Transcript Thelan`s Critical Care Nursing

CHAPTER 26
Shock, Sepsis, and Multiple
Organ Dysfunction Syndrome
Copyright © 2012, 2008, 2004, 2000, 1996, 1992 by Mosby, an imprint of Elsevier Inc.
OBJECTIVES
Describe generalized shock response and
systemic inflammatory response.
 List the etiologies of hypovolemic,
cardiogenic, anaphylactic, neurogenic,
and septic shock and multiple organ
dysfunction syndrome (MODS).
 Explain the pathophysiology of the five
forms of shock and MODS.

(continued)
OBJECTIVES (CONTINUED)
Identify the clinical manifestations of the five
forms of shock and MODS.
 Outline the important aspects of the medical
management of hypovolemic, cardiogenic,
anaphylactic, neurogenic, and septic shock
and multiple organ dysfunction syndrome.
 Summarize the nursing priorities for
managing a patient with each type of shock
or MODS.

SHOCK SYNDROME

Description
 Often

results in MODS
Etiology
 Four
classifications:
 Hypovolemic
 Cardiogenic
 Distributive

Septic, anaphylactic, or neurogenic
PATHOPHYSIOLOGY OF
SHOCK SYNDROME

Four stages:
 Initial
stage
 Compensatory stage
 Progressive stage
 Refractory stage
CONSEQUENCES OF SHOCK

Cardiovascular
Ventricular failure
 Microvascular thrombosis


Neurological
Sympathetic nervous system dysfunction
 Cardiac and respiratory depression
 Thermoregulatory failure
 Coma

(continued)
CONSEQUENCES OF SHOCK (CONTINUED)

Pulmonary
 Acute
respiratory failure
 Acute lung injury (ALI)

Renal
 Acute
tubular necrosis (ATN)
(continued)
CONSEQUENCES OF SHOCK (CONTINUED)

Hematological
 Disseminated

intravascular coagulation (DIC)
Gastrointestinal
 Gastrointestinal
 Hepatic
tract failure
failure
 Pancreatic failure
ASSESSMENT AND DIAGNOSIS OF
SHOCK SYNDROME

Clinical assessment
SBP <90 mm Hg
 Accompanied by:

 Tachycardia
 Altered
mental status
 Varies with specific shock syndromes

Global indicators of systemic perfusion and
oxygenation
Serum lactate
 Base deficit levels

MEDICAL MANAGEMENT OF
SHOCK SYNDROME

Improvement and preservation of tissue
perfusion
Adequate pulmonary gas exchange
 Adequate cardiac output

 Preload

Volume resuscitation
 Afterload
 Contractility
Adequate hemoglobin level
 Optimal metabolic environment

 Nutritional
support
 Glucose control
NURSING MANAGEMENT OF
SHOCK SYNDROME

Nursing priorities in managing the patient’s
psychosocial needs:
Providing information on patient status
 Explaining procedures and routines
 Supporting the family
 Encouraging the expression of feelings
 Facilitating problem solving and decision making
 Involving the family in the patient’s care
 Establishing contacts with necessary resources

COLLABORATIVE MANAGEMENT

Support oxygen transport
Establish a patent airway
 Initiate mechanical ventilation
 Administer oxygen
 Administer fluids (crystalloids, colloids, blood
and other blood products)
 Administer vasoactive medications
 Administer positive inotropic medications
 Ensure sufficient hemoglobin and hematocrit

(continued)
COLLABORATIVE MANAGEMENT
(CONTINUED)

Support oxygen use
 Identify
and correct cause of lactic acidosis
 Ensure adequate organ and extremity
perfusion
 Initiate nutritional support therapy
Identify underlying cause of shock and
treat accordingly
 Provide comfort and emotional support
 Maintain surveillance for complications

QUESTION
Sodium bicarbonate is recommended in the
treatment of shock-related lactic acidosis.
A.
B.
True
False
ANSWER
B.
False
Sodium bicarbonate is not recommended in the
treatment of shock-related lactic acidosis. No overall
benefit has been found. Risks associated with its use
include shifting of the oxyhemoglobin dissociation
curve to the left, rebound increase in lactic acid
production, development of hyperosmolar state, fluid
overload resulting from excessive sodium, and rapid
cellular electrolyte shifts.
HYPOVOLEMIC SHOCK

Description
 Inadequate
fluid volume in the intravascular
space

Etiology
 Absolute
 Relative

Pathophysiology
 Loss
of circulating blood volume
PATHOPHYSIOLOGY OF HYPOVOLEMIC
SHOCK
FIGURE 26-1 The pathophysiology of hypovolemic shock.
ASSESSMENT AND DIAGNOSIS
OF HYPOVOLEMIC SHOCK

