Module 15: Nursing Care of the Individual Experiencing Shock/Trauma/Disaster:
Requiring Critical Care
Shock NOTES
1. Definition: Clinical syndrome characterized by decreased tissue perfusion
and impaired cellular metabolism resulting in an imbalance between the
supply and demand for oxygen and nutrients.
2. Etiology and Pathophysiology

Cardiogenic shock occurs when either systolic or diastolic
dysfunction of the pumping action of the heart results in compromised
cardiac output (CO).
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Precipitating causes of cardiogenic shock include myocardial infarction
(MI), cardiomyopathy, blunt cardiac injury, severe systemic or
pulmonary hypertension, cardiac tamponade, and myocardial
depression from metabolic problems.
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Hemodynamic profile will demonstrate an increase in the pulmonary
artery wedge pressure (PAWP) and pulmonary vascular resistance.
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Clinical manifestations of cardiogenic shock may include tachycardia,
hypotension, a narrowed pulse pressure, tachypnea, pulmonary
congestion, cyanosis, pallor, cool and clammy skin, decreased
capillary refill time, anxiety, confusion, and agitation.

Hypovolemic shock occurs when there is a loss of intravascular fluid
volume.
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Absolute hypovolemia results when fluid is lost through hemorrhage,
gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage,
diabetes insipidus, hyperglycemia, or diuresis.

Relative hypovolemia results when fluid volume moves out of the
vascular space into extravascular space (e.g., interstitial or
intracavitary space) and this is called third spacing.
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The physiologic consequences of hypovolemia include a decrease in
venous return, preload, stroke volume, and CO resulting in decreased
tissue perfusion and impaired cellular metabolism.

Clinical manifestations depend on the extent of injury or insult, age,
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and general state of health and may include anxiety; an increase in
heart rate, CO, and respiratory rate and depth; and a decrease in
stroke volume, PAWP, and urine output.

Neurogenic shock is a 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, or in response to spinal
anesthesia.

Clinical manifestations include hypotension, bradycardia, temperature
dysregulation (resulting in heat loss), dry skin, and poikilothermia
(taking on the temperature of the environment).

Anaphylactic shock is an acute and life-threatening hypersensitivity
(allergic) reaction to a sensitizing substance (e.g., drug, chemical,
vaccine, food, insect venom).

Immediate reaction causes massive vasodilation, release of vasoactive
mediators, and an increase in capillary permeability resulting in fluid
leaks from the vascular space into the interstitial space.

Clinical manifestations can include anxiety, confusion, dizziness, chest
pain, incontinence, swelling of the lips and tongue, wheezing, stridor,
flushing, pruritus, urticaria, and angioedema.

Sepsis is a systemic inflammatory response to a documented or
suspected infection. Severe sepsis is sepsis complicated by organ
dysfunction.

Septic shock is the presence of sepsis with hypotension despite fluid
resuscitation along with the presence of tissue perfusion abnormalities.

In severe sepsis and septic shock, the initiated body response to an
antigen is exaggerated resulting in an increase in inflammation and
coagulation, and a decrease in fibrinolysis.

Endotoxins from the microorganism cell wall stimulate the release of
cytokines and other proinflammatory mediators that act through
secondary mediators such as platelet-activating factor.
o Platelet-activating factor results in the formation of microthrombi
and obstruction of the microvasculature resulting in damage to the
endothelium, vasodilation, increased capillary permeability,
neutrophil and platelet aggregation, and adhesion to the
endothelium.

