Focus on Shock (Relates to Chapter 67, “Nursing Management: Shock, SIRS, and Multiple Organ Dysfunction Syndrome,” in the textbook) Copyright © 2007, 2004, 2000, Mosby, Inc.,
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Transcript Focus on Shock (Relates to Chapter 67, “Nursing Management: Shock, SIRS, and Multiple Organ Dysfunction Syndrome,” in the textbook) Copyright © 2007, 2004, 2000, Mosby, Inc.,
Focus on
Shock
(Relates to Chapter 67,
“Nursing Management: Shock, SIRS,
and Multiple Organ Dysfunction Syndrome,”
in the textbook)
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Shock
Syndrome
characterized by decreased
tissue perfusion and impaired cellular
metabolism
Imbalance in supply/demand for O2
and nutrients
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Shock
Classification of shock
Low blood flow
Cardiogenic
Hypovolemic
Maldistribution of blood flow
Septic
Anaphylactic
Neurogenic
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Low Blood Flow
Cardiogenic Shock
Definition
Systolic
or diastolic dysfunction
Compromised cardiac output (CO)
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Low Blood Flow
Cardiogenic Shock
Precipitating causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic
problems
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Pathophysiology of
Cardiogenic Shock
Fig. 67-2
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Low Blood Flow
Cardiogenic Shock
Early
manifestations
Tachycardia
Hypotension
Narrowed pulse pressure
↑ Myocardial O2 consumption
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Low Blood Flow
Cardiogenic Shock
Physical examination
Tachypnea, pulmonary congestion
Pallor; cool, clammy skin
Decreased capillary refill time
Anxiety, confusion, agitation
↑ in pulmonary artery wedge pressure
Decreased renal perfusion and UO
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Low Blood Flow
Hypovolemic Shock
Absolute
hypovolemia: Loss of
intravascular fluid volume
Hemorrhage
GI loss (e.g., vomiting, diarrhea)
Fistula drainage
Diabetes insipidus
Hyperglycemia
Diuresis
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Low Blood Flow
Hypovolemic Shock
Relative
hypovolemia
Results when fluid volume moves out of
the vascular space into extravascular
space (e.g., interstitial or intracavitary
space)
Termed third spacing
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Pathophysiology of
Hypovolemic Shock
Fig. 67-3
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Low Blood Flow
Hypovolemic Shock
Response
to acute volume loss depends
on
Extent of injury or insult
Age
General state of health
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Low Blood Flow
Hypovolemic Shock
Clinical
manifestations
Anxiety
Tachypnea
Increase in CO, heart rate
Decrease in stroke volume, PAWP, UO
If
loss is >30%, blood volume is
replaced
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Maldistribution of Blood Flow
Neurogenic Shock
Hemodynamic phenomenon that can occur
within 30 minutes of a spinal cord injury at
the fifth thoracic (T5) vertebra or above
and can last up to 6 weeks
Can be in response to spinal anesthesia
Results in massive vasodilation leading to
pooling of blood in vessels
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Pathophysiology of
Neurogenic Shock
Fig. 67-4
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Maldistribution of Blood Flow
Neurogenic Shock
Clinical manifestations
Hypotension
Bradycardia
Temperature dysregulation (resulting in heat
loss)
Dry skin
Poikilothermia (taking on the temperature of
the environment)
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Maldistribution of Blood Flow
Anaphylactic Shock
Acute,
life-threatening hypersensitivity
reaction
Massive vasodilation
Release of mediators
↑ Capillary permeability
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Maldistribution of Blood Flow
Anaphylactic Shock
Clinical
manifestations
Anxiety, confusion, dizziness
Sense of impeding doom
Chest pain
Incontinence
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Maldistribution of Blood Flow
Anaphylactic Shock
Clinical
manifestations
Swelling of the lips and tongue,
angioedema
Wheezing, stridor
Flushing, pruritus, urticaria
Respiratory distress and circulatory
failure
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Maldistribution of Blood Flow
Septic Shock
Sepsis:
Systemic inflammatory
response to documented or suspected
infection
Severe sepsis = Sepsis + Organ
dysfunction
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Maldistribution of Blood Flow
Septic Shock
Septic
shock = Presence of sepsis with
hypotension despite fluid resuscitation
+ Presence of tissue perfusion
abnormalities
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Maldistribution of Blood Flow
Septic Shock
Mortality
rates as high as 50%
Primary causative organisms
Gram-negative and gram-positive
bacteria
Endotoxin stimulates inflammatory
response
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Pathophysiology of Septic Shock
Fig. 67-5
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Maldistribution of Blood Flow