Clinical manifestations
 Based
on severity of fluid loss
 Class
I
 Class II
 Class III
 Class IV

Hemodynamic assessment
 Varies
by stage
MEDICAL MANAGEMENT OF
HYPOVOLEMIC SHOCK

Medical management
 Correct
hypovolemia
 Restore tissue perfusion
NURSING DIAGNOSIS PRIORITIES
HYPOVOLEMIC SHOCK
Deficient fluid volume related to active blood
loss
 Deficient fluid volume related to interstitial fluid
shift
 Decreased cardiac output related to alterations
in preload
 Imbalanced nutrition: less than body
requirements related to increased metabolic
demands or lack of exogenous nutrients

(continued)
NURSING DIAGNOSIS PRIORITIES
HYPOVOLEMIC SHOCK (CONTINUED)
Risk for infection
 Anxiety related to threat to biological,
psychological, and/or social integrity
 Compromised family coping related to a
critically ill family member

NURSING MANAGEMENT OF
HYPOVOLEMIC SHOCK

Nursing priorities are directed toward:
 Minimizing
fluid loss
 Administering volume replacement
 Promoting comfort and emotional support
 Maintaining surveillance for complications
CARDIOGENIC SHOCK

Description
 Failure

of heart to pump blood effectively
Etiology
 Primary
ventricular ischemia
 Structural problems
 Dysrhythmias
PATHOPHYSIOLOGY OF CARDIOGENIC
SHOCK

Pathophysiology
 Impaired
ability of ventricle to pump blood
 Leads to a decrease in stroke volume and an
increase in the blood left in the ventricle at
the end of systole
 Decreased cellular oxygen supply
 Ineffective tissue perfusion
 Caused by a “heart” problem
PATHOPHYSIOLOGY OF CARDIOGENIC
SHOCK
FIGURE 26-2 The pathophysiology of cardiogenic shock.
ASSESSMENT AND DIAGNOSIS OF
CARDIOGENIC SHOCK

Clinical manifestations
 Low
CO and low BP
 Compensatory mechanisms develop

Hemodynamic assessment
 Decreased
cardiac output with a cardiac
index <2.2 L/min/m2s
MEDICAL MANAGEMENT OF
CARDIOGENIC SHOCK

Correct underlying cause of pump failure
 Identify

etiological factors
Enhance the effectiveness of the pump
 Pharmacological

management
Improve tissue perfusion
 Intubation
and mechanical ventilation
 Early revascularization
 Intraaortic balloon pump (IABP) or ventricular
assist device (VAD)
NURSING DIAGNOSIS PRIORITIES
CARDIOGENIC SHOCK
Ineffective cardiopulmonary tissue perfusion
related to acute myocardial ischemia
 Decreased cardiac output related to
alterations in contractility
 Decreased cardiac output related to
alterations in heart rate
 Imbalanced nutrition: less than body
requirements related to increased metabolic
demands or lack of exogenous nutrients

(continued)
NURSING DIAGNOSIS PRIORITIES
CARDIOGENIC SHOCK (CONTINUED)
Risk for infection
 Disturbed body image related to
functional dependence on life-sustaining
technology
 Compromised family coping related to a
critically ill family member

NURSING MANAGEMENT OF
CARDIOGENIC SHOCK

Nursing priorities are directed toward:
 Limiting
myocardial oxygen demand
 Enhancing myocardial oxygen supply
 Providing comfort and emotional support
 Maintaining surveillance for complications
ANAPHYLACTIC SHOCK

Description
 Distributive

shock
Etiology
 Antigen-antibody
reaction
PATHOPHYSIOLOGY OF
ANAPHYLACTIC SHOCK

Immunological stimulation of mast cells
results in release of biochemical mediators
Histamine
 Eosinophil chemotactic factor of anaphylaxis
 Neutrophil chemotactic factor of anaphylaxis
 Platelet-activating factor
 Proteinases
 Heparin, serotonin, leukotrienes
 Prostaglandins

(continued)
PATHOPHYSIOLOGY OF
ANAPHYLACTIC SHOCK (CONTINUED)

Activation of biochemical mediators causes:
Vasodilation
 Increased capillary permeability
 Bronchoconstriction
 Excessive mucus secretion
 Coronary vasoconstriction
 Inflammation
 Cutaneous reactions
 Constriction of smooth muscle in intestinal wall,
bladder, and uterus

PATHOPHYSIOLOGY OF
ANAPHYLACTIC SHOCK
FIGURE 26-3 The pathophysiology of anaphylactic shock.
ASSESSMENT AND DIAGNOSIS
OF ANAPHYLACTIC SHOCK

