Lewis: Medical-Surgical Nursing, 10th Edition

Chapter 66

Shock, Sepsis, and Multiple Organ Dysfunction Syndrome

KEY POINTS

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 O2 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 (MI), cardiomyopathy,
blunt cardiac injury, severe systemic or pulmonary hypertension, and myocardial
depression from metabolic problems.
 Clinical manifestations of cardiogenic shock 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.
 The reaction is caused by a sensitizing substance (e.g., drug, chemical, vaccine,
food, insect 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 adequate fluid
resuscitation along with the presence of inadequate tissue perfusion.
 In severe sepsis and septic shock, the body’s 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, acute
kidney injury with 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 multiple organ dysfunction
system (MODS).
 In the refractory 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 is established
from a detailed history and physical examination findings.
 Studies that assist in the diagnosis include a serum lactate, base deficit, 12-lead ECG,
continuous cardiac monitoring, chest x-ray, continuous pulse oximetry, and hemodynamic
monitoring.
Interprofessional 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 patient’s history,
physical examination, and clinical findings to establish a 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 O2 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
resulting in tissue hypoxia. Vasopressor or vasodilator therapy is used according to
patient needs to maintain the mean arterial pressure at the appropriate level after adequate
volume resuscitation.
 Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in
shock. Early enteral nutrition is vital to decreasing morbidity from shock.

Interprofessional Care: Specific Measures

Cardiogenic Shock
 The overall goal is to restore blood flow to the myocardium by restoring the balance
between O2 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 targeted response based on CVP, ScvO2, cardiac ultrasound, a focused physical
assessment, fluid responsiveness, or other measures. Use of a fluid challenge technique
(crystalloids if associated with hemodynamic improvement [increased MAP and/or other
measures]) is recommended.
 Vasopressor drug therapy may be added for mean arterial pressure (MAP) that does not
respond to initial fluid resuscitation. Vasopressin may be added to patients refractory to
vasopressor therapy.
 IV 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 for patients with septic shock. They
should be started after cultures (e.g., blood, urine) are obtained and within the first hour
 of severe sepsis or 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
 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 crystalloids, 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 assessing responsiveness and ABCs: airway, breathing,
and circulation.
 Further assessment focuses on the assessment of tissue perfusion and includes evaluation
of trends in 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 patient’s ongoing physical and emotional
status, (2) identifying trends to detect changes in the patient’s condition, (3) planning and
implementing nursing interventions and therapy, (4) evaluating the patient’s 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, SvO2,
and pulmonary artery (PA) pressures or arterial pressure wave-form analysis for cardiac
output (APCO); 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, as well as prevention of health
care-associated infections.
  Rehabilitation of the patient who is recovering from shock necessitates correction of the
precipitating cause, prevention or early treatment of complications, and education
focused on disease management and/or prevention of recurrence based on initial cause of
shock.

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.
 Multiple organ dysfunction syndrome (MODS) results from SIRS and is the failure of two
or more organ systems such that homeostasis cannot be maintained without intervention.
 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).
 Cardiovascular changes, neurologic dysfunction, acute kidney injury, DIC, GI
dysfunction, and liver dysfunction are common.

Nursing and Interprofessional 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.
 Interprofessional care for patients with MODS focuses on (1) prevention and treatment of
infection, (2) maintenance of tissue oxygenation, (3) nutritional and metabolic support,
(4) supportive measures for individual failing organs, (5) risk analysis and prevention of
health care-associated infections, and (6) patient education focused on disease
management and/or prevention of recurrence based on initial cause of SIRS and MODS.