water from the vasculature to the brain.

Front 26

Is decreasing the cerebral perfusion pressure during neurosurgery an effective way of reducing cerebral blood flow and "slacking" the brain?

Back 26

No.

Front 27

To reduce intracranial volume to give the neurosurgeon more space to work in the posterior fossa, ETCO2 should be maintained at what level?

Back 27

Between 25-30 mmHg.

Front 28

For what two neurosurgical procedures might controlled hypotension be beneficial? What agents may be used to induce deliberate hypotension for those procedures?

Back 28

1. Cerebral aneurysm repair
2. Brain tumor resection

Isoflurane, nitroprusside and esmolol are most commonly used.

Front 29

Why is isoflurane beneficial during a neurosurgical case using controlled hypotension?

Back 29

1. It enhances the effects of the commonly used hypotensive agents.
2. It blunts the stress-response evoked by deliberate hypotension.
3. Pulmonary shunting is not increased.

Front 30

Mean arterial pressure should be maintained at what level during controlled hypotension for surgery for clipping of a cerebral aneurysm?

Back 30

Between 60-70 mmHg.

Front 31

What is the goal of deliberate hypotension during surgery for cerebral aneurysm?

Back 31

To maintain or reduce transmural pressure as this would decrease the likelihood of aneurysm rupture.

Front 32

When using a hypotensive technique during a craniotomy, what happens to blood flow to ischemic and nonischemic regions of the brain? What is this shift in blood flow called?

Back 32

Vessels in the ischemic regions are already maximally dilated. Decreased blood pressure by the hypotensive technique causes the normal cerebral arteries to dilate, resulting in a shunting of blood away from the ischemic region (intracerebral steal syndrome).

Front 33

List seven causes for disruption of the blood-brain barrier.

Back 33

1. Disease
2. Osmotic shock
3. Acute hypertension
4. Trauma
5. Irradiation
6. Tumor
7. Ischemia

Front 34

What can happen to ICP when isotonic IV fluids are administered to a pt with a disrupted BBB?

Back 34

ICP can increase.

Front 35

List seven signs and symptoms that might indicate the presence of a venous air embolism.

Back 35

1. Decreased ETCO2
2. Decreased oxygenation
3. Detection of end-tidal nitrogen
4. Dysrhythmias
5. Mill wheel murmur
6. Hypotension
7. Sudden appearance of vigorous spontaneous ventilation despite continuing mechanical ventilation.

Front 36

What are pulmonary signs of venous air embolism?

Back 36

1. Decreased PaO2 and SaO2
2. Decreased ETCO2
3. Increased PaCO2
4. Nitrogen is detected in the end-tidal gases.

Front 37

Your healthy young pt is in the sitting position for an open craniotomy under general endotracheal anesthesia when suddenly ETCO2 drops. What is the probable problem?

Back 37

Venous air embolus.

Front 38

Nine actions should be taken in response to venous air embolism.

Back 38

1. Notify the surgeon so he can flood the field with saline or pack the field.
2. Turn off N2O.
3. Administer 100% oxygen.
4. Aspirate the central venous catheter.
5. Irrigate the operative site with fluid and apply occlusive material to all bone edges.
6. Infuse fluid intravenously to increase venous pressure.
7. Give vasopressures.
8. Temporarily compress the right and left jugular veins.
9. Place pt in a horizontal position.

Front 39

Where in the heart would you place the tip of he central venous catheter to aspirate air with a venous air embolism?

Back 39

Right atrium with the catheter tip 3 cm below the junction of the right atrium with the superior vena cava.

Front 40

If your initial actions to treat venous air embolism fail, in what position should the pt be place?

Back 40

Left lateral decubitus position with a slight Trendelenburg.

Front 41

If circulatory arrest persists after the pt with venous air embolism is placed in the left lateral decubitus position, what should be done?

Back 41

Place the pt in the supine position and start cardiac compressions.

Front 42

What is the probable cause of death in a pt with a venous air embolism?

Back 42

Cardiovascular collapse and arterial hypoxemia.

Front 43

Identify the location of appropriate placement of the Doppler for detecting a venous air embolus.