Septic Shock
Clinical
manifestations
↑ Coagulation and inflammation
↓ Fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Hyperdynamic state: Increased CO and
decreased SVR
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Maldistribution of Blood Flow
Septic Shock
Clinical
manifestations
Tachypnea/hyperventilation
Temperature dysregulation
↓ Urine output
Altered neurologic status
GI dysfunction
Respiratory failure is common
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Stages of Shock
Initial Stage
Usually
not clinically apparent
Metabolism changes from aerobic to
anaerobic
Lactic acid accumulates and must be
removed by blood and broken down by
liver
Process requires unavailable O2
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Stages of Shock
Compensatory Stage
Clinically
apparent
Neural
Hormonal
Biochemical compensatory mechanisms
Attempts
are aimed at overcoming
consequences of anaerobic metabolism
and maintaining homeostasis
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Compensatory Stage of Shock
Fig. 67-6
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Stages of Shock
Compensatory Stage
Baroreceptors in carotid and aortic bodies
activate SNS in response to ↓ BP
Vasoconstriction while blood to vital
organs maintained
↓ Blood to kidneys activates renin–
angiotensin system
↑ Venous return to heart, CO, BP
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Stages of Shock
Compensatory Stage
Impaired
Risk for paralytic ileus
Cool,
GI motility
clammy skin from blood
Except septic patient who is warm and
flushed
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Stages of Shock
Compensatory Stage
Shunting
blood from lungs increases
physiologic dead space
↓ Arterial O2 levels
Increase in rate/depth of respirations
V/Q mismatch
SNS
stimulation increases myocardium
O2 demands
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Stages of Shock
Compensatory Stage
If
perfusion deficit corrected, patient
recovers with no residual sequelae
If deficit not corrected, patient enters
progressive stage
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Stages of Shock
Progressive Stage
Begins
when compensatory
mechanisms fail
Aggressive interventions to
prevent multiple organ
dysfunction syndrome
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Progressive Stage of Shock
Fig. 67-7
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Stages of Shock
Progressive Stage
Hallmarks
of ↓ cellular perfusion and
altered capillary permeability:
Leakage of protein into interstitial
space
↑ Systemic interstitial edema
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Stages of Shock
Progressive Stage
Anasarca
Fluid leakage affects solid organs and
peripheral tissues
↓ Blood flow to pulmonary capillaries
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Stages of Shock
Progressive Stage
Movement
of fluid from pulmonary
vasculature to interstitium
Pulmonary edema
Bronchoconstriction
↓ Residual capacity
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Stages of Shock
Progressive Stage
Fluid
moves into alveoli
Edema
Decreased surfactant
Worsening V/Q mismatch
Tachypnea
Crackles
Increased work of breathing
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Stages of Shock
Progressive Stage
CO
begins to fall
Decreased peripheral perfusion
Hypotension
Weak peripheral pulses
Ischemia of distal extremities
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Stages of Shock
Progressive Stage
Myocardial
dysfunction results in
Dysrhythmias
Ischemia
Myocardial infarction
End result: Complete deterioration of
cardiovascular system
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Stages of Shock
Progressive Stage
Mucosal
barrier of GI system becomes
ischemic
Ulcers
Bleeding
Risk of translocation of bacteria
Decreased ability to absorb nutrients
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Stages of Shock
Progressive Stage
Liver
fails to metabolize drugs and
wastes
Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
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Stages of Shock
Progressive Stage
Acute
tubular necrosis/acute renal
failure
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Stages of Shock
Refractory Stage
Exacerbation
of anaerobic metabolism
Accumulation of lactic acid
↑ Capillary permeability
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Refractory Stage of Shock
Fig. 67-8
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Stages of Shock
Refractory Stage
Profound
hypotension and hypoxemia
Tachycardia worsens
Decreased coronary blood flow
Cerebral ischemia
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Stages of Shock
Refractory Stage
Failure
of one organ system affects
others
Recovery unlikely
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Diagnostic Studies
Thorough history and physical examination
No single study to determine shock
Blood studies
Elevation of lactate
Base deficit
12-lead ECG
Chest x-ray
Hemodynamic monitoring
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Diagnostic Tests cont.
