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SIRS
 Systemic inflammatory response syndrome (SIRS)-
systemic inflammatory response to a variety of insults
 Generalized inflammation in organs remote from initial
insult
 Triggers
 Mechanical tissue trauma: burns, crush injuries, surgical procedures
 Abscess formation: intra-abdominal, extremities
 Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
 Microbial invasion: Bacteria, viruses, fungi
 Endotoxin release: Gram-negative bacteria
 Global perfusion deficits: Post–cardiac resuscitation, shock states
 Regional perfusion deficits: Distal perfusion deficits
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MODS
 Multiple organ dysfunction syndrome (MODS)-
failure of two or more organ systems
 Homeostasis cannot be maintained without
intervention-Results from SIRS
 SIRS and MODS represent ends of a continuum
 Transition from SIRS to MODS DOES NOT occur in
a clear-cut manner
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Relationship Shock, Sirs & Mods
SIRS and MODS
 Consequences of inflammatory
response
 Release of mediators
 Direct damage to endothelium
 Hypermetabolism
 Vasodilation leading to dec SVR
 Inc in vascular permeability
 Activation of coagulation cascade
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SIRS and MODS
Pathophysiology
 Organ and metabolic dysfunction
 Hypotension
 Decreased perfusion
 Formation of microemboli
 Redistribution or shunting of blood
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SIRS and MODS
Pathophysiology
 Respiratory system
 Alveolar edema
 Decrease in surfactant
 Increase in shunt
 V/Q mismatch
 End result: ARDS
 Cardiovascular system
 Myocardial depression and
massive vasodilation
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SIRS and MODS
Pathophysiology
 Renal system
 Acute renal failure

Hypoperfusion

Release of mediators

Activation of renin–angiotensin– aldosterone system

Nephrotoxic drugs, especially antibiotics
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SIRS and MODS
Pathophysiology
 GI system
 Motility decreased: Abdominal distention and paralytic ileus
 Decreased perfusion: Risk for ulceration and GI bleeding
 Potential for bacterial translocation
 Hypermetabolic state
 Hyperglycemia–hypoglycemia
 Insulin resistance
 Catabolic state
 Liver dysfunction
 Lactic acidosis

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SIRS and MODS
Pathophysiology
 Hematologic system
 DIC
 Electrolyte imbalances
 Metabolic acidosis
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SIRS and MODS
Collaborative Care
 Prognosis for MODS poor
 Goal: Prevent progression of SIRS to MODS
 Vigilant assessment-ongoing monitoring to detect early
signs of deterioration or organ dysfunction-critical
 Prevention and treatment of infection
 Aggressive infection control strategies to dec risk for
nosocomial infections
 Once an infection suspected, institute interventions to
control source !~
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SIRS and MODS- Collaborative Care
 Maintain tissue oxygenation
 Dec O2 demand
 Sedation
 Mechanical ventilation
 Paralysis
 Analgesia
 Optimize O2 delivery


Maintain normal hemoglobin level
Maintain normal PaO2

Individualize tidal volumes with PEEP
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SIRS and MODS- Collaborative Care
 Maintenance of tissue oxygenation
 Enhance CO
 Inc
preload or myocardial contractility
 Reduce afterload
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SIRS and MODS- Collaborative Care
 Nutritional and metabolic needs
 Goal of nutritional support: Preserve
organ function-total energy expenditureoften inc 1.5 to 2.0 times
 Nutritional and metabolic needs
 Use of enteral route preferred to parenteral nutrition
 Monitor plasma transferrin & prealbumin levels to

