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163 Cards in this Set

  • Front
  • Back
Factors that must be controlled by the anesthetist during neurosurgery
physiologic and pharmacologic factors that influence CBF, CMRO2, ICP
what three factors have important implications in the care of patients with central nervous system disease?
Selection of drugs, ventilation techniques, and choice of monitors.
The cranium is divided into which two compartments?
supratentorial, infratentorial
what is contained in the supratentorial compartment?
Cerebral hemispheres, diencephalon (thalmus, hypothalmus)
what is contained in the infratentorial compartment?
Brainstem, cerebellum.
Describe the main arterial blood supply to the brain:
left and right internal carotid arteries and vertebrobasilar system
describe the Circle of Willis and state its purpose
The anastomoses between the internal carotid arteries and the vertebrobasilar system. It creates collateral blood supply to protect against ischemia.
What is the blood brain barrier composed of and what is its purpose?
Capillary endothelial cells with tight junctions that prevent extracellular passage of macromolecules like proteins. In contrast, lipid soluble substances (carbon dioxide, oxygen, anesthesia) cross easily.
What could cause disruption in the blood brain barrier?
Acute systemic hypertension, trauma, infection, hypoxemia, severe hypercapnea, tumors, for sustained seizure activity.
What is normal cerebral blood flow?
50ml/100g/min
why does the brain receive such a disproportionately large share of cardiac output?
Its high metabolic rate and inability to store energy
name the five determinants of cerebral blood flow:
CMRO2, CPP and autoregulation, PaCO2, PaO2, and anesthetic drugs.
Describe the effect of CMRO2 on cerebral blood flow:
increases or decreases in CMRO2 result in a proportional increase or decrease in CBF.
What is the effect of hypothermia on CMRO2?
It is decreased
what is CPP?
MAP minus ICP or CVP, whichever is higher.
What is cerebral autoregulation?
A protective mechanism that maintains a constant cerebral blood flow in the presence of a changing cerebral perfusion pressure. It is the ability of cerebral arterioles to constrict or relax in response to changes in perfusion pressure.
How long does it take for cerebral autoregulation to kick in?
1 to 3 minutes.
Within which range of CPP does cerebral autoregulation keep blood flow relatively constant in normotensive, healthy individuals?
CPP of 50-150.
What happens to cerebral blood flow when CPP goes outside of the 50 to 150?
Cerebral blood flow will then vary directly with cerebral perfusion pressure.
What effects does chronic hypertension or sympathetic stimulation have on CBF needs?
The autoregulatory curve shifts to the right and these patients require a higher minimum CPP to maintain adequate CBF.
Which way does anesthesia shift the cerebral autoregulatory curve?
To left. And this provides some protection.
Under what circumstances can autoregulation become impaired?
Following dramatic brain injury, intracranial surgery, intracranial tumors (in the proximity of the tumor.)
What affect does inhaled anesthesia have on autoregulation?
Inhaled anesthetics are potent cerebral vasodilators and impair autoregulation and varying degrees in high doses greater than 1 MAC. In contrast, intravenous anesthetics do not disrupt autoregulation.
Describe the physiology associated with the effects of PCO2 on cerebral blood flow:
carbon dioxide mediated alterations in perivascular pH which lead to dilation or constriction of cerebral arterioles.
Why are the effects of PCO2 on cerebral blood flow transient?
Increase in CSF HCO3 concentrations.
How long will it take cerebral blood flow to return to normal even if abnormal CO2 levels are maintained?
6 to 8 hours.
What affect does aggressive prolonged hyperventilation have following dramatic brain injury?
It is probably associated with poorer neurologic outcomes.
What affect does decrease in PaO2 below 50 have on cerebral blood flow?
It results in an exponential increase.
Which anesthesia drugs cerebral vasoconstrictor and decrease CMRO2?
thiopental, propofol, etomidate. They reduce CMRO2 and CBF in parallel and therefore are used frequently for anesthesia in neurosurgery.
Describe the use of ketamine in neuroanesthesia:
there is controversy about the effects of ketamine. When ketamine is given without controlled ventilation, CO2, CBF and ICP all increase. When given alongside another anesthetic drug into the patient with controlled ventilation, these increases do not occur. Nonetheless, ketamine is usually not selected for patients with known intracranial disease.
What affect do benzodiazepines and opioids have on CMRO2 and CBF?
Like thiopental and propofol, the decrease it, although, to a lesser extent.
Why should we be cautious with opioids and benzodiazepines in patients with intracranial disease?
