Ignatavicius: Medical-Surgical Nursing, 7th Edition

Chapter 39: Care of Patients with Shock

Key Points - Print

OVERVIEW

Shock is wide-spread abnormal cellular metabolism that occurs when the bodys
need for oxygenation and tissue perfusion is not met adequately.
It is a condition rather than a disease and represents the whole-body response
that occurs when too little oxygen is delivered to the tissues.
All body organs are affected by shock, and either work harder to adapt and
compensate for reduced oxygenation or fail to function because of hypoxia.
Shock is a syndrome because the cellular, tissue, and organ events that occur in
response to its presence happen in a predictable sequence.
Any problem that impairs oxygen delivery to tissues and organs can start the
syndrome of shock and lead to a life-threatening emergency.
Most often, cardiovascular problems and changes lead to shock.
Patients in acute care settings are at higher risk, but shock can occur in any
setting.
When compensatory mechanisms or health care interventions are not effective
and shock progresses, severe hypoxia can lead to cell loss, multiple organ
dysfunction syndrome, and death.
Shock is most commonly classified by the functional impairment it causes or by
the origin of
the problem.
Many manifestations of shock are similar regardless of what starts the process
or which
tissues are affected first.
The common manifestations result from physiologic adjustments, known as
adaptive or compensatory mechanisms, made by the sympathetic nervous
system, the endocrine system, and the cardiovascular system that attempt to
ensure continued oxygenation of vital organs.
Manifestations unique to any one type of shock result from specific tissue
dysfunction.
More than one type of shock can be present at the same time.
Cardiogenic shock occurs when the actual heart muscle is unhealthy and
pumping is directly impaired.
Myocardial infarction is the most common cause of direct pump failure.
Distributive shock is the type of shock that occurs when blood volume is not lost
from the body but is distributed to the interstitial tissues where it cannot
circulate and deliver oxygen.
Distributive shock can be caused by a loss of sympathetic tone, blood vessel
dilation, pooling of blood in venous and capillary beds, and increased blood
vessel permeability.
Capillary leak syndrome is the response of capillaries to the presence of
biologic chemicals or mediators that change blood vessel integrity and allow
fluid to shift from the blood in the vascular space into the interstitial tissues.
Anaphylaxis is one result of Type I allergic reactions, beginning within seconds
to minutes after exposure to a specific allergen in a susceptible person.
The result is wide-spread loss of blood vessel tone and decreased cardiac output.
Assess all patients at risk for shock for a change in affect, reduced cognition,
altered level of consciousness, and increased anxiety.
Stay with the patient in shock. Reassure patients who are in shock that the
appropriate interventions are being instituted.
Immediately assess vital signs of patients who have a change in level of
consciousness, increased thirst, or anxiety.
Assess for changes in pulse rate and quality rather than blood pressure as an
indicator of shock.
Give oxygen to any patient in shock.

HYPOVOLEMIC SHOCK

Hypovolemic shock occurs when too little circulating blood volume causes the
mean arterial pressure (MAP) to decrease so that the bodys total need for
oxygen is not met.
Common problems leading to hypovolemic shock are hemorrhage and
dehydration.
The result is wide-spread loss of blood vessel tone and decreased cardiac output.
Assess hourly urine output to evaluate the adequacy of treatment for
hypovolemic shock.

