CENTRAL NERVOUS SYSTEM DISEASE

Question 1

What is the arterial blood supply to the brain?

Answer 1

1. The arterial blood supply to the brain is from three blood vessels, including the right and left internal carotids and the vertebrobasilar artery. Anastomoses between these vessels form the circle of Willis, and provide for a collateral blood supply forcerebral protection against ischemia. (476)

Question 2

In what proportion of human brains is the classic depiction of the circle of Willis
found?

Answer 2

2. The classic depiction of the circle of Willis is found in less than half of human
   brains and collateralization may not be complete in all individuals. (476-477,

Question 3

What makes up the blood-brain barrier?

Answer 3

3. The blood-brain barrier is composed of capillary endothelial cells with tight
   junctions. This barrier allows the passage of lipid-soluble substances such as carbon
   dioxide, oxygen, and some anesthetic agents but prevents the passage of large
   macromolecules such as proteins. (476)

Question 4

Name conditions in which the blood-brain barrier may be disrupted.

Answer 4

4. The blood-brain barrier may be disrupted in conditions such as acute systemic hypertension, head trauma, infection, arterial hypoxemia, severe hypercapnia,intracranial tumors, and sustained seizure activity. (476)

Question 5

Name some factors that influence cerebral blood flow.

Answer 5

5. Factors that influence cerebral blood flow include the cerebral metabolic rate,
   cerebral perfusion pressure and autoregulation, the PaO2, the PaCO2, and
   anesthetic drugs.

Question 6

What is normal cerebral blood flow?

Answer 6

6. Normal cerebral blood flow is 50 mL per 100 g of brain tissue per minute and
   represents approximately 15% of cardiac output. Although the brain is a very small
   percent of body weight, its high metabolic rate and inability to store energy account
   for the high percent of cardiac output it receives

Question 7

What is the relationship between cerebral metabolic rate and cerebral blood flow?

Answer 7

7. The cerebral metabolic rate directly affects cerebral blood flow through cerebral
   flow-metabolism coupling. Increases or decreases in metabolic rate result in
   a proportional increase or decrease in cerebral blood flow

Question 8

8. For every 1 C decrease in temperature below normal body temperature, what is thecorresponding decrease in cerebral blood flow?

Answer 8

8. For every 1 C decrease in temperature below normal body temperature there is
   a corresponding decrease in cerebral blood flow by about 7%. This effect is due to the
   decrease in the cerebral metabolic rate caused by the decrease in temperature. (477)

Question 9

Define cerebral perfusion pressure.

Answer 9

9. Cerebral perfusion pressure is defined as the difference between mean arterial
   pressure and central venous pressure or intracranial pressure, whichever is
   greater. (

Question 10

Within what range of mean arterial pressures will cerebral blood flow remain
relatively constant?

Answer 10

10. In healthy, normotensive individuals cerebral blood flow remains relatively
    constant between cerebral perfusion pressures of 50 to 150 mm Hg. Within this
    range the cerebral vasculature is able to vasodilate or vasoconstrict in response to
    changes in mean arterial blood pressure to maintain a constant cerebral blood flow.
    Below a cerebral perfusion pressure of 50 mm Hg (mean arterial pressure of
    about 65 mm Hg assuming an intracranial pressure of 15 mm Hg) cerebral blood
    flow decreases proportionally to mean arterial pressure. Above a cerebral perfusion
    pressure of about 150 mm Hg, cerebral blood flow increases proportionally to
    the mean arterial pressure. This response of the cerebral vasculature to alterations in the mean arterial pressure to maintain a constant cerebral blood flow is termed
    “autoregulation.”

Question 11

What is the time course within which cerebral vasculature changes in response to alterations in mean arterial pressure? What is the clinical implication of this?

Answer 11

11. The time course within which cerebral vasculature changes in response to
    alterations in mean arterial pressure is 1 to 3 minutes. That is, within 1 to 3 minutes
    of an alteration in the mean arterial pressure, the cerebral vasculature is able torespond appropriately to maintain a constant cerebral blood flow. In the interim,
    with drastic increases or decreases in mean arterial pressure, there may be a
    brief period of respective cerebral hyperperfusion or hypoperfusion.

Question 12

What are factors that impair the autoregulation of cerebral blood flow?

Answer 12

12. Autoregulation of cerebral blood flow may be impaired in the presence of
    intracranial mass lesions, head trauma, intracranial surgery, subarachnoid
    hemorrhage, severe hypothermia, or volatile anesthetics. Chronic arterial
    hypertension or sympathetic nervous system stimulation results in a shift of the
    autoregulatory curve to the right, such that cerebral blood flow is maintained
    between pressures higher than 60 to 150 mm Hg. This effect is believed to occur
    after 1 to 2 months of hypertension.

Question 13

Describe the relationship between PaCO2 and cerebral blood flow.

Answer 13

13. Cerebral blood flow is linearly related to the PaCO2, such that increases in the PaCO2
    result in increases in cerebral blood flow and vice versa. This effect of the PaCO2
    occurs as a result of the effect of the arterial carbon dioxide tension on the pH
    of the cerebrospinal fluid. An increase in PaCO2 leads to acidosis, which in turn leads
    to cerebral vascular vasodilation. The duration of this effect is 6 to 8 hours,
    after which cerebral blood flow normalizes through the transfer of bicarbonate out
    of the cerebrospinal fluid. This effect is only in response to respiratory acidosis.
    The cerebral vasculature is not affected by metabolic acidosis, owing to the
    blood-brain barrier protection against the diffusion of hydrogen ions from the
    vascular space. (477-478, Figure 30-2

Question 14

How much does cerebral blood flow change for every 1 mm Hg increase or decrease
in PaCO2 from 40 mm Hg?

