NU371Shock

Alyssa Wallschleger--5/2/16

Shock
Life threatening condition where body does not get enough blood flowcells,
tissues, organs not enough O2, not enough nutrients to fxn properly

When not tx properly can cause MODIS-multiorgan dysfxn syndrome

3 causes
1. Pump failuredamage to heart muscle so improper fxn of heart
2. Vessel failuredilation of BV so much where system expands larger than
volume to fillcauses low BP
3. Content failureblood is lost through injury so blood volume is not sufficient
enough to run the system

4 Stages of Shock {pg.1639 table 67.5 all s/s of each system during phases of
shock}
1. Initial
a. Hypoxiarestlessness, increase pulse/resp, anxiety; lactic acid
build up; small change in BP
2. Compensatory
a. Body starts to compensate use hormones & chemicals to
reverse the shock
b. Acidotic stage starts to pH drops; hyperventilate blow off CO2
c. Epi is released by baroreceptors that causes vasoconstriction
d. Renin-angiotension is activated, ADH released, vasoconstriction in
kidneys/GI tract trying to shunt blood to go to major organsshunt
blood from kidneys which will cause decrease in urine output
e. BP drops we try to get it back up
3. Progressive
a. Compensatory mechanisms are failing, decreased perfusion in
cells, increased Na ions, K leaks out
b. p/t looks increased anxious, increase HR
c. increased metabolic acidosis
d. in anaerobic metabolism state
e. smooth muscles/caps relax blood starts to pool in caps
f. third spacing-fluid shift in interstitial spaces
g. blood gets thickerviscosity increases risk for VTE...small micro clots
travel to lungs end up w/pulmonary edema
h. perfusion to organs still decreased watch out for organ damage
i. GI tract decreased for long period of time it can become ischemic b/c
no blood flow we then get bacteria build up then enters blood
streamendotoxic shock
j. Patient becomes cool, diaphoretic

k. BP here stabilizes maybe a good sign maybe a bad sign

4. Refectory
a. Late stage of shock, vital organs are failing, cells are dying,
decreased blood flow, can lead to brain damage & eventually death
b. Too much ATP converted into adenosine b/c absence of O2 it cannot be
reversed CO2 increases
c. Typically everything craps out
d. BP drops below <50 it dramatically spontaneously drops
e. RR drops <10, pulse very weak & thready if you can even feel it

4 Types of Shock
1. Hypovolemic shockloss of intravascular blood volume {anything lowers
the tank}
a. #1 cause is bleeding
b. Causes= burns, diuresisnausea/vomiting, diabetes insipidus losing
too much urine
c. Look dehydrated, lethargic, decreased LOC, if losing blood then losing
O2, increased anxiety, hypoxia, increased RR, urine output down
d. Replacement formula is 3:1 we replace 3 mL for every 1 mL they loss
2. Obstructive shocksome kind of obstructionsomething is obstruction
blood flow to heart can be anywhere in the body
a. Cardiac tamponade: too much blood/fluid in the pericardium that
prevents inflow of blood to the heart aka prevents venous return
i. Tx w/needle decompression
b. Pericarditis: inflammation or hardening blocks normal operation/blood
flow
c. Tension pneumothorax: occurs b/c increase thoracic pressure
i. Venous blood flow blocked so blood cant get to heart
ii. Tx needle decompression or chest tube
d. Pulmonary embolism: clots in lungsconsequently blood flow not
going back to heart
i. Tx w/blood thinners, or green filter that will prevent these clots
from migrating further
e. Aortic stenosisaortic valve becomes hard does not open/close as
should; hinders circulation
3. Cardiogenic shockrelated to pump failuredamaged heart muscles
a. Causes: MI, dysrhythmias, CHF, cardiomyopathy, any valve failure
b. Aortic stenosis can then may be obstructive & cardiogenic shock
c. Ultimate goal is to restore blood flow especially to heart/brain & restore
O2 demand/supply
d. Tx: depends on the causetake workload off heart, supplemental O2,
fix the problem
i. Smooth muscle relaxers, nitrates
ii. Start inotropic drugs like dopamine or doputomineif low dose it
will increase perfusion to kidneys the higher the dose then
higher perfusion to heart
iii. Anti-plateletsaspirin to decrease platelet aggregation
iv. If necessary loop diuretics