Back 43

Over the right atrium, from the 3rd to 6th intercostal spaces, right of the sternum.

Front 44

Identify the two most sensitive monitors for detection of air emboli.

Back 44

1. TEE
2. Doppler probe over the right side of the heart

Front 45

Which method is the most sensitive for detecting venous air embolism?

Back 45

TEE

Front 46

Transesophageal two-dimensional echocardiography has greater sensitivity the precordial Doppler ultrasound for detecting venous air embolism. Transesophageal two-dimensional echocardiography has an additional benefit; what is this benefit?

Back 46

Evaluation of cardiac function.

Front 47

Identify three more measurements that show intermediate sensitivity for detecting venous air embolism.

Back 47

1. Pulmonary artery pressure
2. ETCO2
3. PaO2

Front 48

What two monitoring methods are least sensitive for detecting venous air embolism?

Back 48

1. PaCO2
2. MAP

Front 49

What is the major intraoperative complication during cerebral aneurysm surgery?

Back 49

Hemorrhage

Front 50

If a cerebral aneurysm ruptures during surgery, what is your plan?

Back 50

1. Immediate, aggressive fluid resuscitation with dextrose-free fluid.
2. Controlled hypotension
3. Maintenance of normocarbia.

Front 51

What should you do if an intracranial aneurysm ruptures before, during or immediately after induction?

Back 51

First hyperventilate with 100% oxygen. Then control blood pressure and give thiopental.

Front 52

Once the bleeding is controlled, what measure can be taken to protect the brain from ischemic damage if an intracranial aneurysm ruptures during the case?

Back 52

Barbiturates and/or thiopental may be given

Front 53

What is cerebral blood flow in ml/min? in ml/100g/min? As a % of cardiac output?

Back 53

1. 750 ml/min
2. 50 ml/100 g/min
3. 15-20% of cardiac output

Front 54

Below what cerebral blood flow does cerebral ischemia occur?

Back 54

50% of normal

Front 55

What are the two determinants of cerebral blood flow?

Back 55

1. Cerebral vascular resistance
2. Cerebral perfusion pressure

Front 56

Cerebral perfusion pressure normally is equal to what?

Back 56

Cerebral perfusion = MAP-ICP

Front 57

When is cerebral perfusion pressure not equal to the difference between mean arterial pressure and intracranial pressure?

Back 57

When right atrial pressure is abnormally elevated and greater than intracranial pressure.

Front 58

What is the cerebral perfusion pressure when intracranial pressure is 15 mmHg, right atrial pressure is 5 mmHg and MAP is 110 mmHg?

Back 58

95 mmHg

Front 59

Identify 3 factors that alter cerebral vascular resistance and hence cerebral blood flow.

Back 59

Changes in:
1. PaCO2
2. PaO2
3. Temperature

Front 60

The single most important determinant of cerebral blood flow so far as the anesthetist is concerned, is what?

Back 60

PaCO2

Front 61

How does hypercarbia alter cerebral blood flow? Hypocarbia?

Back 61

1. Increased with hypercarbia.
2. Decreased with hypocarbia.

Front 62

How would hyperventilation affect cerebral vessels and blood flow? Hypoventilation?

Back 62

1. Hyperventilation would cause constriction of vessels and a decrease in blood flow.
2. Hypoventilation would cause dilatation of vessels and an increase in blood flow.

Front 63

How much does cerebral blood flow decrease in ml/100g tissue/min for each mmHg decrease in PaCO2? How much does it increase for each mmHg increase in PaCO2?

Back 63

1. It decreases 1 ml/100g/min for each mmHg decrease in PaCO2 down to about 20 mmHg.
2. It will increase 1 ml/100g/min for each 1 mmHg increase in PaCO2.

Front 64

What substance is the most potent vasodilator of the cerebral vascular system?

Back 64

CO2

Front 65

What is the only intravenous anesthetic agent that dilates cerebral vasculature and increases cerebral blood flow by 50-60%?

Back 65

Ketamine

Front 66

How does a change in temperature alter cerebral blood flow and cerebral metabolism.