Answer 14

14. Cerebral blood flow increases by 1 mL/100 g of brain tissue per minute for every
    1 mm Hg increase in the PaCO2 from 40 mm Hg. Conversely, cerebral blood flow
    decreases by 1 mL/100 g of brain tissue per minute for every 1 mm Hg decrease
    in the PaCO2 from 40 mm Hg. The impact of this can be marked, given that a decreasein the PaCO2 from 40 to 25 mm Hg can lead to approximately a 33% decrease in
    cerebral blood flow. (478)

Question 15

What is a potential risk of prolonged, aggressive hyperventilation to a PaCO2 of less than 30 mm Hg?

Answer 15

15. A potential risk of prolonged, aggressive hyperventilation to a PaCO2 of less than
    30 mm Hg is cerebral ischemia. Prolonged aggressive hyperventilation following
    traumatic brain injury has been shown to be associated with a poorer neurologic
    outcome. (478)

Question 16

Below what PaO2 will cerebral blood flow increase?

Answer 16

16. Cerebral blood flow increases dramatically when the PaO2 falls below 50 mm Hg.
    (478,

Question 17

What are the effects of volatile anesthetics on cerebral blood flow and intracranial
pressure?

Answer 17

17. Volatile anesthetics are potent cerebral vasodilators. At concentrations above
    0.5 MAC, these anesthetic agents increase cerebral blood flow in a dose-dependent
    manner, most likely through the direct relaxation of vascular smooth muscle
    leading to vasodilation. In contrast, volatile anesthetics decrease the cerebral
    metabolic oxygen requirement profoundly. Normally, a reduction in cerebral
    metabolic rate would produce a reduction in cerebral blood flow through
    flow-metabolism coupling. However, the net effect of volatile anesthetics is to
    increase cerebral blood flow, particularly at high doses. Therefore, volatile
    anesthetics uncouple the normal physiologic relationship between cerebral blood
    flow and metabolism. These effects may lead to increases in intracranial pressure
    and cerebral edema.

Question 18

What are the effects of nitrous oxide on cerebral blood flow and intracranial
pressure?

Answer 18

18. Nitrous oxide increases cerebral blood flow through cerebral vasodilation. The
    effect of nitrous oxide appears to be blunted in the presence of intravenous
    anesthetics and increases cerebral blood flow less than the volatile anesthetics.
    Limitation of the inspired concentration of nitrous oxide to less than 0.7 MAC
    minimizes its effect of cerebral vasodilation and intracranial pressure

Question 19

What are the effects of ketamine on cerebral blood flow and intracranial pressure?

Answer 19

19. The effect of ketamine on cerebral blood flow and intracranial pressure is
    controversial. In isolation, ketamine appears to increase PaCO2, cerebral blood
    flow, and intracranial pressure, limiting its use for patients with increased
    intracranial pressure. These effects appear to be attenuated, however, in the
    presence of other anesthetic agents and controlled ventilation. (478)

Question 20

What are the effects of thiopental on cerebral blood flow and intracranial pressure?

Answer 20

20. Thiopental decreases cerebral blood flow via cerebral vasoconstriction. It also
    decreases cerebral metabolic oxygen requirements and reliably decreases the
    intracranial pressure.

Question 21

What are the effects of propofol on cerebral blood flow and intracranial pressure?

Answer 21

21. Propofol decreases cerebral blood flow via cerebral vasoconstriction in a manner
    similar to thiopental. It also decreases cerebral metabolic oxygen requirements and
    reliably decreases the intracranial pressure.

Question 22

22. What are the effects of etomidate on cerebral blood flow and intracranial pressure?

Answer 22

22. Etomidate decreases cerebral blood flow and cerebral metabolic oxygen
    requirements in the absence of myoclonus or seizure activity.

Question 23

What are the effects of benzodiazepines on cerebral blood flow and intracranial
pressure?

Answer 23

24. Benzodiazepines minimally decrease cerebral blood flow and cerebral metabolic
    rate and do not appear to cause an increase in intracranial pressure. (478)

Question 24

What are the effects of opioids on cerebral blood flow and intracranial pressure?

Answer 24

25. Studies evaluating the effects of opioids on cerebral blood flow and intracranial
    pressure have yielded inconsistent results. Opioids either very minimally decrease
    cerebral blood flow and intracranial pressure or produce no effect at all in the
    absence of respiratory depression and elevated PaCO2

Answer 25

23. Dexmedetomidine and clonidine decrease cerebral blood flow through reductions
    in mean arterial pressure and cerebral perfusion pressure. They have minimal
    effect on cerebral metabolic rate and intracranial pressure. (478)

Question 26

What are the effects of neuromuscular blocking drugs on cerebral blood flow and
intracranial pressure?

Answer 26

26. Succinylcholine may increase intracranial pressure through stimulation of
    muscle spindles, which then increases cerebral metabolic rate and cerebral blood
    flow. These effects are not consistent, and may be attenuated through a deep level
    of anesthesia during the administration of succinylcholine. Nondepolarizing
    neuromuscular blocking drugs do not generally affect intracranial pressure except
    through the potential release of histamine, leading to cerebral vasodilation.

Question 27

What is a normal intracranial pressure?

