Neurophysiology Flashcards
3 main components within the cranial vault that can cause ICP?
- CSF (obstruction, overproduction, decreased clearance) 2. Blood volume (hypotension, high CVP) 3. Brain tissue (edema)
What does cerebral perfusion pressure equal?
CPP = MAP - ICP (or CVP whichever is higher)
What is a normal ICP?
< 10 mmHg
What MAP range is cerebral vascular resistance auto-regulated?
70 mmHg to 150 mmHg, above that, cerebral vascular resistance cannot increase anymore to restrict pressure dependent increase in flow
How does cerebral vascular resistance change with hypercarbia?
CVR and flow increases in a linear fashion until > 80 mmHg where the curve starts to flatten, and gets flat at 120 mmHg
How does cerebral vascular resistance change with hypoxia?
Little effect until PaO2 drops below ~50 mmHg and then rises exponentially; no effect between 60 mmHg and 300 mmHg
How do volatile anesthetics affect cerebral blood flow and cerebral metabolic rate?
VA’s “uncouple” flow from consumption in that O2 consumption decreases and CBF (and therefore oxygen delivery) increases
What is the normal cerebral metabolic rate (CMRO2)?
3.5 cc/ 100g/ min
What is the normal cerebral blood flow?
50 cc/ 100g/ min
How much CSF does an average adult have at any one time? How much CSF is produced per day?
~150 cc, 500cc produced per day
What happens in the brain when the ICP is 30?
CPP decreases -> decreased blood flow -> decreased O2 delivery -> ischemia -> cellular break down -> edema -> increased ICP -> decreases CPP more
What does dexamethasone do to CSF production and absorption?
Decreases production, decreases absorption in animal studies
How does mannitol work?
Increases serum osmolality -> fluid shift into intravascular space -> increased UOP
What do you worry about with mannitol and intracranial hematomas?
Decreased brain swelling can cause a hematoma that was being tamponaded by the swollen brain tissue to expand
What happens to cerebral blood flow with 1 MAC of sevoflurane?
Increases about 20%
How does propofol affect cerebral blood flow and cerebral consumption of oxygen?
Decreases both
What happens in reverse steal of the brain?
Normal brain vasculature vasocontricts to stimulus (i.e. propofol) while ischemic brain cannot response -> normal brain is underperfused
How does hypercarbia affect cerebral blood flow?
Changes the H+ concentration
Mechanisms of action for cerebral ischemia with a PaCO2 less than 20?
- Decrease in cerebral blood flow 2. Left shit in the oxyhemoglobin dissociation curve
Which anesthetic agents decrease cerebral metabolic rate of O2?
Most anesthetic agents except ketamine and N2O
Does hypothermia uncouple CMRO2 and CBF?
No, it just decreases both of them
Is autoregulation affected by high doses of propofol?
No, but propofol does decrease CBF, cerebral blood volume, and ICP
How does thiopental affect CMRO2 and CBF?
Decreases it in a dose dependent manner until 50%
What IV induction agent do you worry about in patients with seizures?
Etomidate (can be epileptogenic in patients with seizure disorders)
Which narcotic can provoke seizures in patients with epilepsy?
Alfentanil
Do volatile anesthetics impair autoregulation and if so, which ones more than the others?
Yes in a dose-dependent manner Sevoflurane impairs less than iso or des, halothane impairs it the most
How does nitrous affect CMRO2, CBF, and ICP?
Increases all three of them
What level of consciousness do you see when an EEG shows delta waves? theta waves? alpha waves? beta waves?
Delta: deep sleep Theta: first stage of sleep/drowsiness Alpha: relaxed bu alert Beta: Highly alert
Which volatile anesthetic has epileptiform discharge during induction and at 2 MAC?
Sevoflurane and Enflurane (not clinically significant)
Blood flow to the brain comes what what two main arteries?
Internal carotid (80%) and vertebrobasilar system (20%)
What are the main areas of aneurysms in the brain?
Anterior communicating artery (25%) MCA (25%) Internal carotid artery between posterior communicating and anterior choroidal arteries (22%) Basilar bifurcation (7%) Internal carotid bifurcation (4%)
Put these in order of most to least sensitive for detecting VAE: TEE, PA pressures, ETN2, Precordial doppler
TEE > Doppler > PA pressure changes > ETN2
What are the first steps needed after diagnosis of a VAE?