They depress consciousness, produce Miosis, and depress ventilation which could be associated with increases in CO2 and ICP.
What affect do a2 agonists have on CBF and CPP?
They reduce CBF and CPP with minimal effects on ICP.
What is the role of a2 agonists?
To reduce the dose of other anesthetics, postoperatively as a sedative, or to attenuate postoperative hypertension and tachycardia.
To what extent are volatile anesthetics cerebral vasodilators?
They are potent cerebral vasodilators. In a normally breathing patient they produce rapid vasodilation and dose-dependent increases in CBF.
What affect do volatile anesthetics have on CMRO2 and how is this related to their vasodilating effect?
They decrease CMRO2. There is an uncoupling.
What affect does nitrous oxide alone have on CBF?
It increases CBF and possibly increases CMRO2 but these effects appear to be attenuated by coadministration of other anesthetics.
What three substances is the intracranial compartment composed of?
Brain, CSF, blood. Increases in any of these three substances can result in increased ICP.
Define increased intracranial pressure:
a sustained increase of ICP above 15.
What affect does increased ICP have on CPP and CBF?
They are decreased, and this can progress to the point of cerebral ischemia.
What initially happens when cerebral volume is increased?
CSF is initially translocated into the spinal canal. Once this compensation is a maximized, ICP starts to rise and cerebral blood vessels are eventually compressed.
With ischemia associated with increased ICP, what else can occur that compounds the problem?
Ischemia will lead to cerebral edema and further increase ICP. It is therefore critical to prevent sustained increases in ICP.
Describe, in brief, the pressure volume compliance curve with ICP:
as intracranial volume starts to increase there is a very sharp increase in ICP which quickly shoots straight up. This is because there is no compliance within the skull.
Describe the danger with the pressure volume compliance curve and a person who has a space occupying lesion:
because of the lesion, they may already have progressed on the pressure volume compliance curve. Additional increases in volume at this point, as produced by increased CBF during anesthesia, could possibly precipitate abrupt increases in ICP.
Name three ways we can decrease intracranial pressure:
reduce CSF, reduce cerebral blood volume, reduce cerebral edema.
In decreasing intracranial pressure, how do we reduce CSF?
External ventricular drain, lumbar drain, Furosemide, Acetazolamide.
In decreasing intracranial pressure, how do we reduce cerebral blood volume?
Decrease cerebral blood flow with intravenous anesthetic drugs, hyperventilation, avoid cerebral vasodilators, and avoid extreme hypertension. We can also increase venous outflow by elevating the head, avoid constriction of the neck, and avoid PEEP and excessive airway pressure.
In decreasing intracranial pressure, how do we reduce cerebral edema?
Mannitol, decompressive craniectomy, resection of space occupying lesion, and prevention of ischemia with associated secondary edema.
Why must you be careful with propofol and thiopental?
Because they can decrease systemic blood pressure and CPP.
Name one important difference between etomidate and thiopental in neuroanesthesia:
Etomidate is associated with an increase in frequency of excitatory peaks on EEG. It should be used cautiously in patients with epilepsy.
Under which ETCO2 is the tendency for volatile anesthetics to increase ICP attenuated?
35
what measure should be taken in choosing anesthesia agent in a patient with abnormal compliance is symptomatic or confirmed by radiologic imaging?
Volatile agents should be avoided.
What affect does succinylcholine have on ICP and how?
It may increase ICP through stimulation of muscle spindles, which in turn either directly or indirectly results in increased CMRO2.
When does hypothermia provide neuroprotection?
During acute injury
what affect does hyperthermia have on ischemic brain injury?
It worsens ischemic injury and should be avoided in patients vulnerable to ischemia.
Describe the effect of nitrous oxide and volatile anesthetics on motor and sensory evoked potentials:
in general, nitrous oxide and volatile anesthetics have a greater effect on motor and sensory evoked potentials when intravenous anesthetics.
What is electrocorticography?
An intraoperative mapping technique used to identify epileptic foci for resection.
What is our concern when electrocorticography is performed?
We need to consider the effects of drugs that change the seizure threshold (benzodiazepines, volatile anesthetics.)
What possible symptoms may see in a patient presenting with a space occupying lesion?
Seizures, altered consciousness, headaches, cranial nerve abnormalities, and motor or sensory deficits.
What possible symptoms may you see in a patient presenting with AVMs?
Severe "thunderclap" headache if ruptured, focal deficits or visual impairment from compression of the optic chiasm when unruptured.
What could imaging possibly show?
