Transcript Shock
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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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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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