Transcript SHOCK: A CLINICAL SYNDROME

SHOCK:
Ruth M. Kolk, RN,MS,CEN
Joy Borrero, RN, MSN
NUR240
Overview of Shock





Definition: Shock can be defined as a clinical clinical
syndrome of decreased blood flow to body tissues
resulting in cellular dysfunction and eventual organ failure.
Tissue perfusion in shock is inadequate to supply to
oxygen and nutrients to cells. Although shock begins as a
cellular phenomenon, it is a dynamic process which has
been described as a final pathway to death.
Risk Factors
MAP: a change in sympathetic tone by dilation or
constriction of blood vessels will affect MAP
MAP= 2D+S
3
CLASSIFICATION OF SHOCK



Hypovolemic: decreased intravascular
volume-dehydration or hemorrhage
Cardiogenic : inability of the heart to pump
blood-MI,valve disorders,dysrhythmias,arrest
Distributive or vasogenic: abnormality in the
vascular system that produces a
maldistribution of blood volume –neurogenic
anaphylactic, septic, capillary leak

Obstructive –tension pneumo, pulmonary embolism,
pulmonary HTN
Hypovolemic shock characterized by
decreased intravascular volume. Inadequate
fluid volume in the intravascular
compartments results in decreased blood
flow and reduced tissue perfusion
Excessive fluid loss
Causes: internal fluid shifts
external fluid loss
Hypovolemia

Decrease in circulating volume –
hemorrhage, plasma volume loss

Untreated will lead to hypovolemic
shock –causes profound alteration in tissue
perfusion . Cellular O2 demand exceeds
available supply
Stages of Hypovolemic shock
1. Initial – MAP decreased less than 10mm
Hg. Compensation is effective. No visible
changes
2. Compensatory –body’s primary goal is to
maintain blood flow to heart & brain through
vasoconstriction
( epinephrine ) &
shunting to vital organs. Anaerobic
metabolism occurs.
Compensatory






continued
Decreased peripheral blood flow
Tachycardia to maintain C.O.
Pulse pressure narrows
Initially BP may be “ normal “
Urine output decreases
Early s/s of shock : thirst,
restless/anxiety , AMS
Shock : late signs & symptoms
Progressive and Refractory Stages







Tachypnea & tachycardia
Weak pulse
Narrow pulse pressure
Flat neck veins
Pale , cool ,clammy skin
Hypotension
Oliguria
Progressive (intermediate )




Vital organs develop hypoxia
Significant changes occur at cellular
level which makes resuscitation difficult
Cardiac dysrhythmias due to inadequate
oxygenation
Microclotting :DIC begins
Refractory ( irreversible )





Tissue perfusion is negligible
Acidosis is prevalent
Cellular necrosis occurs due to lack of
oxygen
Massive DIC
Multi system organ failure
Interventions for shockGOALS?







Position patient – supine vs semifowlers
Large bore vascular access
Oxygen
Crystalloid infusions
Blood transfusions
Vasopressors
Prevent heat loss ( warmed IV fluids) ,
heating blankets
Cardiogenic Shock

Caused by decreased cardiac output
that results from impaired heart
function. Impaired heart function can
be classified as systolic or diastolic.
Pathophysiology of
Cardiogenic Shock

When LV cannot propel blood forward,
two problems occur:


Decreased stroke with resultant declines in
CO, BP & tissue perfusion.
As BP decreases perfusion to coronary
muscles also decreases potentiating
myocardial ischemia & predisposing the
patient to further muscle damage.
Classic cardiogenic shock is secondary to
systolic dysfunction. (the ability of the
heart to pump blood forward). The left
ventricle has a greater workload and
metabolic demand than the right
ventricle. Left ventricular dysfunction
affects forward flow of blood into
systemic circulation.


Death of the heart (MI) places the
patient at risk of developing cardiogenic
shock.
Necrotic heart muscle does not contract
normally leading to decreased CO and
inadequate tissue perfusion.


This type of shock is the leading cause
of in-hospital death
Those at the greatest risk are patients
who have lost a large portion of Left
ventricular muscle mass (anterior wall)
Noncoronary Causes





Valvular defects, such as stenosis or
regurgitation.
Stenosis refers to incomplete opening
of the valve (impedes blood flow )
Decreased stroke volume
Decreased cardiac output
cardiomyopathy
Pathophysiology Cardiogenic
Shock
Impaired Function of LV
Inadequate systolic emptying
LV filling pressures
Stroke
volume
LA pressures
CO
Pulmonary congestion
Tissue perfusion
Pulmonary capillary
pressures
Pulmonary
Interstitial edema
Intra-alveolar edema
Distributive Shock