Clinical manifestations
 Affects

multiple body systems
Hemodynamic assessment
 Decreased
cardiac output–cardiac index
 Vasodilation leads to decrease in systemic
vascular resistance
QUESTION
Clinical manifestations of anaphylactic shock
include:
A.
B.
C.
D.
chest pain and crackles.
decreased urine output and narrowing pulse
pressure.
bradycardia and warm dry skin.
pruritus and hypotension.
ANSWER
D.
Pruritus and hypotension.
Chest pain and crackles are symptoms of cardiogenic
shock. Decreased urine output and narrowing pulse
pressure are symptoms of hypovolemic shock.
Bradycardia and warm dry skin are symptoms of
neurogenic shock.
MEDICAL MANAGEMENT OF
ANAPHYLACTIC SHOCK

Immediate and direct approach
 Remove
antigen
 Reverse effects of biochemical mediators
 Promote adequate tissue perfusion
 Fluid
replacement
 Oxygen
 Epinephrine
 Benadryl
NURSING DIAGNOSIS PRIORITIES
ANAPHYLACTIC SHOCK





Deficient fluid volume related to relative loss
Decreased cardiac output related to alterations in
preload
Decreased cardiac output related to alterations in
afterload
Ineffective breathing pattern related to decreased
lung expansion
Impaired gas exchange related to ventilation/
perfusion mismatching or intrapulmonary shunting
(continued)
NURSING DIAGNOSIS PRIORITIES
ANAPHYLACTIC SHOCK (CONTINUED)
Imbalanced nutrition: less than body
requirements related to increased
metabolic demands or lack of exogenous
nutrients
 Risk for infection
 Ineffective coping related to situational
crisis and personal vulnerability
 Compromised family coping related to a
critically ill family member

NURSING MANAGEMENT OF
ANAPHYLACTIC SHOCK

Nursing priorities are directed toward:
 Facilitating
ventilation
 Administering volume replacement
 Providing comfort and emotional support
 Maintaining surveillance for complications
NEUROGENIC SHOCK

Description
 Distributive

shock
Etiology
 Disruption
(SNS)
of sympathetic nervous system
PATHOPHYSIOLOGY OF
NEUROGENIC SHOCK

Loss of sympathetic tone results in:
 Massive
peripheral vasodilation
 Inhibition of the baroreceptor response
 Impaired thermoregulation
PATHOPHYSIOLOGY OF
NEUROGENIC SHOCK
FIGURE 26-4 The pathophysiology of neurogenic shock.
ASSESSMENT AND DIAGNOSIS OF
NEUROGENIC SHOCK

Clinical manifestations
 Hypotension
 Bradycardia
 Warm
dry skin
 Hypothermia

Hemodynamic assessment
 Decreased
cardiac output/cardiac index
 Decrease in systemic vascular resistance due
to vasodilation
MEDICAL MANAGEMENT OF
NEUROGENIC SHOCK

Careful approach
 Remove
cause of neurogenic shock
 Prevent cardiovascular instability
 Promote optimal tissue perfusion
NURSING DIAGNOSIS PRIORITIES
NEUROGENIC SHOCK
Deficient fluid volume related to relative loss
 Decreased cardiac output related to
sympathetic blockade
 Hypothermia related to exposure to cold
environment trauma or damage to the
hypothalamus
 Imbalanced nutrition: less than body
requirements related to increased metabolic
demands or lack of exogenous nutrients

(continued)
NURSING DIAGNOSIS PRIORITIES
NEUROGENIC SHOCK (CONTINUED)
Risk for infection
 Anxiety related to threat to biological,
psychological, or social integrity
 Compromised family coping related to a
critically ill family member

NURSING MANAGEMENT OF
NEUROGENIC SHOCK

Nursing priorities are directed toward:
 Treating
hypovolemia
 Maintaining normothermia
 Monitoring for dysrhythmias
 Providing comfort and emotional support
 Maintaining surveillance for complications
SEVERE SEPSIS AND
SEPTIC SHOCK

Description
 Occurs
when microorganisms invade the
body and initiate a systemic inflammatory
response
 Host response results in perfusion
abnormalities with organ dysfunction (severe
sepsis) and eventually hypotension (septic
shock)
 Primary mechanism of shock is
maldistribution of blood flow to the tissues
ETIOLOGY OF SEVERE SEPSIS
AND SEPTIC SHOCK

Caused by a wide variety of microorganisms
Gram-negative and gram-positive aerobes
 Anaerobes
 Fungi
 Viruses


