Neuroanesthesia Flashcards
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
True
T or F: visual evoked potentials (VEPs) are most sensitive to the effects of volatile anesthesia.
True
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.
True
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.
True
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.
True
T or F: volatile agents cause cerebral vasodilation, with the order of vasodilation going from halothane (most), enflurane, desflurane, isoflurane, and sevoflurane (least).
True
T or F:TBI patients usually have low CBF in the first 24 hours of injury.
True
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.
True
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?
CPP = MAP - ICP
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.
True
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.