Clinical presentation for sepsis is complex and no single or group of
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symptoms are specific to the diagnosis.
o Patients will usually experience a hyperdynamic state characterized
by increased CO and decreased SVR.
o Persistence of a high CO and a low SVR beyond 24 hours is
ominous and often associated with hypotension and multiple organ
dysfunction syndrome (MODS).
o Initially patients will hyperventilate as a compensatory mechanism,
resulting in respiratory alkalosis followed by respiratory acidosis
and respiratory failure.
o Other clinical signs include alteration in neurologic status,
decreased urine output, and GI dysfunction.
3. Diagnostic tests for clients in shock p. 1775 table 67-3
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Blood: RBC, hemoglobin and hematocrit
Arterial Blood Gases: respiratory alkalosis and metabolic acidosis
Electrolytes (Na level increased early, decreased later if hypotonic fluid
given) K dec, later inc. K with cellular breakdown and renal failure
BUN and creatinine increased , specific gravity increased then fixed at
1.010
Blood cultures: identify causative organism in septic shock; treat
Cardiac enzymes: diagnosis of cardiogenic shock
Glucose- increased early then decreased
DIC screen: FSP, fibrinogen level, platelet count, PTT and PT,
thrombin time and d-dimer
Lactic acid- increased
Liver enzymes, ALT, AST and GGT increased
4. Common Nursing Diagnoses
 Decreased Cardiac Output
 Altered Tissue Perfusion
 Fluid volume deficit
 Anxiety
 Fear
5. Stages of Shock
1) Compensatory Shock (p. 1779)
a) MAP below normal levels
b) Decrease in circulating blood volume
c) Sympathetic nervous system stimulated; release
catecholamines (epinephrine and norepinephrine);
bronchodilation and increased cardiac output occurs. To
maintain blood pressure: inc. heart rate and contractility; inc. in
peripheral vasoconstriction due to stimulation of beta adrenergic
fibers (cause vasoconstriction of blood vessels of skin and
abdominal viscera) and inc. in heart rate and contractility
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d) Renin-angiotensin release of aldosterone- reabsorb H2O and
sodium; Get fluid shift from interstitial to capillaries due to
decrease in hydrostatic pressure in capillaries
e) Shunting blood from the lungs- ventilation- perfusion mismatchincreased RR
f) Circulation maintained, but only sustained short time without
harm to tissues; must treat underlying cause of shock; will
progress to next stage
2) Progressive shock
a) Altered capillary permeability (3rd spacing)
b) In the lungs- alveolar or pulmonary edema- ARDS, increased
PA pressures
c) Cardiac output decreases and coronary perfusion is decreased.
Decreased myocardial perfusion-arrhythmias and myocardial
ischemia- even MI
d) Kidneys- ATN- worsened by nephrotoxic drugs- elevated BUN
and Creatinine
e) Metabolic acidosis- anaerobic metabolism and kidneys can’t
excrete acids and reabsorb bicarbonate
f) GI- ischemia causes ulcers and GI bleed
g) Liver- can’t eliminate waste products- elevated NH3 and lactate,
bilirubin (jaundice) Bacteria released in bloodstream.
h) Hematologic- DIC3) Refractory shock (also called MODS…multiple organ
dysfunction> death)
a) Anaerobic metabolism- Lactic acid build-up
b) Increased capillary blood leak- worsens hypotension and
tachycardia, also get cerebral ischemia.
c) **Get profound hypotension and hypoxemia
d) Cellular death leads > tissue death > vital organs fail and death
occurs (lungs, liver and kidneys result in accumulation of waste
products. One organ failure leads to another.
e) Recovery unlikely
6. Common Manifestation/Complications
a) Effects of Shock on Body Systems (See text p. 1781 Multsystem
effects of Shock)