Midline shift more than 0.5 cm, encroachment of expanding brain on ventricles, cerebral edema, hydrocephalus, or any combination of the signs.
Do we give preoperative sedation to patients presenting with intracranial processes?
No. This is because drug-induced depression of ventilation can lead to increased PCO2 and subsequent increases in ICP.
Name six signs of increased intracranial pressure on the preoperative examination:
positional headache, nausea and vomiting, hypertension with bradycardia, altered level of consciousness, altered pattern of breathing, papilledema (checked by ophthalmoscopy or fundus photography, and possibly slit lamp examination.)
Why is EKG monitoring important?
It allows prompt detection of cardiac dysrhythmias caused by surgical manipulation of cardiovascular centers.
Describe the two main monitors inserted by neurosurgeons for ICP:
EVD, subarachnoid or subdural bolt.
Name one advantage and one to disadvantage to a bolt over and EVD:
the bolt can be placed through a burr hole and can be inserted quickly in an emergency setting. It does not, however, allow for the drainage of CSF.
for which cranis do we do supine or lateral position?
supratentorial and intracranial vascular lesions.
for whch cranis do we do or sitting or prone position?
Posterior fossa and infratentorial tumors.
The sitting position facilitates surgical exposure of posterior fossa tumors. So why do we go through the trouble of placing them prone?
Because in sitting position there is high risk of venous air embolism (greater than 25%.)
Name some other risks, in addition to venous air embolism, with the sitting position:
upper airway edema as a result of venous obstruction from excessive cervical flexion, quadriplegia from spinal cord compression and ischemia especially with pre-existing cervical stenosis.
Describe park bench position:
lateral, but rolled slightly forward with the head rotated facing the floor. This allows full access to the posterior fossa and minimizes risk of venous air embolism .
When are we allowed to give standard preoperative sedation?
If the patient is not symptomatic and ICP is not elevated.
Describe additional monitoring with sitting position:
since there is a high frequency of VAE use standard monitors plus CVP, precolonial Doppler, or TEE.
What is the dose of mannitol?
0.25 to 1 g per kilogram.
What is our goal for volume maintenance with craniotomy?
euvolemia.
Postoperatively, what do we want to avoid with craniotomy?
Coughing, straining, and systemic hypertension during tracheal extubation.
Describe the goals of induction with craniotomy:
achieve a sufficient level of anesthesia to blunt the stimulation of direct laryngoscopy and intubation without compromising CPP by increasing ICP or decreasing MAP.
Describe the severity of increased ICP with succinylcholine:
it is variable and usually short-lived.
What range should we keep ETCO2 with craniotomy?
30 to 35. There is no evidence of additional therapeutic benefit when below this range.
Should we use PEEP with craniotomy?
No, because it could impair cerebral venous drainage and increase ICP.
Describe maintenance for craniotomy:
combination of opioid, propofol infusion, volatile agent that less than 0.5 Mac with or without nitrous oxide.
What affect do direct acting vasodialators like hydralazine, nitroglycerin, nipride and calcium channel blockers have?
They increase CBF and ICP despite causing simultaneous decreases in systemic blood pressure. Therefore, the use of these drugs, particularly before the dura is open, is not encouraged.
Why is movement and coughing avoided with craniotomy?
Because these responses can lead to increased ICP, bleeding from the operative site, and a brain bulge into the operative site that makes surgical exposure difficult.
What measures can be taken if cerebral swelling occurs?
Additional doses of diuretics to decrease brain water.
Describe the pharmacodynamics of mannitol:
it is an osmotic diuretic that reduces cerebral water content.
What is the onset of action of mannitol?
5 to 10 min.
when does the affect of mannitol peak?
20 to 30 min.
how long does the affect of mannitol last?
2 to 4 hours.
What could happen if mannitol was given too quickly?
Peripheral vasodilation, hypotension and a short term increase in intravascular volume which could result in increased ICP.
What are the signs of acute mannitol toxicity ?
Hyponatremia, high serum osmolality, a gap between the measured and calculated serum osmolality of greater than 10 mOsm with higher doses (2 to 3 g per kilogram.)
What effect does furosemide have?
It is effective in decreasing ICP, though less than mannitol.
What else can be done to decrease ICP besides diuresis?
Intermittent doses of thiopental or propofol, placing the patient in head up position, discontinuation of volatile anesthetics, and hyperventilation.
Why do we avoid dextrose containing solutions?
They are rapidly distributed throughout body water, and if blood glucose concentrations decrease more rapidly than brain glucose concentrations, water will cross the blood brain barrier resulting in cerebral edema.
