Transcript Shock

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Syndrome characterized by decreased tissue
perfusion and impaired cellular metabolism
 Imbalance in supply/demand for O2 and nutrients
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Classification of shock
 Cardiogenic
 Hypovolemic
 Distributive
 Obstructive
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Preload
 Right atrial pressure (RAP) or centrol venous pressure (CVP) = _____________
 Pulmonary artery wedge pressure (PAWP)or left atrial pressure (LAP)=________
 Pulmomary diastolic pressure (PADP)= _________________________________
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Afterload
 Systemic vascular resistance (SVR)= (MAP –CVP) X 8O
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8O
 Mean arterial pressure (MAP)= Systolic BP + 2 (Diastolic BP) =_________
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Nursing Management: Shock and
Multiple Organ Dysfunction Syndrome
Sirs > MODS
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Fig. 67-1. Relationship of shock, systemic inflammatory response syndrome, and multiple
organ dysfunction syndrome. CNS, Central nervous system.
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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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Early manifestations
 Tachycardia
 Hypotension
 Narrowed pulse pressure
 ↑ myocardial O2 consumption
Person in
cardiogenic shock
 What would you expect to see on physical exam?
 What about PAWP? Low or high?
 Urinary output?
 What lab studies helpful?
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Clinical Manifestations:
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Increased SVR, CVP, and PAWP
Pulmonary congestion
Cyanosis
Cool, clammy skin
Confusion/ agitation
Decreased capillary refill time
Initially, what clinical condition does this sound
similar to?
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Restore blood flow to the myocardium by restoring the
balance between O2 supply and demand.
Thrombolytic therapy ; Angioplasty with stenting
Emergency revascularization
Valve replacement
Circulatory assist devices (e.g., intraaortic balloon pump,
ventricular assist device
 Hemodynamic monitoring PAWP
 Intraaortic balloon pump (IABP) IABP
 Ventricular assist device VAD video
 Transplant (rarely
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 Drug therapy (e.g., diuretics to
reduce preload); Medications
(depends on cause cause):
▪
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▪
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Aspirin
heparin
Dopamine
Norepinephrine
dobutamine
Diuretics
Vasodilators
Amiodarone
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Absolute hypovolemia: loss of intravascular fluid volume
 Hemorrhage
 GI loss (e.g., vomiting, diarrhea)
 Fistula drainage
 Diabetes insipidus
 Hyperglycemia
 Diuresis
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Relative hypovolemia
 Results when fluid volume moves out of the vascular space into
extravascular space (e.g., interstitial or intracavitary space)
 Also known as _________
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Fig. 67-3. The pathophysiology of hypovolemic shock.
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Response to acute volume loss depends on
 Extent of injury or insult
 Age
 General state of health
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Clinical manifestations
 What signs/symptoms? _______, _______
 ________in CO, _____ heart rate
 Inc or decrease in stroke volume, PAWP, urinary output
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If loss is >30%, blood volume is replaced.
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1)
What is often the priority in the treatment of
hypovolemic shock?
2)
How might you recognize the development
of hypovolemic shock?
3)
What would you do about it?
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Lab/ Diagnostic Tests:
 Find the source of blood loss
▪ CT, ultrasound, surgery
 CBC, electrolytes, blood gases, lactate level
 SpO2
 Hourly urine output monitoring
Treatment Stop source of fluid loss
 Restore circulating volume
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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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Neurogenic- hemodynamic phenomenon
associated with spinal cord injury at T5 or
above; anesthesia
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Anaphylactic-hypersensitivity reaction
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Septic-systemic inflammatory reaction
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 Hemodynamic phenomenon occuring after spinal
injury at T5 or above
 Usually within 30 minutes of injury, can last up to
6 weeks
 Causes massive vasodilation without
compensation secondary to the loss of
sympathetic nervous system vasoconstrictor tone
 Can also be caused by spinal anesthesia
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Clinical manifestations Bradycardia (from unopposed parasympathetic stimulation)
 Hypotension (from massive vasodilation) (dec BP, MAP)
Hypothermia (due to heat loss)
▪ Initially, skin may be warm due to vasodilation
▪ Later, skin may be cool, depending on ambient temperature
 Bladder dysfunction
 Paralysis below level of lesion
 Bowel dysfunction
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Clinical manifestations
 Temperature dysregulation (resulting in heat loss)
 Dry skin
 Poikilothermia (taking on the temperature of the
environment)
 WHY?
 Late- skin cool and pale
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Fig. 67-4. The pathophysiology of neurogenic shock. BP, Blood pressure.