Answer 27

27. Normal intracranial pressure is lower than 15 mm Hg. (478)

Question 28

How does the body compensate for increasing intracranial pressure? What
implications does this have clinically?

Answer 28

28. The intracranial pressure is determined by the intracranial contents occupying
    a fixed space. The intracranial compartment is composed of brain tissue,
    cerebrospinal fluid, and blood. Increases in brain tissue or fluid, such as by brain
    tumor and edema, are space occupying and could potentially increase the
    intracranial pressure. Initially, the displacement of cerebrospinal fluid from the
    cranium compensates for increases in the space-occupying mass, but as the mass
    enlarges an increase in intracranial pressure becomes apparent clinically.
    The relationship between the intracranial volume and intracranial pressure is such
    that after compensatory mechanisms are exhausted, minimal increases in the
    intracranial volume result in marked increases in the intracranial pressure. Increases
    in a patient’s intracranial pressure can interfere with cerebral perfusion and
    result in cerebral ischemia.

Question 29

How do drug-induced increases in cerebral blood flow affect the intracranial
pressures of normal patients and of patients with intracranial tumors?

Answer 29

29. Although drug-induced increases in cerebral blood flow do not greatly affect
    the intracranial pressure of normal patients, patients with intracranial space-
    occupying lesions are not able to compensate for the changes in cerebral blood flow
    and are vulnerable to developing increased intracranial pressure.

Question 30

30. Name some methods used to decrease elevated intracranial pressure.

Answer 30

30. Reductions in elevated intracranial pressure are achieved through reductions in
    cerebral spinal fluid, cerebral blood volume, and cerebral edema. Cerebral spinal
    fluid may be drained through an external ventricular or lumbar drain, or its
    production decreased by drugs such as furosemide and acetazolamide. Methods of
    reducing cerebral blood volume include positioning of the head to facilitate
    venous drainage, avoidance of high ventilatory pressures and PEEP, avoidance
    of hypertension, and hyperventilation. Finally, osmotic diuretics such as
    mannitol, as well as surgical resection of space-occupying lesions and
    decompressive craniectomy, may reduce intracranial pressure from cerebral
    edema

Question 31

. Name some signs and symptoms that may be noted preoperatively that provide
evidence that a patient may have an increased intracranial pressure.

Answer 31

31. Signs and symptoms of an increased intracranial pressure include nausea and
    vomiting, hypertension, bradycardia, personality changes, altered levels
    of consciousness, altered patterns of breathing, papilledema, and seizures.

Question 32

What is the current recommendation regarding the use of induced hypothermia
for neuroprotection?

Answer 32

32. The use of induced hypothermia in neurosurgical procedures was widespread based
    on laboratory studies. An international multicenter study in 2005 of 1001 patients
    did not show any benefit in neurologic outcome, however. Because there has
    been no verifiable benefit ascribed to hypothermia for neuroprotection in humans,
    the routine use of hypothermia in neurosurgery is no longer recommended. Indeed,
    the routine use of hypothermia in neurosurgery is unlikely to continue.

Question 33

What is the current recommendation regarding the use of intravenous anesthetics
for neuroprotection?

Answer 33

33. Although intravenous anesthetics have been shown to decrease the cerebral
    metabolic rate and intracranial pressure, there has not been any evidence to prove that
    neurologic outcome is improved with their use. A concern with the use of intravenous
    anesthetics such as propofol or barbiturates for this purpose is that the moderate
    benefit they may provide for neuroprotection can be readily offset by alterations in
    the cardiovascular or hemodynamic status of the patient. When these drugs are being
    administered, vigilance is required to avoid exacerbation of cerebral injury, thus
    limiting their usefulness. Rather it is recommended that other physiologic parameters
    (cerebral perfusion pressure, oxygenation, normocapnia, temperature, and control
    of hyperglycemia) are attended to for maximal neuroprotection.

Question 34

What monitors are typically used for intracranial neurosurgery?

Answer 34

34. In addition to standard monitors, continuous monitoring of systemic blood pressure
    is commonly employed using a peripheral arterial catheter to monitor the
    hemodynamic changes that occur around induction of anesthesia, laryngoscopy,
    application of Mayfield head frame, surgery, and emergence from anesthesia.
    Abnormally low or high systemic blood pressure may compromise cerebral
    perfusion or increase cerebral swelling, respectively. In addition, these catheters
    permit blood sampling and accurate determination of PaCO2. Other monitors should
    include a peripheral nerve stimulator to monitor the level of paralysis and a
    bladder catheter, particularly if diuretics are used. Central venous catheters are
    not routinely employed but may be considered for patient or surgical indications.

Question 35

What two devices can be used to measure the intracranial pressure?

Answer 35

35. An external ventricular device or a subdural bolt placed through a burr hole can be
    used to measure the intracranial pressure. The external ventricular device has the
    additional advantage of also allowing for drainage of cerebral spinal fluid

Question 36

What measures can an anesthesiologist undertake to attenuate increases in arterial
blood pressure and intracranial pressure during direct laryngoscopy?

Answer 36

36. Before direct laryngoscopy and intubation of the trachea, there are several measures
    that can be taken to attenuate increases in arterial blood pressure and intracranial
    pressure. Neuromuscular blockade should be confirmed with a peripheral nerve
    stimulator. This ensures that dangerous rises in intracranial pressure due to
    coughing or bucking in response to direct laryngoscopy do not occur. The
    administration of an additional dose of propofol, thiopental, opioids, deeper levels
    of a volatile agent, a bolus of intravenous lidocaine, or a short-acting b-adrenergic
    antagonist (e.g., esmolol) prior to direct laryngoscopy are all methods that may
    be used to attenuate an increase in intracranial pressure. Finally, the duration
    of direct laryngoscopy should be minimized. (

Question 37

How is maintenance anesthesia usually achieved in patients undergoing
intracranial neurosurgery?

