Clinical aspects of cerebral perfusion & ICP Flashcards
Cerebral blood flow is what percentage of cardiac output
15%
Brain ischaemia occurs at what perfusion rate
20ml/100g tissue/min
What pressure determines cerebral blood flow at any given time
Cerebral perfusion pressure
Cerebral perfusion pressure (CPP) =
MAP - ICP (intracranial pressure)
MAP =
Diastolic pressure + 1/3 pulse pressure
Increased ICP causes cerebral perfusion pressure to increase or decrease
Decrease
Remember CPP = MAP - ICP
Factors that regulate cerebral blood flow (3)
CPP
Conc. of arterial PCO2
Conc. of arterial PO2
Weight of brain
1300-1400g
Name 3 types of oedema
Vasogenic (extracellular)
Cytotoxic (intracellular)
Interstitial
Vasogenic oedema
- what is it due to
- location of oedema
- composition of oedema
- extracellular fluid levels increased or decreased
- effect of steroids
- effect of mannitol
Increased capillary permeability Mainly white matter Plasma filtrate Increased Effective Effective
Cytotoxic oedema
- what is it due to
- location of oedema
- composition of oedema
- extracellular fluid levels increased or decreased
- effect of steroids
- effect of mannitol
Cellular swelling (of neurons and glial cells) due to failure of Na/K pump
Grey and white matter
Increased intracellular water and sodium
Decreased
No effect of steroids
Mannitol effective
Interstitial oedema
- what is it due to
- location of oedema
- composition of oedema
- extracellular levels increased or decreased
- effect of steroids
- effect of mannitol
increased brain water due to impairment of absorption of CSF
periventricular white matter
CSF based
Extracellular fluid increased
No effect of steroids
Mannitol sometimes has an effect, sometimes doesn’t
Causes of vasogenic oedema (4)
Tumour
Abscess
Late stage infarction
Trauma
Causes of cytotoxic oedema (2)
Early stages of infarction
Water intoxication
Cause of interstitial oedema
Hydrocephalus (communicating or non-communicating)
What condition do you get interstitial oedema
Hydrocephalus
Percentage of brain substance, blood and CSF within the cranium
80%
10%
10%
What is the munro-kelly doctrine
Pressure-volume relationship that aims to keep a dynamic equilibrium among the essential non-compressible components inside the rigid compartment of the skull
Essentially meaning that the sum of the volumes of brain substance , CSF, and intracranial blood is constant (i.e. total intracranial volume is always constant)
When a new intracranial mass is introduced, what happens in respect to the munro-kelly doctrine
a compensatory change in volume must occur through a reciprocal decrease in venous blood or CSF to keep the total intracranial volume constant
Define compliance
change in volume observed for a given change in pressure
Define elastance + what does the term mean in association with intracranial masses
change in pressure observed for a given change in volume (INVERSE OF COMPLIANCE)
Refers to the accommodation to outward expansion of an intracranial mass
Homeostatic compensatory mechanisms in response to intracranial masses (2)
1) Venous system can collapse to squeeze blood out jugular veins or emissary and scalp veins
2) CSF can be displaced into subarachnoid space
What happens when homeostatic compensatory mechanisms in response to intracranial masses have been exhausted
The innate homeostatic pressure-buffering mechanisms keep compliance flat until a “critical volume” is reached
After this critical volume, small changes in volume produce significant increase in pressures, and intracranial hypertension naturally follows
As compliance decreases, does ICP increase or decrease
Increase
What is the cushing’s reflex
AKA vasopressor (anti-hypotensive) response
physiological response to raised ICP (causing decreased CPP), resulting in CUSHING’S TRIAD
What does the Cushing’s triad consist of
Hypertension
Irregular breathing
Bradycardia
Cushing’s reflex comes about due to raised ICP (causing decreased CPP), the decreased CPP activates what system (1) which brings about what response (2) to cause the cushing’s triad
AUTONOMIC NERVOUS SYSTEM
Sympathetic response – a1 adrenergic receptors stimulated to cause HYPERTENSION & TACHYCARDIA
Aortic baroreceptors stimulate vagus nerve –> BRADYCARDIA
Management of raised ICP (6)
Head elevation - to improve venous return to heart
Mannitol/hypertonic saline - short acting
Hyperventilation - to decrease CPP, short acting
Barbiturate coma - to decrease cerebral metabolism & CPP
Surgical decompression
Brain tissue oxygenation monitoring with probe
Normal ICP range
7-15 mmHg
3 types of ICP pulse waveforms (Correlate to arterial pressure)
P1 wave = percussion wave
P2 wave = tidal wave
P3 wave = dicrotic wave
What are Lundberg A waves
Steep increases in ICP lasting for 5 to 10 minutes.
They are always pathological and represent reduced intracranial hypertension indicative of early brain herniation
What are Lundberg B waves
oscillations of ICP at a frequency of 0.5 to 2 waves/min and are associated with an unstable ICP
What are Lundberg C waves
oscillations with a frequency of 4-8 waves/min. They have been documented in healthy subjects and are probably caused by interaction between the cardiac and respiratory cycles.
Related to waves of systemic BP
What is cerebral autoregulation
ability to maintain constant blood flow to the brain over a WIDE RANGE OF CPP (50-150mmHg)
If CPP low, what do cerebral arterioles do
dilate to compensate for the decreased pressure and vice versa if CPP is high
In some pathologies, cerebral blood flow can’t be autoregulated (ability to maintain constant blood flow to the brain over CPP range of 50-150mmHg) - describe some of these pathologies (3)
if CPP exceeds 150mmHg, such has in HYPERTENSIVE CRISIS, the autoregulatory system fails as it’s not within the range
Toxins like CO2 can cause diffuse cerebrovascular dilation and inhibit proper autoregulation
During first 4-5 days of head trauma, many patients can experience disruption in cerebral autoregulation
