Neuroanesthesia Flashcards
What are the stimulation and response sites for SSEPs and MEPs?
SSEPs:
Stimulation - median nerve
Response - scalp electrodes over sensory cortex
MEPs:
Stimulation - scalp electrodes over motor cortex
Response - EMG in abductor pollicis brevis
What is normal ICP?
15 mm Hg or less
What is the equation for cerebral perfusion pressure (CPP)?
CPP = MAP - (the greater of CVP or ICP)
What is the ideal EtCO2 range for reduction in ICP? What PaCO2 does it reflect?
EtCO2 of 25 to 30 mm Hg, which reflects a PaCO2 of 30 to 35 mm Hg
Describe cerebral blood flow autoregulation? What are its limits?
The intrinsic ability of the cerebral vasculature to adjust resistance to maintain constant CBF over a wide range of MAPs
Autoregulation occurs from 60 to 160 mm Hg
- Above or below this range, CBF is pressure dependent
How do changes in PCO2 effect CBF?
For every 1 mm Hg change in PCO2, CBF will change by 1mL/100g/min in the same direction
What is autonomic hyperreflexia? Where is the transection usually located? What anesthetic technique is preferred? How is it treated?
Autonomic hyperreflexia is a disorder of sympathetic dysinhibition seen after spinal cord transection
- Stimulation below the level can result in generalized vasoconstriction and hypertension
- Bradycardia can occur secondary to activation of baroreceptor reflexes
Above lesion, parasympathetic predominantly - flushing and sweating
Below lesion, sympathetic predominantly - pale, cool, and goosebumps
About 85% of pts have transection above T6
Anesthetic technique should involve deep general or spinal/epidural with local anesthetic
Treatment of acute episode is with alpha-antagonists and vasodilators
- beta-blockers should not be used
What is the normal cerebral metabolic rate for oxygen per minute?
3.5 mL/100 g brain tissue
Order (most to least) of neuromonitoring sensitivity to interference from anesthetics
Visual evoked potentials
Somatosensory evoked potentials
Brainstem auditory evoked responses
What are the most sensitive monitors for venous air embolism?
TEE is the gold standard
Precordial doppler is the most sensitive non-invasive monitor
- can detect as little as 0.25 mL of air
What is normal cerebral blood flow? What is the critical low value?
Normal CBF is 50cc/100g tissue/min
The critical low value is 20cc/100g tissue/min, under which EEG changes begin to occur
How does ischemia effect autoregulation? What is the difference between intracerebral steal syndrome and Robin Hood syndrome?
During focal cerebral ischemia, ischemia areas of the brain are unable to participate in autoregulatory changes of vessel resistance
Intracerebral steal syndrome occurs with hypercarbia, when normal vessels vasodilate shunting blood away from the unchanged ischemic area
Robin Hood syndrome is reverse steal caused by hypocarbia, when normal vessels constrict shunting blood to the “poor” ischemic areas
What is the treatment for venous air embolism?
Flood the field and pack the wound 100% O2 Jugular venous compression Aspirate air through central line Place pt head down and in left lateral position
Describe the Glascow Coma Scale
Motor response: Obeys commands - 6 Localizes stimulus - 5 Withdraws from pain - 4 Flexion posture - 3 Extension posture - 2 No response - 1
Verbal response: Oriented - 5 Confused - 4 Inappropriate - 3 Incomprehensible - 2 No response - 1
Eye opening: Spontaneous - 4 To speech - 3 To pain - 2 Nothing - 1
What is neurogenic pulmonary edema?
NPE is pulmonary edema caused by massive sympathetic discharge after neurologic/spine injury
Occurs in up to 20% of pts with severe head injury
Typically develops within 4 hours of inciting event
How do the following agents effect CMRO2, CBF, and ICP?
- Volatile anesthetics
- Nitrous oxide
- Xenon
- Propofol
Volatiles decrease CMRO2, increase CBF, and increase ICP
N2O increases CMRO2, CBF, and ICP
- Increase in CBF can be blunted by the simultaneous administration of IV or volatile anesthetics
Xenon decreases CMRO2, but increases both CBF and ICP
Propofol decreases CMRO2, CBF, and ICP
What are the physiologic effects of ECT?