Types:



Neurogenic
Vasogenic ( anaphylactic, septic,
endotoxins)
Septic
Sepsis-Induced Distributive
Shock
Neurogenic Shock



Massive vasodilatation secondary to loss
of sympathetic tone.
Cause is usually spinal cord injury or
head injury
Rare and usually transitory
Neurogenic Pathophysiology

Massive Vasodilatation
Venous Dilation
Venous return
Ventricular filling
Arterial Dilation
Peripheral vascular
resistance
Stroke volume
CO
Blood Pressure
Tissue Perfusion
Anaphylactic Shock


Characterized by massive dilatation and increased
capillary permeability. Potentially life threatening.
Causes: Antigen – Antibody Reaction
Anaphylactic Shock Patho
Antibody
Antigen Antibody Reaction
Histamine
Release of Vasoactive Mediators
Massive Vasodilatation
Veins
Venous
return
CO
Arteries
SVR
Blood Pressure
Tissue Perfusion
Prosglandin
Serotonin
Capillary Refill
Septic Shock



Severe overwhelming infection.
It develops as a result of invasion of
foreign microorganisms and subsequent
over- activity & dysfunction of body’s
defense system.
Septic shock & its sequelue are
described as part of a clinical
continuum.
Septic Shock Continuum



At one end of the continuum is
infection.
Presence of microorganisms stimulate
the body to activate the inflammatory
response.
As inflammatory response becomes
more widespread, SIR (Systemic
Inflammatory Response) develops.


Sepsis can then progress to severe
sepsis, in which the inflammatory
response, initiated to help the body,
begins to have harmful effects.
Imbalance between coagulation &
fibrinolysis
Pathophysiology of sepsis





Severe sepsis, organ dysfunction
hypoperfusion begins
Hypotension despite adequate fluid
resuscitation
Lactic acidosis
MODS
Most common cause of ICU death
NCLEX time
In planning an in-service for a group of health
care providers employed in an assisted-living
facility, the nurse identifies which of the
following as risk factors for sepsis? (Choose all
that apply.
A.Cardiomyopathy
B.Low serum albumin level
C.History of anaphylaxis
D.Prolonged use of corticosteroids
E.Age older than 85
F.Chemotherapy treatment for cancer
NCLEX TIME





The nurse monitors the client for which
clinical manifestation as a
compensatory mechanism to the initial
stage of shock?
A.Vascular vasodilation
B.Increased heart rate
C.Decreased mean arterial pressure
D.Elevated body temperature
NCLEX Time





The nurse recognizes the client with
which disorder is at greatest risk for
hypovolemic shock?
A.Myopathies
B.Sepsis
C.Pericarditis
D.Burns
NCLEX TIME





The nurse understands that the
rationale for the administration of
positive inotropic medications to the
client in shock is to :
A.Increase heart rate
B.Increase cardiac contractility
C.Increase cellular metabolism
D.Increase oxygen consumption
Critical Thinking Challenge





Your client is a 33-year-old woman who is returned to
your outpatient unit after having a surgical tubal ligation
by colposcopy. After moving her from the stretcher to her
bed, you take her vital signs. Her pulse is 110 and
thready, blood pressure is 90/72, respiratory rate is 28,
and pulse oximetry is 89%. When you shake her
shoulder, she opens her eyes but does not answer any
questions.
What should you do first?
What other assessment data should you obtain?
Given the type of surgery, where would you expect
bleeding to occur and what manifestations would you
expect to find?
She still has an IV in her left hand infusing dextrose 5%
in 0.45% saline. The postsurgical orders indicate that it
should be removed when she is stable. Should you
remove it now? Why or why not?
NCLEX Time





Which blood product is indicated for the
client with hypovolemic shock
secondary to large blood loss?
A.Packed red blood cells
B.Fresh frozen plasma
C.Platelets
D.Whole blood
NCLEX Time





Which clinical finding does the nurse
look for in the client responding
effectively to treatment for the initial
stage of shock?
A.Increased urine output
B.Increased heart rate
C.Decreased bowel sounds
D.Decreased blood pressure
NCLEX Time





Which of the following clinical
manifestations would indicate a worsening
in the condition of a client in the late stage
of septic shock?
A.Warm, flushed skin
B.Bleeding, oozing from intravenous sites
C.Increasing body temperature
D.Urine output of 20 mL/hr
Your client who had tubal ligation by colposcopy
has no external bleeding, but her abdomen is
enlarging and you observe skin discoloration
on her lower back.
Is O2 an appropriate tx for her?
Should you apply pressure to the abd area?
Why or why not?
What type(s) of IV fluid would be indicated for
her? Why?