Week 22 - Head Injury Flashcards
What are the 3 anatomical components of consciousness? What are they responsible for?
Brainstem (reticular formation)
- level of consciousness, processes afferent sensory info, modifies neuronal processing in CNS via neurotransmitters
Thalamus
- determines how responsive you are to your environment
Cortex
- Establishes significance and meaning to experience of consciousness
Describe the neurotransmitter systems and what they do.
Norepinephrine (pons) - allows you to focus on salient inputs
Dopamine (ventral tegmental area) - responsible for behavioural arousal and waking
Serotonin (Raphe nuclei) - calming influence in wakeful state
Histamine (midbrain) - stimulates wakefulness
Acetylcholine (pons) - Increases thalamocortical activation and arousal
What is the thalamic reticular nucleus (TRN) and what does it do?
It is the gatekeeper of consciousness. It’s a thin mesh of neurons just outside of thalamus that has dense reciprocal connections with other thalamic nuclei, the ARAS, and the cortex.
It is an interconnected network of GABAergic neurons that coordinates the synchronous 40 Hz firing between cortex and thalamus necessary for consciousness.
Describe the two broad forms of selective attention.
Top-down (volitional)
- we decide what to focus on
Bottom-up
- rapid and automatic
What is the role of the prefrontal cortex in attention?
Has executive function over consciousness. It’s an important association area that allows us to associate self with societal expectations.
Define mild, moderate, and severe traumatic brain injury (TBI) using the Glasgow Coma Scale.
Mild = 12-15
Moderate = 9-11
Severe =
Define the Monro-Kellie doctrine.
A change in volume of one intracranial compartment can only occur as a result of a compensatory decrease in another compartment.
What are the intracranial compartments? Which ones will change?
Brain matter, CSF, arteries, veins.
Venous and CSF compartments will decrease upon increased pressure as they are low pressure systems.
Walk through the pathophysiology of traumatic brain injury.
Direct tissue damage -> neuronal dysfunction & endothelial injury…
When is ICP monitoring recommended? What are the methods of ICP monitoring?
Severe TBI + abnormal CT head
Severe TBI with normal CT head with:
- age >40, SBP
What is the equation for cerebral oxygen delivery?
= Cerebral blood flow x O2 blood content
Cerebral blood flow = cerebral perfusion pressure = MAP - ICP
What are some methods to decrease ICP?
Sedation - reducing metabolic demands Osmotic therapy - draws intracellular water out of cells CSF catheter - reduce CSF Temperature control Decompression
Describe the factors that regulate cerebral blood flow.
Blood gases
- hypocapnia will cause cerebral vasoconstriction, whereas hypercapnia will cause vasodilation
Temperature & sedation
- hypothermia leads to a suppression of cerebral metabolic activity, thus decreasing CBF. 1 deg change leads to 5-7% change in CBF.
Medications
- inhalation anaesthetics cause decreased metabolism, but increased cerebral vasodilation (impaired flow metabolic coupling.
- IV agents like propofol, barbiturates, and benzos maintain flow metabolic coupling
- Opiates have no effect
What are the general components of general anaesthesia?
Hypnotic (knock out), analgesic (kill pain), amnesia (kill memory), immobility and inhibition of reflexes (kill movement), muscle relaxation (kill muscles)
What does the partition coefficient of a general anaesthetic tell you?
It’s solubility in the blood (low partition coefficient means very poor solubility). Lower coefficients are used currently.
How does the solubility of a general anaesthetic in the blood influence the rate of induction?
The more soluble it is in blood, the longer it takes to saturate the blood and thus takes longer to hit the brain. If the drug is more insoluble in blood, the brain and the alveoli can equilibrate more quickly.
Describe the MOA of inhaled anaesthetics.
Lipid theory is not true. They suppress excitable tissues by facilitating inhibition (increase GABA transmission) and inhibiting excitation (decrease glutamate and Ach transmission).
Why does the metabolism of a general anaesthetic matter?
Metabolites may be toxic (especially to liver and kidneys) and the degree of metabolism may affect the decrease in alveolar pressure at the end of procedure.
Rate of metabolism generally follows solubility in the blood.
(Desflurane is breathed out in full form).
What is the minimal alveolar concentration (MAC) with respect to a general anaesthetic?
It is the minimal concentration of an anaesthetic in the alveoli at 1 atm that prevents movement in response to a painful stimulus in 50% of the patients.
Basically the ED50.
Usually 1.2 MAC will prevent movement in 95% of patients.
What are some factors that will decreases an agent’s MAC with particular patients? And why does it matter?
Volatile anaesthetics are the most dangerous drugs used clinically. They have a very steep dose-response curve and have a very low therapeutic index (twice the therapeutic dose can kill you).
Increased age, decreased temperature, pregnancy, opioids, other anaesthetics.
What is the Meyer-Overton rule?
An agent’s MAC inversely correlates with it’s lipid solubility.
Describe the effects of inhaled anaesthetics on the CNS, cardio system, respiratory system, kidneys, skeletal muscle, and uterus.
CNS - dec in cerebral metabolic rate - cerebral vasodilation Cardio - dec in MAP due to dec in CO and TPR Respiratory - inc rate and dec depth of breathing (tidal volume) - dec response to PaCO2 elevation Kidneys - reduction of RBF (less CO) leads to dec GFR and output Skeletal muscle - relaxation. Uterus - relaxation. May lead to prolonged uterine atony and severe blood loss in parturients (thus, spinal tap..)
What is thiopental? Describe it.
It’s an IV anaesthetic (barbiturate) that was used for rapid induction of hypnosis (no analgesia). Facilitates neurotransmission of GABA. Was used for executions.
Rapid induction time, but brain concentration rapidly drops due to redistribution (wake up after 5 mins).
Saturated tissues via infusion result in elimination determining the time of emergence (11 hrs).