assess hepatic protein synthesis
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SIRS and MODS- Collaborative Care
 Support of failing organs
 ARDS: Aggressive O2 therapy and mechanical ventilation
 DIC: Appropriate blood products
 Renal failure: Continuous renal replacement therapy or
dialysis
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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
 Cardiogenic
 Hypovolemic
 Distributive
 Obstructive
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Low Blood Flow- Cardiogenic Shock
 Definition
 Systolic or diastolic dysfunction
 Compromised cardiac output (CO)
 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. 67-1. Relationship of shock, systemic inflammatory response syndrome, and multiple
organ dysfunction syndrome. CNS, Central nervous system.
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Low Blood Flow-Cardiogenic Shock
 Early manifestations
 Tachycardia; Hypotension
 Narrowed pulse pressure
 ↑ myocardial O2 consumption
 Physical examination
 Tachypnea, pulmonary congestion
 Pallor; cool, clammy skin
 Dec capillary refill time
 Anxiety, confusion, agitation
 ↑ in pulmonary artery wedge pressure
 Dec 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
 Relative hypovolemia
 Results when fluid volume moves out of vascular space
into extravascular space (e.g., interstitial or intracavitary
space)
 Termed third spacing
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Pathophysiology of Hypovolemic Shock
Response to acute volume loss depends
on:
•Extent of injury or insult
•Age
•General state of health
Fig. 67-3. The pathophysiology of hypovolemic shock.
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Low Blood Flow
Hypovolemic Shock
 Clinical manifestations
 Anxiety
 Tachypnea
 Inc in CO, heart rate
 Dec in stroke volume, PAWP, urinary output
 If loss is >30%, blood volume is replaced.
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Distributive Shock
Neurogenic Shock
 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
 Can occur in response to
spinal anesthesia
 Results in massive
vasodilation > lead to pooling
of blood in vessels
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Distributive Shock-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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Distributive Shock-Anaphylactic Shock
 Acute, life-threatening hypersensitivity reaction
 Massive vasodilation; Release of mediators
 ↑ capillary permeability
 Clinical manifestations
 Anxiety, confusion, dizziness
 Sense of impending doom; Chest pain
 Incontinence
 Swelling of the lips and tongue, angioedema
 Wheezing, stridor; Flushing, pruritus, urticaria
 Respiratory distress and circulatory failure
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Distributive Shock-Septic Shock
 Sepsis: systemic inflammatory
response to documented or
suspected infection
 Severe sepsis = Sepsis + Organ
dysfunction
 Presence of sepsis with
hypotension despite fluid
resuscitation
 Presence of tissue perfusion
abnormalities
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Distributive Shock-Septic Shock
 Clinical manifestations
 ↑ coagulation and inflammation
 ↓ fibrinolysis
Formation of microthrombi
 Obstruction of microvasculature
Hyperdynamic state: inc CO and dec SVR
Tachypnea/hyperventilation
Temperature dysregulation
↓ urine output
Altered neurologic status
GI dysfunction
Respiratory failure common.








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Obstructive Shock
 Develops when physical obstruction to blood flow
occurs with dec CO
 From restriction to diastolic filling of right ventricle
due to compression
 Abdominal compartment syndrome
 Patient experience
 Dec CO
 Inc afterload
 Variable left ventricular filling pressures
 Rapid assessment and immediate treatment
important
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Stages of Shock
Initial Stage
 Usually not clinically apparent
 Metabolism changes from aerobic to anaerobic.
 Lactic acid accumulates -must be removed by blood and
broken down by liver.
 Process requires unavailable O2.
 Clinically apparent –Neural, Hormonal &Biochemical
compensatory mechanisms
 Attempts aimed to overcome consequences of
anaerobic metabolism and maintaining homeostasis.
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Compensatory Stage of Shock
•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
•Impaired GI motility- Risk for paralytic
ileus
•Cool, clammy skin from blood
Except septic patient who is warm
and flushed
Fig. 67-7. Compensatory stage: reversible stage during which compensatory mechanisms are
effective and homeostasis is maintained.
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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 myocardial O2 demands.
 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 (MODS)
 Hallmarks -↓ cellular perfusion &
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
 Movement of fluid from pulmonary vasculature to
interstitium



Pulmonary edema
Bronchoconstriction
↓ residual capacity
 Fluid moves into alveoli




Edema-Dec surfactant
Worsening V/Q mismatch
Tachypnea, Crackles
Inc work of breathing
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Stages of Shock-Progressive Stage
 CO begins to fall




Dec peripheral perfusion
Hypotension
Weak peripheral pulses
Ischemia of distal extremities
 Myocardial dysfunction results in



Dysrhythmias
Ischemia; Myocardial infarction
End result: complete deterioration of cardiovascular system
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Stages of Shock-Progressive Stage
 Liver fails to metabolize drugs and waste.