What is the effect of hyperglycemia on brain injury?
It augments neuronal cell damage by promoting neuronal lactate production, which worsens cellular injury.
Which intravenous solutions are recommended for craniotomy?
Normal saline or lactated ringers. In addition, colloids may be used, but there has been no improvement in outcomes noted.
What can be done to help prevent coughing on emergence with craniotomy?
Lidocaine, opioid. Also a good idea to have labetalol on standby for hypertension.
What should be done if a patient has delayed awakening or neurologic deterioration in the postoperative period with craniotomy?
CT scan, MRI.
Name one potential postoperative complication associated with craniotomy if nitrous oxide was used during the case:
tension pneumocephalus.
Why is the labetalol recommended with craniotomy?
Because it decreases systemic blood pressure without causing cerebral vasodilation.
Why is there increased risk of VAE with craniotomy?
The operative site is often above the heart. Plus, the venous sinuses on the cut edge of bone or dura may not collapse when transected. Air could enter the pulmonary circulation and become trapped in small vessels, causing an acute increase in dead space.
Describe how right ventricular failure may occur with massive vae:
air trapping in the right ventricle.
Describe how reflex bronchoconstriction could occur with vae:
microvascular bubbles which cause reflex bronchoconstriction and activation of endothelial mediators causing pulmonary edema.
How does death usually occur with vae?
Cardiovascular collapse and arterial hypoxemia.
With vae, how could air get into the cerebral or coronary circulation (paradoxical air embolism?)
By crossing a probe patent foramen ovale, which is present in 20 to 30% of adults. Also, transpulmonary passage of venous air could occur in patients who do not have a patent foramen ovale.
What is the most sensitive method for detecting vae?
TEE
what is the drawback to using tee to assess for vae?
It is invasive and cumbersome
what is the second most sensitive method for detecting vae?
Precordial doppler
where is the precordial doppler placed?
Over the right side of the heart, second or third intercostal space to the right of the sternum to maximize audible signals from the right atrium.
Describe why there is a sudden loss of etco2 with massive vae:
increased dead space secondary to continued revelation of alveoli no longer being perfused because of obstruction of their vascular supply by air bubbles.
Which end tidal monitor could possibly detect vae?
end tidal nitrogen. But it is rarely available.
How could cvp line be used to detect vae?
Aspiration of air. But the tip of the catheter would have to be placed correctly (at the junction of the svc and ra.)
What signs would you see with vae?
Hypotension, tachycardia, attempts by a ventilated patient to gasp, dysrhythmia, cyanosis.
What could you hear on the chest which would indicate vae?
mill wheel murmur. This is a late sign.
What would happen with pa pressure during vae?
It would increase.
Give two signs of vae in an awake patient:
chest pain, coughing.
What should you do if you suspect vae?
Notify the surgeon immediately. They can irrigate the operative site and apply occlusive material to all bone edges so that sites of venous air entry are occluded. Gentle compression of the internal jugular veins. Placement of the patient and head down position.
In which age group are brain tumors are usually seen?
40 to 60
what did the initial signs and symptoms of brain tumors are indicate?
Increased ICP
what seizures are present in previously healthy adults suggest?
Brain tumor
what is the number one goal in delivering anesthesia to patients with brain tumors?
Avoidance of increases in ICP.
What additional considerations are there with anesthesia plan with posterior fossa tumors?
If done in sitting position, it properly positioned CVP catheter and precordial Doppler should be used, given the high incidence of vae.
What is the unique surgical danger with posterior fossa tumors?
They can injure vital brainstem respiratory and circulatory nuclei and results in intraoperative hemodynamic fluctuations and postoperative depression of ventilation. In addition, the cranial nerves can be affected and lead to impairment of protective airway reflexes.
Describe the unique concerns when extubation posterior fossa craniotomy:
we need to know if the patient can protect their airway and breathing sufficiently. Postoperative mechanical ventilation may be required.
What is the most common cause of intracranial hemorrhage?
Intracranial aneurysms.
What is the occurrence of intracranial aneurysms in the population?
2 to 4%.
What percentage of intracranial aneurysms rupture every year?
1 to 2%.
What are the signs and symptoms of aneurysm rupture?
Sudden severe headache, nausea, vomiting, focal neurologic signs, and depressed consciousness.
what of the major complications of aneurysm rupture?
Death,rebleeding, vasospasm.
How are intracranial aneurysms treated?
Endovascular coiling or surgery.
When does vasospasm generally occur with subarachnoid hemorrhage?