Back 66

An increase in temperature causes an increase in cerebral blood flow and cerebral metabolism. A decrease in temperature causes a decrease in cerebral blood flow and cerebral metabolism.

Front 67

How much does cerebral blood flow decrease for each 1 degree C decrease in temperature?

Back 67

By 7%

Front 68

For each 1 degree C decrease in temperature, cerebral metabolic rate decreases by what percent?

Back 68

6-7%

Front 69

Does acute metabolic acidosis or alkalosis alter cerebral blood flow? Why or why not?

Back 69

No, because ions including H+ and HCO3 do not cross the BBB.

Front 70

When PaO2 falls below what level will cerebral blood flow increase?

Back 70

50 mmHg

Front 71

Normally, how does a change in cerebral perfusion pressure affect cerebral blood flow?

Back 71

Changing perfusion pressure does not normally alter CBF, because CBF is autoregulated over the range of MAP from 50-150 mmHg.

Front 72

When is autoregulation of cerebral blood flow lost?

Back 72

When MAP falls below 50 mmHg or rises above 150 mmHg.

Front 73

What happens to autoregulation in pts with chronic arterial hypertension.

Back 73

The range of pressures for autoregulation increases.

Front 74

Where in the brain may autoregulation of blood flow be diminished/impaired?

Back 74

In diseased or traumatized regions of brain.

Front 75

Distinguish between focal and global cerebral ischemia.

Back 75

1. Global ischemia occurs when the entire brain is unperfused.
2. Focal ischemia has 3 zones of brain tissue:
a. the penumbra
b. an inner zone
c. normally perfused tissue

Front 76

At what intracranial pressures does focal ischemia occur? At what intracranial pressures does global ischemia occur?

Back 76

1. Focal ischemia develops between 25-55 mmHg.
2. Global ischemia occurs at about 55 mmHg.

Front 77

The pt with an intracranial pressure of 40 mmHg will exhibit what type of cerebral ischemia, focal or global?

Back 77

Focal ischemia

Front 78

How is cerebral "steal" syndrome triggered during anesthesia?

Back 78

It could be triggered if the pt is given a vasodilator or if the pt is hypoventilated.

Front 79

What two actions can the anesthetist take to prevent cerebral steal?

Back 79

1. Hyperventilate the pt
2. Reduce metabolism by given an agent such as a barbiturate.

Front 80

What is Robin Hood effect? What are other names for the Robin Hood effect?

Back 80

A shunting of blood from adequately perfused cerebral tissues to compromised, potentially ischemic areas. Other names include reverse steal and inverse steal.

Front 81

What triggers the Robin Hood effect? Explain?

Back 81

Hypocarbia. It constricts cerebral vessels in nonischemic tissues. Blood is diverted from nonischemic to ischemic regions.

Front 82

What happens to cerebrovascular tone and blood flow in ischemic and nonischemic regions of the brain when the pt is hyperventilated.

Back 82

Blood vessel diameters in ischemic areas remain unchanged; they remain maximally dilated because of the presence of local metabolic factors so blood flow to ischemic issue increases.

Front 83

What happens to cerebrovascular tone and blood flow in ischemic and nonischemic regions of the brain when the pt is hypoventilated?

Back 83

Cerebrovascular tone in ischemic areas remains unchanged, but blood flow decreases because blood is diverted to non-ischemic regions.

Front 84

What is the function of the circle of Willis?

Back 84

It provides collateral blood flow to the brain if a major vessel carrying blood to the brain become obliterated.

Front 85

How is intracranial pressure affected by cerebral blood flow?

Back 85

The greater the blood flow, the greater the intracranial pressure.

Front 86

What is the normal intracranial pressure?

Back 86

5-15 mmHg

Front 87

What % of the intracranial volume is occupied by brain, by blood, and by cerebrospinal fluid?

Back 87

1. 80% brain matter and intracellular water
2. 12% blood
3. 8% CSF

Front 88

What keeps intracranial pressure from increasing initially when one of the intracranial compartments begins expanding because of a pathological condition?

