Apex Flashcards
What is the formula for CBF? What is the normal value?
CBF = CPP/cerebral vascular resistance
50mL/100g/min
What are the 5 determinants of CBF?
CMRO2 CPP Venous pressure PaCO2 PaO2
What is the normal value for CMRO2?
3.0-3.8mL/100g/min
50mL/min
What factors cause CMRO2 to increase?
hyperthermia
seizures
Ketamine
N2O
What factors cause CMRO2 to decrease?
hypothermia (7% per 1 C) Halogenated agents propofol etomidate barbiturates
What is the formula for CPP? What is normal?
CPP = MAP - ICP (or CVP)
50-150mmHg
What is normal ICP range?
10-15mmHg
What are the consequences of a CPP that exceeds the limits of auto regulation (too low)?
Vessels are maximally dilated
CBF becomes pressure dependent
Risk of cerebral hypoperfusion
What are the consequences of a CPP that exceeds the limits of auto regulation (too high)?
Vessels are maximally constricted CBF becomes pressure dependent
Risk of cerebral edema and hemorrhage
What is the relationship between PaCO2 and CBF?
Linear. Decreasing PaCO2 decreases CBF and therefore ICP.
At what PaCO2 does maximal cerebral vasoconstriction occur?
25mmHg
At what PaCO2 does maximal cerebral vasodilation occur?
80-100mmHg
For every 1mmHg increase or decrease in PaCO2, how much will CBF increase or decrease?
By 1-2ml/100/min
What is the relationship between CMRO2 and CBF?
Things that increase CMRO2 tend to cause vasodilation and increase CBF.
Things that decrease CMRO2 tend to cause cerebral vasoconstriction and decrease CBF.
What is the exception to the relationship between CMRO2 and CBF?
Halogenated agents. They decouple the relationship, they reduce CMRO2 but cause cerebral vasodilation.
How does acidosis and alkalosis affect CBF?
Respiratory acidosis increases CBF
Respiratory alkalosis decreases CBF
Metabolic acidosis and alkalosis have not affect on CBF because H+ does not cross the BBB.
How does PaO2 affect CBF?
PaO2 below 50-60mmHg causes cerebral vasodilation and increases CBF.
PaO2 above 60mmHg does not affect CBF
What is normal ICP?
5-15mmHg (10 or less she says)
What level is considered intracerebral hypertension?
> 20mmHg
When is ICP measurement indicated?
When Glasgow coma scale is 7 or less
What is the gold standard for ICP measurement? What are other ways to measure ICP?
Gold standard: intraventricular catheter
Subdural bolt
Catheter over the convexity of the cerebral cortex
List the signs and symptoms of intracranial hypertension
Headache N/V Papilledema Focal neuro deficits Decreased LOC Seizure Coma
What is the Monro-Kellie Doctrine?
Describes the pressure-volume equilibrium between the brain, blood, and CSF. An increase in one of the components must be countered with a decrease in one or both of the others otherwise ICP will increase
What is Cushing’s triad? What are the symptoms?
It indicates intracranial hypertension.
Hypertension
Bradycardia
Irregular respirations
Explain why the symptoms of Cushing’s triad occur with intracranial hypertension.
Increased ICP reduces CPP and in an effort to preserve perfusion BP increases.
Hypertension activates the baroreceptor reflex leading to bradycardia.
Compression of the medulla causes irregular respirations.
How does hyperventilation affect CBF? What is the ideal PaCO2 to achieve this effect?
CO2 dilates the cerebral vessels which decreases cerebral vascular resistance increasing CBF and ICP.
Hyperventilation to the point of 30-35mmHg constricts the cerebral blood vessels increases cerebral vascular resistance and decreasing CBF and ICP.
Why should PaCO2 not be decreased below 30-35mmHg?
PaCO2 below 30mmHg increases the risk of cerebral ischemia due to vasoconstriction and shifting the oxyhemoglobin dissociation curve to the left reducing O2 offloading.
How do NTG and nitroprusside affect ICP?
Both are cerebral vasodilators and increase CBF and ICP
How does head position affect ICP?
Head elevated > 30 degrees facilitates venous drainage from the brain.
Neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV and ICP.
Head down (TBurg) increases CBV and ICP.
How does mannitol reduce ICP? What problems can arise when mannitol is used in this way?
Increases serum osmolarity and pulls water across the BBB into the bloodstream.
This transiently increases blood volume which can increase ICP and stress a failing heart.
If the BBB is disrupted mannitol cross and pull water into the brain (cerebral edema).
What is the relationship between hyperglycemia and cerebral hypoxia?
During cerebral hypoxia, glucose in converted to lactic acid. Cerebral acidosis destroys brain tissue and is associated with worse outcomes.
What is transmural pressure?
The balance between MAP using out on the walls of an aneurysm and the ICP pushing in on the aneurysm. It’s a tamponade effect. Increases predispose the aneurysm to rupture.
How is transmural pressure calculated? What increases it?
Transmural pressure = MAP - ICP
Increased by: hypertension and/or an acute reduction in ICP.
What does aneurysm rupture cause? (condition)
Subarachnoid Hemorrhage
What are the signs and symptoms of a SAH?
Intense HA* LOC Focal neuro deficits N/V photophobia fever
What is the most significant source of morbidity and mortality in a patient with SAH?
Cerebral vessel vasospasm
What is cerebral vessel vasospasm?
Delayed contraction of the cerebral arteries that can lead to cerebral infarct
When is cerebral vasospasm most likely to occur?
4-9 days following SAH
What is the treatment for cerebral vasospasm?
Triple H Therapy:
hypervolemia
hypertension
hemodilution
Explain the purpose of triple H therapy?
Liberal hydration supports BP and CPP.
Hemodilution reduces blood viscosity and cerebrovascular resistance.
What are 2 common ways of reducing ICP that should specifically be avoided in a traumatic brain injury?
Hyperventilation - can worsen cerebral ischemia with TBI.
Steroids - worsens neurologic outcome
