Advanced Neurophysiology And Neurosurgery Flashcards
(39 cards)
How does acute hypoglycemia lead to global brain injury? Which cells are most likely to be injured? Acute hypoglycemia vs starvation:
Acute, sustained hypoglycaemia produces brain injury in a pattern similar to that of global hypoxia, in that the entire brain is affected, and those cells that are most metabolically active are the most likely to have the greatest injury
25 year old man following traumatic brain injury (TBI) has a measured intracranial pressure (ICP) of 28 cc H20 through an external ventricular drain (EVD), and mean arterial pressure (MAP) of 60. The EVD has been draining 12 cc of cerebral spinal fluid (CSF) an hour and is set to drain above a pressure of 20 cm H20. Which of the following is the next most important step in this patient’s management:
A. Decrease the level of the drain to 15 cm H20
B. Apply intermittent suction to the EVD
C. Flush the EVD with 20 cc of warm saline
D. Start a phenylephrine drip
E. Measure a CVP
An EVD can be placed both to measure the ICP as well as drain fluid. When the ICP is greater than the EVD ‘pop-off’ pressure, CSF fluid is drained. In cases of rapid ICP increases, the CSF cannot drain as quickly as ICP increases. Other causes of an ICP being elevated with EVD in place include insufficient amount of CSF, restrictions on how much CSF can be drained per hour, and a kinked or obstructed (including misplaced) catheter. Flushing 20 cc of saline into the ventricle with high ICPs is dangerous as it may further increase ICP. Applying suction to an EVD is idiotic, hopefully for obvious reasons. Decreasing the ‘pop-off’ of the EVD to 15 cm H20 will not help as the ICP is already greater than the level of the drain. Lowering the CVP would only help if it were greater than CSF, and there is no indication in the stem that the CVP would be greater than 28 cm H20 (which would likely be an error anyway if it read that high). Phenylephrine will raise the MAP to increase perfusion (MAP – ICP).
What is the formula for CPP?
Cerebral perfusion pressure (CPP) = MAP – ICP
Which of the following conditions would blood flow to the brain expect to rise to the greatest extent in an otherwise healthy patient:
A. MAP of 100 mm Hg B. MAP of 180 mm Hg C. PaCO2 75 mm Hg D. PaO2 of 20 mm Hg E. 50% decrease in viscosity
D: PaO2 of 20 mm Hg
Cerebral vascular resistance decreased with hypercarbia and hypoxia and is autoregulated from approximately 50-60 mmHg to 150-160 mm Hg. In autoregulation, increases in MAP do not result in increased flow, because vascular resistance proportionately increases to ‘match’ the MAP up to a MAP of 160 mm Hg. Recall Ohm’s law, where Flow = MAP / Resistance; therefore a proportional increase of resistance in the setting of increasing MAP will essentially cancel each other out. Above a MAP of 160 mm Hg, cerebral vascular resistance can no longer increase to restrict pressure dependent increases in flow. In general, very high MAPs will not increase flow as much as moderately bad hypercarbia or hypoxia (which vasodilate the cerebral vasculature). Cerebral vascular resistance (and therefore flow) increases nearly in a linear inverse fashion with increased PaCO2. As PaCO2 rises above 80, the curve starts to flatten and above 120 or so very little further increases are possible with increased PaCO2. Oxygen has little effect on cerebral blood flow until PaO2 drops below (about) 50, at which point in rises exponentially. Therefore, a very low PaO2 such as 25 will produce extremely high cerebral blood flow. Viscosity has very little effect of cerebral blood flow as it is only a minor contributory to cerebral vascular resistance.
Which of the following would likely be associated with the highest cerebral blood flows: (ABG: pH/ PaO2/ PaCO2):
A. 7.30/ 65 / 63
B. 7.15 / 350 / 75
C. 7.05/ 65/ 40
D. 6.95 / 60 / 65
B: 7.15 / 350 / 75
As discussed above, both hypoxia and hypercarbia can affect cerebral blood flow. Normal and even moderately low PaO2 have almost no effect on blood flow as compared to very high oxygen tensions. Only when hypoxia is severe (< 50) does cerebral blood flow start to rapidly climb. Also, as stated above, cerebral blood flow increases almost linearly with PaCO2 from 20 to 80. Therefore since answer B had the highest PaCO2, one would expect that patient to have the highest blood flow. The mechanism appears to be CO2 crossing into the CSF, causing an acidosis. This is why even though answers C & D have lower pH’s (due to either pure or mixed metabolic acidosis), the blood flow is lower (since donated H+ from acids in the plasma do not cross the blood brain barrier (BBB) into the CSF
What does coupling mean?