Back 88

CSF passes through the foramen magnum into the spinal cord.

Front 89

What is papilledema? What usually causes papilledema?

Back 89

It is edema and hyperemia of the optic disk. It is usually associated with an increased ICP.

Front 90

Papilledema involves which cranial nerve?

Back 90

Cranial nerve II (optic nerve)

Front 91

Continuous readings of ICP in neurotrauma pts reveal 3 distinct pathological wave forms. Names these 3 waveforms, and indicate which two are not useful in guiding therapy or predicting outcome.

Back 91

1. A-waves
2. B-waves
3. C-waves

B and C waves are not useful in relation to therapy or outcome.

Front 92

When are plateau waves (A-waves) observed, and what causes them?

Back 92

They are found in pts with increased ICP. It is caused by an abrupt increase in cerebral blood volume in regions where cerebral blood flow is decreased.

Front 93

The anterior, middle and posterior cranial fossa contain what structures? What herniates through the foramen magnum when intracranial pressure becomes excessive?

Back 93

1. The frontal lobe rests on the anterior cranial fossa.
2. The temporal lobe rests on the middle cranial fossa.
3. The brainstem and cerebellum rest on the posterior cranial fossa.

The brainstem herniates when ICP becomes excessive.

Front 94

What are 12 signs and symptoms of increased ICP?

Back 94

1. Headache
2. Nausea and vomiting
3. Blurred vision
4. Unilateral pupillary dilation
5. Papilledema
6. Cranial nerve III paralysis
7. Cranial nerve VI paralysis
8. Hypertension
9. Altered level of consciousness
10. Seizures
11. Bradycardia
12. Irregular respirations

Front 95

What will you see if the pt's ICP is 35 mmHg?

Back 95

Any or all of the signs of increased ICP, including Cushing's triad.

Front 96

What is Cushing's triad?

Back 96

1. Hypertension
2. Bradycardia
3. Irregular respirations

Front 97

What 8 steps can the anesthetist take to treat an increase in ICP?

Back 97

1. Hyperventilate
2. Administer a corticosteroid
3. Restrict fluids
4. Dehydrate the brain rapidly
5. Control blood pressure
6. Administer a potent cerebral vasoconstrictor
7. Cool the pt to 34 degrees celsius
8. Elevate the head to 30 degrees

Front 98

Dexamethasone, furosemide, hyperventilation, and/or mannitol are common therapies to reduce elevated ICP. Rank these treatments from fastest to slowest response time and duration.

Back 98

1. Hyperventilation
2. Mannitol
3. Lasix
4. Corticosteroid treatment

Front 99

What is the preferred drug for decreasing brain swelling?

Back 99

Mannitol

Front 100

Why is mannitol effective for reducing ICP?

Back 100

It cannot permeate the cerebral capillary and is thus capable of exerting a high osmotic pressure across the cerebral capillary wall.

Front 101

What does of mannitol is appropriate to treat elevated ICP? What is the initial dose of mannitol for decreasing ICP?

Back 101

Appropriate dose is 0.25-1 g/kg. The initial dose is 0.25-1 g/kg.

Front 102

List 9 adverse effects of mannitol administration.

Back 102

1. Hypovolemia
2. Hyponatremia
3. Hypernatremia
4. Hyperkalemia
5. Acidosis
6. Dehydration
7. Acute hemodilution
8. Pulmonary edema and cardia decompensation in pts with poor left ventricular function due to mannitol-induced increase in intravascular fluid volume.
9. Rebound increase in ICP if the BBB is not intact

Front 103

Will mannitol alter serum glucose levels? Why or why not?

Back 103

No. It is an inert 6-carbon sugar that is neither metabolized nor converted, so it should not alter blood glucose levels.

Front 104

What is the mainstay therapy of acute and subacute management of increased ICP?

Back 104

Hyperventilation of the lungs to maintain PaCO2 between 25-30 mmHg.

Front 105

Is the decrease in cerebral vascular resistance and cerebral blood flow associated with acute hyperventilation and hypocapnia sustained during chronic hyperventilation of treat increased ICP?

Back 105

No.