Blood Type and cross
BAL- 20-50% of trauma have alcohol
involved
Urine drug screen
CBC
Electrolytes
Bun, Creat, specific gravity
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Collaborative Care
Successful
management includes
Identification of patients at risk for shock
Integration of the patient’s history,
physical examination, and clinical
findings to establish a diagnosis
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Collaborative Care
Successful
management includes
Interventions to control or eliminate the
cause of the decreased perfusion
Protection of target and distal organs
from dysfunction
Provision of multisystem supportive care
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Collaborative Care
General
management strategies
Ensure patent airway
Maximize oxygen delivery
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Collaborative Care
Cornerstone
of therapy for septic,
hypovolemic, and anaphylactic shock
= volume expansion
Isotonic crystalloids (e.g., normal saline)
for initial resuscitation of shock
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Collaborative Care
Volume
expansion
If the patient does not respond to 2 to 3 L
of crystalloids, blood administration and
central venous monitoring may be
instituted
Complications of fluid resuscitation
Hypothermia
Coagulopathy
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Collaborative Care
Primary
goal of drug therapy =
correction of decreased tissue perfusion
Vasopressor drugs (e.g., epinephrine)
Achieve/maintain MAP >60 to 65 mm Hg
Reserved for patients unresponsive to
other therapies
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Collaborative Care
Primary
goal of drug therapy =
correction of decreased tissue perfusion
Vasodilator therapy (e.g., nitroglycerin
[cardiogenic shock], nitroprusside
[noncardiogenic shock])
Achieve/maintain MAP >60 to 65 mm Hg
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Collaborative Care
Nutrition
is vital to decreasing
morbidity from shock
Initiate enteral nutrition within the first 24
hours
Initiate parenteral nutrition if enteral feedings
contraindicated or fail to meet at least 80% of
the caloric requirements
Monitor protein, nitrogen balance, BUN,
glucose, electrolytes
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Collaborative Care
Cardiogenic Shock
Restore
blood flow to the myocardium
by restoring the balance between O2
supply and demand
Thrombolytic therapy
Angioplasty with stenting
Emergency revascularization
Valve replacement
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Collaborative Care
Cardiogenic Shock
Hemodynamic
monitoring
Drug therapy (e.g., diuretics to reduce
preload)
Circulatory assist devices (e.g., intraaortic balloon pump, ventricular
assist device)
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Collaborative Care
Hypovolemic Shock
Management
focuses on stopping the
loss of fluid and restoring the
circulating volume
Fluid replacement is calculated using
a 3:1 rule (3 ml of isotonic crystalloid
for every 1 ml of estimated blood loss)
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Collaborative Care
Septic Shock
Fluid
replacement (e.g., 6 to 10 L of
isotonic crystalloids and 2 to 4 L of
colloids) to restore perfusion
Hemodynamic monitoring
Vasopressor
drug therapy;
vasopressin for patients refractory to
vasopressor therapy
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Collaborative Care
Septic Shock
Intravenous
corticosteroids for
patients who require vasopressor
therapy, despite fluid resuscitation, to
maintain adequate BP
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Collaborative Care
Septic Shock
Antibiotics
after obtaining cultures
(e.g., blood, wound exudate, urine,
stool, sputum)
Drotrecogin alfa (Xigris)
Major side effect: Bleeding
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Collaborative Care
Septic Shock
Glucose
levels <150 mg/dl
Stress ulcer prophylaxis with
histamine (H2)-receptor blockers
Deep vein thrombosis prophylaxis
with low-dose unfractionated heparin
or low-molecular-weight heparin
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Collaborative Care
Neurogenic Shock
In
spinal cord injury: Spinal stability
