Brain injury ppt

peripheral vs central chemoreceptors

peripheral detects CO2 and O2 via aortic and carotid

central detects pH via medulla

dorsal resp group: location, fxn

w/i medulla

initiates insp phase, maintaining rate + depth and varying via signals from pneumotaxic center. neurons in upper pons act as insp cut off

ventral resp group

w/i medulla

controls forceful breathing (exercising!) sending impulses to apneustic center

pontine resp group

fine tunes and regulates normal RR/depth, stimulating DRG to prolong Ti

pneumotaxic center

w/i pontines

controls ending inhalation, signaling doral group to speed up/down. damage to this makes breathing impossible

apneustic center

controls deep breathing, signaling dorsal group to delay insp off

airway protection reflexes + location

cough = medulla

gag = cranial IX, X

tracheal tone = Cranial X, C6

CSF

cerebrospinal fluid

colorless in brain/spine buffering from impacts, circulating hormones, NTs and metabolic products and is produced by ventricles

meninges

membranes enveloping in CNS with:

1. dura = outer layer

2. arachnoid = vasculature

3. subarachnoid = CSF

4. Pia mater = inner layer

circle of willis

cerebral arteries for redundant/collateral BF for brain

brain stem

located in posterior fossa

contains midbrain, pons (pneumotaxic + apneustic center) and medulla (ventral/dorsal)

cranium

forms casing for brain

what is the most compressible part?

the brain

biot’s breathing

ataxic breathing w/ periodic breathing due to neuron damage

kussmaul’s

met acidosis

cheyne-stoke

crescendo/decrescendo breathing w/ intermittent apnea

DAI and types (3)

worst TBI, never gaining consciousness resulting from shearing of axons

1. tensional (stretch)

2. rotational (twist)

3. shearing force (tear)

concussion

milder DAI

anoxic brain injury

MC via CARDIAC ARREST! (>20min bad!) due to it being through lack of O2 in brain. this quickly affects guts/kidneys as body responds by increasing and redirecting BF.

strokes, drowning, OD, choking, CO poisoning

what happens if O2 is restores?

damage can still be done if brain been deprived for a long time.

anoxic brain injury diagnoses

1. MRI

2. EEG

3. SSEP

4. CK-BB (cerebral taps, dx. meningitis)

ischemic vs hemorrhagic stroke

hemorrhagic = bleeding into brain

ischemic = clot blocking BF to brain

aneurysm

bulging of BV wall causing weakening of wall that can the lead to burst/hemorrhagic shock

AV malformation

arteriovenous malformation (AVM) is the abnormal connection b/w A and V which can lead to locked-in syndrome. there are no signs/symptoms to show if you have it as it is congenital.

what happens if ICPs are too high

comes out spinal cord!

ICP treatments

1. decompressive craniotomy

2. mannitol

3. 23.4% sodium chloride

4. mechanical hyperventilation

this is to increase ammonia levels!

why does hyperventilation help ICPs?

decreased CO2 → vasoconstriction → reduced BF → reduce ICP

Licox

measures PbO2 (partial pressures in brain)

normal = 20-45mmHg

CPP

CPP = MAP - ICP, being pressure gradient that drives DO2 to brain tissue.

normal = 60-80mmHg (low = ischemia, high = increased ICP)

ventriculostomy

catheter draining fluid from ventricles that must be clamped during stimulating procedures (CPT, sxn, etc.)

what happens when brain herniates (and pt doesn’t die)

1. loss of brainstem reflexes (cough, gag)

2. irregular breathing patterns + pulses

3. coma

4. arrest

5. brain death

paroxysmal sympathetic hyperacitivty

aka neuro storming

random desats/spikes due to increased sympathetic activity, increasing recovery time (not mortality). this causes longer time on vents = trach! most times will transfer them to trach collar so brain can figure out stuff.

issue with fevers in neuro storming

cannot prove if the fever is from storm or infection. this prevents pt from leaving hospital as facilities won’t take pt. with fever.

how to treat storms?

1. BBlockers = prevents episodes from starting

2. morphine = stops episodes that have started

persistent vegetative state

awake but not aware (ex., eyes can open and some times track, variable response to stimulation)

locked in syndrome

pseudocoma via injury to pons. Pt. is AWARE but cannot act (TT so sad bruh) as they are paralyzed besides eye movement.

brain death steps

1. prereqs (warm, no meds given, etc.)

2. clinical exam

   1. must be in coma

   2. brainstem reflexes

      1. doll’s eyes (no eye movement)

      2. cold calorics (no eye deviation)

      3. no cough/gag

   3. apnea test (preox + disconnect vent → let CO2 rise to either 60mmHg or +20 baseline)

   4. ancillary test (only if needed like EEG, angiography, nuc scan)

2 methods for anoxic brain injury

1. hypoxic/ischemic = blood/perfusion issue! no BF to go to brain (cardiac arrest, shock, stroke, etc.)

2. anemic/histotoxic = O2 content/carrier issue! O2 can be delivered to brain but cannot be carried or used properly like decreased Hb (anemia) or cyanide poisoning (histotoxic).