Cardiovascular/hematologic
1) Initially: slight tachycardia, normal blood pressure
2) Progresses to weak, rapid pulse with dysrhythmias
3) Progressive dec. in systolic and diastolic blood pressures with
narrowing of pulse pressure; blood pressure > inaudible
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4) DIC [disseminated intravascular coagulation
Respiratory
1) Initially: inc. respiratory rate
2) Gas exchange impaired >leads to anaerobic metabolism and
acidosis
3) Acute Respiratory Distress Syndrome (ARDS):
Gastrointestinal and Hepatic
1) GI organs > ischemic, with blood circulation shunted to heart
and brain > Stress Ulcers and Paralytic Ileus
2) Altered liver metabolism: initially glucose made available, then
hypoglycemia toxic materials; anoxic liver does not detoxify.
Neurologic
1) Develops cerebral hypoxia (cerebral edema due to hypoxia)
2) Restlessness initially > altered level of consciousness, lethargy,
coma
Renal:
1) Dec. kidney perfusion - oliguria to anuria (develop ATN)
elevated BUN and Creat, inc. renin, inc. aldosterone, inc. ADH,
2) metabolic acidosis
Skin,
1) temperature cool, warm and flushed early septic shock, thirst;
2) Skin: cool to cold, pale, and clammy
3) later stage mottled and cyanotic
b) Types of Shock
 Low Blood Flow Shock
1) Cardiogenic- when either diastolic or systolic dysfunction of the
pumping action of the heart results in dec. cardiac output and
adequate tissue perfusion
i. Common causes: MI, cardiomyopathy, cardiac trauma,
severe systemic or pulmonary hypertension, myocardial
depression from metabolic problems. Diastolic
dysfunction is caused by cardiac tamponade and
cardiomyopathy.
ii. Mortality rate 50-85%
iii. Leads to left and right sided heart failure
iv. Manifestations
a) Tachycardia, hypotension, and a narrowed pulse pressure.
b) Elevated SVR and increased O2 demand
c) Tachypnea and crackles
d) Elevated pulmonary wedge pressure(PAWP)
e) Cyanosis, pallor, cool and clammy skin, dec. capillary refill
f) Dec. renal blood flow- Na and water retention and dec. urine
output
g) Anxiety, confusion, and agitation
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h) Diagnostics- cardiac enzymes, troponin, EKG, CXR,
echocardiaogram
2) Hypovolemic; loss of intravascular volume – Table 67-4,(Clinical
Presentation of the Major Types of Shock)
a) Absolute hypovolemia- hemorrhage, GI loss, fistula
drainage, diabetes insipidus, hyperglycemia, or diuresis.
b) Relativehypovolemia-third spacing of fluids- sepsis, burns,
liver failure(ascites), bowel obstruction, fractures
c) Manifestations- decreased preload, dec. stroke volume and
dec. cardiac output
d) Loss of up to 15%-30% of total blood volume- body
compensates- Sympathetic nervous system
e) Loss of more than 30%- body can’t compensate, need
immediate fluid replacement
f) Diagnostics- H and H, urine specific gravity, serum
electrolytes, ABG’s and lactic acid.

Maldistribution of blood flow (Vasogenic); includes several
types of shock-result in widespread vasodilatation and dec.
peripheral resistance;
1) Neurogenic Shock P.1776 Table 67-4 Clinical Presentation in
Clients in Neurogenic shock
a) Occurs within 30 minutes of spinal cord injury at T5 or above
and can last up to 6 weeks. Get dec. sympathetic control of
vasomotor responses; parasympathetic stimulation
unchecked > **sustained peripheral vasodilation and pooling
of blood.
b) Other causes- spinal anesthesia, narcotics
c) Most important clinical manifestations are: Bradycardia (from
unopposed parasympathetic) and hypotension (massive
vasodiation)
d) May have hypothermia- due to heat loss. Initially warm due
to vasodiation but later hypothermia.. Later takes on temp of
the room since can’t regulate temp (poikilothermia).
e) Early neurogenic shock: blood pools in venous & capillary
beds; skin warm and pink; pulse slow and bounding; dec.
BP; dec. temperature; have vasodilation and dec. MAP; Late
skin pale and cool and heart rate inc.
2) Anaphylactic Shock p.1776 Table 67-4
a) Acute and life-threatening allergic reaction to a sensitizing
substance
b) Substances- drugs, chemicals, vaccine, food, insect venom
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c) Immediate reaction- vasodiation, release of vasoactive
mediators and increase in capillary permeability- fluid leaks
(3rd spacing)
d) Leads to respiratory distress due to laryngeal edema or
severe bronchospasm. Also circulatory failure due to
massive vasodilation
e) Symptoms- dizziness, chest pain, incontinence, swelling of
the lips and tongue, wheezing and stridor
f) Skin changes- flushing, pruritis, and swelling
g) Feeling of impending doom
3) Septic - p. 1776, Table 67-4 Clinical Presentation of Clients with
Septic Shock)
a) Septic shock is the presence of sepsis with hypotension
despite fluid resuscitation along with the presence of
decreased tissue perfusion.
b) Common stimuli: Gram negative bacteria most often
causative agent; others (pseudomonas, E coli); Gram
positive bacterial infections (staphylococcus and
streptococcus) up to 50% mortality rate despite treatment
c) Course: Septicemia (bacteremia initially) causes the
inflammatory cascade and it is exaggerated causing
increase in inflammation and coagulation and a decrease in
fibrinolysis. This results in damage to the endothelium,
vasodilation, increased capillary permeability, and neutrophil
and platelet aggregation. blood > endotoxins disrupt
circulation > cause massive vasodilation in response to
pathogen’s release of toxins into bloodstream> normal
coagulation mechanisms altered> inflammatory response
triggered > DIC
d) Signs and symptoms-hyperdynamic with increased cardiac
output and decreased SVR
e) Respiratory failure (85%) and ARDS (40%) is also common
f) Other- decreased in level of consciousness, decreased urine
output, GI bleeding and paralytic ileus.
7. Therapeutic Interventions/Collaborative Care
Successful management of the patient in shock includes the following: (1)
identification of patients at risk for the development of shock; (2)
integration of the patient’s history, physical examination, and clinical
findings to establish a diagnosis; (3) interventions to control or eliminate
the cause of the decreased perfusion; (4) protection of target and distal
organs from dysfunction; and (5) provision of multisystem supportive care.
 General management strategies for a patient in shock begin with
ensuring that the patient has a patent airway and oxygen delivery is
optimized. The cornerstone of therapy for septic, hypovolemic, and
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anaphylactic shock is volume expansion with the administration of the
appropriate fluid.
It is generally accepted that isotonic crystalloids, such as normal
saline, are used in the initial resuscitation of shock. If the patient does
not respond to 2 to 3 L of crystalloids, blood administration and central
venous monitoring may be instituted. Two major complications of fluid
resuscitation are hypothermia and coagulopathy.