SEPSIS AND SEPTIC SHOCK

Sepsis is a wide-spread infection that triggers a whole body inflammatory
response leading to distributive or septic shock when organisms are present in
the blood.
Prevention is the best management strategy for sepsis and septic shock. Evaluate
all patients for their risk for sepsis, especially older adults, because the death
rate from sepsis in people over age 65 years is nearly twice that of younger
adults.
Identify patients at high risk for infection due to age, disease, or the
environment.
Assess the immunocompromised patient every shift for infection.
Assess the skin integrity of the patient with reduced immune function at least
every shift.
The syndrome of shock progresses in four stages when the conditions that cause
shock remain uncorrected and poor cellular oxygenation continues.
The stages are the initial stage, nonprogressive stage, progressive stage, and
refractory stage.
The stages are defined on the basis of how well compensatory mechanisms are
working, the severity of the clinical manifestations, and whether tissue damage
is reversible.
During the initial stage of shock, adaptive mechanisms are so effective at
returning MAP to normal levels that oxygenated blood flow to all vital organs is
maintained.
During the nonprogressive or compensatory stage of shock, kidney and
hormonal adaptive mechanisms are activated because cardiovascular
adjustments alone are not enough to maintain MAP and supply needed oxygen to
the vital organs.
In the life-threatening progressive stage of shock, adaptive or compensatory
mechanisms are functioning but can no longer deliver sufficient oxygen, even to
vital organs.
Vital organs develop hypoxia, and less vital organs become anoxic and ischemic
resulting in tissue damage or death.
The refractory stage or irreversible stage of shock occurs when too much cell
death and tissue damage results from too little oxygen reaching the tissues.
Therapy is not effective in saving the patients life, even if the cause of shock is
corrected and MAP temporarily returns to normal.
The sequence of cell damage caused by the massive release of toxic metabolites
and enzymes is termed multiple organ dysfunction syndrome.
Most manifestations of hypovolemic shock are caused by the changes resulting
from compensatory efforts, which are physiologic adjustments or responses that
try to keep an adequate blood flow to vital organs.
The earliest clinical signs of hypovolemic shock are cardiovascular, often starting
with decreased mean arterial pressure.
Since changes in systolic blood pressure are not always present in the initial
stage of shock, assess for changes in pulse rate and quality.
Respiratory rate and depth increase during hypovolemic shock to increase
oxygen intake and combat lactic acidosis.
Renal and urinary changes occur with shock to adapt or compensate for
decreased arterial pressure by conserving body fluids through decreased
filtration and increased water reabsorption.
Ensure that vital sign measurements are accurate and monitor them for trends
indicating shock.
Skin changes occur in shock because of blood vessel constriction in the skin.
Central nervous system changes with shock often first manifest as thirst and are
followed by changes in level of consciousness and orientation to person, place,
and time.
Skeletal muscle changes during shock are muscle weakness and pain in response
to tissue hypoxia, anaerobic metabolism.
The goals of shock management are to maintain tissue oxygenation, increase
vascular volume to normal range, and support compensatory mechanisms.
Oxygen therapy, fluid replacement therapy, and drug therapies are useful for this
problem.
Drug therapy may be needed if the volume deficit is severe and the patient does
not respond sufficiently to the replacement of fluid volume and blood products.
The actions of drugs for shock increase venous return, improve cardiac
contractility, or improve cardiac perfusion by dilating the coronary vessels.
Early detection of sepsis before progression to septic shock is a major nursing
responsibility.
Assess vital signs often for changes from baseline levels.
Review laboratory data for changes in serum lactate levels, total white blood cell
count, and in the differential.
Other biologic indicators of severe sepsis and septic shock are changes in plasma
d-dimer levels and specific cytokine (interleukin-6 [IL-6] and interleukin-10 [IL-
10]) levels.
These indicators have a lag time and changes may not be present soon enough to
identify sepsis with systemic inflammatory response syndrome, SIRS, before
severe sepsis or septic shock develops.
Sepsis is different from other types of shock, as the syndrome may occur over
many hours to days and the manifestations usually are less obvious.
Secondly, the cause of sepsis is often less obvious than for other types of shock.
The presence of bacteria in the blood supports the diagnosis of sepsis although
this finding may not be present in up to 30% of patients with sepsis.
Obtain specimens of urine, blood, sputum, and any culture and drainage to
identify the causative organisms.
The actual diagnosis of sepsis is difficult to make, yet the best outcome is
dependent on an early diagnosis and the implementation of aggressive
interventions.
Identify patients at high risk for infection as a result of age, disease, work
environment, or leisure activities.
Assess all patients at risk for shock for a change in affect, reduced cognition,
altered level of consciousness, and increased anxiety.
Immediately assess vital signs of patients who have a change in level of
consciousness, increased thirst, or anxiety.
Use strict aseptic techniques when performing invasive procedures, dressing
changes, or handling nonintact skin.
Use good handwashing techniques before providing any care to a patient who is
either immunocompromised or immunodeficient.
Teach the patient and family about the clinical manifestations of infection and
when to seek medical advice.
Explain all diagnostic and treatment procedures to the patient and family.