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Flashcards in Neuroanesthesia Deck (64)

Describe cerebral salt wasting.

Hyponatremia, volume contraction, and urinary sodium level > 50 mmol/L. Believed to be mediated by the release of natriuretic peptide of the injured brain.


Describe SIADH.

Syndrome of inappropriate antidiuretic hormone, characterized by normovolemia or hypervolemia and treated with fluid restriction.


For the management of anesthesia for surgery of intracranial aneurysmal clipping, what agents must you give?

1- Agents that facilitate brain relaxation like mannitol.
2- Maintain precise blood pressure control and high-normal MAP to ensure adequate CBF into recently damaged and marginally perfused areas of the brain.


T or F: brainstem evoked potentials are the LEAST sensitive modality of sensory evoked potentials clinically used. Volatile anesthetics cause an increased latency in BAEPs, but this effect is less than is seen with SSEPs and VEPs.

T- usually do one sided monitoring, nitrous oxide causes no further change.


T or F: subcortical and spinal somatosensory evoked potentials (SSEPs) are less sensitive to the effects of volatile anesthetics than cortical SSEPs



T or F: visual evoked potentials (VEPs) are most sensitive to the effects of volatile anesthesia.



T or F: in general, for all types of sensory evoked potentials, IV anesthetics affect the evoked potentials less than volatile anesthetics when given in equipotent doses.

True- This effect is less important when monitoring BAEPs, because BAEPs are relatively resistant to the effects of volatile anesthesia.


T or F: patients with high spinal cord lesions can have difficulty with thermogenesis.

True- there is an inability to shiver below the level of the spinal cord lesion, and there may be cutaneous vasodilation below the lesion, leading to hypothermia. It is also possible for hyperthermia to develop because normal sweating is impaired below the spinal cord lesion.


Describe autonomic dysreflexia. When are patients the most susceptible to this?

Autonomic dysreflexia is a life-threatening condition and medical emergency that occurs in spinal cord injured patients with injuries typically above T6.

It is characterized by hypertension, bradycardia, and flushing above the lesion. It is typically stimulated by visceral stimulation like a full bladder.

Occurs after the acute phase of spinal shock. Can occur within weeks to years of spinal cord injury, but 80% of patients susceptible to this syndrome will exhibit this within the first year of injury.


T or F: patients with high spinal cord lesions exhibit hyporeflexia for the first 4 days of the injury and then develop hyperreflexia.



T or F: light anesthesia is NOT indicated in patients with high spinal cord lesions because significant visceral reflexes can be evoked even if the patient feels no pain.



T or F: autonomic hyperreflexia is most commonly associated with hypertension, bradycardia, flushing, and diaphoresis above the spinal cord lesion.

T- bradycardia is often seen because the only intact efferent component of the baroreflex pathways in quadriplegic patients is the vagus. When the systemic blood pressure rises as a result of the mass reflex, the baroreceptor reflex is activated, resulting in bradycardia.


T or F: there is evidence of supersensitivity of adrenergic receptors in patients with high spinal cord lesions.

True- quadriplegic patients are extremely sensitive to the effects of angiotensin and catecholamines.


T or F: patients with diabetes are at risk for silent ischemia and aspiration from gastroparesis.

T- The gastroparesis seen in diabetic autonomic neuropathy is amenable to treatment with metoclopramide. Patients treated with 10 mg po metoclopramide preoperatively had significant lower residual gastric contents measured than the placebo group.


Describe the trigeminal cardiac reflex.

- Manifested by sudden onset of parasympathetic activity, sympathetic hypotension, and apnea or gastric hypermotility during central or peripheral stimulation of any branches of the trigeminal nerve.

- Reported to occur during craniofacial surgery, manipulation of the trigeminal ganglion, and surgery for leesions in the CPA, cavernous sinus, and pituitary fossa.

- Treatment is to have the surgeon cease manipulating in the relevant area, but in some cases an anticholinergic agent may need to be given.


What is Cushing's triad? When does it occur?

1- Hypertension
2- Bradycardia
3- Apnea

(Occurs in response to elevated ICP)


T or F: most IV anesthetics, with the exception of ketamine, are associated with a decrease in cerebral metabolic rate and a reduction in CBF.