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Treatment Depends on the cause
 If spinal cord injury, promote spinal stability
 Vasopressors and atropine for hypotension and
bradycardia (respectively)
 Fluids administered cautiously
 Monitor for hypothermia
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Treatment If spinal cord injury, promote spinal stability
 Vasopressors and atropine for hypotension and
bradycardia (respectively)
 Fluids administered cautiously
 Monitor for hypothermia
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 Acute and life-threatening allergic reaction
(hypersensitivity) reaction
 Can be caused by drugs, chemicals, vaccines, food insect
venom
 Causes massive vasodilation, release of vasoactive
mediators, and an increase in capillary permeability
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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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Epinephrine, diphenhydramine-block massive release of
histamine
Maintaining a patent airway
▪ Nebulized bronchodilators
▪ Intubation or cricothyroidotomy (video) maybe needed
Aggressive fluid replacement
IV corticosteroids if significant hypotension after 1 to 2 hours of
aggressive therapy
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From Seton. Educational use only.
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What are you worried about with a
medication reaction?
What are you watching for?
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Sepsis: systemic inflammatory response to documented or
suspected infection (SIRS)
Severe sepsis = Sepsis + Organ dysfunction
 Presence of sepsis with hypotension despite fluid resuscitation
 Presence of tissue perfusion abnormalities
•*Over 750,000 clients diagnosed with severe sepsis annually and 28%
to 50% die
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Course Septicemia (initially bacteremia) causes
inflammatory cascade
 Main organisms > sepsis are gram-negative and
gram-positive bacteria also parasites, fungi, and
viruses > sepsis and septic shock.
 If gram positive infection (Staphylococcus and
streptococcus), up to 50% mortality rate
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Clinical manifestations
 ↑ Coagulation and inflammation
 ↓ Fibrinolysis > DIC
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▪ formation of microthrombi
▪ obstruction of microvasculature
Hyperdynamic state: inc CO and dec SVR
Tachypnea/hyperventilation
Temperature dysregulation *Warm shock > cold shock
↓ urine output; GI dysfunction
Altered neurologic status
Respiratory failure is common (ARDS)
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Fig. 67-5. The pathophysiology of septic shock. CNS, Central nervous system.
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Hemorrhagic Rash
DIC
Aftermath septic shock
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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>maintain adequate BP
Antibiotics after cultures obtained (e.g., blood, wound etc)
Drotrecogin alfa (Xigris) *not used ;major side effect: bleeding
Glucose less than 150
Stress ulcer prophylaxis with H2- receptor blockers and DVT
prophylaxis
**Question- when to give pressors in septic shock
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From Seton. Educational use only.
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Develops when physical obstruction to blood flow occurs
with dec CO
 Restriction to diastolic filling of right ventricle due to
compression
 Abdominal compartment syndrome
Patient will have
 Dec CO
PE
 Inc afterload
 Variable left ventricular filling pressures
**Rapid assessment/immediate treatment critical
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*Fix the underlying problem is primary treatment
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Early recognition and treatment is primary
strategy.
Mechanical decompression
Radiation or removal of mass
Decompressive laparotomy
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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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Identify cause
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CBC
BMP
Arterial blood gases
Blood cultures
Cardiac enzymes (cardiogenic shock)
Glucose
DIC (Disseminated Intravascular Coagulation) screen:
FSP, fibrogen level, platelet count, PTT and PT/INR, and
D-dimer
Lactic Acid
Liver enzymes- ALT, AST, GGT
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Electrolytes Sodium level increased early, decreased later if
hypotonic fluid administered
 *Potassium decreased in early shock, then
increased later with cellular breakdown and renal
failure
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DIC (Disseminated Intravascular Coagulation)
screen: FSP, fibrogen level, platelet count, PTT and
PT/INR, and D-dimer
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Decreased cardiac output
Fluid volume deficit
Anxiety
Fear
LVAD implantation (23 minutes into clip
Ineffective tissue perfusion: renal, cerebral,
cardiopulmonary, gastrointestinal, hepatic, and
peripheral
 Potential complication: organ ischemia/dysfunction
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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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Clinically apparent
 Neural
 Hormonal
 Biochemical compensatory mechanisms
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Attempts are aimed at overcoming
consequences of anaerobic metabolism and
maintaining homeostasis.
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Compensatory Shock Mean Arterial Pressure (MAP)
 blood pressure (but adequate to perfuse vital organs)
 cardiac output
Sympathetic nervous system (SNS) stimulation >
vasoconstriction. Blood flow to heart and brain
maintained; blood flow to kidneys, GI tract, skin, and
lungs diverted
 Dec blood flow to kidneys > activation of reninangiotensin system > sodium retention and potassium
excretion
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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
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Shunting blood from lungs inc physiologic dead space.
