The Reticular Activating System (RAS)

affects what?

altered by what?

houses where in the brain?

Affects Arousal

Altered by trauma, medication, infection, hydration, and other stressors

Housed in the core of the brain stem

What does the brain stem maintain as to body systems?

A severely decreased level of consciousness immediately following trauma upon admission are an indicatior of?

heart rate, blood pressure, and respirations

Poor prognosis

Why is a severly decreased level of consciousness immediately after trauma a poor prognosis?

What are 2 things that are considered Parmacologically induced for unconsciousness?

heart rate, B/P, and the Patients ability to maintain their own respiratory rate and volume are likely to be affected

1-Anestesia

2-Continuous heavy sedation

head tauma and brain swelling, as well as electrolyte changes, opioid or benzidiazapine OD, heavy metal poisoning and anoxic brain injury

may be a few causes

What is being assesed in the Glascow Coma Scale?

When is the Glascow Coma Scale used in the Neuro Unit?

Best Motor Response (M)

Best Verbal Response (V)

Reaction of the patients eys in response to voice or painful stimuli

On a daily basis or upon any reassessment or change in the pt neurologic status

What if the Glascow Coma Scale is less than 8 upon admission?

What are the 6 grades for Motor Response?

Less than 8 associated with a poor prognosis

Motor

6-Follows commands

5-Localizes pain

4-Withdraws to pain

3-Decorticate flexion

2-Decerebrate extension

1-No Response

Glascow Coma Scale

Verbal Scale 1-5  ?

Eyes Scale 1-4  ?

Verbal                           Eyes

5-Oriented and Alert          4-Open

4-Disoriented                        3-To Voice

3-Nonsensical Speech           2-To Pain

    2-Moans, unintelligible              1-No Response

1-No response                                    

Monroe-Kelly hypothesis

ICP (Normal Ranges)?

What is considered abnormally elevated w/ ICP?

What is CPP?

How do you find CPP?

ICP Normal- from 0-15mm Hg

Abnormally elevated ICP is >15mm Hg for mor than 5 minutes

CPP- is the greatest pressure required to maintain cerebral perfusion;dependent on autoregulation of cerebral blood flow

CPP= MAP-ICP

CPP= MAP-ICP

What is the Normal Range?

What does CPP have to be at least to ensure adequate cerebral oxygenation?

What is the amount to maintain perfusion at all?

What CPP range is imcompatible to life?

 Normal = 80-100mm Hg

Adequate cerebral O2 = >70mm Hg

Maintaining = at least 50mm Hg

Incompatible to life = <30mm Hg

What are causes of ICP?

What are  the many S/S of ICP? (9)

Hematoma, Tumor, Trauma, Changes in blood flow, or if a pt is making excess Spinal Fluid

S/S of ICP= depressed level of consciousness, HTN, +/- Bradycardia, Irregular Respiratory Pattern, HA, N/V, Papiledema, Cranial Nerve Changes, Cushing's Triad

What is Cushings Triad?

What does this indicate in a neuro patient?

HTN w/ (widened pulse pressure), bradycardia,

irregular respirations-(late sign)

Very late sign as it indicates herniation changes and displacement of the brain stem

3 complications to ICP are?

What does DI do in terms with fluctuations in the Body?

Diabetes Insipidus

Syndrome of Inappropriate Antidiuretic Hormone

Cerebral Salt Wasting

DI  -Inadequate ADH

-High Urine (hypovolemia)

-High Serum Sodium

-High Serum Osmoality

-Low Specific Gravity

Free water replacement

DDAVP (Synthetic ADH)

Too much ADH

Hypervolemia

Hyponatremia

Low Urine Output

Low Serum Osmoality

High Specific Gravity

Dilution of all other serum electrolytes

Sodium Replacement

Fluid Restriction

What is Cerebral Salt Wasting and the fluctuations?