Treatment of the hypotension and
bradycardia with vasopressors and
atropine
Fluids used cautiously as hypotension is
generally not related to fluid loss
Monitor for hypothermia
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Collaborative Care
Anaphylactic Shock
Epinephrine,
diphenhydramine
Maintaining a patent airway
Nebulized bronchodilators
Endotracheal intubation or
cricothyroidotomy may be necessary
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Collaborative Care
Anaphylactic Shock
Aggressive
fluid replacement
Intravenous corticosteroids if
significant hypotension persists after
1 to 2 hours of aggressive therapy
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Nursing Assessment
ABCs: Airway,
breathing, and
circulation
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Nursing Assessment
Focused
assessment of tissue perfusion
Vital signs
Peripheral pulses
Level of consciousness
Capillary refill
Skin (e.g., temperature, color, moisture)
Urine output
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Nursing Assessment
Brief
history
Events leading to shock
Onset and duration of symptoms
Details of care received before
hospitalization
Allergies
Vaccinations
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Nursing Diagnoses
Ineffective
tissue perfusion: Renal,
cerebral, cardiopulmonary,
gastrointestinal, hepatic, and
peripheral
Fear
Potential complication: Organ
ischemia/dysfunction
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Planning
Goals
for patient
Assurance of adequate tissue perfusion
Restoration of normal or baseline BP
Return/recovery of organ function
Avoidance of complications from
prolonged states of hypoperfusion
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Nursing Implementation
Health
Promotion
Identify patients at risk (e.g., elderly
patients, those with debilitating illnesses
or who are immunocompromised,
surgical or accidental trauma patients)
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Nursing Implementation
Health
Promotion
Planning to prevent shock
(e.g., monitoring fluid balance to prevent
hypovolemic shock, maintenance of
handwashing to prevent spread of
infection)
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Nursing Implementation
Acute
Interventions
Monitor the patient’s ongoing physical
and emotional status to detect subtle
changes in the patient’s condition
Plan and implement nursing
interventions and therapy
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Nursing Implementation
Acute
Interventions
Evaluate the patient’s response to
therapy
Provide emotional support to the
patient and family
Collaborate with other members of
the health team when warranted
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Nursing Implementation
Neurologic status: Orientation and level of
consciousness
Cardiac status
Continuous ECG
VS, capillary refill
Hemodynamic parameters: central
venous pressure, PA pressures, CO,
PAWP
Heart sounds: Murmurs, S3, S4
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Nursing Implementation
Respiratory status
Respiratory rate and rhythm
Breath sounds
Continuous pulse oximetry
Arterial blood gases
Most patients will be intubated and
mechanically ventilated
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Nursing Implementation
Urine
output
Tympanic or pulmonary arterial
temperature
Skin: Temperature, pallor, flushing,
cyanosis, diaphoresis, piloerection
Bowel sounds
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Nursing Implementation
Nasogastric
drainage/stools for occult
blood
I&O, fluid and electrolyte balance
Oral care/hygiene based on O2
requirements
Passive/active range of motion
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Nursing Implementation
Assess
level of anxiety and fear
Medication PRN
Talk to patient
Visit from clergy
Family involvement
Comfort measures
Privacy
Call light within reach
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Evaluation
Normal or baseline, ECG, BP, CVP, and
PAWP
Normal temperature
Warm, dry skin
Urinary output >0.5 ml/kg/hr
Normal RR and SaO2 ≥90%
Verbalization of fears, anxiety
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