CENTRAL NERVOUS SYSTEM DISEASE Flashcards
1
Q
What is the arterial blood supply to the brain?
A
- 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)
2
Q
In what proportion of human brains is the classic depiction of the circle of Willis
found?
A
- 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,
3
Q
What makes up the blood-brain barrier?
A
- 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)
4
Q
Name conditions in which the blood-brain barrier may be disrupted.
A
- 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)
5
Q
Name some factors that influence cerebral blood flow.
A
- Factors that influence cerebral blood flow include the cerebral metabolic rate,
cerebral perfusion pressure and autoregulation, the PaO2, the PaCO2, and
anesthetic drugs.
6
Q
What is normal cerebral blood flow?
A
- 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
7
Q
What is the relationship between cerebral metabolic rate and cerebral blood flow?
A
- 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
8
Q
- For every 1 C decrease in temperature below normal body temperature, what is thecorresponding decrease in cerebral blood flow?
A
- 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)
9
Q
Define cerebral perfusion pressure.
A
- Cerebral perfusion pressure is defined as the difference between mean arterial
pressure and central venous pressure or intracranial pressure, whichever is
greater. (
10
Q
Within what range of mean arterial pressures will cerebral blood flow remain
relatively constant?
A
- 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.”
11
Q
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?
A
- 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.
12
Q
What are factors that impair the autoregulation of cerebral blood flow?
A
- 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.
13
Q
Describe the relationship between PaCO2 and cerebral blood flow.
A
- 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
14
Q
How much does cerebral blood flow change for every 1 mm Hg increase or decrease
in PaCO2 from 40 mm Hg?
A
- 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)
15
Q
What is a potential risk of prolonged, aggressive hyperventilation to a PaCO2 of less than 30 mm Hg?
A
- 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)
16
Q
Below what PaO2 will cerebral blood flow increase?
A
- Cerebral blood flow increases dramatically when the PaO2 falls below 50 mm Hg.
(478,
17
Q
What are the effects of volatile anesthetics on cerebral blood flow and intracranial
pressure?
A
- 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.
18
Q
What are the effects of nitrous oxide on cerebral blood flow and intracranial
pressure?
A
- 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
19
Q
What are the effects of ketamine on cerebral blood flow and intracranial pressure?
A
- 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)
20
Q
What are the effects of thiopental on cerebral blood flow and intracranial pressure?
A
- Thiopental decreases cerebral blood flow via cerebral vasoconstriction. It also
decreases cerebral metabolic oxygen requirements and reliably decreases the
intracranial pressure.
21
Q
What are the effects of propofol on cerebral blood flow and intracranial pressure?
A
- 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.
22
Q
- What are the effects of etomidate on cerebral blood flow and intracranial pressure?
A
- Etomidate decreases cerebral blood flow and cerebral metabolic oxygen
requirements in the absence of myoclonus or seizure activity.
23
Q
What are the effects of benzodiazepines on cerebral blood flow and intracranial
pressure?
A
- Benzodiazepines minimally decrease cerebral blood flow and cerebral metabolic
rate and do not appear to cause an increase in intracranial pressure. (478)
24
Q
What are the effects of opioids on cerebral blood flow and intracranial pressure?
A
- 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
25
Q
A
- 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)
26
Q
What are the effects of neuromuscular blocking drugs on cerebral blood flow and
intracranial pressure?
A
- 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.
27
Q
What is a normal intracranial pressure?
A
- Normal intracranial pressure is lower than 15 mm Hg. (478)
28
Q
How does the body compensate for increasing intracranial pressure? What
implications does this have clinically?
A
- 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.
29
Q
How do drug-induced increases in cerebral blood flow affect the intracranial
pressures of normal patients and of patients with intracranial tumors?
A
- 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.
30
Q
- Name some methods used to decrease elevated intracranial pressure.
A
- 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
31
Q
. Name some signs and symptoms that may be noted preoperatively that provide
evidence that a patient may have an increased intracranial pressure.
A
- 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.
32
Q
What is the current recommendation regarding the use of induced hypothermia
for neuroprotection?
A
- 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.
33
Q
What is the current recommendation regarding the use of intravenous anesthetics
for neuroprotection?
A
- 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.
34
Q
What monitors are typically used for intracranial neurosurgery?
A
- 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.
35
Q
What two devices can be used to measure the intracranial pressure?
A
- 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
36
Q
What measures can an anesthesiologist undertake to attenuate increases in arterial
blood pressure and intracranial pressure during direct laryngoscopy?
A
- 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. (
37
Q
How is maintenance anesthesia usually achieved in patients undergoing
intracranial neurosurgery?
A
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.
38
Q
What minimum alveolar concentration (MAC) of volatile anesthetic should be
administered when used for maintenance anesthesia in patients undergoing
intracranial neurosurgery?
A
- 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.
39
Q
What is the desired range of PaCO2 to optimize cerebral blood flow intraoperatively?
A
- 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.
40
Q
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?
A
- 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.