It is an overall status of dehydration

-Neurogenic sodium loss

-Hyponatremia

-Hypovolemia

-High urine sodium and osmolarity

-Low serum sodium and osmolarity

What is the treatment for Cerebral Salt Wasting?

Client with DI have a high urine osmolarity?

True or False

Treatment: 

Replace fluids and sodium

False

What is autoregulation?

When SBP increases and decreases the cerebral arterioles contrict or dialate?

Autoregulation-the ability of cerebral vessels to maintain constant perfusion pressure despite MAP

SBP increases-constrict

SBP decreases-dilate

Autoregulation

MEAN ABP  <>

When can ischemia in the brain develop?

When can vasocongestion develop?

ischemia <60 Mean ABP

vasocongestion >140 Mean ABP

Chemoregulation-What is it?

What is the sensitivity to CO2?

What is the sensitivity to PO2?

When does vasoconstriction happen?

Chemoregulation:  Vasodilation with acidosis or hypoxia

(CO2>45 q 1 point above dilates the blood flow 3%)

(PO2 <50 vasodilates to get more oxygen)

Vasoconstriction with alkalosis or hyperoxygenation

Chemoregulation

Every Degree above 37 degrees C increases what?

The Brain accepts how much % of CO?

What is the Tx to reduce of CO2?

37> =  O2 demands by 6%

Brain accepts 15-20% of CO

Reduce CO2 for the ventilated pt by turning up the respiratory rate to try to cause vasoconstriction of the cerebral arterioles

Hypoxia-does it increase or decrease ICP?

When demands are not met for the Brain what can the body use to compensate?

Hypoxia increases ICP

Compensates with anaerobic metabolism and ischemia and can have accumulation of edema

Intra-Ventricualar Catheter-monitors and/or drains (Gold Standard)

Sub Arachnoid Bolt-monitoring

Microsensor-monitoring

What does SjVO2 measure?

What is the normal range?

What is AVDO2?

What is the normal range?

SjVO2 measured from jugular vein to obtain blood directly from cerebrum

Normal= 50-70%

AVDO2 is the calculation for cerebral O2 consumption

Normal= 4-9 mL/dl

What is used for direct monitoring for cerebral oxygenation?

Where is this device placed?

What does this device allow for measurement?

Licox/Camino

The catheter is placed directly in the cerebrum

Allows for early warning of differences between brain tissue oxygen supply and demand

What is the temperature the body must be for Hypothermic Therapy?

How long is this therapy maintained for?

What are the downfalls of this therapy?

The temp needs to be reduced to 32-34 degrees Celsius

The therapy is maintained for 24-48 hours then slowly re-warmed

Electrolyte shifts can cause problems

What is the difference between

Primary and Secondary

Brain Injury?

Primary Injury: occurs immediately upon impact of mechanical force

Neurons are basicall ripped apart

Secondary Injury: Intracellular pathologic cascade

Hypoxia, hypercapnea, systemic hypotension, vasospasms, hypoglycemia, hyperglycemia, acid-base imbalance, hyperthermia

What are the 3 types of Edema in the brain?

Why does Cytotoxic happen?

Cytotoxic, Vasogenic and Ischemic

Cytotoxic: neuronal degeneration.  Each neuron is equipped with a sodium pump to maintain fluid and electrolyte balance.  Tramatic injury can cause dysfunction to this pump and consequent influx of sodium and water into the cells.

Why does Vasogenic Edema happen to the brain?

Why does Ischemic Edema happen to the brain?

Vasogenic edema is due to compromise of blood-brain barrier by damaged capillaries that allow plasma leakage into the brain tissue

Ischemic edema is due to a combonation of cytoxic and vasogenic processes.

What happens when the brain senses increased ICP?

What is a major contributor to increased ICP?

What happens between 1-18 hrs after injury and peaks at day 3?

It tries to shunt blood out of the brain to decrease that pressure.

Edema

and

Edema

What can alcohol do if it is on board during a traumatic head injury?

What are Hematomas?

