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Neurosurgery - VAE, N2O, CNS Monitoring
Terms in this set (71)
Identify the signs and symptoms of venous air embolism (VAE).
Signs of venous air embolism are proportionate to the volume of entrained air, and unfortunately, are not apparent until large volumes of air have been entrained. Because VA causes increased dead-space, increases in end-tidal nitrogen, a sudden decrease in end-tidal CO, and arterial hypoxemia are seen. Late signs of VAE are hypotension, tachycardia, cardiac arrhythmias, and cyanosis. A characteristic " millwheel murmur, as heard through an esophageal stethoscope, is late sign of catastrophic venous air embolism.
List three causes of death from venous air embolism.
Death from venous air embolism is usually due to:
(1) a vapor lock causing right-side cardiac output to plummet,
(2) acute cor pulmonale, or
(3) arterial hypoxemia from combined cardiac and pulmonary insults.
What are pulmonary signs of venous air embolism?
With venous air embolism, PaO2 and SaO2 decrease while PaCO2 increases and end-tidal CO2. (EtCO2) decreases. The changes in arterial and end-tidal gases occurs secondary to the increase in dead space. In addition, nitrogen is detected in the end-tidal gases.
What surgical positioning predispose to venous air embolism?
Venous air embolism (VAE) is a potential hazard whenever the operative site is above the level of the patient's heart, such that pressure in the exposed veins is subatmospheric. In other words, VAE may occur in any position where a negative pressure gradient exists between the right atrium and the veins at the operative site.
What specific surgical positioning are most associated with venous air embolism?
The sitting position, and a modification of the sitting position-the c "beach chair" position -are associated with a greater incidence of venous air embolism.
The greatest incidence of venous air embolism (VAE) is associated with the sitting, or modified sitting (beach chair) position, as you know. What are the incidences of VAE during neurological surgery in the sitting, supine, prone, and lateral positions?
The incidences of venous air embolism (VAE) in patients undergoing neurologic surgical procedures in various positions are:
(1) sitting = = 25%; (2) supine 18%; (3) prone = 10%; and, (4) lateral = 8%.
Your healthy young patient is in the sitting position for an open craniotomy under general endotracheal anesthesia when suddenly ETCO2 drops. What is the probable problem?
A sudden drop in ETCO, followed by a sudden rise in end-tidal nitrogen is caused by venous atmospheric air entrainment (venous air embolus).
Nine actions should be taken in response to venous air embolism. List five of them. (You will be asked in the next question to identify the other four.)
(1) Notify surgeon so he/she can flood the field with saline or pack the field;
(2) turn off the N2O, if used;
(3) administer 100% 02;
(4) aspirate the central venous catheter to remove entrained air;
(5) prevent further air entry by irrigating the operative site with fluid and applying occlusive material to all bone edges so as to occlude sites of venous air entry.
In addition to five actions taken in response to venous air embolism previously specified, list four more.
(1) Infuse fluids intravenously to increase venous pressure;
(2) give vasopressors to correct hypotension;
(3) temporarily compress the right and left jugular veins to increase cerebral venous pressure and slow air entrainment; and
(4) place the patient in a horizontal position if possible.
List five (5) steps to manage a gas embolism during laparoscopic surgery.
Management of a gas embolism during laparoscopic surgery includes:
(1) halting the insufflation of gas,
(2) eliminating nitrous oxide N2O) from the anesthetic gases,
(3) releasing the pneumoperitoneum,
(4) placing the patient in the left lateral decubitus position (Durant maneuver), and
(5) aspirating the gas through a central venous catheter.
What is the optimal position for the tip of a single orifice catheter for aspirating entrained air from the right atrium?
To aspirate entrained air from the right atrium, it is suggested that the optimal position for the tip of a single orifice catheter is 3.0 cm above the junction of the superior vena cava and the right atrium.
What is the optimal position for the tip of a multi-orifice catheter for aspirating entrained air from the right atrium?
To aspirate entrained air from the right atrium, the tip of a multi-orifice catheter should be placed high in the right atrium, at the junction of the superior vena cava and the right atrium.