The primary goal of drug therapy for shock is the correction of
decreased tissue perfusion.
o Sympathomimetic drugs cause peripheral vasoconstriction and are
referred to as vasopressor drugs (e.g., epinephrine,
norepinephrine).
 The goals of vasopressor therapy are to achieve and maintain a
mean arterial pressure (MAP) of 60 to 65 mm Hg and the use of
these drugs is reserved for patients unresponsive to other
therapies.
o The goal of vasodilator therapy, as in vasopressor therapy, is to
maintain MAP at 60 to 65 mm Hg or greater.
 Vasodilator agents most often used are nitroglycerin (in
cardiogenic shock) and nitroprusside (in noncardiogenic shock).
Collaborative Care: Specific Measures
Cardiogenic Shock
 Overall goal is to restore blood flow to the myocardium by restoring the
balance between oxygen supply and demand.
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Definitive measures include thrombolytic therapy, angioplasty with
stenting, emergency revascularization, and valve replacement.
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Care involves hemodynamic monitoring, drug therapy (e.g., diuretics to
reduce preload), and use of circulatory assist devices (e.g., intraaortic
balloon pump, ventricular assist device).
Hypovolemic Shock
 The underlying principles of managing patients with hypovolemic shock
focus on stopping the loss of fluid and restoring the circulating volume.
o 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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Septic Shock
 Patients in septic shock require large amounts of fluid replacement,
sometimes as much as 6 to 10 L of isotonic crystalloids and 2 to 4 L of
colloids, to restore perfusion.
o Hemodynamic monitoring and arterial pressure monitoring are often
necessary.
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Vasopressor drug therapy may be added and vasopressin may be given
to patients refractory to vasopressor therapy.
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Intravenous corticosteroids are recommended for patients who require
vasopressor therapy, despite fluid resuscitation, to maintain adequate BP.
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Antibiotics are early component of therapy and are started after obtaining
cultures (e.g., blood, wound exudate, urine, stool, sputum).