T or F: volatile agents cause cerebral vasodilation, with the order of vasodilation going from halothane (most), enflurane, desflurane, isoflurane, and sevoflurane (least).



T or F:TBI patients usually have low CBF in the first 24 hours of injury.



T or F: hypocapnia should be reserved for specific time-limited episodes in which it is necessary. These include preventing imminent herniation, minimizing retractor pressure, facilitating surgical access, and acutely lowering ICP to less than 20 mm Hg.



T or F: In general, the effects of hypocapnia are not sustained, with the pH of the CSF and extracellular fluids and the CBF returning to normal within 6-24 hours of the institution of hypocapnia.

True- thus it is important not to abruptly cease hypoventilation of a patient who has been hyperventilated for a prolonged period of time to prevent hyperperfusion.


What is the formula for cerebral perfusion pressure?



What is the formula for CBF?

CBF = CPP / cerebral vascular resistance


T or F: in general, in humans cerebral autoregulation begins to become impaired at a mean blood pressure of 70 mm Hg. The upper limit of autoregulation is a mean arterial pressure of about 150 mm Hg.



Why should hyperventilation be titrated to PaCO2 as opposed to etCO2?

Controlled hyperventilation is considered to be effective to temporarily decrease ICP because a reduction in PaCO2 causes a decrease in CBF.

Hypocarbia below PaCO2 of 25 mm Hg can result in a significant enough decrease in CBF that ischemia can occur. Target PaCO2 of 30-35.

Check the PaCO2! etCO2 can differ markedly from PaCO2 due to changes in physiological dead space during general anesthesia. It may be possible to correlate the PaCO2 with the etCO2 when the first ABG sample is checked, but relying only on etCO2 is not sufficient.


What are strategies to prevent increased ICP?

In hyperventilation, you want to maintain adequate cerebral perfusion pressure while preventing increased intracranial pressure. Strategies for this include diuretics, hyperosmotic solutions like mannitol, steroids, maintain MAP, head of bed elevation, and hyperventilation.


What is the ASA recommendations during an airway fire?

Remove the ETT, stop the flow of all airway gases, remove sponges and other flammable material from the airway, and pour saline into the airway.`


Why is hypothermia dangerous in an intraoperative setting?

CAn cause coagulopathy, increased oxygen consumption from shivering, vasoconstriction, decreased oxygen delivery, and if severe enough, decreased heart rate and blood pressure and cardiac irritability leading to v-fib.


What are the American College of Radiology's recommended treatment protocols for patients at increased risk for reaction to IV contrast dye?

There are two protocols: 1- corticosteroid therapy alone, 1- combination of an antihistamine with the corticosteroid.


To prevent contrast-induced nephropathy, what are the American College of Radiology's guidelines?

1- for inpatients, hydrate for 12 hours before and after the procedure with NS
2- for outpatients, hydrate with NS or Bicarb 3-6 hours before and 6 hours after
3- discontinue metformin
4- n-acetylcysteine is neither recommended nor refuted


What is the treatment of cyanide poisoning?

2 steps:

1- administration of amyl nitrate or sodium nitrite (these nitrites convert oxyhemoglobin to methemoglobin by oxidizing the iron group of hemoglobin from ferrous state to ferric state)
2- administration of a sulfur atom compound, usually thiosulfate.

From wikipedia:

The United States standard cyanide antidote kit first uses a small inhaled dose of amyl nitrite, followed by intravenous sodium nitrite, followed by intravenous sodium thiosulfate.


T or F: cyanide poisoning may occur with the use of sodium nitroprusside for vasodilation.



In a patient on a sodium nitroprusside drip, what are indicators of cyanide poisoning?

1- Metabolic acidosis
2- Elevated mixed venous oxygen --> leads to cherry red skin tachyphylaxis to sodium nitroprusside


T or F: In the setting of pulmonary aspiration, prophylactic use of saline lavage, steroids, or antibiotics has not been shown to decrease mortality in pulmonary aspiration.



T or F: intraoperative heat loss occurs in four main manners- radiation, convection, conduction, and evaporation.

True- of these, radiation and convection are the first and second major causes of intraoperative hypothermia.


T or F: All of the halogenated inhaled anesthetics cause roughly equivalent dose-dependent decreases in amplitude and increases in latency that are further worsened by the addition of 60% nitrous oxide.