If your initial actions to treat venous air embolism fail, in what position should the patient be placed?
If the initial actions to treat venous air embolism fail, place the patient in the left lateral decubitus position with a slight head-down (Trendelenburg) tilt in an attempt to dislodge a possible air lock. Persistent circulatory arrest necessitates supine position and resuscitation efforts.
If circulatory arrest persists after the patient with venous air embolism is placed in the left lateral decubitus position, what should be done?
Place the patient in the supine position and begin resuscitation by cardiac compression.
What is the probable cause of death in a patient with a venous air embolism?
Death is probably due to cardiovascular collapse and arterial hypoxemia.
Identify the location of appropriate placement of the Doppler for detecting a venous air embolism.
Over the right atrium, from the third to sixth intercostal spaces, to the right of the sternum.
Identify three measurements that show intermediate sensitivity for detecting venous air embolism.
(1) Pulmonary artery pressure; (2) end-tidal CO2; and (3) PaO2.
What two monitoring methods are least sensitive for detecting venous air embolism?
(1) PaCO2; and (2) mean arterial blood pressure.
What is the major intraoperative complication during cerebral aneurysm surgery?
If a cerebral aneurysm ruptures during surgery, what is your plan?
Cerebral aneurysm rupture during surgery requires immediate, aggressive fluid resuscitation and controlled hypotension via nitroprusside, labetalol, propranolol, or esmolol. These agents are preferred because they do not affect cerebral blood flow or intracranial pressure.
Use dextrose-free fluids since increased neurologic defects are seen with hyperglycemia.
Note: this is the classic answer found in most texts. These same texts are now favoring the use of a temporary clip on the parent vessel to allow the surgeon to gain control of the ruptured vessel. If controlled hypotension was instituted before the temporary clip was placed, restore the systemic blood pressure after the clipping to improve collateral blood flow.
Additionally, if the temporary clip IS in place for more than 10 minutes, thiopental and mild hypothermia are often implemented for cerebral protection.
Normocarbia should be maintained whenever possible regardless of which protocol is used.
During intracranial aneurysm surgery, the risk of intraoperative aneurysm rupture is 7%. A temporary clip may be placed to gain control of the ruptured aneurysm; where will the surgeon place the temporary clip? How should arterial blood pressure be managed while the temporary clip is in place?
If an intracranial aneurysm ruptures intraoperatively, a temporary clip may be placed on the feeding vessel is to gain control of a ruptured aneurysm. The systemic blood pressure can be returned to normal or even slightly elevated levels to improve collateral blood flow while the vessel is obstructed by the occlusion clip.
Q22. IVA10c: Neurosurgery; Venous Air Embolism Identify 3 actions for intraoperative rupture of a cerebral aneurysm.
Intraoperative aneurysmal rupture necessitates
(1) maintenance of MAP between 40 and 50 mm-Hg or lower to facilitate surgical control of the neck of the aneurysm or of the parent vessel. Alternatively,
(2) one or both carotid arteries may be compressed for up to 3 minutes to produce a bloodless field.
(3) Blood that is lost should be continuously replaced with whole blood, blood products, or colloid solution so that intravascular volume is maintained.
What should you do if an intracranial aneurysm ruptures before, during, or immediately after induction?
If the aneurysm bleeds before, during, or after induction, the patient is first hyperventilated with 100% oxygen. Next, blood pressure is controlled and thiopental may be given.
Once the bleeding is controlled, what measures can be taken to protect the brain from ischemic damage if an intracranial aneurysm ruptures during the case?
Animal studies have shown that barbiturates are the only useful drugs in situations of temporary intracranial vessel occlusion.
Barbiturates may be administered up to 30 to 60 minutes after occlusion and still be beneficial.
Thiopental administration is started with small 100 to 200 mg boluses. Approximately 15 to 30 mg/kg is administered over a 30 minute period.
List four contraindications to the use of N2O.
(1) Presence of a closed pneumothorax,
(2) tympanoplasty or other middle ear surgery,
(3) pneumocephalus, and
(4) venous air embolism.
List four adverse side-effects of N2O.