▪ ↓ arterial O2 levels
▪ Inc. rate/depth of respirations
▪ V/Q mismatch
SNS stimulation inc 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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Fig. 67-7. Compensatory stage: reversible stage during which compensatory mechanisms are
effective and homeostasis is maintained.
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Begins when compensatory mechanisms fail
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Aggressive interventions to prevent multiple
organ dysfunction syndrome
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**Hallmarks of ↓ cellular perfusion and
altered capillary permeability
▪ Leakage of protein into interstitial space
▪ ↑ systemic interstitial edema
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Altered capillary permeability (3rd spacing)
Alveolar and pulmonary edema, ARDS,  PA pressures
 cardiac output,  coronary perfusion> arrhythmias & MI
Movement of fluid from pulmonary vasculature to interstitium
>pulmonary edema
▪ Bronchoconstriction & dec residual capacity
Fluid moves into alveoli >Edema, dec surfactant inc V/Q mismatch
▪ Tachypnea; Crackles; inc work of breathing
Acute tubular necrosis
Jaundice,  ALT,AST GGT
DIC
Cold, clammy skin
Anasarca
▪ Fluid leakage affects solid organs and peripheral tissues.
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Mucosal barrier of GI system becomes ischemic
▪ Ulcers
▪ Bleeding
▪ Risk of translocation of bacteria
▪ Decreased ability to absorb nutrients
Liver fails to metabolize drugs and waste.
▪ Jaundice
▪ Elevated enzymes
▪ Loss of immune function
▪ Risk for DIC and significant bleeding
 Lactic acidosis
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Fig. 67-8. Progressive stage: compensatory mechanisms are becoming ineffective and
fail to maintain perfusion to vital organs.
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Exacerbation of anaerobic metabolism
 Accumulation of lactic acid
 ↑ capillary permeability
 Profound hypotension and hypoxemia
 Tachycardia worsens.
 Failure one organ system affects others.
 Recovery unlikely
 Respiratory failure
 Unresponsive
 Anuria
 DIC
 hypothermia
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Fig. 67-9. Irreversible or refractory stage: compensatory mechanisms are not functioning or are
totally ineffective, leading to multiple organ dysfunction syndrome.
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Successful management includes
 Identification of patients at risk for shock
 Integration of patient’s history, physical
examination, and clinical findings > 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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General management strategies
 Ensure patent airway.
 Maximize oxygen delivery.
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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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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
Primary goal of drug therapy = Correction dec tissue perfusion
 Vasopressor drugs (e.g., norepinephrine)
▪ Achieve/maintain MAP >60 to 65 mm Hg.
▪ Reserved for patients unresponsive to fluid resuscitation
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*Nutrition vital to dec morbidity from shock.
 Initiate enteral nutrition within 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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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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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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Health promotion
 Identify patients at risk.
▪ Elderly patients
▪ Those with debilitating illness
▪ Those who are immunocompromised
▪ Surgical or accidental trauma patients
Focused assessment of tissue perfusion
 Vital signs; Peripheral pulses; Level of consciousness
 Capillary refill; Skin (e.g., temperature, color, moisture)
 Urine output
 Planning to prevent shock
▪ Monitoring fluid balance to prevent hypovolemic shock
▪ Maintenance of hand washing to prevent spread of infection
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Acute interventions
 Monitor patient’s ongoing physical/emotional status to detect subtle
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changes in patient’s condition.
 Plan/implement nursing interventions and therapy.
 Evaluate patient’s response to therapy.
 Provide emotional support to patient and family.
 Collaborate with members of health team when warranted
Respiratory status
 Respiratory rate and rhythm; Breath sounds
 Continuous pulse oximetry ; Arterial blood gases
 Most patients -intubated and mechanically ventilated.
Urine output
Tympanic or pulmonary arterial temperature
Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
Bowel sounds
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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
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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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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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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Systemic Inflammatory Response Syndrome (SIRS)- a
systemic inflammatory response to a variety of
insults, including infection, ischemia, infarction, and
injury
 Characterized by generalized inflammation of organs
 Two or more of the following conditions: temperature
>38.5°C (101.3 F) or <35.0°C (95.0 F); heart rate of >90
beats/min; respiratory rate of >20 breaths/min or PaCO2
of <32 mm Hg; and WBC count of >12,000 cells/mL, <4000
cells/mL, or >10 percent immature (band) forms
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 Results from SIRS
 Characterized by failure of two or more organ
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systems such that homeostasis can not be
obtained without intervention
Often culminates in ARDS
Can cause massive vasodilation and myocardial
depression
Commonly manifests as changes in LOC
Acute renal failure common
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GI tract highly vulnerable to ischemic injury
secondary to shunting in early stages
At risk for ulceration and GI bleeding
Potential for bacterial translocation from GI tract to
cirulation
Causes hypermetabolic state
Failure of coagulation system manifests as DIC
Electrolyte changes and fluid shifts
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Care of the critically ill patient
Invasive monitoring capabilities
Bedside procedures possible
2 to 1 patient to nurse ratio
Intensivists or pulmonary/ critical care
physicians and advanced practice nurses
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Post-surgical pathways often include going to ICU
Certain medications, devices, and frequency of
testing require placement in ICU
 Medications must be reconciled with any move to or
from critical care to other level of care
 Notify family members
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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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26-year-old man arrives via paramedics to ED
with multiple gun shot wounds to abdomen.
