what are the 3 diff ways to classify ischemic stroke?
(1) Territory affected (E.g., middle cerebral artery) (2) Underlying cause (3) Size of vessels involved
what is the infarct called if it is in a large vessel? Small vessel?
Territorial infarct= large vessel. Lacunar infarct= small vessel ( Often seen in the thalamus)
*what are clinical signs of an ischemic stroke? (where is there predilection?)
PERACUTE onset of FOCAL disease. Signs reflect lesion localization. Predilection for the cerebellum
which is the better dx tool for ischemic stroke- MRI or CT?
MRI is superior, it even has Special sequences for imaging stroke
prog for neuro function after an ischemic stroke?
typically good, Recovery within 24-72 hr (Degree to which they recover varies)
how to tx ischemic stroke?
treat underlying condition+supportive care
Global Brain Ischemia-- in what situation(s) do you most commonly see this situation?
Can be seen after anesthesia or CPR (in class she said: "get a call that a dog isnt quite right after a dental" is almost always the case)
how long before hypoxia is lethal to neurons?
clinical signs of global brain ischemia?
blindness, recumbency, seizures
how do animals recover from global brain ischemia/ prog?
Signs typically abate with time (to varying degrees). Good prognosis but requires a long time
ischemic vs global brain ischemia vs hemorrhagic stroke?
Ischemic is thromboembolic dz, where a clot is blocking a vessel and that localized part of the brain suffers hypoxia. GBI is when they basically arent breathing (anesthesia complication/CPR), and a hemorrhagic stroke is either a brain aneurysm burst or a weakened blood vessel leak. Blood spills into or around the brain and creates swelling and pressure, damaging cells and tissue in the brain
3 major underlying etiologies of hemorrhagic stroke?
4 major causes of hypertension which might lead to hemorrhagic stroke?
Hyperadrenocorticism (cortisol's enhancement of epinephrine's vasoconstrictive effect), Pheochromocytoma (inc epi), Renal failure (anuric? sthing to do with RAAS?), hyperthyroidism (Increases in heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption)
(said in class) if you're gonna have a stroke, youre gonna wanna have a _________ stoke
most common signalment for a stroke?
Middle-aged to old dogs and cats
which signalment is prone to global brain ischemia?
Brachycephalic animals are predisposed to global hypoxia (anesthetic accident)
clinical signs of a stroke?
Reflect localization--- FOCAL SIGNS. PERACUTE onset. there can also be Transient ischemic attacks (mini strokes)
Trauma (contusions (coup and countercoup), skull fractures, laceration (hge, edema) ), Cerebrovascular accident (stroke), Global cerebral hypoxia (anesthetic accident)
explain the pathophys of 2* brain injury (what is the main inciting problem)
ATP DEPLETION. Without ATP the pumps dont work...which means only channels are working...sooo you get Na influx (should be extracellular), Ca++ influx (most is extracellular), and there is glutamate release (excitatory), and lactic acidosis
The anatomy of an infarct- the diff parts (pic)
what is a penumbra?
wiki says: the penumbra is the area surrounding an ischemic event such as thrombotic or embolic stroke. Immediately following the event, blood flow and therefore oxygen transport is reduced locally, leading to hypoxia of the cells near the location of the original insult. This can lead to hypoxic cell death (infarction) and amplify the original damage from the ischemia; however, the penumbra area may remain viable for several hours after an ischemic event due to the collateral arteries that supply the penumbral zone.
what is intracranial pressure? What is normal? what are the 3 components of the ICP?
ICP is the Pressure exerted by tissue and fluid within the cranial vault. (Normal= 5-12 mmHg). the components are: Cerebral blood volume (10%), Cerebrospinal fluid (10%), Brain tissue (80%)
what is the Monroe-Kellie Doctrine?
The (fused) skull is a rigid compartment filled to capacity with 3 contents: Vc= V blood + V CSF + V brain. These volumes remain in equilibrium so ICP
remains the same. If one rises...the other must decrease.
what are the compensatory mechanisms if the ICP starts rising? (what doctrine is this following?)
(Monroe-Kellie Doctrine) Note: THEY ARE LIMITED! CSF redistribution, ↓ cerebral blood flow (vasoconstriction), ↓ CSF production (chronic)
what does the pressure/volume curve look like for intracranial?
Autoregulation: Cerebral blood flow is maintained within limits whereby metabolic demands of the brain can be met. So, the Cerebral blood vessels respond to what 3 things?
