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Transcript of SHOCK idol/shock-to-the- system/USCA30800056 idol/shock-to-the- system/USCA30800056.
SHOCK
http://www.vevo.com/watch/billy-id
ol/shock-to-the-system/USCA3080
0056
Definit
ion
A complex clinical syndrome of decreased blood flow
to body tissues resulting in cellular
Dysfunction and eventual organ death
http://www.youtube.com/watch
?v=9a7N9AU1GiQ&feature=rel
ated
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thogenesi
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Tissue perfusion decreases
Compensatory mechanisms
triggered Blood goes to primary organs
only Vascular system fails
(refractory hypotension)
Hypoxia at cellular level with
massive acidosis Increased capillary
permeability with leakage
Coagulation cascade activated
Blood pools in periphery
Organ death
Progre
ssio
n o
f Shock Initial stageCompensatory stage
Progressive stageRefractory stage
Init
ial S
tage
Tissue perfusion is decreasedDecreased oxygen to
cells/tissuesAnaerobic metabolism
increasesExcess lactic acid producedNo clinical signs
Com
pensa
tory
Sta
ge
Goal: restore cardiac
output and tissue perfusion to vital organs Interrelated mechanisms: Neural compensation
Hormonal compensation
Chemical compensation
Clin
ical
Manifest
ati
ons
duri
ng
Com
pensa
tory
Phase
Blood pressure normal
Tachycardia Cool, pale, moist skin Thirst Urine output <30 cc/hour
Restless, confused, agitated Able to respond to verbal
commands Tachypnea
Progre
ssiv
e
Phase Third StageSevere hypoperfusion
leads to multiple organ dysfunction and
failure
Progre
ssiv
e:
Card
iova
scula
r
Decreased preload r/t
loss of autoregulation &
increased capillary permeabilityFluid leaves capillaries
Blood flow sluggish Imbalance of supply &
demand to heart muscle
ArrhythmiasHypotension appears
Progre
ssiv
e:
Pulm
onary
Pulmonary arterioles constrict r/t
hypoxia, edema, mediator release
Develop pulmonary hypertension
Decreased pulmonary blood flow,
increased physiologic dead space
Impaired gas exchange -
decreased PaO2, increased PCO2
Alveoli collapse/edema r/t
decreased surfactant production
& increased capillary permeability
Further decreased oxygen
diffusion Respiratory failure with ARDS
development
Progre
ssiv
e:
Neuro
logic
Decreased cerebral perfusion with decreased cardiac output & blood pressureDeteriorating LOC
Responds only to painful stimuli becoming totally flaccid and nonresponsive to pain
Progre
ssiv
e:
Renal
ATN r/t prolonged hypoperfusionAcute renal failure
developsCreatinine & BUN retained in blood
Develop metabolic acidosis
Progre
ssiv
e:
GI
Develop ischemic gut
syndrome r/t prolonged hypoperfusion and vasoconstriction
Develop paralytic ileus
Mucosa erodes: Increased chance of GI
bleed Release of bacteria into
gut – “translocation”
Progre
ssiv
e:
Hem
ato
logic
Hyperdynamic = hyperglycemicClotting cascade
Altered due to mediator
release and inflammatory process
Develop DIC (Disseminated Intravascular Coagulation)
Progre
ssiv
e: C
linic
al
Manifest
ati
ons
Cardiovascular: Weak peripheral pulses,
extremities cyanotic & cold, B/P
falling, decreased urine output,
decreased LOC, increased HR
Pulmonary: respiratory failure
with ARDS, increased RR
Neuro: decreased LOC without
response to pain at end
Renal: acute renal failure with
increased creatinine/BUN
GI: s/s sepsis and/or GI bleed
Hematologic: DIC & hyperglycemia
Refr
act
ory
Sta
ge
of
Shock
Cell destruction severe
Condition refractory to
treatmentMultiple organ failure Refractory hypotension
Refractory hypoxemia Renal shutdown GI failure (no absorption
of nutrients) Neurological failure (no
response)
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www.youtube.com/watch?v=CbM4UihE1
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Hypovolemic
Shock
Definit
ion
Decreased intravascular volume Inadequate fluid
volume in the intravascular compartment results in
decreased blood flow
and reduced tissue perfusion Can result from loss of
either blood, plasma, or
extracellular fluid.
