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

Basi

c Pa

thogenesi

s

htt

p:/

/v.y

ouku

.com

/v_s

how

/id_X

MTU

2N

Tc3M

TIw

.htm

l

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)

htt

p:/

/

ww

w.y

outu

be.c

om

/watc

h?v

=Pr

kNm

VPI9

sc

http://

www.youtube.com/watch?v=CbM4UihE1

TQ

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