Answer 37

Maintenance anesthesia in patients undergoing intracranial neurosurgery is often
achieved with the administration of a low concentration of volatile anesthetic in
conjunction with nitrous oxide and an opioid. The volatile anesthetic contributes to
decreased awareness and the blunting of sympathetic nervous system responses.
The disadvantage of volatile anesthetics during the resection of an intracranial
tumor is its potential to increase cerebral blood flow. Alternatively, anesthesia may
be maintained with a combination of intravenous anesthetic agents, most
commonly propofol in conjunction with an opioid such as fentanyl or remifentanil.
The use of intravenous anesthesia may be preferred in patients with elevated
intracranial pressure due to a reduction of cerebral blood flow associated with these
agents, as well as their compatibility with intraoperative neuromonitoring with
evoked potentials.

Question 38

What minimum alveolar concentration (MAC) of volatile anesthetic should be
administered when used for maintenance anesthesia in patients undergoing
intracranial neurosurgery?

Answer 38

38. To limit the degree of increase in cerebral blood flow associated with its
    administration, the MAC of volatile anesthetic administered should not exceed
    0.5 MAC when administered for maintenance anesthesia in patients undergoing
    intracranial neurosurgery. It may be prudent to avoid the administration of volatile
    anesthetics altogether in patients with elevated intracranial pressure, since
    even slight increases in cerebral blood flow and intracranial pressure are potentially
    harmful. Likewise, the administration of a volatile anesthetic should be
    discontinued intraoperatively if cerebral swelling develops.

Question 39

What is the desired range of PaCO2 to optimize cerebral blood flow intraoperatively?

Answer 39

39. The PaCO2 should be maintained between 30 and 35 mm Hg to optimize cerebral
    blood flow intraoperatively. Below a PaCO2 of 30 mm Hg there is no evidence
    of any additional benefit.

Question 40

What is a potential problem of the administration of positive end-expiratory
pressure (PEEP) during mechanical ventilation of the lungs in patients undergoing
intracranial neurosurgery?

Answer 40

40. Excessive use of PEEP during mechanical ventilation of the lungs in patients
    undergoing intracranial neurosurgery may lead to an increase in intracranial
    pressure by increasing the central venous pressure and impairing cerebral venous
    drainage.

Question 41

How do peripheral vasodilators affect cerebral blood flow? What is the
recommendation regarding the use of these drugs intraoperatively in patients
undergoing intracranial neurosurgery?

Answer 41

41. Peripheral vasodilators may increase cerebral blood flow by causing cerebral
    vascular vasodilation while simultaneously decreasing mean arterial blood pressure
    and cerebral perfusion pressure. Examples include nitroglycerin, nitroprusside,
    adenosine, calcium channel blockers, and hydralazine. The use of these drugs is not
    recommended for use in neurosurgical patients, particularly before the dura is
    open in patients with elevated intracranial pressure.

Question 42

Why might neuromuscular blockade be maintained throughout intracranial
surgical procedures?

Answer 42

42. Neuromuscular blockade is commonly maintained throughout intracranial surgical
    procedures to minimize the risk of patient movement, coughing, or bucking
    that may result in dangerous increases in intracranial pressure. Patient movement
    may also result in an increase in operative site bleeding and bulging of the brain
    into the operative site with difficult surgical exposure

Question 43

How can cerebral swelling be treated intraoperatively?

Answer 43

43. Cerebral swelling occurring intraoperatively can be treated a number of ways.
    First, it should be confirmed that the maximal benefit is being derived from
    hyperventilation of the lungs with a PaCO2 between 30 and 35 mm Hg. Next, drugs
    that will cause cerebral dehydration may be administered. Mannitol at a dose of
    0.25 to 1 g/kg or furosemide at a dose of 0.5 to 1 mg/kg is frequently used for this
    purpose. Intermittent injections of an intravenous anesthetic such as thiopental
    or propofol may also be administered. If surgically possible, placing the patient
    in a head-up position may improve venous drainage and reduce swelling.
    Discontinuing volatile anesthetic agents and using intravenous agents such as
    propofol should be considered to reduce cerebral blood flow.

Question 44

What are some potential problems that can occur with the administration of
mannitol?

Answer 44

44. Mannitol is an osmotic diuretic whose onset of action is within 5 to 10 minutes, and
    whose maximum benefit lasts for 2 to 4 hours. There are some potential problems
    that can occur with the administration of mannitol, however. If given rapidly,
    hypotension through peripheral vasodilation combined with a short-term increase
    in intravascular fluid volume can lead to a decrease in the cerebral perfusion
    pressure. If large doses of mannitol are administered, there is a risk of acute
    mannitol toxicity, manifested by hyponatremia and a high measured serum
    osmolality.

Question 45

How should intravenous fluid administration be managed intraoperatively in
patients undergoing intracranial neurosurgery?

Answer 45

45. Maintenance of euvolemia with isotonic intravenous fluids, such as normal saline
    or lactated Ringer solution, during intracranial neurosurgery is recommended.
    Hypotonic solutions are not recommended due to increases in free water and
    possible cerebral edema. Colloids such as 5% albumin are acceptable but no
    improvement in outcome has been demonstrated.