Source of microorganisms
Exogenous
 Endogenous


Intrinsic and extrinsic precipitating factors
PATHOPHYSIOLOGY OF SEVERE
SEPSIS AND SEPTIC SHOCK

Complex system response
Initiated when a microorganism enters the body
 Stimulates inflammatory/immune system


Release of toxins and other substances
activated the plasma enzyme cascades as
well as platelets, neutrophils, monocytes,
and macrophages
(continued)
PATHOPHYSIOLOGY OF SEVERE
SEPSIS AND SEPTIC SHOCK (CONTINUED)

Hallmarks of severe sepsis
 Endothelial
damage
 Coagulation dysfunction
PATHOPHYSIOLOGY OF SEVERE
SEPSIS AND SEPTIC SHOCK
FIGURE 26-5 The pathophysiology of septic shock.
ASSESSMENT AND DIAGNOSIS OF
SEVERE SEPSIS AND SEPTIC SHOCK
Effective treatment depends on timely
recognition
 Diagnosis based on identification of three
conditions

 Known
or suspected infection
 Two or more of the clinical indicators of the
systemic inflammatory response
 Evidence of at least one organ dysfunction
MEDICAL MANAGEMENT OF SEVERE
SEPSIS AND SEPTIC SHOCK
Multifaceted approach
 Goals of treatment

 Reverse
pathophysiological responses
 Control and eliminate infection
 Promote metabolic support
SEVERE SEPSIS AND SEPTIC SHOCK
MANAGEMENT GUIDELINES
Initial resuscitation
 Diagnosis
 Antibiotic therapy
 Source identification and control
 Fluid therapy
 Vasopressors
 Inotropic therapy
 Steroids

(continued)
SEVERE SEPSIS AND SEPTIC SHOCK
MANAGEMENT GUIDELINES (CONTINUED)
Recombinant human activated protein C
 Blood product administration
 Mechanical ventilation of sepsis-induced
ALI/ARDS
 Sedation, analgesia, and neuromuscular
blockade in sepsis
 Glucose control
 Renal replacement

(continued)
SEVERE SEPSIS AND SEPTIC SHOCK
MANAGEMENT GUIDELINES (CONTINUED)
Bicarbonate therapy
 Deep Vein thrombosis prophylaxis
 Stress ulcer prophylaxis
 Consideration for limitation of support

NURSING DIAGNOSIS PRIORITIES
SEVERE SEPSIS AND SEPTIC SHOCK





Deficient fluid volume related to relative loss
Decreased cardiac output related to alterations in
preload
Decreased cardiac output related to alterations in
afterload
Decreased cardiac output related to alterations in
contractility
Impaired gas exchange related to ventilation/perfusion
mismatching or intrapulmonary shunting
(continued)
NURSING DIAGNOSIS PRIORITIES SEVERE
SEPSIS AND SEPTIC SHOCK (CONTINUED)
Imbalanced nutrition: less than body
requirements related to increased
metabolic demands or lack of exogenous
nutrients
 Risk for infection
 Anxiety related to threat to biological,
psychological, or social integrity
 Compromised family coping related to a
critically ill family member

NURSING MANAGEMENT OF SEVERE
SEPSIS AND SEPTIC SHOCK
Prevention is one of the primary
responsibilities of the critical care nurse
 Nursing priorities are directed toward:

 Early
identification of the sepsis syndrome
 Administering prescribed fluids and
medications
 Providing comfort and emotional support
 Maintaining surveillance for complications
MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

Description
MODS results from progressive physiological
function of two or more separate organ systems
 Trauma patients are particularly vulnerable
 Other high-risk patients include those who have
experienced:

 Infection
 Shock
episodes
 Ischemia-reperfusion events
 Acute pancreatitis
 Burns
ETIOLOGY OF MODS

Primary MODS
 Occurs

as a direct consequence of the insult
Secondary MODS
 Manifests
latently and involves organs not
affected in the initial insult

Systemic inflammatory response
syndrome (SIRS)
PATHOPHYSIOLOGY OF MODS
FIGURE 26-6 Pathogenesis of multiple organ dysfunction syndrome. GI, gastrointestinal; MDF, myocardial depressant
factor; MODS, multiple organ dysfunction syndrome; PAF, platelet activating factor; WBCs, white blood cells. (From
Cheek DJ, et al: Shock, multiple organ dysfunction syndrome, and burns in adults. In McCance KL, Huether SE,
editors: Pathophysiology: the biologic basis for disease in adults and children ed 6, St Louis, 2010, Mosby.)
PATHOPHYSIOLOGY OF MODS
INFLAMMATORY MEDIATORS

