Interventions for Clients in Shock

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Transcript Interventions for Clients in Shock

Interventions for Clients
in Shock
Shock
Can occur when any part of the
cardiovascular system does not
function properly for any reason
 Begins with abnormal cellular
metabolism that occurs when too
little oxygen is delivered to tissues

Review of tissue perfusion

Organ perfusion is related to mean arterial pressure (MAP).
Because the cardiovascular system is a closed but continuous
circuit, the factors that influence MAP include the following:
– Total blood volume
– Cardiac output
– Size of the vascular bed


Total blood volume and cardiac output are directly related to MAP —
increases in either total blood volume or cardiac output usually raise
MAP. Decreases in either total blood volume or cardiac output
eventually lower MAP.
The size of the vascular bed is inversely (negatively) related to MAP
— increases in the size of the vascular bed lower MAP, and
decreases raise MAP
Processes of Shock
Initial stage (early shock)
 Nonprogressive stage (compensatory
stage)
 Progressive stage (intermediate
stage)
 Refractory stage (irreversible stage)

Multiple Organ Dysfunction
Syndrome
Cell damage is caused by the massive
release of toxic metabolites and
enzyme.
 Metabolites trigger small clots to
form that block tissue oxygenation
and damage more cells, continuing
the devastating cycle.

Hypovolemic Shock
Occurs when low circulating blood
volume causes a mean arterial
pressure decrease; the body’s
oxygen need is not met
 Caused by external hemorrhage;
common after trauma and surgery or
reduction in levels of clotting factors

(Continued)
Hypovolemic Shock
(Continued)

Caused by internal hemorrhage as
occurs with blunt trauma,
gastrointestinal ulcers, and poor
control of surgical bleeding
Cardiogenic Shock
Actual heart muscle is unhealthy and
pumping is directly impaired.
 Cardiac output and afterload are
reduced, thus reducing mean arterial
pressure.

Distributive Shock
Caused by loss of sympathetic tone,
blood vessel dilation, pooling of
blood in venous and capillary beds,
and increased blood vessel
permeability
 Neural-induced distributive shock
 Chemical-induced distributive shock

(Continued)
Distributive Shock (Continued)
Anaphylaxis
 Sepsis
 Capillary leak syndrome

Obstructive Shock
Shock is caused by problems that
impair the ability of the normal heart
muscle to pump effectively.
 Heart is normal but conditions
outside the heart prevent either
adequate filling of the heart or
adequate contraction of the healthy
heart muscle.

Physical Assessment/Clinical
Manifestations
Cardiovascular changes
 Pulse
 Blood pressure
 Oxygen saturation
 Skin changes
 Respiratory changes
 Renal and urinary changes
 Central nervous system changes
 Musculoskeletal changes

Interventions
Reverse the shock.
 Restore fluid volume.
 Prevent complications through
supportive and drug therapies.
 Nonsurgical management includes
oxygen therapy, fluid replacement,
and monitoring.

Drug Therapies
Vasoconstrictors, such as dopamine,
epinephrine, norepinephrine,
phenylephrine
 Agents that enhance contractility
 Agents that enhance myocardial
perfusion

Collaborative Management
of Septic Shock
Manifestations of the first phase:
unique to septic shock and often
opposite from those seen with all
other types of shock
 Cardiovascular changes
 Respiratory changes
 Skin changes: in the hyperdynamic
phase of septic shock, the skin is
warm with no cyanosis evident

Interventions for Septic
Shock
Focus on correcting conditions causing
shock and preventing complications.
 Give oxygen therapy.
 Drug therapy: antibiotics and
anticoagulants, clotting factors and blood
products, activated protein C, and
antibodies, such as interleukin-1,
interleukin-6, and tumor necrosis factor