Question 46

Why should glucose-containing intravenous solutions be avoided in neurosurgical patients?

Answer 46

46. Glucose-containing solutions should be avoided as hyperglycemia augments
    ischemic neuronal cell damage in the brain.

Question 47

Why should coughing and straining by patients awakening from anesthesia be
avoided after intracranial surgery? What are some methods by which these
responses by the patient can be avoided?

Answer 47

47. Coughing and straining in patients awakening from anesthesia after intracranial
    surgery can result in dangerous increases in the intracranial pressure, increases in
    cerebral edema, and precipitate postoperative bleeding. A small dose of opioid,
    intravenous lidocaine, or both at the conclusion of the procedure may decrease
    the likelihood of coughing during extubation. The emergence from anesthesia is
    better timed to follow placement of the head dressings because movement of
    the head at the conclusion of surgery in the lightly anesthetized patient can
    stimulate coughing on the endotracheal tube.

Question 48

Why is rapid awakening desirable in neurosurgical procedures?

Answer 48

48. Rapid awakening is desirable in neurosurgical procedures to allow for a timely
    assessment of neurologic status after surgery. (

Question 49

How should delayed recovery after intracranial surgery be evaluated? When should tension pneumocephalus be considered as a possible cause of postoperative delayed recovery?

Answer 49

49. Delayed recovery as well as worsening neurologic function after intracranial
    surgery without obvious cause warrant evaluation by computed tomography or
    magnetic resonance imaging. A tension pneumocephalus may be considered as
    a possible cause of postoperative delayed recovery when nitrous oxide was
    administered intraoperatively, particularly after posterior fossa surgeries in the
    sitting position. Tension pneumocephalus occurs as a result of air entering the
    subdural cavities and the treatment is burr hole removal of the gas

Question 50

What drug is commonly used to treat hypertension on emergence from anesthesia
for intracranial neurosurgery?

Answer 50

50. Labetalol is commonly used to treat hypertension on emergence from anesthesia
    for intracranial neurosurgery due to its ability to reduce mean arterial blood
    pressure without causing cerebral vasodilation and with rapid onset.

Question 51

Why are patients undergoing neurosurgical procedures at an increased risk for venous air embolism?

Answer 51

51. Patients undergoing neurosurgical procedures are at an increased risk for a venous
    air embolism due to positioning of the patient’s head above the level of the heart.
    In addition, veins that are opened intraoperatively in the cranial vault may
    remain tented open unlike in other body sites. Patients undergoing posterior fossa
    craniotomies in the sitting position are at particular risk of an intraoperative venous
    air embolism. For this reason, many neurosurgeons prefer to do posterior fossa
    craniotomies with the patient in the prone or park bench position.

Question 52

Describe the pathophysiology of a venous air embolism. What percent of adult
patients have a probe patent foramen ovale?

Answer 52

52. A venous air embolism is characterized by entry of air into the venous circulation
    and the right heart. After entry into the heart, the air may take three paths. First, it
    may stay in the right ventricle, interfering with blood flow into the pulmonary
    artery. Second, it may enter the pulmonary circulation and precipitate acute
    pulmonary hypertension as well as traverse the pulmonary circulation and enter the
    arterial circulation. Finally, from the right atrium it could enter the left atrium
    through a patent foramen ovale, which is present in approximately 25% of adults.
    Arterial emboli in the cerebral and coronary circulation can lead to neurologic and
    coronary infarctions, respectively.

Question 53

What are methods by which a venous air embolism can be detected? Which of these
is the most sensitive?

Answer 53

53. Methods by which a venous air embolism can be detected include transesophageal
    echocardiography, precordial Doppler ultrasound transducer, an acute decrease
    in the exhaled carbon dioxide concentration, increased end-tidal nitrogen
    concentration, and changes in pulmonary and systemic pressures. In response to a
    pulmonary embolus, patients may have bronchoconstriction, pulmonary edema,
    elevated right atrial or pulmonary artery pressure, and elevated peak inspiratory
    pressure. The most sensitive method to detect a venous air embolism is through
    the use of transesophageal echocardiography. It is also beneficial in that it allows
    for the identification of right-to-left air shunting. The drawbacks of routine
    transesophageal echocardiography monitoring for venous air embolism are its
    invasiveness, bulk, and cost. An acceptable alternative to transesophageal
    echocardiography for monitoring is through the combined use of a precordial
    Doppler transducer and monitoring exhaled concentrations of carbon dioxide.
    The transducer should be placed between the second or third intercostal spaces to
    the right of the sternum. The Doppler transducer is able to recognize small volumes of intracardiac air, but it is not able to distinguish between small volumes and large
    volumes of air. (

Question 54

What are some signs of a clinically significant venous air embolism?

Answer 54

54. Signs and symptoms of a clinically significant venous air embolism include a
    decrease in end-tidal carbon dioxide, hypotension, hypoxemia, tachycardia, cardiac
    dysrhythmias, cyanosis, and a characteristic “mill wheel” murmur. The awake
    patient may experience anxiety, chest pain, and coughing

Question 55

What is the treatment for a venous air embolism?