Drotrecogin alpha (Xigris), a recombinant form of activated protein C, has
demonstrated promise in treating patients with severe sepsis. Bleeding is
the most common serious adverse effect.
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Glucose levels should be maintained at less than 150 mg/dl.
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Stress ulcer prophylaxis with histamine (H2)-receptor blockers and deep
vein thrombosis prophylaxis with low dose unfractionated heparin or low
molecular weight heparin are recommended.
Neurogenic Shock
 Treatment of neurogenic shock is dependent on the cause.
o In spinal cord injury, general measures to promote spinal stability are
initially used.
o Definitive treatment of the hypotension and bradycardia involves the
use of vasopressors and atropine respectively.
o Fluids are administered cautiously as the cause of the hypotension is
generally not related to fluid loss.
o The patient is monitored for hypothermia.
Anaphylactic Shock
 Epinephrine is the drug of choice to treat anaphylactic shock.
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Diphenhydramine is administered to block the massive release of
histamine.
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Maintaining a patent airway is critical and the use of nebulized
bronchodilators is highly effective.
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Endotracheal intubation or cricothyroidotomy may be necessary.
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Aggressive fluid replacement, predominantly with colloids, is necessary.
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Intravenous corticosteroids may be helpful in anaphylactic shock if
significant hypotension persists after 1 to 2 hours of aggressive therapy.
Nursing Management: Shock
Nursing Assessment
 The initial assessment is geared toward the ABCs: airway, breathing, and
circulation.
 Further assessment focuses on the assessment of tissue perfusion and
includes evaluation of vital signs, peripheral pulses, level of
consciousness, capillary refill, skin (e.g., temperature, color, moisture),
and urine output.
Planning
 The overall goals for a patient in shock include (1) assurance of adequate
tissue perfusion, (2) restoration of normal BP, (3) return/recovery of organ
function, and (4) avoidance of complications from prolonged states of
hypoperfusion.
Nursing Implementation
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Health Promotion
o To prevent shock, the nurse needs to identify patients at risk (e.g.,
patients who are older, those with debilitating illnesses, those who are
immunocompromised, surgical or accidental trauma patients).
o Planning is essential to help prevent shock after a susceptible
individual has been identified (e.g., monitoring fluid balance to prevent
hypovolemic shock, maintenance of hand washing to prevent spread of
infection).
Acute Intervention
o The role of the nurse in shock involves (1) monitoring the patient’s
ongoing physical and emotional status to detect subtle changes in the
patient’s condition; (2) planning and implementing nursing
interventions and therapy; (3) evaluating the patient’s response to
therapy; (4) providing emotional support to the patient and family; and
(5) collaborating with other members of the health team when
warranted by the patient’s condition.
o Neurologic status, including orientation and level of consciousness,
should be assessed every hour or more often.
o Heart rate/rhythm, BP, central venous pressure, and PA pressures
including continuous cardiac output (if available) should be assessed
at least every 15 minutes and PAWP every 1 to 2 hours.
 Trends in these parameters yield more important information than
individual numbers.
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
o
o
o
o
o
o
o
o
Trendelenburg (head down) position during hypotensive crisis is not
supported by research and may compromise pulmonary function
and increase intracranial pressure.
 The patient’s ECG should be continuously monitored to detect
dysrhythmias that may result from the cardiovascular and metabolic
derangements associated with shock. Heart sounds should be
assessed for the presence of an S3 or S4 sound or new murmurs.
The presence of an S3 sound in an adult usually indicates heart
failure. The frequency of this monitoring is decreased as the
patient’s condition improves.
The respiratory status of the patient in shock must be frequently
assessed to ensure adequate oxygenation, detect complications early,
and provide data regarding the patient’s acid-base status.
 Pulse oximetry is used to continuously monitor oxygen saturation.
 Arterial blood gases (ABGs) provide definitive information on
ventilation and oxygenation status, and acid-base balance.
 Most patients in shock will be intubated and on mechanical
ventilation.
Hourly urine output measurements assess the adequacy of renal
perfusion and a urine output of less than 0.5 ml/kg/hour may indicate
inadequate kidney perfusion.
 BUN and serum creatinine values are also used to assess renal
function.
Tympanic or pulmonary arterial temperatures should be obtained
hourly if temperature is elevated or subnormal, otherwise every 4
hours.
Capillary refill should be assessed and skin monitored for temperature,
pallor, flushing, cyanosis, diaphoresis, or piloerection.
Bowel sounds should be auscultated at least every 4 hours, and
abdominal distention should be assessed.
 If a nasogastric tube is inserted, drainage should be checked for
occult blood as should stools.
Oral care for the patient in shock is essential and passive range of
motion should be performed three or four times per day.
Anxiety, fear, and pain may aggravate respiratory distress and
increase the release of catecholamines.
The nurse should talk to the patient, even if the patient is intubated,
sedated, and paralyzed or appears comatose. If the intubated patient
is capable of writing, a “magic slate” or a pencil and paper should be
provided.
 Family and significant others (1) link the patient to the outside
world; (2) facilitate decision-making and advise the patient; (3)
assist with activities of daily living; (4) act as liaisons to advise the
health care team of the patient’s wishes for care; and (5) provide
safe, caring, familiar relationships for the patient. Family time with
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the patient should be facilitated, provided this time is perceived as
comforting by the patient.
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTIPLE
ORGAN DYSFUNCTION SYNDROME
 Systemic inflammatory response syndrome (SIRS) is a systemic
inflammatory response to a variety of insults, including infection (referred
to as sepsis), ischemia, infarction, and injury.