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Unresponsive, BP 58/30, HR 146
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Three units type O packed RBC given for
profuse blood loss before surgery
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Surgery successful in removing bullets and
repairing blood vessels
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Surgeon estimated he lost at least
3 L of blood before surgery and 1 L more during
surgery.
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He is admitted to ICU.
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1.
What complications will you anticipate with
this amount of blood loss?
2.
What fluids can you expect to administer?
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3.
What medications will likely be ordered?
4.
What should you monitor hourly or every 2
hr?
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A client’s nursing diagnosis is Fluid Volume Deficit
Related to Excessive Fluid Loss. Which action
related to fluid management should be delegated
to a nursing assistant?
a.
b.
c.
d.
Administer IV fluids as prescribed by the physician.
Provide straws and offer fluids between meals.
Develop plan for added fluid intake over 24 hours.
Teach family members to assist client with fluid intake.
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The client also has the nursing diagnosis
Decreased Cardiac Output related to decreased
plasma volume. Which finding on assessment
supports this diagnosis?
a.
b.
c.
d.
Flattened neck veins when client is in supine position.
Full and bounding pedal and post-tibial pulses.
Pitting edema located in feet, ankles, and calves.
Shallow respirations with crackles on auscultation.
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Which of these clients in the neurologic ICU will be
best to assign to an RN who has floated from the
medical unit?
A 26-yr-old client with a basilar skull fracture who has
clear drainage coming out of the nose.
b. A 42-yr-old client admitted several hours ago with a
headache and diagnosed with a ruptured berry
aneurysm.
c. A 46-yr-old client who was admitted 48 hours ago with
bacterial meningitis and has an antibiotic dose due.
d. A 65-yr-old client with an astrocytoma who has just
returned to the unit after having a craniotomy.
a.
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You are monitoring blood administration to a
trauma victim in shock. Which of the following
assessments indicate a dangerous transfusion
reaction?
a. Red raised areas on the skin that itch
b. An increase in body temp by 3 degrees
c. Decreasing BP and dyspnea
d. Increasing BP and pulse
86

A 17 yr old male presents to the Emergency
Department via EMS. He was riding his dirt bike on
a cross country trail when he struck a tree. He has
bruising over his right upper quadrant and is
complaining of severe pain with palpation. VS are
86/50, HR 122, RR 24 T 96.5 and his O2 sat is 94% on
room air. The patient is cool and sweaty and
appears confused.
Hypovolemic Shock
87

A listless 2 year old is rushed into the Emergency
Department in his mother’s arms. She relates he was eating
a peanut butter cookie when he began crying and rubbing
his mouth. Within seconds his lips and eyes became swollen
and he developed a raised rash over his trunk and
extremities. His breathing became labored and audible
wheezing could be heard. His mother states he has never
eaten nuts before. VS are BP 86/33 P185 R52 T 97.6 axillary
and O2 Sat 88% on room air
Distributive - Anaphylaxis
88

A 72 year old male is brought to the Emergency
Department via EMS. He sustained a 10 foot fall
from a ladder onto his back. He is awake and alert.
BP is 80/50 P 55 R 26 T 96.6 O2 sat 91% on room air
The patient complains of mid low back pain and
decreased ability to move his legs. His legs are
pink, warm and dry but you notice above his
waistline that he is pale, cool and clammy.
Distributive - Neurogenic
89

A 55 yr old diabetic female presents to the
Emergency Department complaining of
bilateral flank pain, foul smelling urine,
vomiting and chills for 3 days. She is
lethargic and her skin is pale and cool. VS are
BP 90/60 P 112 T 96.6 R22 O2 sat 93% room
air
Septic Shock
90

A 68 yr old male presents to the Emergency
Department complaining of severe midsternal chest
pain that radiates to his left arm and jaw. He
reports shortness of breath, nausea and dizziness.
He is lethargic, pale and diaphoretic with mottled
extremities. Rales are heard bilaterally upon
auscultation of his lung sounds. VS are 72/50 P 118
T 96.8 R 22 O2 sat 89% on room air
Cardiogenic Shock
91