Answer 55

55. The treatment for a venous air embolism includes the prompt administration
    of 100% oxygen and the discontinuation of nitrous oxide administration. The
    surgeons should be asked to irrigate the operative field with fluid and to occlude
    the bone edges to prevent the further entry of air. Lowering the operative field
    (Trendelenburg position) in conjunction with aggressive volume resuscitation may
    also prevent further entrainment of air and improve hemodynamics. Gentle
    compression of the jugular veins can be instituted. In addition, if a central venous
    catheter is in place, aspiration on the catheter to retrieve the air may be attempted
    to confirm the diagnosis. Other treatment methods of a venous air embolus are
    supportive as needed for hypotension, decreased cardiac output,
    bronchoconstriction, or other manifestations.

Question 56

Why should nitrous oxide administration be discontinued in the presence of a
venous air embolism?

Answer 56

56. Nitrous oxide administration should be discontinued in the presence of a venous air
    embolism. The diffusion of nitrous oxide into the air embolus could potentially
    increase its size and worsen its clinical effects. Some clinicians choose to avoid the
    administration of nitrous oxide in patients at risk for a venous air embolus

Question 57

What are the advantages of a pulmonary artery catheter in the presence of a venous
air embolism?

Answer 57

57. Although a pulmonary artery catheter is not useful for aspirating air from the
    venous circulation because of its small catheter size, it may detect increases in
    pulmonary artery pressure caused by a pulmonary air embolus. In practice,
    pulmonary artery catheters are rarely used.

Question 58

How efficacious is the use of PEEP in the prevention of a venous air embolism?

Answer 58

58. PEEP has not been shown to be efficacious in the prevention of a venous air
    embolism. (

Question 59

What typically causes death in a fatal venous air embolism?

Answer 59

59. Death occurring as a result of a venous air embolism is usually due to an obstruction
    of forward flow from the right side of the heart. Acute cor pulmonale,
    cardiovascular collapse, and arterial hypoxemia result.

Question 60

What are some of the presenting signs and symptoms of patients with an
intracranial tumor?

Answer 60

60. Presenting signs and symptoms of patients with an intracranial tumor are typically
    reflective of an elevated intracranial pressure due to a space-occupying mass.
    Manifestations of elevated intracranial pressure include nausea and vomiting,
    hypertension, bradycardia, personality changes, altered levels of consciousness,
    altered patterns of breathing, and papilledema. Patients may also present with
    seizures depending on the location of the tumor. New-onset seizures in a previously
    asymptomatic adult are suggestive of an intracranial tumor.

Question 61

What are the anesthetic goals for patients undergoing surgical resection of an
intracranial tumor?

Answer 61

61. The anesthetic goals in patients undergoing surgical resection of an intracranial
    tumor are to reduce intracranial pressure using medications, and avoid drugs or
    events (e.g., hypercarbia) that will cause undesirable changes in cerebral blood flow
    or intracranial pressure.

Question 62

Why is it important to limit drug-induced depression of ventilation with
preoperative medicines in patients who are scheduled to undergo surgical resection
of an intracranial tumor?

Answer 62

62. Preoperative sedative medications may result in depression of ventilation and
    increases in PaCO2 in patients with an intracranial tumor. This in turn could lead
    to an increase in cerebral blood flow and a corresponding increase in the
    intracranial pressure.

Question 63

ow is the induction of general anesthesia in patients undergoing surgical resection
of an intracranial tumor achieved?

Answer 63

63. The induction of general anesthesia in patients scheduled to undergo surgical
    resection of an intracranial tumor can be achieved with the administration of
    thiopental or propofol to produce adequate anesthesia and minimize increases in
    intracranial pressure with direct laryngoscopy. Cerebral perfusion pressure must be
    maintained, however, to prevent cerebral ischemia in compromised patients.
    Etomidate may be useful in situations in which patients have a suspected elevated intracranial pressure but are also hemodynamically unstable or hypovolemic, such
    as trauma patients.

Question 64

What are the advantages and disadvantages of the sitting position for the resection
of intracranial tumors?

Answer 64

64. The sitting position facilitates surgical exposure of posterior fossa tumors and reduces
    retraction of brain structures, potentially preventing unwanted trauma. The high
    risk of venous air embolism (>25%), however, limits the use of the sitting position and
    many surgeons prefer the prone position instead. Other disadvantages of the
    sitting position include upper airway edema as a result of venous obstruction from
    cervical flexion and quadriplegia from spinal cord compression and ischemia.

Question 65

Name some anesthetic considerations that are unique to posterior fossa tumors.

Answer 65

65. There are some anesthetic considerations that are unique to posterior fossa tumors.
    Posterior fossa tumors place the patient at a higher risk for venous air embolism.
    In addition, resection of tumors in this area may injure vital brainstem structures
    and result in intraoperative hemodynamic fluctuations as well as respiratory
    depression in the postoperative period. Finally, injury to the cranial nerves may result
    in a loss of protective airway reflexes that necessitates postoperative ventilation.

Question 66

How do patients with ruptured intracranial aneurysms usually present?

Answer 66

66. Ruptured intracranial aneurysms have a mortality of 40% to 50%. Patients with
    ruptured intracranial aneurysms usually present with a sudden, severe headache,
    nausea, vomiting, focal neurologic signs, hypertension, and a depressed level of
    consciousness. Many of these symptoms are indications of an elevated intracranial
    pressure. The immediate management of patients with a ruptured intracranial
    aneurysm is to treat elevations in the intracranial pressure.

Question 67

. What is the goal of the anesthetic management of a patient undergoing resection
of an intracranial aneurysm or arteriovenous malformation?