Front 106

What agents are suitable for induction if a pt has a high ICP?

Back 106

1. Barbiturates
2. Benzos
3. Etomidate
4. Propofol

Front 107

What fluid should not be used on a pt with elevated ICP and cerebral injury? Why?

Back 107

Dextrose containing solutions because hyperglycemia has been shown to exaggerate neuro deficits after incomplete neuro ischemia.

Front 108

What intravenous anesthetic would you not administer to a pt with an elevated ICP? Why?

Back 108

Ketamine because it increased cerebral blood flow and ICP.

Front 109

What is the specific gravity of CSF?

Back 109

1.003-1.009

Front 110

What is the rate of CSF?

Back 110

500-700 ml/day

Front 111

Where is CSF formed?

Back 111

By the choroid plexus

Front 112

Where is the choroid plexus located?

Back 112

In the temporal horn of each lateral ventricle, the posterior portion of the 3rd ventricle, and the roof of the 4th ventricle.

Front 113

Name the connection between the 3rd and 4th ventricle.

Back 113

The aqueduct of Sylvius

Front 114

Where does CSF leave the ventricle system?

Back 114

Via the 4th ventricle through the single foramen of Magendie and the two foramina of Luschke and enters the cerebral and spinal subarachnoid space.

Front 115

CSF is located between what two meningeal layers?

Back 115

The pia and the arachnoid.

Front 116

What is the volume of CSF?

Back 116

150 ml

Front 117

What volume of the total CSF is found in the subarachnoid space?

Back 117

25-35 ml

Front 118

What is the result of interference with CSF drainage?

Back 118

Hydrocephalus

Front 119

Where is the most common site of obstruction leading to hydrocephalus?

Back 119

The aqueduct of Sylvius

Front 120

Distinguish between communicating and non-communicating hydrocephalus.

Back 120

1. Communicating - CSF flows readily through the cerebral ventricles into the subarachnoid space, but reabsorption of CSF is blocked so CSF volume and pressure increase.
2. Non-communicating - Fluid does not flow out of one of the cerebral ventricles because the exit is blocked, so CSF volume and pressure increase behind the block.

Front 121

How do the brain capillaries differ anatomically from other capillaries? What is the significance of this difference?

Back 121

Endothelial cells of cerebral capillaries are so tightly connected, most substances cannot take this route to cross the capillary wall - this is the BB.

Front 122

What is the function of the BBB?

Back 122

It serves to protect the brain from sudden changes in plasma composition.

Front 123

What substances cross the BBB?

Back 123

1. Ions
2. Polar molecules

Front 124

What four factors determine how much of a substance will diffuse across the BBB?

Back 124

1. Size
2. Charge
3. Lipid solubility
4. Degree of protein binding

Front 125

How do vital hydrophilic substances such as glucose and amino acids cross the BBB?

Back 125

By using specific protein channels to cross the BBB.

Front 126

What regions of the brain have no BBB?

Back 126

1. Chemoreceptor trigger zone
2. Capillaries of the choroid plexis
3. Area around the posterior pituitary

Front 127

Damage to the reticular activating system causes what?

Back 127

Coma

Front 128

Decorticate rigidity occurs with damage where? Describe the posturing associated with decorticate rigidity.

Back 128

When there are lesions of the cerebral hemispheres. There is upper extremity flexion and lower extremity extension.

Front 129

Coma will be associated with which type of rigidity, decerebrate or decorticate? Ventilatory depression is associated with which type of rigidity? Why?

Back 129

1. Coma is associated with both decerebrate and decorticate rigidities.
2. Ventilatory depression is associated with decerebrate rigidity. The vital centers in the medulla are damaged.

Front 130

Excessive brain dopamine appears to be associated with what disease?

Back 130

Schizophrenia

Front 131

The extrapyramidal system is involved in regulating what physiological functions?

Back 131

Maintenance of posture and involuntary movements.

Front 132

What are the possible results of a lesion involving the extrapyramidal system? What is the most common disorder involving the extrapyramidal system?

Back 132

Lesions are characterized by movement disturbances . Parkinson's disease is the most common.