4. Distributive shockoccurs when there is excessive vasodilation & impaired

blood flow disruption
a. 4 Types
i. Neurogenic distributive shockspinal cord or CNS damage,
occurs as a result of major vasodilation caused by loss of
sympathetic peripheral vessel tone
1. Low BP, low pulse, decrease tissue perfusion,
hypothermia, blood may still pool below site of injury
where that site might feel warm, this is where
poikilothermia body cannot regulate their temperature
might take the temp of the room
2. Tx the cause, s/s, major vasodilation so give fluids, help
regulate the p/ts temperature
ii. Anaphylactic shockhypersensitivity rxn within seconds to
minutes to being exposed to something
1. Ultimate severe allergic rxn to something
2. Histamine released, vasodilation, increased cap
permeability
3. 1st thing we see is anxiety may or may not know they are
allergic to something
4. BP drops, skin becomes red, get hives
5. First thing concerned with is AIRWAY!! Hear wheezing,
stridor (upper airway constricts), chest pain
6. Get anti-histamines in them with Benadryl!! IV epi, IV
Benadryl all depends on severityfollowed by
corticosteroids
7. Watch BP can have significant drop 1-2hrs after
anaphylactic rxn
iii. Septic shock systemic inflammatory response
1. Occurs from severe infection, illness, or tissue death.
2. Common in ICU patients due to being bedridden for a long
time.
3. Two different phases of septic shock ]
a. Warm shock hyperdynamic shock this is the first
phase in septic shock
i. Characterized by high cardiac output
ii. Vasodilation effect from histamine release,
bradykinin, serotonin, caps more permeable
causing fluid shiftthird spacing
iii. High RR >20 might have a fever--100.4 or
higher, pulse about 100, WBC may be normal
like 12 may be caused by gram negative
bacteria, pulses increasedcheck urinary
outputprofound diuresis
iv. To compensate for diminished blood volume
increased CO, increased
cardiomyocontractility initially but eventually
tissue perfusion is inadequate loss cellular

energylactic acid production pH becomes

acidotic we should run anion gap we start to
see this occur before s/s
v. Early metabolic acidosis
vi. Whatever the cause the high RR can actually
cause profound respiratory alkalosis might
see a shift toward respiratory alkalosis,
important to check metabolic acidosis early!!
vii. Check clotting factors with INRmay be
excessive activation of clotting mechanisms
clots may block up caps may notice
petachiae rash usually starts below in the
lower legs works way up this is called
modeling
viii. Other labs may be ordered that measure
different levels of different clotting factors
ix. Decreased cerebral perfusionrestlessness,
confusion, not all p/t have but one of the first
signs
x. Bodys endorphins are keeping person
comfortable may appear resting
comfortable
xi. In warmth stage they have normal urine
outputblood starting to level GI system
first clue decreased bowel sounds
xii. VS might look normalish as mentioned above
we want to CHECK history!!!
b. Cold stagemay enter as early as 6hours after
warmth stage
i. Late and nearly irreversible stage of septic
shock
ii. Persons temp drops they become
hypothermic they have subnormal
temperature, WBC count is normal or low
iii. Hypotension, cold, more modeled
iv. Looking at VS drop in 40 mmHG systolic this
is bad sign!!
v. If BP below 90 bad sign
vi. Lactic acidosis
vii. Little to no urine outputoliguria
viii. Severe change in mental status
ix. Looking at organ involvement here in this
stageMODS most likely 2 or more of organs
are shut down
4. Precipitants of Septic shockAbdominal or digestive
infections; lung infections such as pneumonia/bronchitis,

septic shock precipitated by something, UTI/repro

infections
5. Tx: with O2 first! Antibiotics, fluid resuscitation,
vasopressors, corticosteroids decrease inflammation,
watch K/insulin b/c cell breakdown
iv. Capillary leak syndromefluid shifts from blood to interstitial
space usually self-resolving & rare
1. Lasts about 1-3 days in which 70% total plasma volume
invades the cavities orthostatic hypotension, they feel
dizzy, light headed, fainting
2. Third spacing all that edema, end up in circulatory shock
major risk for pulmonary collapse & organ damage
3. Acute renal failure due to acute tubular necrosis
4. Look for s/s of compartment syndrome
5. Fluid in interstitial spaces cannot overhydrate them
6. Watch for flash pulmonary edemawatch urine output
polyuria
7. Give large doses of diuretics
8. Tx cause of infection, tx each organ affected accordingly
we want O2 ventilation maybe intubation
9. Kidneyscath, watch electrolytes, watch urine output,
temporary dialysis
10.Feed them enteral want to prevent ischemia in the gut
support p/t temperature, replace F/E, give analgesic for
comfort
Psychogenic shocksomething psychologically affects the p/t

Such as site of blood, love one being injured, blood drains in hear pools
in abdomen causing person to faint
Temp dilation of BV for no physical cause
Once they pass out it all returns back to normal