Nitrous oxide may promote:
(1) aplastic anemia (immature red blood cells),
(2) congenital anomalies,
(3) spontaneous abortion, and
(4) CNS toxicity.
What may happen to the volume of gas in the stomach immediately after the onset of administration of 50% N2O?
It will increase (double).
N2O can cause a decrease in blood pressure and cardiac output when added to a high dose of what intravenous anesthetics?
Does ETCO2 increase, decrease, or remain unchanged when N2O is turned off? Why? What law applies?
ETCO2 decreases. When N2O is discontinued, N2O rushes into the alveoli from the blood. The alveoli enlarge and gases that are present, including CO2, are diluted.
Fick's law of diffusion applies.
How does N70 alter pulmonary vascular resistance and pulmonary artery blood pressure?
N2O increases pulmonary vascular resistance and pulmonary arterial blood pressure, especially when administered to patients with pulmonary hypertension.
Why does N2O by itself produce an increase in both systemic vascular resistance and pulmonary vascular resistance?
N2O has a mild sympathomimetic effect.
Does nitrous oxide administered alone increase cerebral blood flow and intracranial pressure?
Which inhaled agent is most associated with postoperative nausea and vomiting (PONV). Rank the inhaled agents, from greatest to least, with respect to causing PONV.
Nitrous oxide has the greatest capacity to cause postoperative nausea and vomiting (PONV). From greatest to least, the likelihood of an inhaled agent causing PONV is:
nitrous oxide > desflurane = isoflurane = sevoflurane.
Nitrous oxide is turned on and held at the same concentration for 6 hours. At 6 hours, is the uptake of nitrous oxide increasing, decreasing, or remaining unchanged?
Nitrous oxide equilibrates with all tissues within 6 hours, so uptake of nitrous oxide remains unchanged at this time; the amount of nitrous oxide inhaled essentially equals the amount of nitrous oxide exhaled.
In general, how much does N2O reduce the MAC of a volatile agent?
There is approximately a 1% reduction in MAC for every 1% of nitrous oxide delivery.
List four (4) indications for electroencephalographic monitoring during anesthesia.
Four indications for EEG monitoring during anesthesia are:
(1) carotid endarterectomy (perfusion jeopardized during cross-clamping of the carotid artery),
(2) cardiopulmonary bypass procedures,
(3) cerebrovascular surgery, for example, temporary clipping during aneurysm surgery or vascular bypass procedures, and
(4) when burst suppression is desirable for cerebral protection.
List two (2) indications for electroencephalographic monitoring in the intensive care unit.
In the intensive care unit, EEG monitoring is indicated
(1) for barbiturate coma for patients with traumatic brain injury, and (2) when sub-clinical seizures are suspected.
How many millivolts (mV) are generated on the skin by electroencephalographic (EEG) signals? How many microvolts (V) is this?
EEG potentials on the skin are generally close to 0.1 millivolts (mV), which is 100 microvolts (V).
Brain waves are generally in the 10-100 microvolt range.
Electroencephalogram (EEG) waves are categorized as alpha, beta, delta, and theta, based upon frequency and amplitude. Give the frequency range (in Hz) of each of these EEG waveforms and the brain region(s) from which each is recorded.
Delta waves are the lowest frequency (0-4 Hz), greatest amplitude waves in the electroencephalogram (EEG).
Theta waves range from 4 to 7 Hz and exhibit a slightly lower amplitude than delta waves.
Alpha waves are typically recorded over the posterior aspect of the head during awake, alert, but relaxed activities. Alpha waves have an intermediate amplitude-less than delta and theta, but greater than beta waves -and a frequency range of 8-12 Hz.
Finally, beta waves are the highest frequency (> 12 Hz), lowest amplitude waveforms, and are recorded predominantly over the frontal areas of the head, but can be seen from all brain regions.
Briefly describe the typical brain activities associated with each electroencephalogram (EEG) waveform. Reminder: the waveforms are delta, theta, alpha, and beta.
Delta waves (0-4 Hz) are seen in the sleeping adult but are considered abnormal in the awake adult. Delta waves are also seen in encephalopathy, deep coma, and deep anesthesia.