Jaundice; Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
 Mucosal barrier of GI system becomes ischemic




Ulcers
Bleeding
Risk of translocation of bacteria
Dec ability to absorb nutrients
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Stages of Shock--Irreversible Stage
 Exacerbation of anaerobic
metabolism
 Accumulation of lactic acid
 ↑ capillary permeability
 Profound hypotension and
hypoxemia
 Tachycardia worsens.
 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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Collaborative Care
 Successful management includes
 Identification of patients at risk for shock
 Integration of patient’s history, physical examination,
and clinical findings to establish diagnosis
 Interventions to control or eliminate cause of dec
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.
 Cornerstone of therapy for septic, hypovolemic, and
anaphylactic shock = Volume expansion
 Isotonic crystalloids (e.g., normal saline) for initial
resuscitation of shock
 Volume expansion
 If patient does not respond to 2 to 3 L of crystalloids,
blood administration & 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., norepinephrine)


Achieve/maintain MAP >60 to 65 mm Hg.
Reserved for patients unresponsive to fluid resuscitation
 Vasodilator therapy (e.g., nitroglycerin, nitroprusside)

Achieve/maintain MAP >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 caloric
requirements
 Monitor protein, nitrogen balance, BUN, glucose,
electrolytes
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Collaborative Care-Cardiogenic Shock
 Restore blood flow to myocardium by restoring
balance between O2 supply and demand.
 Thrombolytic therapy
 Angioplasty with stenting
 Emergency revascularization
 Valve replacement
 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 loss of fluid and
restoring 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 to restore perfusion

Hemodynamic monitoring
 Vasopressor drug therapy
 Vasopressin for patients refractory to vasopressor
therapy
 IV corticosteroids for patients who require vasopressor
therapy, despite fluid resuscitation, to maintain
adequate BP
 Antibiotics after cultures obtained (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 hypotension and bradycardia with
vasopressors and atropine
 Fluids used cautiously as hypotension generally is not
related to fluid loss
 Monitor for hypothermia.
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Collaborative Care-Anaphylactic Shock
 Epinephrine, diphenhydramine
 Maintaining patent airway


Nebulized bronchodilators
Endotracheal intubation or cricothyroidotomy may be
necessary.
 Aggressive fluid replacement
 Intravenous corticosteroids if significant hypotension
persists after 1 to 2 hours of aggressive therapy
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Collaborative Care
Obstructive Shock
 Early recognition and treatment is primary strategy.
 Mechanical decompression
 Radiation or removal of mass
 Decompressive laparotomy
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Nursing Assessment
 ABCs: airway, breathing, and circulation
 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, GI, hepatic, and peripheral
 Fear
 Potential complication: organ ischemia/dysfunction
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
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Nursing Implementation
 Health promotion
 Identify patients at risk.




Elderly patients
Those with debilitating illness
Those who are immunocompromised
Surgical or accidental trauma patients
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Nursing Implementation
 Health promotion (cont’d)
 Planning to prevent shock


Monitoring fluid balance to prevent hypovolemic shock
Maintenance of hand washing 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 patient and family.
 Collaborate with other members of 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
 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
 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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Audience Response Question
When assessing a patient in shock, the nurse recognizes that
the hemodynamics of shock include:
1. Normal cardiac output in cardiogenic shock.
2. Increase in central venous pressure in hypovolemic shock.
3. Increase in systemic vascular resistance in all types of
shock.
4. Variations in cardiac output and decreased systemic
vascular resistance in septic shock.
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Audience Response Question
The nurse determines that the patient in shock has
progressed beyond the compensated stage when laboratory
tests reveal:
1. Increased blood glucose levels.
2. Increased serum sodium levels.
3. Increased serum potassium levels.
4. Increased serum calcium levels.
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65
Case Study
 26-year-old man arrives via paramedics to ED with
multiple gun shot wounds to abdomen.
 Unresponsive, BP 58/30, HR 146
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Case Study
 Three units type O packed RBC given for profuse
blood loss before surgery
 Surgery successful in removing bullets and repairing
blood vessels
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Case Study
 Surgeon estimated he lost at least
3 L of blood before surgery and 1 L more during surgery.
 He is admitted to ICU.
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Discussion Questions
1.
What complications will you anticipate with this
amount of blood loss?
2. What fluids can you expect to administer?
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Discussion Questions
3.
What medications will likely be ordered?
4.
What should you monitor hourly or every 2 hr?
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