Flood the field, stop N2O, 100% O2, T-berg, positive pressure vent (pressure on SVC), compression of jugular vein, fluids/pressors, aspiration of central line
If you have an unruptured aneurysm and surgeon asks for hyperventilation and mannitol, what do you do?
No! Since transmural pressure of the aneurysm is MAP - ICP, once the cranial vault is open, ICP is 0 and then you can do it to prevent rupture since transmural pressure = MAP
What ECG changes do you see with subarachnoid hemorrhages?
Sympathetic stimulation can cause dysrythmias (i.e. PVCs, prolonged QT, ventricular tachyarrythmias)
What is Cushing’s response?
From high ICP: bradycardia, HTN, irregular breathing (Cheyne Stokes)
When is the peak time you would expect cerebral vasospasm after SAH?
1 week peak (rarely occurs after 2 weeks): thought to be from oxy-Hgb in subarachnoid space leading to free radical production = decreased NO = more vasoconstriction
What is the treatment for cerebral vasospasms?
HHH: Hypertension (SBP ~160), hypervolemia (CVP >8), and hemodilution (Hct of ~30) Nimodipine (CCB)
Lucid interval following head trauma, lenticular appearance on CT
Epidural hematoma
Associated with old age, crescent shape on CT expanding past skull sutures
Subdural hematoma
RBCs in CSF means what?
Subarachnoid hematoma
Diffuse bleeding into an area of cerebral contusion is what kind of hemorrhage?
Intracerebral hematoma
What is neurogenic pulmonary edema?
ARDS in the setting of TBI
Patient after TBI has a sodium of 154 and nearly 200cc of urine in an hour. Diagnosis and treatment?
Diabetes insipidus Tx: DDAVP
What is neurogenic diabetes insipidus?
Lack of ADH secretion
What is syndrome of inappropriate ADH secretion?
Too much ADH leading to hyponatremia and fluid retention (patients normally euvolemic)
What is cerebral salt wasting syndrome?
After brain injury, salt wasting (hyponatremia) poorly responsive to fluid restriction and are often hypovolemic from fluid losses (SIADH patients are euvolemic)
Treatment for cerebral salt wasting syndrome?
Replacing fluid loss with NS and generally resolves over days to weeks
Treatment for SIADH?
Fluid restriction + salt tablets (symptomatic) + “vaptan” drugs - vasopressin analogues
What is the Monro-Kellie hypothesis?
Cranial compartment is incompressible and the volume inside is fixed made up of: blood, CSF, and brain tissues
What does line A, B, and C represent?
A: O2
B: CO2
C: MAP
Which actually slightly increases cerebral blood flow: sufentanil, alfentanil, fentanyl, remifentanil
Sufentanil (the rest slightly decreases CBF)
The blood brain barrier prevents the passage of: glucose, water, CO2, lipid soluble compounds
Glucose
What two drugs decrease CSF production?
Acetazolamide and furosemide
Which decreases cerebral blood flow and cerebral metabolic rate: fentanyl, ketamine, isoflurane, lidocaine
Lidocaine (remember that isoflurane and other volatile anesthetics uncouple CMRO2 and CBF)
Compared to serum, which is proportionately the lowest in CSF: protein, glucose, sodium, bicarbonate
Protein
Class C nerves are used in what?
Nociception and post-ganglionic autonomic system
Where are the cell bodies of the first order neurons for pain signaling? 2nd order neurons?
1st: Dorsal root ganglion
2nd: Dorsal horn of the spinal cord
What tracts does pain and temperature go up in the spinal cord?
Spinothalamic tract (after crossing over to the contralateral side)
What is the precentral gyrus responsible for? Postcentral gyrus?
Pre: motor cortex
Post: sensory cortex
What does beta-1 activation do? Beta-2 activation?
1: increased chronotropy/inotropy/lusitropy, lipolysis, renin secretion
2: bronchodilation, smooth muscle relaxation, glycogenolysis
How does the SNS affect GU organs? ADH secretion?
Relaxes GU organs (i.e. uterus, etc.) and increase ADH secretion (to increase BP)