Theta waves (4-7 Hz) are seen in sleep and in deep anesthesia.
Prominent alpha wave activity (7-12 Hz) is characteristic of awake, alert, but relaxed activities. An eyes-closed" resting alpha pattern is the baseline awake pattern used when anesthetic effects on the EEG are described.
Beta waves (> 12 Hz) are characteristic of aroused, attentive, active thinking.
What happens to the electroencephalography (EEG) waveforms as anesthetic depth increases?
Increasing depth of anesthesia from the awake state is characterized by increased amplitude and synchrony in the EEG waveforms.
As anesthetic depth increases, periods of electrical silence occupy greater proportions of the electroencephalogram (EEG). Give a synonym for "electric silence" in the EEG.
A7. IID01: CNS Monitoring A period of electrical silence in an EEG is called an isoelectric EEG pattern. [Barash, Clin. Anes., 6th. 2009 p1009] ©2020 www.valleyanesthesia.com
What MAC correlates with an isoelectric EEG pattern?**
An isoelectric pattern dominates the EEG in the range of 1.5 to 2.0 MAC.
During certain surgical procedures, maximal suppression of cerebral metabolic rate is desirable to protect the brain during an ischemic insult. Under such circumstances, the anesthetic agent can be titrated against the EEG until the desired effect is achieved. Typically, instead of an isoelectric EEG, the goal is a state called burst suppression. Characterize "burst suppression" on the electroencephalogram (EEG).
Electroencephalogram (EEG) burst suppression is characterized by periods of isoelectric EEG punctuated by "bursts" of EEG activity.
The "burst" is high-frequency activity and the "suppression" is 0.5 - to several-second periods of isoelectric activity.
The electroencephalogram (EEG) is occasionally used during cerebrovascular surgery to confirm adequate cerebral oxygenation. Identify four conditions or agents that can produce EEG changes mimicking cerebral ischemia.
The electroencephalogram (EEG) changes that accompany cerebral ischemia can be mimicked by (1) hypothermia, (2) electrolyte disturbances, (3) marked hypocapnia, and (4) anesthetic agents.
When would you use sensory evoked potential monitoring?
The primary application of sensory-evoked potential monitoring (somatosensory, brainstem auditory, visual) is to assess continually the function and integrity of neural pathways including the spinal cord (somatosensory), or cranial nerve VIII (brainstem auditory), or cranial nerve II (visual).
Evoked potentials are used during resection of spinal cord tumors, corrective surgery of the spine and cranial tumor resection.
How are somatosensory evoked potentials elicited?
Somatosensory evoked potentials are elicited by electrically stimulating tibial, ulnar or radial nerves. Low threshold sensory neurons (those that carry touch and pressure sensations) are excited.
What is the value of somatosensory evoked potential monitoring?
Somatosensory evoked potentials are recorded to monitor the integrity of the posterior (dorsal) spinal cord where the sensory tracts (cuneatus and gracilis) of the dorsal-lemniscal system are located.
Somatosensory evoked potential (SEP) monitoring assesses the integrity of which region of the spinal cord: dorsal, lateral, or ventral?
SEP monitoring assesses the integrity of the dorsal cord.
Where are recording electrodes placed for somatosensory evoked potential monitoring if the tibial nerves are stimulated bilaterally?
Somatosensory evoked potentials are recorded from electrodes placed between the ears on the scalp. The crucial electrode is placed midway between each ear.
What happens to the somatosensory evoked potential (SSEP) when the patient undergoing laminectomy is paralyzed with a muscle relaxant?
Nothing. Neuromuscular blockade will not alter the transmission of action potentials in the sensory tracts.
All anesthetic agents except muscle relaxants depress SEPs to varying degrees.
How are evoked potentials altered by volatile anesthetics?
Volatile aesthetics, especially high concentrations (>1 MAC), produce dose-dependent increases in latency and decreases in amplitude of evoked potentials.
Which volatile inhalational agent LEAST depresses the amplitude and increases the latency of the somatosensory evoked potential (SSEP)? Which volatile inhalational agent MOST depresses the amplitude and increases the latency of the SSEP?