(1) BP (2) blood viscosity (3) ** Metabolic by-products (CO 2 ) <--this is what they REALLY respond to...high CO2= dilate BVs to get that outta there
what is the equation explaining what makes up cerebral perfusion pressure (CCP)?
(wiki says: It is is a physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and a reduction of the heart rate.) So, Basically you see systemic hypertension and bradycardia as an attempt to protect cerebral blood flow (remember CPP=MAP-ICP--- so if intracranial pressure increases, the MAP has to increase as well to overcome this, but then there has to be a reflex bradycardia to protect the CO bc CO=HRxSV.) So, systemic hypertension with bradycardia in case of a head injury may indicate intracranial hypertension. [[to reiterate-- you have a head injury. The ICP increases. The brain needs blood, so the mean arterial pressure has to increase in order to maintain cerebral perfusion pressure]
what are the three types of brain herniation? what are the sequelae from this (And what are the sequelae stemming from)
3 types= Subfalcine, Transtentorial, Foramen magnum herniation (she didn't define these). You get sequelae related to compression of the midbrain(brainstem): Mydriasis, Tetraparesis, altered level of consiousness.
6 respiratory patterns which might be associated with brain injury (she just lists them, doesn't define them)
Hypoventilation, Hyperventilation, Cheyne-Stokes respiration (abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnea), Apneustic respiration (abnormal pattern of breathing characterized by deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release.) Biot’s/ataxic respiration (abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea), Apnea
4 things to look for in your neuro exam in your ER assessment
Small animal coma scale, Cushing’s response (hypertension+reflex bradycardia), Breathing pattern (6 possible resp patterns), eye exam (look for Mydriasis)....HOWEVER: dont forget about the rest of the pt!! (Volume status, hemorrhage, pulmonary parenchymal and/or pleural space disease, arrhythmias, abdominal trauma, etc. )
what does the Small Animal Coma Scale assess? what is it useful for?
Assesses motor activity, brain stem reflexes, and level of consciousness. This scale is An objective means of monitoring head trauma patients, and often can be used as a prognostic tool
explain that parts of the small animal coma scale and how you put it all together
there is a scale for rating their motor activity, brain stem reflexes, and level of consciousness. You assign a number for each assessment part, add them together, and this sum is used to determine a prognosis (higher number=better prog)
what is the name of the posture that makes her worry about brainstem problems?
what is Decerebrate Rigidity? What does it tell you and what does it look like?
This position indicates a Brainstem lesion (midbrain). You will see Rigid extension of all limbs, and +/- opisthotonus (extension of head and neck). Along with this you will see an ABNORMAL LEVEL ON CONSCIOUSNESS (hence brainstem aka middle brain lesion)) seen as depressed/dull, stuporous, coma
does two major things: (1) Osmotic gradient in the IV space (2) Free radical scavenger. (See effects in 5-10 min; effects last 3-5 hr)
side effects of using mannitol as a tx for brain injury? Things you must consider before using?
Must be euvolemic first!! Can cause Diuresis (electrolyte abnormalities, hypovolemia), Acute renal failure (tubular necrosis), Cerebral edema (theoretical- Mannitol can accumulate extravascularly and raise brain osmolarity) (Dose: 0.25 – 2 g/kg over 5-30 min)
what is the MOA of hypertonic saline?
Osmotic agent- Also helps restore intravascular volume (Increases cardiac output and blood pressure)
How helpful are corticosteroids with brain injury?
NEVER USE THEM JFC. NEVER. OH MAN. doesnt help and can be harmful
SEs of using corticosteroids with brain trauma?
HAVE I MENTIONED NEVER USE THEM??? GI bleeding, hyperglycemia (contributes to poor prognosis), immunosuppression, increased risk of infection, death
supportive care: 2 Measures to prevent venous obstruction?
(1) Head elevated (30º) (2) No neck leads or jugular venipuncture
how can you help avoid inc the ICP even more with supportive care?
Avoid excitement and dysphoria
where do you want to maintain MAP in brain trauma? Why might they be hypotensive?
want it to be >90mmHg. Hypotension usually due to hypovolemia or hemorrhage (trauma patients)
if the pt is hypertensive, what should your FIRST worry be?
If the patient has systemic hypertension your first worry should be about intracranial hypertension (Cushing’s reflex= you will see hypertension and bradycardia in response to inc in ICP...so you know you should be worrying about the pressure up thur)
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