Eti
olo
gy:
H
ypovo
lem
ia
Internal fluid shifts Internal hemorrhage Increased capillary
permeability r/t thermal
injuries, sepsis, anaphylaxis Third spacing - ascites
External fluid losses Trauma – GSW GI upset Large exudative lesions
Path
ophys
iolo
gy:
H
ypovo
lem
ia
Clinical Manifestations: Hypovolemic Shock S/S of compensatory
changes Altered mentation Cool, clammy skin Tachypnea U/O decreased and dark
Poor peripheral pulses
Treatm
ent
of
Hyp
ovo
lem
ic S
hock
Treat the cause RESUSCITATE with fluids
Fluid challenge of 500 cc or
greater Crystalloids, Colloids or
Blood products Monitor response – WHAT
TO ASSESS???? Administer vasoactives
Oxygen support Cardiac monitor,
hemodynamic lines
Fluid
s &
Resu
scit
ati
on
(Cry
stallo
ids)
Isotonic Osmolarity = to serum:
expands intravascular
volume Example: LR, NSHypotonic Osmolarity less than
serumHypertonic Osmolarity greater than
serum
Collo
ids
or
Blo
od
Product
s
Colloids Do not diffuse through
capillary walls Increases osmotic pressure = fluid stays in
vascular compartment
Examples Albumin, dextranBlood/blood products
Cardiogenic
Shock
Eti
olo
gy
“Pump failure”= decreased cardiac outputMainly “systolic”
dysfunctionEtiology: MI Open heart surgery Cardiomyopathies Severe systemic or
pulmonary hypertension
Path
ophys
iolo
gy:
C
ard
iogenic
Narrow pulse pressure
JVD & pulmonary congestion Arrhythmias Chest pain Cool, pale, moist skin
Oliguria Decreased LOC Increased HR, Increased
RR, SBP <85, decreased
CO
Treatm
ent
– C
ard
iogenic
Cardiac monitorABGs w/serum lactateMultiple labsSwan catheterMeds Vasopressors Diuretics Nitrates IABP
Obstructive
Shock
Obst
ruct
ive
Shock
Heart compression with
obstruction to atrial filling and/or outflow
from the heart Etiology: Cardiac tamponade Tension Pneumothorax or
massive PE Dissecting aneurysm Clinical manifestations:
Muffled heart sounds, s/s
decreased perfusion
Treatm
ent
of
Obst
ruct
ive S
hock
Address causePericardiocentesisPericardial window
(chronic)Chest tubeOxygen therapyFluid resuscitationOngoing monitoring
(cardiac, renal, resp)
Distributive ShockNeurogenic, Anaphylactic, Septic
Neurogenic Shock
Neuro
genic
Shock
An abnormality in the
vasculature that changes the
normal distribution of
vascular volume Massive vasodilation due to
loss of sympathetic tone/vasomotor control
Etiology: Spinal cord injury (spinal
shock) Spinal anesthesia Adrenergic blocking drugs
Barbituate overdose Severe emotional distress
Path
ophys
iolo
gy:
N
euro
genic
Clinical Manifestations:
Neurogenic Hypotension Bradycardia Loss of temperature control Loss of or diminished
sensation, motor movement, and reflexes
Skin dry (warmth dependent on temperature of environment)
Treatm
ent
of
Neuro
genic
Shock
Supportive careSolumedrol therapyOxygen therapy Judicial fluid resuscitationMay require vasoactive drips
Monitor closelyV/S, u/o, LOC, skin, hemodynamics
Anaphylactic
Shock
http://www.youtube.com/wat
ch?v=QM_cRFvkzl4
Anaphyl
act
ic
Shock
Massive vasodilation,
decreased peripheral
resistance, and increased capillary permeabilityEtiology:Allergic reaction Drugs Food Bee stings Latex
Path
ophys
iolo
gy:
A
naphyl
axi
s
Clinical Manifestations:
Anaphylaxis Generalized erythema
Urticaria Pruritus Angioedema Decreased respiratory
status: stridor, bronchoconstriction
Hypotension Decreased LOC
Anaphyl
axi
s Tr
eatm
ent
Avoidance #1Epinephrine #1Fluid resuscitationBenadryl (liquid vs.
pill???)H2 BlockersBronchodilatorsMagnesium Sulfate
Sepsis
Sepsi
s -
Septi
c Shock
Severe, overwhelming
infection & massive inflammatory responseContinuum developmentRisk: MultipleEtiology Any microorganism