Elevations in CBF and ICP
Long- and short-term memory loss
Initial increase in parasympathetic stimulation
- increased secretions
- bradycardia
- asystole
Quickly followed by increased sympathetic stimulation
- hypertension
- tachycardia
- ST segment and T wave changes
What methods are available for CNS monitoring during carotid endarterectomy? What can they detect?
Carotid stump pressures
- can detect global ischemia but not emboli
EEG
- can detect global ischemia but not emboli
SSEPs
- can detect even subcortical ischemia
Transcranial doppler
- can detect emboli but not ischemia
What are the requirements for the determination of brain death?
Evaluation by two physicians
No other causes that could mimic brain death
Coma with absent brainstem reflexes
Lack of respiratory drive by apnea testing
- if apnea testing can not be performed, confirmatory testing (cerebral perfusion scintigraphy) is necessary
Describe the timing of the morbidity/mortality of SAH? Are there any predictors of outcome? What is the treatment?
Re-bleeding can occur in the first 48 hours
Vasospasm can occur 3-7 days after initial event
Higher admission hemoglobin has been associated with decreased cerebral ischemia and improved outcomes
Traditional treatment involved Triple H therapy, but studies have not proven benefit
- hypertension
- hemodilution
- hypervolemia
Calcium channel blockers (Nimodipine) can improve outcome and decrease cerebral infarction
Chemical angioplasty can also be used to treat vasospasm
What physiologic changes can negatively impact SSEP monitoring?
Hypotension
Hypo-/Hyper-thermia
Hypoxia
Anemia
Acid-base status does not affect SSEPs
What is Cushing’s Triad? What causes it?
Cushing’s Triad:
- Hypertension
- Bradycardia
- Breathing alterations
Caused by brainstem compression, usually due to surgical manipulation or severe cerebral edema
What is jugular bulb venous oxygen saturation (SjVO2)?
SjVO2 is a monitoring modality which can assess the oxygen extraction of brain tissue
Values represent the balance between global cerebral oxygen supply and demand
- focal ischemia cannot be assessed
Which fluids should be avoided during surgery for an intracranial aneurysm and why?
Hypotonic solutions - may worsen cerebral edema
Glucose containing solutions - may exacerbate neuronal injury
What drug should be avoided in a patient with myotonic dystrophy?
Succinylcholine
- known precipitating factor for myotonia
What are the differences between Myasthenic Syndrome (Lambert-Eaton) and Myasthenia Gravis?
Myasthenic Syndrome (Lambert-Eaton)
- Dysfunction of presynaptic calcium channels leading to decreased release of Ach
- Muscle weakness improves with use
- Muscle pain is common; reduced DTRs
- Associated with small cell lung cancer
- MORE sensitive to both succinylcholine and non-depolarizing NMBs
Myasthenia Gravis
- Destruction of postsynaptic Ach receptors
- Muscle weakness worsens with use
- No muscle pain; normal DTRs
- Associated with thymoma
- Resistant to succinylcholine; MORE sensitive to non-depolarizing NMBs
What factors can predict increased likelihood of the need for postoperative mechanical ventilation in patients with Myasthenia Gravis?
Risk Factors:
- Duration of disease over 72 months (6 years)
- History of chronic respiratory disease (ie. asthma or COPD)
- Pyridostigmine dose over 750mg/day
- Vital capacity of less than 2.9 liters
Describe the potential causes of postoperative visual loss
Ischemic optic neuritis (ION)
- occurs due to hypoperfusion or decreased oxygen delivery to the optic nerve
- presents with painless visual loss and impaired color vision
Retinal artery occlusion
- occurs due to external compression, retrobulbar hemorrhage, or embolism
- presents with painless visual loss and “cherry red macula”
Acute angle glaucoma
- occurs due to increased IOP from blockade of aqueous humor outfow
- presents with painful and red globe, blurry vision, headache, N/V