Alcohol promotes cerebral edema by increasing the permeability of the blood brain barrier,

so it complicates the process greatly.

Bleeding in a space of the brain, usually between the meninges or in the brain tissue itself.

What bleed is below the dura?

What bleed is within the dura?

What bleed is beneath the arachnoid space?

What bleed is within the brain tissure itself?

Subdural

Epidural

Subarachnoid

Intracerebral

If you have chronic bleeds, esp. sub dural hematomas, what can be done?

What is the more common chronic bleed?

What if there is rapid bleeding, what will be done?

Drains can be placed within these bleeds to try to evacuate then and decrease ICP

Chronic Sub Dural Hematomas

Patients may have surgery to remove some sort of clot or repair an artery

What happens with Herniation Syndromes with fluid volume and brain volume?

What are the types of Herniation in the Brain and where are they located?

Both fluid volume and brain volume increases

Cingulate

Central

Uncle

Tonsillar

Where are the types of heniation located?

Cingulate

Central

Uncal

Tonsilar

Cingulate-lateral shift of hemisphere

Central-Downward shift above tentorium

Uncal-lateral and downward shift below tentorium

Tonsilar-Downward shift through foramen magnum

(impalement of the brain stem on the tentorium-death)

What fracture should we NOT insert an NG tube in the head?

Why would we hyperventilate a patient with a brain injury?

From a pharmacological standpoint, what is used to pull fluid in an effort to decrease swelling in the brain?

Basilar skull fracture

To decrease CO2 and allow for constriction of cerebral arterioles for ICP

Osmotic diuretics

What is used pharmacologically to decrease cerebral metabolic demand and to prevent hypoxia that will cause dilation?(2)

Whatis used for seizure activity that can cause great O2 demand? (2)

sedatives and paralytics

barbituates and anticonvulsants

What if a person is admitted and has battle's sign (bruising behind the ear), and racoon's eyes?

Why is it important to not place an NG tube?

These are signs of a basilar sull fracture

because the barrier between the nasal passage and the brain may be fractured or missing and the NG tubes could enter cerebral tissue

What is a simple partial seizure?

Complex partial?

Simple partial -pt is awake and experiences variable motor, auditory, sensory, autonomic, or psychic sensations, however they remain awake and alert and aware of what is going on.

Complex partial-when the pt appears to be awake in that their eyes are open but they are unable to make eye contact or communicate

Absence seizure?

Absence-immediate loss of awareness, the pt often appears to be blanking out and after a short period of time, they immediately regain awareness, but may not have memory of the event.

Tonic-loss of  consciousness, skeletal contractions toward the body

Clonic phase-rapid contractions and relaxation of muscle convulsions, ranges from twitching to violent shaking, eyes roll back, Incontinence

How long for convulsions to be in order to be termed status epilepticus?

What may be necessary with meds to attempt to reoxygentate the pt and the brain?

What is the postictal state?

IV Benzodiazepines, sedatives, paralytics and intubation

Postictal State-following a seizure, varies from person to person

How long can a Tonic phase last?

What kind of stimulation is turned on?

How lon can a Clonic phase last?

10-30 seconds

Autonomic

30-60 seconds

What are 3 anti-seizure meds and what do they do in the brain?

What part of the brain is affected with seizures?

Phenytoin (Dilantin) PO or IV-Reduces voltage frequency and spread of electrical discharges

Carbamazepine (Tegretol) PO-Reduces synaptic reaction

Phenobarbital (Luminal) PO, IM, IV-Works like a circuit breaker in seizure activity

Motor Cortex

What are the issues around taking ant-seizure/anti-convulsant medication?

What should you watch for in each individual Med for side effects?

Dilantin

Tegretol

Phenobarbital

Levels need to be maintained, cannot abruptly stop medication, Seizures that cause memory loss can cause patients to take multiple medication doses a day.

Dilantin-gingival hyperplasia, bradycardia

Tegretol-visual problems, ataxia, vertigo

Phenobarbital-drowsiness, dependence, habit forming

What are the 3 steps to stroke recognition?

