Thelan`s Critical Care Nursing
Download
Report
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