Halothane has the least and enflurane the most pronounced effects on amplitude and latency of the SSEP.
How does nitrous oxide affect latency and amplitude of the somatosensory evoked potential?
Nitrous oxide causes a decrease in amplitude without a change in latency of the somatosensory evoked potential when used alone or when added to opioid or volatile anesthetics.
List 5 physiologic factors that may alter sensory evoked potentials (SEPs).
Five physiologic factors which may alter sensory evoked potentials are:
(1) temperature, (2) hypotension, (3) hypoxia, (4) hypocarbia, and (5) isovolemic hemodilution.
Which physiologic factor has the greatest effect on sensory evoked potentials? The least?
Based upon the data, we believe that altered temperature affects SEPs the most, whereas hemodilution affects SEPs the least.
Following are the details.
(1) Hypothermia will increase latency and decrease the amplitude of SEPs (latency increases by 1 ms for each 1° C decrease in temperature) and hyperthermia will decrease amplitude by up to 15%. Miller states that SEPs are lost at 42; C.
(2) With a mean arterial pressure less than 40 mm-Hg, there is a progressive decrease in amplitude of SEPs.
(3) A decrease in SEP amplitude 1S seen with hypoxia, probably due to alterations in blood flow.
(4) With an ETCO, ≤ 25 mm-Hg, SEP latency increases.
(5) With isovolemic hemodilution, SEP latency does not increase until the hematocrit is less than 15%, and SEP amplitude does not decrease until the hematocrit IS less than 7%.
Flow-through what spinal arterial vessel(s) is monitored by somatosensory evoked potentials (SSEPs)?
SEPs monitor flow through the posterior spinal arteries.
Arterial blood is delivered to the spinal cord via one anterior spinal artery, two posterior spinal arteries and small segmental (radicular) arteries that augment flow to the anterior and posterior arteries.
The major source of blood is the anterior and posterior arteries.
SEPs monitor sensory action potentials, which ascend in tracts located in the posterior cord, so posterior cord ischemia resulting from hypoperfusion of the posterior spinal arteries would result in increased latency and decreased amplitude of the SEP.
Brainstem auditory evoked potential monitoring is useful during operations involving what cranial nerve?
Cranial nerve VIII.
Is brainstem auditory evoked potential monitoring appropriate for surgery for acoustic neuroma? Why or why not?
Yes it is appropriate since cranial nerve VIII carries acoustic messages.
Monitoring of what evoked potential may be useful during pituitary surgery?
Visual evoked potential monitoring may be used during pituitary surgery to assess direct compression of, or compromise of the blood supply to, the optic nerve and optic chiasm.
What evoked potential (somatosensory, brainstem auditory, or visual) is monitored during transsphenoidal surgery?
Visual evoked potential monitoring may be employed for transsphenoidal surgery if the tumor is large and involves the optic nerves (cranial nerve II).
Multiple drugs used in the perioperative period can influence the ability to accurately monitor sensory-evoked responses (SER; e.g. somatosensory, visual, and brainstem (auditory) evoked potentials). Compare and contrast the effects of intravenous versus inhalational anesthetics on sensory-evoked responses (evoked potentials).
Several general concepts summarize the influence of intravenous and inhalational agents on sensory-evoked responses.
(1) Inhalational agents, including nitrous oxide, generally have a more depressant effect on evoked potentials than equipotent doses of intravenous agents.
(2) Combinations of drugs generally produce additive effects.
(3) Propofol and thiopental attenuate the amplitude of virtually all evoked potential modalities but do not obliterate them.
(4) Opioids and benzodiazepines have negligible effects on the recording of all evoked potentials.
(5) Ketamine and etomidate have been reported to enhance the quality of signals in patients with weak baseline somatosensory evoked potential (SSEP) signals.
Rank the three major sensory-evoked responses-somatosensory (SSEP), visual (VEP), and brainstem/auditory (BAPE) -based upon sensitivity to anesthetic agents.
