Lewis: Medical-Surgical Nursing, 8th Edition

Chapter 67: Nursing Management: Shock, Systemic Inflammatory Response

Syndrome, and Multiple Organ Dysfunction Syndrome
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SHOCK
Shock is a syndrome characterized by decreased tissue perfusion and impaired
cellular metabolism resulting in an imbalance between the supply of and demand
for oxygen and nutrients.
The four main categories of shock are cardiogenic, hypovolemic, distributive
(includes septic, anaphylactic, and neurogenic shock), and obstructive.
Cardiogenic Shock
Cardiogenic shock occurs when either systolic or diastolic dysfunction of the
pumping action of the heart results in reduced cardiac output (CO).
Causes of cardiogenic shock include acute myocardial infarction (AMI),
cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension,
and myocardial depression from metabolic problems.
Clinical manifestations include tachycardia, hypotension, a narrowed pulse
pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy
skin, diaphoresis, decreased capillary refill time, anxiety, confusion, and agitation.
Hypovolemic Shock
Hypovolemic shock occurs when there is a loss of intravascular fluid volume.
Absolute hypovolemia results when fluid is lost through hemorrhage,
gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes
insipidus, or diuresis.
Relative hypovolemia results when fluid volume moves out of the vascular space
into extravascular space, such as with sepsis and burns.
Clinical manifestations depend on the extent of injury or insult, age, and general
state of health and may include anxiety; an increase in heart rate, CO, and
respiratory rate and depth; and a decrease in stroke volume, pulmonary artery
wedge pressure (PAWP), and urine output.
Neurogenic Shock
Neurogenic shock is a hemodynamic phenomenon that can occur within 30
minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last
up to 6 weeks, or in response to spinal anesthesia.
Clinical manifestations include hypotension, bradycardia, temperature
dysregulation (resulting in heat loss), dry skin, and poikilothermia.
Anaphylactic Shock
Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic)
reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect
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venom).
Immediate reaction causes massive vasodilation, release of vasoactive mediators,
and an increase in capillary permeability resulting in fluid leaks from the vascular
space into the interstitial space.
Clinical manifestations can include anxiety, confusion, dizziness, chest pain,
incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus,
urticaria, and angioedema.

Septic Shock
Sepsis is a systemic inflammatory response to a documented or suspected
infection. Severe sepsis is sepsis complicated by organ dysfunction.
Septic shock is the presence of sepsis with hypotension despite fluid resuscitation
along with the presence of inadequate tissue perfusion.
In severe sepsis and septic shock, the bodys response to infection is exaggerated,
resulting in an increase in inflammation and coagulation, and a decrease in
fibrinolysis.
Septic shock has three major pathophysiologic effects: vasodilation,
maldistribution of blood flow, and myocardial depression.
Patients often have hypotension, respiratory failure, alteration in neurologic
status, decreased urine output, and GI dysfunction.
Stages of Shock
The initial stage of shock that occurs at a cellular level is usually not clinically
apparent.
The compensatory stage is clinically apparent and involves neural, hormonal, and
biochemical compensatory mechanisms in an attempt to overcome the increasing
consequences of anaerobic metabolism and to maintain homeostasis.
The progressive stage of shock begins as compensatory mechanisms fail and
aggressive interventions are necessary to prevent the development of multipleorgan dysfunction system (MODS).
In the irreversible stage, decreased perfusion from peripheral vasoconstriction and
decreased CO exacerbate anaerobic metabolism. The patient will demonstrate
profound hypotension and hypoxemia, as well as organ failure; at this stage,
recovery is unlikely.
Diagnostic Studies
There is no specific diagnostic study to determine shock. The diagnosis depends
on the history and physical.
Studies that assist in diagnosis include a serum lactate, base deficit, 12-lead ECG,
continuous cardiac monitoring, chest x-ray, continuous pulse oximetry, and
hemodynamic monitoring.
Collaborative Care: General Measures
Successful management of the patient in shock includes the following: (1)
identification of patients at risk for the development of shock; (2) integration of
the patients history, physical examination, and clinical findings to establish a

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diagnosis; (3) interventions to control or eliminate the cause of the decreased

perfusion; (4) protection of target and distal organs from dysfunction; and (5)
provision of multisystem supportive care.
General management strategies for a patient in shock begin with ensuring that the
patient has a patent airway and oxygen delivery is optimized. The cornerstone of
therapy for septic, hypovolemic, and anaphylactic shock is volume expansion
with the administration of the appropriate fluid.
The primary goal of drug therapy for shock is the correction of decreased tissue
perfusion. Vasopressor or vasodilator therapy is used according to patient needs to
maintain the mean arterial pressure at the appropriate level.
Protein-calorie malnutrition is one of the main manifestations of hypermetabolism
in shock; nutrition is vital to decreasing morbidity from shock.