Answer 67

67. The goals of the anesthetic management of a patient undergoing resection of an
    intracranial aneurysm are (1) avoidance of sudden increases in systemic arterial
    blood pressure, and therefore transmural pressure of the aneurysm, which could
    result in rupture; and (2) facilitate surgical exposure and access to the aneurysm.
    Exaggerated increases in arterial blood pressure during direct laryngoscopy
    and surgical frame pinning must be attenuated. The anesthetic goals for resection or
    embolization of arteriovenous malformations are similar to those of aneurysms with
    a few distinct considerations. These vascular abnormalities are low pressure and
    high flow, and therefore increases in systemic blood pressure are less likely to result
    in rupture of the lesion. Hypertension should still be avoided, however, due to the
    high incidence of aneurysms associated with arteriovenous malformations. In
    addition, prolonged arteriovenous malformation resection has been associated with
    massive blood loss and severe cerebral swelling.

Question 68

What are the major complications of intracranial aneurysm rupture?

Answer 68

68. Major complications of intracranial aneurysm rupture include death, rebleeding,
    and vasospasm. Early treatment has been shown to reduce the incidence of
    rebleeding but may be technically more difficult due to swelling and inflammation.
    Other complications of aneurysm rupture include seizures, acute and chronic
    hydrocephalus, and systemic complications, such as neurogenic pulmonary edema
    and hyponatremia. (

Question 69

How might the electrocardiogram of patients with a ruptured intracranial aneurysm
appear?

Answer 69

69. The electrocardiogram of patients with a ruptured intracranial aneurysm often appears
    abnormal and may mimic myocardial ischemia. These changes are usually due to
    a neurologic mechanism and are not usually related to underlying coronary artery
    disease. Changes frequently seen on the electrocardiogram of these patients include
    arrhythmias, Q waves, U waves, T wave inversion, prolonged QT intervals, and ST
    segment depression or elevation. Mild elevations in cardiac enzymes are common
    but usually do not correlate with significant myocardial dysfunction.

Question 70

When is vasospasm after cerebral aneurysm rupture most likely to occur? How is it
diagnosed?

Answer 70

70. A major cause of mortality and morbidity after rupture of an intracranial aneurysm
    is vasospasm of the cerebral arteries. Vasospasm occurs in about 70% of these
    patients and typically has onset 3 to 5 days after rupture of an intracranial
    aneurysm, but may occur as late as 12 days after rupture. Drowsiness is the most
    common clinical sign of vasospasm, and transcranial Doppler ultrasound or
    radiologic studies can confirm its presence

Question 71

What is the treatment for vasospasm after cerebral aneurysm rupture?

Answer 71

71. Vasospasm that occurs after cerebral aneurysm rupture is treated with “Triple H”
    therapy (hypertension, hypervolemia, and hemodilution) through an increase
    in cardiac output and the administration of intravenous fluids. Administration of
    the calcium channel blocker nimodipine has been shown to decrease the morbidity
    and mortality from vasospasm. Finally, cerebral vasospasm may be treated using
    the selective injection of vasodilators into the cerebral circulation or angioplasty
    in the interventional radiology suite.

Question 72

What are the different treatment options for intracranial aneurysms?

Answer 72

72. Intracranial aneurysms may be treated using endovascular coiling or surgical
    resection. Outcomes are similar between patients treated surgically and with
    endovascular insertion of coils. Certain patients may be unsuitable candidates for
    endovascular coiling due to the anatomy and location of their aneurysms; these
    patients require surgery

Question 73

What are the different treatment options for intracranial arteriovenous
malformations?

Answer 73

73. Arteriovenous malformations may be treated expectantly, with open resection,
    endovascular embolization, or with stereotactic radiosurgery (gamma knife).
    Preoperative embolization is often used prior to open resection to reduce blood loss
    and facilitate surgical resection.

Question 74

What are special considerations during temporary clip placement during resection
of intracranial aneurysms?

Answer 74

74. Temporary clips are often applied to a major feeding artery of an aneurysm to
    facilitate resection and permanent clip placement. These clips may create regional
    hypoperfusion to the areas perfused by these vessels. Anesthetic management
    during temporary clip placement should involve maintenance of normal or slightly
    increased systemic arterial blood pressure to maintain perfusion through the
    collateral circulation. Drugs such as thiopental or propofol may be used to
    achieve burst suppression on the electroencephalogram in the hope that this
    provides some protection from ischemia. Rarely, hypothermic circulatory arrest
    may be required for very large or complex aneurysms

Question 75

What are the indications for carotid endarterectomy?

Answer 75

75. Carotid endarterectomy is indicated in symptomatic patients with 70% to 99%
    stenosis of the carotid artery. Carotid endarterectomy may be beneficial in
    asymptomatic patients. However, the perioperative risk of stroke and death
    (approximately 4% to 7%) must be taken into account given a reduced benefit.
    Data suggest carotid endarterectomy should be optimally performed within 2 weeks
    of symptom onset.

Question 76

How should patients scheduled for a carotid endarterectomy be evaluated
preoperatively?

Answer 76

76. Patients undergoing a carotid endarterectomy often have coexisting coronary
    artery and other atherosclerotic disease. The perioperative risk of myocardial
    ischemia should be evaluated preoperatively and medically optimized. The range
    of normal blood pressures for the patient should be determined. Neurologic
    symptoms and deficits should be documented preoperatively to prevent any
    dysfunction noted postoperatively from being incorrectly attributed to the surgical
    procedure or intraoperative events

Question 77

What are the anesthetic goals for patients undergoing a carotid endarterectomy?
What is the critical period during this surgery?