In general, cortical evoked potentials with long latency involving multiple synapses are exquisitely sensitive to the influence of anesthetic while short-latency brainstem and spinal components are resistant to anesthetic influence.
Thus, BAEP can be recorded under any anesthetic technique, whereas VEP and SSEP are very sensitive to anesthetic agents.
Mnemonic: Visual are Very, Somatosensory are Somewhat, and Brainstem are Barely sensitive.
Brainstem auditory evoked potentials (BAEP) are generally very resistant to alteration by anything other than structural pathology in the brainstem. What operating room environmental variable will decrease latency and prolong interpeak intervals in BAEPs?
Mild hypothermia has been associated with decreased latency and prolonged interpeak intervals during brainstem auditory (BAEP).
Where are motor evoked potentials stimulated? How are they stimulated?
Motor evoked potentials (MEPs) are stimulated over or in the motor region of the cerebral cortex.
MEPs may be stimulated by transcranial electrical stimulation (teMEP), transcranial magnetic stimulation (tmMEP) or by direct stimulation of the motor cortex with an electrode.
Where may motor evoked potentials be monitored?
Motor evoked potentials (MEPs) are recorded over or at:
(1) the spinal cord, (2) a peripheral nerve, or (3) the involved muscle.
Note: Neither sensory evoked potentials (SEPs) nor motor evoked potentials (MEPs) can be recorded at the site of stimulation.
What is the wake-up test, and how is it performed?
The wake-up test is used to assess the integrity of the spinal motor pathways, which are found in the anterior (ventral) cord.
It is performed by lightening the anesthetic depth. The patient is asked to squeeze a hand and move his/her feet and toes.
After these maneuvers are performed, anesthesia is quickly deepened.
The wake-up test monitors what region of the spinal cord (dorsal, lateral, or ventral)?
The wake-up test monitors the ventral cord, which is supplied by the anterior spinal artery. When the patient is awakened, he or she is asked to squeeze the anesthetist's hand and move his or her feet and toes.
Motor tracts are found in the ventral cord. Recall that the somatosensory-evoked potential monitors the dorsal cord.
What complications can occur during the wake-up test?
Complications of the wake-up test include extubation in the prone position, recall of intraoperative events (incidence, 0-20%), myocardial ischemia, self-injury, dislodgement of instrumentation, and air embolus from open sinuses if the patient is breathing spontaneously and inhales vigorously.
An air embolus from open venous sinuses can occur if the patient is breathing spontaneously and inhales vigorously. Recall of intraoperative events is rare. Pain is very rare.
What agents will not alter bispectral index (BIS) monitoring?
Since the bispectral index (BIS) is based upon the hypnotic action of agents, the BIS is not affected by opioids or analgesics.
Nitrous oxide alone will have no effect on BIS.
Ketamine has minimal effect on BIS, and may slightly increase BIS transiently.
What is cerebral oximetry?
Cerebral oximetry is a noninvasive monitor used to measure regional blood hemoglobin saturation (rSO2) via near-infrared optical spectroscopy (NIRS).
This technology is similar to that of pulse oximetry and can be used for patients at risk for stroke (neurosurgical patients, cardiac or vascular surgery patients, patients with a history of stroke).
Briefly describe the technique of cerebral oximetry via near-infrared optical spectroscopy (NIRS).
To measure regional hemoglobin oxygen saturation (rSO2) via trans cranial near-infrared spectroscopy (NIRS), an infrared light source contained in a self-adhesive patch is affixed to the forehead.
Because the human skull is translucent to infrared light, photons are transmitted through the skull and underlying tissues to the outer layers of the cerebral cortex. Adjacent sensors separate photons reflected from the skin, muscle, skull, and dura from those of the brain tissue.
NIRS measures all hemoglobin, pulsatile and non-pulsatile, in a mixed microvascular bed. The measurement is thought to reflect approximately 75% venous blood.
The ratio remains nearly constant in normoxia, hypoxia, and hypocapnia. Cerebral oximetry appears to both reliably quantify change from an individualized baseline and offer an objective measure of regional hypoperfusion. Cerebral oximetry has the advantage that it may be used during non-pulsatile CPB and circulatory arrest.
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