41
Q
How do peripheral vasodilators affect cerebral blood flow? What is the
recommendation regarding the use of these drugs intraoperatively in patients
undergoing intracranial neurosurgery?
A
- 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.
42
Q
Why might neuromuscular blockade be maintained throughout intracranial
surgical procedures?
A
- 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
43
Q
How can cerebral swelling be treated intraoperatively?
A
- 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.
44
Q
What are some potential problems that can occur with the administration of
mannitol?
A
- 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.
45
Q
How should intravenous fluid administration be managed intraoperatively in
patients undergoing intracranial neurosurgery?
A
- 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.
46
Q
Why should glucose-containing intravenous solutions be avoided in neurosurgical patients?
A
- Glucose-containing solutions should be avoided as hyperglycemia augments
ischemic neuronal cell damage in the brain.
47
Q
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?
A
- 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.
48
Q
Why is rapid awakening desirable in neurosurgical procedures?
A
- Rapid awakening is desirable in neurosurgical procedures to allow for a timely
assessment of neurologic status after surgery. (
49
Q
How should delayed recovery after intracranial surgery be evaluated? When should tension pneumocephalus be considered as a possible cause of postoperative delayed recovery?
A
- 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
50
Q
What drug is commonly used to treat hypertension on emergence from anesthesia
for intracranial neurosurgery?
A
- 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.
51
Q
Why are patients undergoing neurosurgical procedures at an increased risk for venous air embolism?
A
- 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.
52
Q
Describe the pathophysiology of a venous air embolism. What percent of adult
patients have a probe patent foramen ovale?
A
- 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.
53
Q
What are methods by which a venous air embolism can be detected? Which of these
is the most sensitive?
A
- 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. (
54
Q
What are some signs of a clinically significant venous air embolism?
A
- 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
55
Q
What is the treatment for a venous air embolism?
A
- 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.
56
Q
Why should nitrous oxide administration be discontinued in the presence of a
venous air embolism?
A
- 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
57
Q
What are the advantages of a pulmonary artery catheter in the presence of a venous
air embolism?
A
- 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.
58
Q
How efficacious is the use of PEEP in the prevention of a venous air embolism?
A
- PEEP has not been shown to be efficacious in the prevention of a venous air
embolism. (
59
Q
What typically causes death in a fatal venous air embolism?
A
- 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.
60
Q
What are some of the presenting signs and symptoms of patients with an
intracranial tumor?
A
- 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.
61
Q
What are the anesthetic goals for patients undergoing surgical resection of an
intracranial tumor?
A
- 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.
62
Q
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?
A
- 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.
63
Q
ow is the induction of general anesthesia in patients undergoing surgical resection
of an intracranial tumor achieved?
A
- 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.
64
Q
What are the advantages and disadvantages of the sitting position for the resection
of intracranial tumors?
A
- 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.
65
Q
Name some anesthetic considerations that are unique to posterior fossa tumors.
A
- 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.
66
Q
How do patients with ruptured intracranial aneurysms usually present?
A
- 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.
67
Q
. What is the goal of the anesthetic management of a patient undergoing resection
of an intracranial aneurysm or arteriovenous malformation?
A
- 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.
68
Q
What are the major complications of intracranial aneurysm rupture?
A
- 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. (
69
Q
How might the electrocardiogram of patients with a ruptured intracranial aneurysm
appear?
A
- 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.
70
Q
When is vasospasm after cerebral aneurysm rupture most likely to occur? How is it
diagnosed?
A
- 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
71
Q
What is the treatment for vasospasm after cerebral aneurysm rupture?
A
- 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.
72
Q
What are the different treatment options for intracranial aneurysms?
A
- 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
73
Q
What are the different treatment options for intracranial arteriovenous
malformations?
A
- 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.
74
Q
What are special considerations during temporary clip placement during resection
of intracranial aneurysms?
A
- 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
75
Q
What are the indications for carotid endarterectomy?
A
- 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.
76
Q
How should patients scheduled for a carotid endarterectomy be evaluated
preoperatively?
A
- 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
77
Q
What are the anesthetic goals for patients undergoing a carotid endarterectomy?
What is the critical period during this surgery?
A
- 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.
78
Q
How should the arterial blood pressure be managed during a carotid
endarterectomy?
A
- 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
79
Q
How should the PaCO2 be managed during a carotid endarterectomy?
A
- 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.
80
Q
What is the purpose of intraoperative neurologic monitoring during a carotid
endarterectomy? What are some methods of intraoperative neurologic monitoring?
A
- 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.
81
Q
Does local or general anesthesia have better outcomes for carotid endarterectomy?
A
- 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
82
Q
How is local anesthesia for a carotid endarterectomy achieved? What is an
advantage of local anesthesia for this procedure?
A
- 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.
83
Q
How is general anesthesia for a carotid endarterectomy usually achieved? What is
an advantage of general anesthesia for this procedure?
A
- 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
84
Q
What are some potential postoperative complications after carotid endarterectomy?
A
- 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.
85
Q
What are the consequences of postoperative hypertension after carotid
endarterectomy?
A
- 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.