Collaborative Care: Specific Measures

Cardiogenic Shock
The overall goal is to restore blood flow to the myocardium by restoring the
balance between oxygen supply and demand.
Definitive measures include thrombolytic therapy, angioplasty with stenting,
emergency revascularization, and valve replacement.
Care involves hemodynamic monitoring, drug therapy (e.g., diuretics to reduce
preload), and use of circulatory assist devices (e.g., intraaortic balloon pump,
ventricular assist device).
Hypovolemic Shock
The underlying principles of managing patients with hypovolemic shock focus on
stopping the loss of fluid and restoring the circulating volume.
Septic Shock
Patients in septic shock require large amounts of fluid replacement; the goal is to
achieve a target central venous pressure (CVP) of 8 to 12 mm Hg.
Vasopressor drug therapy may be added once CVP is 8 mm Hg; vasopressin may
be given to patients refractory to vasopressor therapy.
Intravenous corticosteroids are only recommended for patients who cannot
maintain an adequate blood pressure (BP) with vasopressor therapy, despite fluid
resuscitation.
Antibiotics are an important component of therapy and should be started within
the first hour of septic shock.
Neurogenic Shock
The treatment of neurogenic shock is dependent on the cause. In spinal cord
injury, general measures to promote spinal stability are initially used.
Treatment of hypotension and bradycardia involves the use of vasopressors and
atropine, respectively. Fluids are administered cautiously; the patient is monitored
for hypothermia.
Anaphylactic Shock

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Epinephrine is the drug of choice to treat anaphylactic shock.

Maintaining the airway is critical; endotracheal intubation or cricothyroidotomy
may be necessary.
Aggressive fluid replacement, predominantly with colloids, is necessary.

Obstructive Shock
The primary strategy in treating obstructive shock is early recognition and
treatment to relieve or manage the obstruction.
NURSING MANAGEMENT: SHOCK
Nursing Assessment
The initial assessment focuses on the ABCs: airway, breathing, and circulation.
Further assessment focuses on the assessment of tissue perfusion and includes
evaluation of vital signs, peripheral pulses, level of consciousness, capillary refill,
skin (e.g., temperature, color, moisture), and urine output.
Planning
The overall goals for a patient in shock include (1) evidence of adequate tissue
perfusion, (2) restoration of normal BP, (3) return/recovery of organ function, and
(4) avoidance of complications from prolonged states of hypoperfusion.
Nursing Implementation
Your role in shock involves (1) monitoring the patients ongoing physical and
emotional status, (2) identifying trends to detect changes in the patients
condition, (3) planning and implementing nursing interventions and therapy, (4)
evaluating the patients response to therapy, (5) providing emotional support to
the patient and caregiver, and (6) collaborating with other members of the health
team to coordinate care.
The patient in shock requires frequent assessment of heart rate/rhythm, BP, CVP,
and pulmonary artery (PA) pressures; neurologic status; respiratory status, urine
output, and temperature; capillary refill; skin for temperature, pallor, flushing,
cyanosis, diaphoresis, or piloerection; and bowel sounds and abdominal
distention.
Rehabilitation of the patient who is recovering from shock necessitates correction
of the precipitating cause and prevention or early treatment of complications.
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTIPLE
ORGAN DYSFUNCTION SYNDROME
Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory
response to a variety of insults, including infection (referred to as sepsis),
ischemia, infarction, and injury.
SIRS is characterized by generalized inflammation in organs remote from the
initial insult and can be triggered by mechanical tissue trauma (e.g., burns, crush
injuries), abscess formation, ischemic or necrotic tissue (e.g., pancreatitis,
myocardial infarction), microbial invasion, and global and regional perfusion
deficits.

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MODS results from SIRS and is the failure of two or more organ systems such
that homeostasis cannot be maintained without intervention.
o The respiratory system is often the first system to show signs of
dysfunction in SIRS and MODS, often culminating in acute respiratory
distress syndrome (ARDS).
o Cardiovascular changes, neurologic dysfunction, acute renal failure, DIC,
GI dysfunction, and liver dysfunction are common.

Nursing and Collaborative Management: SIRS and MODS

The prognosis for the patient with MODS is poor; the most important goal is to
prevent the progression of SIRS to MODS.
A critical component of your role is vigilant assessment and ongoing monitoring
to detect early signs of deterioration or organ dysfunction.
Collaborative care for patients with MODS focuses on (1) prevention and
treatment of infection, (2) maintenance of tissue oxygenation, (3) nutritional and
metabolic support, and (4) appropriate support of individual failing organs.

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