Cerebral blood flow to oxygen consumption
Volatile agents-coupled or uncoupled?
Volatile agents uncouple flow CBF and CMRO2 in that oxygen consumption decreases and flow (and therefore oxygen delivery) increases.
Opioids and coupling:
Ketamine and coupling?
Fentanyl and opioids have rather minor effects on both CBF and CMRO2; and ketamine (depending on the source) increases CBF with minor changes, if any, in CMRO2.
Normal CMRO2 and CBF:
A normal CMRO2 of 3.5 ml/ 100g/ min and a cerebral blood flow of 50 ml/ 100g/ min are probably worth knowing for the boards
Which of the following would NOT be expected to disrupt the blood brain barrier (BBB):
A. Extreme hypercapnea B. Extreme hypertension C. Extreme hyperglycaemia D. Extreme hypoxia E. Sustained seizures
C: Extreme hyperglycaemia
Extremes of hypercapnea & hypoxia, sustained seizures, tumors, strokes, infection, and trauma can lead to disruption of the BBB. Even extreme and prolonged levels of hyperglycaemia, such as seen with hyperosmolar coma, will have an intact BBB.
What does the BBB prevent from going through? What does it let in?
The BBB slows, or in some cases, prevents the entry of larger, charged, or hydrophilic compounds into the brain. Water, CO2, and lipophilic molecules cross easily.
How many times a day does the entire CSF volume replace itself?
About three times a day
Which of the following is NOT a normal compensatory mechanism to decrease intracranial pressure (ICP) in the setting of intracranial hypertension:
A. Displacement of the cerebellar tonsil below the foramen magnum
B. Displacement of intracranial CSF below the foramen magnum
C. Increased CSF absorption at the arachnoid granulations
D. Decreased CSF production at the choroids plexus
E. Decreased intracranial venous blood volume
: A: Displacement of the cerebellar tonsil below the foramen magnum
Displacing the cerebellar tonsil below foramen magnum is referred to as herniation and is uniformly fatal. The other answers are normal compensatory mechanisms so that answer A is avoided.
Which of the following processes are most likely to be occurring with an ICP of 30:
A. Cerebral perfusion pressure (CPP) decreases, leading to brain ischaemia and swelling, further increasing the ICP
B. CPP decreases, leading to brain ischaemia and shrinking, lowering the ICP
Optimal MAP?
Normal ICP 5-15
A: Cerebral perfusion pressure (CPP) decreases, leading to brain ischaemia and swelling, further increasing the ICP
CPP = MAP – ICP. If ICP increases, then CPP decreases, making answers D & E wrong. With decreased CPP, comes decreased blood flow, and therefore decreased oxygen delivery leading to ischaemia. Ischaemia results in cellular breakdown, inability to extrude sodium, and swelling, increasing brain mass and therefore ICP. As ICP increases further, CPP continues to decrease, and the process continues to worsen and worsen. This is why it is essential that MAP be raised when dealing with high ICPs, even though the intracranial blood volume may rise a bit. Decreased heart rate is part of the Cushing response, along with hypertension with a widened pulse pressure and irregular breathing, often with periods of apnea. The Cushing response (reflex) is secondary to increased ICP, not lowered CPP.
Finding the optimal MAP, or CPP, is a complicated discussion and we won’t get into the specifics, needless to say picking a value of 60 mm Hg to apply to everyone may be insufficient for some and more than needed for others. The basic thing you should take away are two important points. First, at CPPs that are too low, ICP will increase via additional edema secondary to the hypo perfusion (tissue hypoxia). At CPPs that are to high the ICP will increase simply due to hyperaemia (one of the three components of intracranial mass - brain and CSF being the other two). Therefore, the optimum CPP is not too low and not too high, and 60 mm Hg works well for most people so we typically pick that. Second, hyperaemic intracranial hypertension is always better than oligaemic intracranial hypertension. At least in the former the brain is getting oxygen.
Cushing’s is a response to what?
Increased ICP
How does mannitol work? Why can pulmonary edema and heart failure result? After mannitol treatment, what can happen? How can giving mannitol expand hematomas?how can aneurysms rupture with mannitol? Electrolyte abnormalities with mannitol?
Mannitol increases serum osmolality, therefore drawing intracellular and interstitial water into the intravascular space and out into the urine (as mannitol passes freely through the glomerulus but is not reabsorbed).