What are the most likely affected areas for stroke pts? (4)

1-Ask the person to smile and stick out tongue

2-Ask the person to make a complete sentence

3-Ask the person to raise both arms

Occlusion of middle, posterior, anterior cerebral artery, and the Cerebellum

Cellular Changes During Ischemia

Mild to moderate?

Severe?

Mild to moderate-insufficent O2 and glucose, inadequate energy supply-failure of neuronal activity and regional brain dysfunction

Severe-Influx of water(Na, Cl)-(cytotoxic edema), Influx of Ca (irreversible cellular injury), anaerobic metabolism (accumulating lactic acid and H compromise neuronal integrity.

Cellular Changes During Ischemia

Advanced?

What is the treatment for a stroke?

Rapid Identification

FAST test (Face, Arm, Speech, Test)

Facial weakness

Arm weakness

Speech disturbances

What are the reasons for Hemorrhagic stroke (2)?

What is the Pathophysiology for a Hemorragic stroke?

usually due to some sort of micro vessel aneurysm due to long standing HTN, or Arterial Venous Malformation

Bleeding leads to ischemia and vasospasm from blood irritation cellular changes, Re-bleeding leads to vasospasm 4-14 days after initial event, Body trying to break down blood-oxyhemoglobin release from digesting erythrocytes

What is the management for Subarachnoid Hemorrhage?

"worst HA of my life!!"

Decommpensate fast, evacuation of hematomas, shunting and drainage-ventriculaostomy placed. 

May drain CSF,

Antihypertensives (Preop control SBP keep <150 to prevent rebleeding,

Anticonvulsants,

Triple H Therapy-Hypervolemia, HTN, and Hemodilution

What is a poor outcome for Hemorrhagic stroke patient?

What is the Treatment after surgery for a Subarachnoid hemorrhagic stroke?

If there is bleeding in the arterial, and if there is a rebleeding which is a high risk after initial bleed 4-14 days

Ventriculostomy placed for shunting and drainage of CFS because pt will have significant edema after surgery.  Intense anti-HTN control <150 SBP to prevent rebleeding.

Anticonvulsants

Triple H Therapy in subarachnoid hemorrhage-hypervolemia, hypertension, and hemodilution after surgery to prevent vasospasms.

What are some reasons that patients can get Ischemic Strokes? (4)

Where do clots form in the heart to get an Ischemic Stoke?

Carodtid stenosis, A fib, not appropriately anti-coagulated with Coumadin or undiagnosed, Coagulopathy's and CA that make clots easier

In the ventricles, I think Left side primarily

Olegemia, Ischemia, Cellular ischemic cascade

Disturbances in Ca lead to Lactic Acidosis causing O2 free Radicals to accumulate and leading to cell death

edema

Infarction

Penumbra surrounds infarct

Cellular ischemic cascade repeats

STAT noncontrast CT within the first 30 minutes

Lumbar puncture (if Hemmorrhagic)

12-Lead EKG and Chest X-ray

Labs: CBC, Coags, Chem, ABGs, toxicology

Carotid Doppler Cerebral angiogram(flow and plaque)

Do Not treate BP unless SBP>220; DBP >140; or Mean >130

What do we treat with if BP of SBP>220, DBP >140, and Mean >130?

What Anticoagulant therapy do we use for Strokes? (4)

What Antiplatelet therapy do we use for Strokes? (3)

Labeltolol, Nipride or Nicardipine

Tissue plasminogen activator (TPA), Streptokinase, Heparin, Coumadin

Aspirin (325 mg must be given within 24 hr if pt did not get TPA), Ticlid, or Plavix

Why are Anticonvulsants given for ischemic stroke attacks?

Whay do we give osmotic agents and diuretics during?

It is highly likely for pts to seize as cells are going through ischemic changes, and this will cause worse O2 consumption and increase metabolic demand.

To derease cerebral edema in an attempt to decrease ICP