T or F: During distraction of the spinal column in scoliosis surgery (or other critical parts of surgery), it is important to minimize interventions that will lower MAP or deepen anesthetic levels acutely.

T- you want to allow differentiation of changes in SSEP waveforms from anesthetic effect.


Address the effects of the following on SSEP monitoring:
1- temperature
2- Hypoxia
3- Hypotension
4- Hypocarbia
5- Isovolemic hemodilution

1- Hypothermia increases latency
2- Hypoxia decreases amplitude
3- Hypotension decreases amplitude
4- Hypocarbia increases latency
5- Latency is not increased until the hematocrit is <7%.


T or F: carotid endarterectomy is not indicated for most patients with moderate (30-69%) stenoses, even if they are symptomatic.

True- however, the rate of stroke or TIA increases dramatically with increasing stenosis, and symptomatic patients and asymptomatic patients with a stenosis > 79% are candidates for a CEA.


Describe cerebral autoregulation. How is it affected in cerebrovascular disease?

Cerebral autoregulation refers to the brain's ability to maintain cerebral blood flow relatively constant (40-60 ml/100gm/min) over a wide range (50-150 mmHg) of arterial pressures.

Stenosis or obstruction in the internal carotid artery causes a pressure drop beyond the obstruction. In an effort to maintain CBF, the cerebral vasculature dilates. As the degree of carotid obstruction progresses, the cerebral vasculature distal to the obstruction maximally dilates. At this point, the cerebral vasculature loses its autoregulatory ability. CBF then becomes passive and depends on systemic blood pressure.

It thus becomes important to maintain the blood pressure of patients with carotid stenosis because they have minimal or no autoregulatory reserve to counter anesthetic-induced reductions in CBF.


T or F: normal cerebral vessels are highly sensitive to arterial carbon dioxide partial pressure, dilating in response to hypercapnia and constricting in response to hypocapnia.

True- however, in ischemic and maximally vasodilated areas of the brain, this relationship breaks down and responses to hypercapnia and hypocapnia may be paradoxical.


What is the phenomenon of "steal?"

Because cerebral vessels in an area of ischemia are already maximally dilated, hypercapnia may result in dilation of only normally responsive vessels outside the area of ischemia. This phenomenon, named "steal," may divert blood flow away from the ischemic area, further compromising perfusion.


What is "Robin Hood" or "inverse steal?"

Hypocapnia may cause vessels in normal areas to undergo constriction, diverting blood to marginally perfused areas.


What is normal cerebral blood flow?

Normal cerebral blood flow is 40-60 mL/100g/min (15% cardiac output).


What is the cerebral metabolic rate?

3-4 mL/100g/min (20% of whole body oxygen consumption)


What is the cerebral blood flow at which ischemia becomes apparent on EEG?

This is refered to as critical regional cerebral blood flow and is 18-20 mL/100g/min.


How do inhalational anesthetics affect cerebral perfusion and cerebral metabolic rate?

In the normal brain, CBF varies directly with CMR. Inhalational agents uncouple this relationship by decreasing CMR for oxygen but causing concurrent dilation of cerebral blood vessels, thus increasing cerebral blood flow.


Which afferent pathways are involved in the oculocardiac reflex?

Ciliary nerves go to ciliary ganglion behind the orbit, and from the ciliary ganglion it travels to the first division of the trigeminal nerve to the trigeminal ganglion, aka the gasserian ganglion.


What is the treatment fo stroke secondary to air embolism?

Hyperbaric oxygen.


Why can cyanide poisoning be lethal?

Cyanide poisoning is a form of histotoxic hypoxia because THE CELLS OF AN ORGANISM ARE UNABLE TO USE OXYGEN, primarily through the inhibition of cytochrome c oxidase.

A cherry red skin color may be present as the result of increased venous hemoglobin oxygen saturation.


Describe mechanism of mannitol.

As an osmotic diuretic, mannitol decreases ICP by shifting fluids from the extracellular compartment to the vascular compartment. Administration of mannitol may produce a biphasic effect on CPP.

An increase in plasma osmolality has been reported to produce cerebral vasodilation, thereby increasing ICP. In addition, the increase in intravascular volume associated with mannitol administration will produce a transient increase in CVP, which could have a negative impact on CPP. Both of these effects tend to be offset by the increase in MAP that occurs as a result of increased preload stemming from the augmentation of intravascular volume. The primary effect of mannitol, however, is to decrease ICP, thereby producing an increase in CPP.


