Critical Care Exam 3

Front 1

5-15

Back 1

ICP

Front 2

80-100

Back 2

CPP

Front 3

required CPP pressure to perfuse the brain

Back 3

60

Front 4

how do you get a very low cpp

Back 4

very low bp, very high ICP

Front 5

Primary cause of head trauma

Back 5

aneurysms, trauma, arteriovenous malformations,

Front 6

create a direct path from venule to arteriole without going thru the capillary beds

gets very conjested so easily ruptured, does not perfuse brain well

Back 6

arteriovenous malformations

Front 7

HTN, HYPOXIA
HYPERCAPNIA
HYPOTENSION

Back 7

SECONDARY CAUSES OF HEAD TRAUMA
(CAN BE INTERRELATED)

Front 8

between skull and dura matter

Back 8

Hematomas, Epidural hemorraghe

Front 9

caused by a skull injury

Back 9

Hematomas, Epidural hemorraghe

Front 10

s/s
brief Loss of consciousness, wake up lucid,

Back 10

Hematomas, Epidural hemorraghe

Front 11

S/S brief loss of consciousness, wake up lucid or confused then los sof conssciousness, in the next 12 hrs will worsen!
Contralateral hemiparesis
ipsilateral dilated and fixed pupils
-same side of injury, eyes will fix, wont react to light, and will be dilated
headache and sleepiness
patient may sleep just check pt frequently for mental status
DIAGNOSTIC: CONFIRM W CT SCAN
looks alot like stroke symptoms

Back 11

Hematomas, Epidural hemorraghe

Front 12

between dura matter and pia matter
either subarachnoid or arachnoid layer

Back 12

hematomas; subdural hemorraghe

Front 13

venous slow bleed

Back 13

hematomas; subdural hemorraghe

Front 14

caused by arteriovenous ruptures, usuall not always

Back 14

hematomas; subdural hemorraghe

Front 15

3 TYPES:
acute, subacute, chronic

Back 15

hematomas; subdural hemorraghe

Front 16

create a direct path from venule to arteriole without going thru the capillary beds

gets very conjested so easily ruptured, does not perfuse brain well

Back 16

arteriovenous malformations

Front 17

HTN, HYPOXIA
HYPERCAPNIA
HYPOTENSION

Back 17

SECONDARY CAUSES OF HEAD TRAUMA
(CAN BE INTERRELATED)

Front 18

between skull and dura matter

Back 18

Hematomas, Epidural hemorraghe

Front 19

caused by a skull injury

Back 19

Hematomas, Epidural hemorraghe

Front 20

you singular gen.

Back 20

tui

Front 21

WORSE onset, FAST! ist 48hrs of time of injury

Back 21

ACUTE SUBDURAL hemorrhage

Front 22

s/s
headche
drowsiness
agiation
confusion
decreasing LOC (patient acting weird)
ipsilateral fixed and dilated pupils
(late sign)
contralateral hemiparesis
profound come (verylate sign)

Back 22

ACUTE SUBDURAL hemorrhage

Front 23

SAME as Acute s/s, but takes
2-14 days to see symptoms

Back 23

SUBACUTE SUBDURAL HEMORRHAGE

Front 24

takeS OVER 14 days

Back 24

Chronic subdural hemorrhage

Front 25

SAME as Acute s/s, but takes
2-14 days to see symptoms

Back 25

SUBACUTE SUBDURAL HEMORRHAGE

Front 26

takeS OVER 14 days

Back 26

Chronic subdural hemorrhage

Front 27

s/s
Progressive lethargy (hard to wake up, ragdoll)
absent mindedness, headache,
vomiting caused by central trigger zone stimulated by sight, sound, smell, and blood in subdural area pushingin on brain and stimulating CT zone.
Seizures(late sign)
ipsilateral pupil dilation
contralateral hemiparesis
diagnostic ct scan

Back 27

chronic subdurral hemorrhage

Front 28

arterial or venous bleed caused by
depressed skull fracture
acceleration/decelaration injuries
penetrating injuries

Back 28

intracerebral hemorrahge

Front 29

s/s
vary depending on location
brainstem: hr and breathing stop, affect memory, speech and emotion
UP to 6-10 days after traumatic event
sometime bleed fast or slow
DIAGNOSTIC CT SCAN
TX:REQUIRE SURGERY

Back 29

INTRACEREBRAL HEMORRHAGE

Front 30

brain is still intact, nothing wrong w brain but you have a brief LOC of neuro function few sesconds-temporary
could lose consciousnees, motor control, confused
can cause permanent if repeated trauma

Back 30

concussion

Front 31

deep bruise in brain,
can occur over 3-5 days
EX: Coup/contracoup, caused by acceleration, decelration injuries

Back 31

contusion

Front 32

axon gets stretched or twisted bc of injury but does not break or tear, it is still intact
NO BLEEDING or fractures, no distress to brain,
XRAYS NEGATIVE
but see signs of head injury

Back 32

diffuse axonal injuires

Front 33

s/s LOC, COMA, POSTURING
Autonomic dysfunction: bradycardia, hypotension, poikilothermia cant control body temp to 105 brain fry or 92, so heating cooling blanket, (get core temp) EXTENSIVE HTN, EXTREME diaphoresis RECTUM IV TEMP