3 to 5 days afterward
what is the foremost cause of morbidity and death with subarachnoid hemorrhage?
Vasospasm.
What monitors can be used to detect vasospasm?
Transcranial Doppler and cerebral arterography.
What are the signs of vasospasm in an awake patient?
Worsening headache, neurologic deterioration, and loss of consciousness
how is vasospasm treated?
Triple H
what is triple H?
Hypervolemia, hypertension, hemodilution.
How is nimodipine helpful?
As a calcium entry blocker, it decreases the risk of morbidity and death from vasospasm.
Interventionally, how can vasospasm be treated?
Intra-arterial injection of vasodilators, balloon angioplasty of the affected cerebral vessels using interventional radiology.
Besides vasospasm, what are some other complications of subarachnoid hemorrhage?
Seizures (10%), acute and chronic hydrocephalus, intracerebral hematoma.
Describe EKG changes with subarachnoid hemorrhage:
T wave inversions, u waves, st depression, and rarely, q waves.
Which electrolyte abnormality is commonly seen after subarachnoid hemorrhage ?
Hyponatremia.
Describe anesthesia management for resection of intracranial aneurysm:
prevent sudden increases in arterial blood pressure which could increase transmural pressure, facilitate surgical exposure and access to the aneurysm. We need to be careful during induction and avoid hypertension. At the same time, we want to maintain CPP to prevent ischemia during retraction or temporary vessel occlusion or as a result of vasospasm.
Where should we keep our blood pressure with aneurysm clipping?
Normal to increased, to prevent ischemia.
How are aneurysms managed postoperatively?
Normal to high blood pressure, early awakening for neurological exam, hhh therapy as needed.
Why do we keep normal to high blood pressure with aneurysm clipping?
Because temporary occlusive clips can create regional hypotension without the need for systemic hypotension and its risk on multiple organ systems. Normal, or even increased systolic blood pressure should be instituted to facilitate perfusion through collateral circulation.
What is the incidence of AVM in the general population?
2 to 4%.
What percentage of AVMs rupture annually?
2%.
What percentage of patients with AVM have an associated aneurysm?
Up to 10%.
How can AVMs be treated?
Open resection, endovascular embolization, or stereotactic radiosurgery (gamma knife.)
What interventional measure could be taken prior to surgery for AVM that will reduce blood loss?
Preoperative embolization.
Are AVMs likely to rupture during acute systemic hypertension?
Not as much as aneurysms. This is because their flow characteristics are different. They are low-pressure, high flow shunts. Hypertension, however, should still be avoided, given the frequent rate of associated aneurysms.
Give two considerations with anesthesia for AVM that are distinct from anesthesia for aneurysm:
you should prepare for massive, persistent blood loss and postoperative cerebral swelling.
At which percentage stenosis is CEA warranted?
70 to 99% stenosis.
In a patient with asymptomatic carotid stenosis, when should CEA be performed?
Optimally, within two weeks of the onset of symptoms, given the presence of unstable artherosclerotic plaque.
Discuss the cardiac risks in a patient undergoing CEA:
there is risk of perioperative cardiac ischemia. These patients typically have CAD.
Discuss awake CEA:
it is done with a cervical plexus block. This approach is controversial because it requires a cooperative and motionless patient.
Discuss preoperative evaluation and a patient with carotid stenosis:
neurologic examination to evaluate for preoperative deficits, screening for associated CAD.
How high do we want blood pressure for carotid clamping?
20% above baseline.
Discuss postoperative concerns with CEA:
avoid coughing, straining, and hypertension when removing endotracheal tube. Quick awakening allows early neurologic assessment. Monitor for hyperperfusion syndrome and airway compromise.
List the goals of anesthesia during CEA:
prevention of cerebral ischemia through maintenance of adequate cerebral perfusion pressure. Prevention of myocardial ischemia through avoidance of acute peaks in blood pressure.
Why do we increase blood pressure by 20% with carotid cross clamping?
To ensure adequate collateral flow through the Circle of Willis.
Should we promote hypocarbia with CEA?
No. This should be avoided. There is risk of cerebral vasoconstriction and ischemia.
What can be done to detect cerebral ischemia and the need for shunting with CEA?
Transcranial Doppler, stump pressure. Although, none of these things have been shown to definitively improve outcome.
Discuss possible postoperative complications with CEA:
cardiovascular ischemia, neurologic deficits secondary to intraoperative emboli. Hypertension may lead to neck hematoma with airway compromise and hyperperfusion syndrome should be avoided.