Front 133

What is the mechanism of spinal shock?

Back 133

When the spinal cord is suddenly transected, all cord functions below the transection are depressed to the point of oblivion.

Front 134

For the pt in acute spinal shock, what happens to blood pressure, heart rate, and systemic vascular resistance?

Back 134

1. Hypotension
2. Bradycardia if the lesion involves the cardiac accelerator nerves
3. Vasodilation

Front 135

A trauma pt has a fracture at T1. At the time of injury, what happens to blood pressure and heart rate?

Back 135

Hypotension and bradycardia occur.

Front 136

List three cardiovascular signs and symptoms of acute spinal shock in addition to hypotension, bradycardia, and decreased SVR.

Back 136

1. The pt feels warm and dry
2. Functional hypovolemia
3. Hypothermia

Front 137

What skeletal muscles are paralyzed in a pt with complete transection of the spinal cord at C5?

Back 137

1. Deltoid
2. Biceps
3. Brachialis
4. Brachioradialis
5. Partial diaphragmatic paralysis.

Front 138

What cardiovascular changes occur after the acute phase of spinal shock?

Back 138

Vasodilation and profound hypotension is reversed.

Front 139

List four efferent responses that develop after the acute phase of spinal shock? Can surgical stimulation trigger these responses?

Back 139

1. Late return of extensor reflexes
2. Motor hyperreflexia
3. Flexor responses
4. Autonomic hyperreflexia

Surgical stimulation can trigger these.

Front 140

From what does autonomic hyperreflexia result?

Back 140

Reflex stimulation of the sympathetic preganglionic neurons arising in the anterolateral column of the spinal cord below the level of a spinal cord lesion.

Front 141

What triggers autonomic hyperreflexia?

Back 141

1. Pain or any noxious stimuli
2. Stimulation of the bladder or bowel

Front 142

What is the typical time-frame for onset of autonomic hyperreflexia following spinal cord injury?

Back 142

1-3 weeks.

Front 143

Transection of the spinal cord at what level is most likely to lead to episodes of autonomic hyperreflexia?

Back 143

At or above T5 or T6.

Front 144

What percent of pts with complete spinal cord transection above T5 exhibit autonomic hyperreflexia? What are the signs and symptoms of autonomic hyperreflexia?

Back 144

85%

1. Severe paroxysmal hypertension
2. Bradycardia
3. Dysrhythmias
4. Cutaneous vasodilation above the injury
5. Cutaneous vasoconstriction below the injury

Front 145

How does surgical stimulation cause hyperreflexia in the pt with spinal cord injury?

Back 145

Loss of supraspinal inhibitory influences causes hyperrlflexia during surgical stimulation. The sensory input from dermatomes below the injury are unrestrained by feedback from the higher center.

Front 146

Can autonomic hyperreflexia be life-threatening in the paraplegic undergoing a cystoscopy or transurethral procedure?

Back 146

Yes

Front 147

What is the most important goal during management of the anesthetic for a pt with chronic transection of the spinal cord

Back 147

Prevent autonomic hyperreflexia.

Front 148

What anesthetic technique is effective for preventing autonomic hyperreflexia?

Back 148

Spinal anesthesia.

Front 149

What is the treatment of choice for autonomic hyperreflexia during surgery? Once the treatment of choice has been accomplished, what other treatments may be instituted to treat autonomic hyperreflexia during surgery?

Back 149

The treatment of choice is the removal of the causative stimulus. Other actions may include deepening anesthesia and, if necessary, administering a direct-acting vasodilator.

Front 150

During a rhizotomy, motor function was preserved but sensory function was lost. Which nerve root was lysed? What was this procedure performed?

Back 150

The posterior nerve roots were lysed. It was performed to relieve pain.

Front 151

A posterior left sided rhizotomy would result in loss of what sensations from what sides?

Back 151

1. Pain, temperature, crude touch, tickle and itch would be lost on the opposite side.
2. Touch, pressure and position would be lost on the same side.

Front 152

Why are the anterior rhizotomies performed?

Back 152

To relieve skeletal muscle spastic disorders.