At what receptor does baclofen work?

GABA-B agonist, The most common side effects of baclofen are drowsiness, vertigo, insomnia, hypotonia, ataxia, skeletal muscle weakness, and nausea.


Why is the co-administration of TCAs and SSRIs dangerous? What is the treatment for TCA poisoning?

SSRIs inhibit a liver enzyme responsible for the metabolism of TCAs. Thus, coadministration can lead to dangerously elevated levels of TCAs and also increase the risk of excess central serotonin levels.

TCAs are highly protein bound, lipophilic, and have a large volume of distribution, making them resistant to forced diuresis or hemodialysis. The treatment of choice for cardiac dysrhythmia or QRS complex duration > 100 ms in the setting of TCA poisoning is SODIUM BICARBONATE. Sodium bicarbonate increases the gradient of sodium across neuronal membranes helping to overcome the blockade of sodium channels produced by the TCA, and the elevation in pH helps keep the TCA in its neutral form, which is less available to bind cardiac sodium channels.


Describe the triad of symptoms of Parkinson's disease. What is the etiology to Parkinson's disease?

Parkinson disease is a neurodegenerative disorder in which there is a characteristic loss of dopaminergic fibers in the basal ganglia, specifically the substantia nigra, leading to
tremor, rigidity, and bradykinesia.


Drugs not to use in parkinson's disease.

Many useful drugs have antidopaminergic effects that, by themselves, may cause parkinsonism. This makes them unsuitable for use in patients with Parkinson disease as they may lead to a worsening of signs and symptoms.

Haloperidol, droperidol, chlorpromazine, and metoclopramide have prominent antidopaminergic effects and should be used with extreme caution, if used at all, in patients with Parkinson disease.


T or F: the benefits of hyperventilation are not sustained and generally last only 8-18 hours after institution.

T- in hyperventilation, the CO2 levels of the extracellular CSF rapidly change and through mediators such as NO and prostaglandins, cerebral blood flow through cerebral vessels decreases.


T or F: respiratory changes alter cerebral blood flow much more than metabolic changes.

True- PaCO2 can rapidly diffuse into the CSF but hydrogen ions cannot. This effect is greatest in areas of normal to increased flow as well as within the range of physiologic PaCO2. The effect of hyperventilation is diminished below a PaCO2 of 25 mmHg.


T or F: one of the downsides of hypeventilation is that it is necesary to slowly wean the individual from a hyperventilated state, especially if the patient has been hyperventilated for a prolonged period of time.

True- becasue the effects of hyperventilation are not sustained, after about 8 hours, the CBF is back to baseline levels. Rapid return to normocapnia will cause a rapid increase in CBF and could be harmful to the patient.


T or F: pts hyperventilated to a level of PaCO2 of 25 mmHg have a poorer outcome compared with patients hyperventilated to a level of PaCO2 35 mmHg. Jugular venous bulb oxygen tensions are decreased in patients who are vigourously hyperventilated.



The afferent and efferent branches of the oculocardiac reflex include which two nerves respectively?

afferent: trigeminal
efferent: vagal

The first step in treatment is to eliminate the offending stimulus, followed by anticholinergic agent like atropine or glycopyrrollate if the bradycardia persists.


T or F: the most sensitive monitor available for the detection of venous air embolism is a TEE, followed by a precordial doppler.



T or F: nitrous oxide is unique amonst inhaled anesthetics in that it causes a dose-dependent decrease ina mplitude without significant changes in latency.

True- etomidate and ketamine increase the latency and amplitude of SSEPs, while volatile anesthetics cause a decrease in amplitude and an increase in latency. Opioids have minimal effect on SSEPs.


T or F: mannitol initially draws water into the vascular space before it is excreted, so rapid dosing can cause a transient increase in ICP and thus mannitol should be infused voer 20-30 minutes.



T or F: if mannitol does not provide adequate surgical conditions, loop diuretics like furosemide may be used.

True- in a naive adult patient, a dose as low as 5 mg might be adequate.

The combination of mannitol and furosemide can cause electrolyte abnormalities and severe systemic dehydration, necessitating fluid resuscitation.