Answer 77

77. The goals of the anesthetic management for patients undergoing a carotid
    endarterectomy include (1) prevention of cerebral ischemia through maintenance of
    adequate cerebral perfusion pressure and (2) prevention of myocardial ischemia
    through avoidance of acute peaks in blood pressure and heart rate. The critical
    period of the procedure occurs intraoperatively while the carotid artery is clamped.
    Mean arterial pressure should be maintained above the patient’s baseline blood
    pressure (within 20%) to ensure adequate blood flow through the circle of Willis.
    Finally, rapid emergence from anesthesia is recommended to facilitate early
    neurologic assessment.

Question 78

How should the arterial blood pressure be managed during a carotid
endarterectomy?

Answer 78

78. During a carotid endarterectomy procedure, the arterial blood pressure should
    be maintained in a normal or slightly elevated range specific to that patient.
    It may be helpful to blunt sympathetic nervous system responses to direct
    laryngoscopy to avoid acute hypertension. A high-normal range of mean arterial
    pressures should be maintained during carotid artery clamping to increase collateral blood flow and prevent cerebral ischemia, particularly when there is
    no intraluminal shunt in place. Intraoperative hypotension is often treated with
    phenylephrine

Question 79

How should the PaCO2 be managed during a carotid endarterectomy?

Answer 79

79. During a carotid endarterectomy the PaCO2 should be maintained near normal,
    between 35 and 40 mm Hg. Hypocarbia should be avoided given the risk of cerebral
    vasoconstriction and ischemia.

Question 80

What is the purpose of intraoperative neurologic monitoring during a carotid
endarterectomy? What are some methods of intraoperative neurologic monitoring?

Answer 80

80. The purpose of intraoperative neurologic monitoring during a carotid
    endarterectomy is to identify cerebral ischemia and the potential need for an
    intraluminal shunt placed for perfusion to the ipsilateral brain while the diseased
    carotid artery is clamped. Several methods of monitoring for cerebral ischemia have
    been used, including stump pressure measurement (blood pressure in the carotid
    artery distal to the placement of the surgical clamp as an indication of adequate
    collateral flow), electroencephalogram, and somatosensory evoked potentials,
    direct measurement of cerebral blood flow, and transcranial Doppler
    ultrasonography. Alternatively, an intraluminal shunt is routinely placed regardless
    of whether cerebral ischemia is detected.

Question 81

Does local or general anesthesia have better outcomes for carotid endarterectomy?

Answer 81

81. The administration of either local or general anesthesia for carotid endarterectomy
    is acceptable. Neither has been shown to have better outcomes or reduced
    morbidity or mortality

Question 82

How is local anesthesia for a carotid endarterectomy achieved? What is an
advantage of local anesthesia for this procedure?

Answer 82

82. Local anesthesia for a carotid endarterectomy is achieved with the administration of
    a deep and superficial cervical plexus block. A deep cervical plexus block provides
    anesthesia to the C1-C4 nerve roots and blocks the greater auricular, lesser occipital,
    transverse cervical, and supraclavicular peripheral nerves. The superficial
    cervical plexus block anesthetizes the cutaneous nerves. The advantages of local
    anesthesia for this procedure include a more accurate assessment of the patient’s
    neurologic status intraoperatively and improved hemodynamic stability.
    Neurologic status is typically monitored using the patient’s contralateral grip
    strength, level of consciousness, and quality of prompted speech. Disadvantages of
    this technique include the need for a cooperative and motionless patient.

Question 83

How is general anesthesia for a carotid endarterectomy usually achieved? What is
an advantage of general anesthesia for this procedure?

Answer 83

83. The induction of general anesthesia for a carotid endarterectomy is usually achieved
    with the administration of an opioid, an intravenous induction agent, and a
    neuromuscular blocking drug. The maintenance of anesthesia is typically achieved
    by the administration of a volatile anesthetic in conjunction with nitrous oxide
    and an opioid. Neuromuscular blockade is usually maintained throughout the course
    of the procedure to minimize the risk of intraoperative movement. Advantages of
    general anesthesia include the ability to manipulate cerebral blood flow and the
    cerebral metabolic oxygen requirement, as well as the security of a protected airway.
    General anesthesia may also be advantageous when patients are unable to
    communicate or when their neck anatomy appears difficult for the administration of
    local anesthesia. Disadvantages include reliance on surrogate indicators to monitor
    neurologic status and greater hemodynamic instability

Question 84

What are some potential postoperative complications after carotid endarterectomy?

Answer 84

84. Potential postoperative complications after a carotid endarterectomy include
    recurrent laryngeal nerve injury, hemodynamic instability, airway compression
    secondary to neck hematoma, loss of carotid body function, myocardial infarction,
    and neurologic dysfunction. Neurologic dysfunction after carotid endarterectomy is
    usually due to intraoperative embolization or hypoperfusion during carotid artery
    clamping.

Question 85

What are the consequences of postoperative hypertension after carotid
endarterectomy?

Answer 85

85. Postoperative hypertension is common after a carotid endarterectomy as the majority
    of patients undergoing carotid endarterectomy have chronic hypertension.
    Hypertension may also occur secondary to the loss of function of the carotid sinus
    or the loss of innervation to the carotid sinus during surgery. Hypertension may
    result in an increased incidence of postoperative complications such as neck
    hematoma, myocardial ischemia, and hyperperfusion syndrome, and should be
    strenuously avoided.