Back 33

diffuse axonal injuries

Front 34

check for posturing, no sternal rubs, just trapezius squeeze and nail bed pressure

Back 34

diffuse axonal injury

Front 35

touches the skull furthest from brain

Back 35

dura mater

Front 36

space where CSF fluid floats around CSF LUBE

Back 36

ARACHNOID MATER

Front 37

LAYERS all the way down spinal cod, huggin brain tight, wraps around brain

Back 37

pia matter

Front 38

Increased metabolic needs (seizures, shivering, restlessness, pain, hyperthermia)

Back 38

INCREASES DEMAND

Front 39

Intracapillary distance
Capillary permeability (r/t inflammation)
Oxyhemoglobin dissociation curve
Capillary surface area (r/t coagulopathy, inflammation) clots, microclots

Back 39

decreases extraction of o2

Front 40

O2 Transport
Circulatory patency (r/t coagulopathy, inflammation)

Back 40

decreases supply of o2

Front 41

oxygen consumption determined by comparing O2 content of mixed venous blood to that of arterial blood – indicator of the proportion of delivered O2 that is consumed

Back 41

N 225 to 275 ml/min or 20 to 30 %

Front 42

seizure, shivering, restlessness, agitation, pain, hyperthermia
From your experience: What type of patients are usually sedated? (Because brain requires so much O2 – 20% of CO and uses 20% of what it receives)

Back 42

Increased demand r/t increased metabolic needs:

Front 43

Even if enough O2 is delivered to meet demand, it is useless to the tissues if it cannot be extracted from the blood
O2 Extraction Index measures this

Back 43

by comparing arterial and venous oxygen saturation N is about 25%

Front 44

(incr. with interstitial edema)

Back 44

Intracapillary distance

Front 45

(r/t inflamation)

Back 45

Capillary permeability

Front 46

How much of all oxygen in the blood is carried on the hemoglobin? 97% of oxygen is carried on the hemoglobin
So anything that effects the amount of hemoglobin available to carry oxygen or the ability of available hemoglobin to carry O2 will effect O2 delivery.
What is a normal Hgb? 12-18 g/dl
In the units, what types of patients have you noticed have low Hgbs?
Abnormal hgb – methemoglobin (nitric), carboxyhemoglobin (burns), hemoglobin S (sickle cell)

Back 46

The transportation of oxygen by the blood to the tissues is dependent upon three factors:
Hemoglobin

Front 47

Ventilation – A&B of ABCs – oxygen must get to the hemoglobin if it is to saturate it
So all the things that go along with ventilation – patent airway, free of secretions, swelling, maximizing alveolar recruitment through vent pressures (PEEP, PS), these also impact the driving pressure behind O2 and, if you’ll remember Boyd’s Law, impact the partial pressure of O2 in the plasma (PaO2) which, if you’ll remember the oxyhemoglobin dissociation curve determines O2 saturation

Back 47

What do you suppose will be a big factor in determining oxygen saturation

Front 48

more saturated for a given PaO2 and gives it up less readily at the tissues
Alkalemia, hypothermia, hypocapnia, decreased 2,3-DPG

Back 48

A shift to the left increases the affinity of Hgb for O2

Front 49

gives it up more readily at the tissues but less saturated at a given PaO2
Acidemia, hyperthermia, hypercapnia, increased 2,3-DPG (diphosphoglycerate)

Back 49

A shift to the right decrease affinity of Hgb for O2

Front 50

What is a parasympatholytic? Name one commonly used in the ICU, CCU in particular?

Back 50

(atropine)

Front 51

How does the SNS effect HR? SV?

Back 51

(ie. Preload, contractility, afterload)

Front 52

should increase CO UNLESS decreased filling time of the ventricle therefore stroke volume is decreased, if greater than the offset of HR then decreased CO

Back 52

Tachycardia

Front 53

fewer beats in a minute means lower output

Back 53

Bradycardia

Front 54

again decreased filling due to lack of kick (30% of EF) and if too fast even more decrease

Back 54

Loss of atrial contraction

Front 55

because it is not the best hemodynamic parameter upon which to base treatment
Granted, often other parameters are not available to the nurse, but not because they can’t be measured
Usually because MD’s aren’t aware of the preferred parameters

Back 55

First I want to explain title of this slide:
BP is a red herring, or distraction,

Front 56

↓ CO and impaired tissue perfusion, lactic acidemia, more cellular damage

Back 56

Initial stage

Front 57

SNS stimulation: neural (adrenergic),constrict vasculature to improve pressure in pipes, incresase hr, hormonal (renin-angiotensin-aldosterone), and chemical (respiratory compensation for metabolic acidosis) responses breath off coa

Back 57

Compensatory stage

Front 58

Compensatory mechanisms fail, Na+-K+pump failure, cell lysis, impair O2 utilization, autodigestion

Back 58

Progressive stage

Front 59

Unresponsive to treatment, MODS, death

Back 59

Refractory stage