Inflammatory cells
 Neutrophils
 Macrophages
or monocytes
 Mast
 Lymphocytes
 Endothelial
(continued)
PATHOPHYSIOLOGY OF MODS
INFLAMMATORY MEDIATORS (CONTINUED)

Biochemical mediators
 Reactive
oxygen species
 Superoxide
radical
 Hydroxyl radical
 Hydrogen peroxide
 Tumor
necrosis factor
 Interleukins
 Platelet activating factor
(continued)
PATHOPHYSIOLOGY OF MODS
INFLAMMATORY MEDIATORS (CONTINUED)
 Arachidonic
acid metabolites
 Prostaglandins
 Leukotrienes
 Thromboxanes
 Proteases

Plasma protein systems
 Complement
 Kinin
 Coagulation
ASSESSMENT AND DIAGNOSIS OF
MODS

Clinical manifestation of organ
dysfunction
 GI
dysfunction
 Hepatobiliary dysfunction
 Pulmonary dysfunction
 Renal dysfunction
 Cardiovascular dysfunction
 Coagulation dysfunction
QUESTION
The primarily mechanism of bacterial
translocation has been associated with:
A.
B.
C.
D.
gastrointestinal mucosal edema.
dysfunction of Kupffer cells.
intestinal bacterial overgrowth.
colonization of the oropharynx.
ANSWER
C.
Intestinal bacterial overgrowth.
The gastrointestinal tract harbors organisms that
present an inflammatory focus when translocated from
the gut into the portal circulation and are inadequately
cleared by the liver. The primary mechanism of bacterial
translocation has been associated with intestinal
bacterial overgrowth.
MEDICAL MANAGEMENT OF MODS
Interdisciplinary collaboration in clinical
management
 Goals of medical management include:

 Prevention
and treatment of infection
 Maintenance of tissue oxygenation
 Nutritional and metabolic support
 Comfort and emotional support
 Support for individual organ function
COLLABORATIVE MANAGEMENT OF MODS

Support oxygen transport:
Establish a patent airway
 Initiate mechanical ventilation
 Administer oxygen
 Administer fluids (crystalloids, colloids, blood
and other blood products)
 Administer vasoactive medications
 Administer positive inotropic medications
 Administer antidysrhythmic medications
 Ensure sufficient hemoglobin and hematocrit

(continued)
COLLABORATIVE MANAGEMENT OF
MODS (CONTINUED)

Support oxygen use:
Identify and correct cause of lactic acidosis
 Ensure adequate organ and extremity perfusion


Decrease oxygen demand:
Administer sedation or paralytics
 Administer antipyretics and external cooling
measures
 Administer pain medications

(continued)
COLLABORATIVE MANAGEMENT OF
MODS (CONTINUED)

Identify the underlying cause of
inflammation and treat accordingly
Remove infected organs or tissue
 Administer antibiotics

Initiate nutritional support
 Treat individual organ dysfunction

Gastrointestinal
 Hepatobiliary
 Pulmonary

(continued)
COLLABORATIVE MANAGEMENT OF
MODS (CONTINUED)

Treat individual organ dysfunction
(continued)
 Renal
 Cardiovascular
 Coagulation

system
Maintain surveillance for complications
 Infection

Provide comfort and emotional support
NURSING DIAGNOSIS PRIORITIES
MODS
Decreased cardiac output related to
alterations in preload
 Decreased cardiac output related to
alterations in afterload
 Decreased cardiac output related to
alterations in contractility
 Impaired gas exchange related to
ventilation/perfusion mismatching or
intrapulmonary shunting

(continued)
NURSING DIAGNOSIS PRIORITIES
MODS (CONTINUED)
Ineffective renal tissue perfusion related to
decreased renal blood flow
 Ineffective cardiopulmonary tissue perfusion
related to decreased coronary blood flow
 Imbalanced nutrition: less than body
requirements related to increased metabolic
demands or lack of exogenous nutrients
 Risk for infection

(continued)
NURSING DIAGNOSIS PRIORITIES
MODS (CONTINUED)
Acute pain related to transmission and
perception of cutaneous, visceral, muscular,
or ischemic impulses
 Acute confusion related to sensory overload,
sensory deprivation, and sleep pattern
disturbance
 Anxiety related to threat to biological,
psychological, or social integrity
 Compromised family coping related to a
critically ill family member

NURSING MANAGEMENT OF MODS

Nursing priorities are directed toward:
 Preventing
development of infections
 Facilitating tissue oxygen delivery and limiting
tissue oxygen demand
 Facilitating nutritional support
 Providing comfort and emotional support
 Maintaining surveillance for complications