By decreasing brain swelling, haematomas that are being tamponaded by the swollen brain tissue can expand.
Cerebral aneurysms can rupture when transmural pressures increase (Transmural pressure = MAP – (either ICP or CVP), either by increasing MAP or decreasing ICP (as with mannitol). As an osmotic diuretic, loss of electrolytes are common resulting in hypokalaemia.
How are propofol’s effects on CMRO2 and CBF similar to thiopental?
Both propofol and barbiturates powerfully decrease CMRO2 and CBF.
Reverse steal, or Robin Hood phenomenon, is where:
In reverse steal, normal brain vasculature vasoconstricts due to some stimulus such as anesthetics (barbiturates, propofol, etomidate, benzodiazepines) or hypocarbia, while ischaemic brain vasculature is unable to respond. Therefore, blood is preferentially directed away from oxygen rich brain (normal) to oxygen poor brain (ischaemic
In a patient with elevated ICP, the role of opioids are to:
A: Blunt the sympathetic surge from intubation
Opioids have very little effects on ICP, CSF production, CBF, or CMRO2. Opioids, in general, have minor effects in increasing CSF absorption, but the primary role of these drugs are to decrease hypertension and increased intracranial blood volume during stimulations, as with intubation.
Which of the following is the most to least SENSITIVE monitor for intraoperative VAE
> Doppler > PA pressure changes > ETN2
TEE is most sensitive and can detect very small bubbles. Precordial Doppler requires at least 0.25 cc of air for detection. PA pressure changes and ETN2 increases require far larger volumes of air. A popular estimate is it requires about 300 cc of air to prove lethal for an average adult.
VAE-position, what. Am you be doing? Why no PEEP onVAE?
The correct answer is: C: Change the position from sitting to left lateral decubitus reverse-trendelenberg position
After diagnosing a VAE, the surgeon should be notified to flood the field with saline and bone wax, nitrous oxide should be stopped (so the VAE does not expand) and 100% oxygen begun, and the patient should be repositioned so the head and heart are at least at the same level. Change the position from sitting to left lateral decubitus reverse-trendelenberg position is partially correct that an obstructing (air-lock) bubble of air at the right outflow tract might be moved away towards the right ventricular apex in the left lateral position, but only when in Trendelenberg, not Reverse-Trendelenberg. Application of prolonged positive pressure to the thorax can increase superior vena cava venous pressures to stop or slow the entrainment of air. Compression of the jugular veins is an attempt to accomplish the same goal. In the setting of cardiovascular instability, fluids, pressors, and chest compressions might be helpful, with the latter theoretically disrupting a large air lock. Hyperbaric oxygen therapy and aspiration of air from the central line might also be helpful; at least theoretically. On the boards, PEEP is probably contraindicated, as it may lead to increased right heart pressures and a paradoxical VAE through an ASD or VSD and ultimately stroke.
EKG and central line
biphasic p-wave indicated a mid atrial position of the catheter, and supposedly pulling back one centimeter (not sonometer, don’t be that guy…and, no, thats not how its pronounced in England either) from here puts it at the SVC/ right atrial positio
What causes aneurysmal rupture?
Why do you want to wait u til the cranial vault is opened?
Rupture results when the transmural pressure increases above a threshold. Since transmural pressure = MAP –ICP, a decrease in ICP (as with hyperventilation and mannitol) or CVP can increase this pressure as well as increased MAPs.
After the cranial vault is opened, ICP drops to 0, and transmural pressure = MAP. At this time MAP can be dropped, but a MAP of 40 (answer E) would likely lead to hypoperfusion of critical organs including normal brain. The concern with giving ICP lowering measures prior to cranial vault opening is that the ICP is unknown and MAP needs to be maintained to avoid ischaemia; leading to the possibility of an increased transmural pressure and aneurysm rupture before the vault is opened (leading to rapidly increasing ICP).
Tell me about the 2 general strategies in clipping an aneurysm:
The traditional approach is placing the clips directly beside the aneurysm. In this case, a low MAP is associated with a decreased chance of bleeding, and it is even reasonable to induce hypotension with propofol, thiopental, nicardipine, nipride, or other drugs just prior to the clip placement. Even administration of adenosine to temporarily stop cardiac output is a reasonable option in some cases. The second strategy is to place a temporary clip on feeding vessel(s) so that the blood flow at the aneurysm is decreased (or even absent). In this case, induced hypertension may be needed to maintain perfusion pressure in collateral distributions to the feeding artery.