SIRS is characterized by generalized inflammation in organs remote from
the initial insult and can be triggered by mechanical tissue trauma (e.g.,
burns, crush injuries), abscess formation, ischemic or necrotic tissue (e.g.,
pancreatitis, myocardial infarction), microbial invasion, and global and
regional perfusion deficits.

Multiple organ dysfunction syndrome (MODS) results from SIRS and is
the failure of two or more organ systems such that homeostasis cannot be
maintained without intervention.
o The respiratory system is often the first system to show signs of
dysfunction in SIRS and MODS often culminating in ARDS.
o Cardiovascular changes include myocardial depression and massive
vasodilation in response to increasing tissue demands.
o Neurologic dysfunction commonly manifests as mental status changes
with SIRS and MODS.
o Acute renal failure (ARF) is frequently seen in SIRS and MODS.
o In the early stages of SIRS and MODS, blood is shunted away from
the GI mucosa, making it highly vulnerable to ischemic injury.
 Risk for ulceration and GI bleeding.
 Potential for bacterial translocation from the GI tract into circulation.
o Both syndromes trigger a hypermetabolic response.
 Catecholamines and glucocorticoids are released and result in
hyperglycemia and insulin resistance.
 Net result is a catabolic state, and a reduction in lean body mass
(muscle).
 May see liver dysfunction as a result of hypermetabolic state.
o Failure of the coagulation system manifests as DIC.
o Electrolyte imbalances, which are common, are related to hormonal
and metabolic changes and fluid shifts.
 These changes exacerbate mental status changes, neuromuscular
dysfunction, and dysrhythmias.
 The release of antidiuretic hormone and aldosterone results in
sodium and water retention.
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Nursing and Collaborative Management: SIRS and MODS
 The prognosis for the patient with MODS is poor and the most important
goal is to prevent the progression of SIRS to MODS.

A critical component of the nursing role is vigilant assessment and
ongoing monitoring to detect early signs of deterioration or organ
dysfunction.
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Collaborative care for patients with MODS focuses on (1) prevention and
treatment of infection, (2) maintenance of tissue oxygenation, (3)
nutritional and metabolic support, and (4) appropriate support of individual
failing organs.

Prevention and treatment of infection:
o Aggressive infection control strategies are essential to decrease the
risk for nosocomial infections.
o Once an infection is suspected, interventions to control the source
must be instituted.

Maintenance of tissue oxygenation:
o Interventions that decrease oxygen demand are essential and may
include sedation, mechanical ventilation, analgesia, paralysis, and rest.
o Oxygen delivery may be optimized by maintaining normal levels of
hemoglobin and PaO2, using individualized tidal volumes with positive
end-expiratory pressure, increasing preload or myocardial contractility
to enhance CO, or reducing afterload to increase CO.

Nutritional and metabolic needs:
o Hypermetabolism in SIRS or MODS can result in profound weight loss,
cachexia, and further organ failure.
o Total energy expenditure is often increased 1.5 to 2 times the normal
metabolic rate.
o Plasma transferrin and prealbumin levels are monitored to assess
hepatic protein synthesis.
o The goal of nutritional support is to preserve organ function and the
use of the enteral route is preferable to parenteral nutrition.

Support of failing organs:
o Support of any failing organ is a primary goal of therapy (e.g., the
patient with ARDS requires aggressive oxygen therapy and
mechanical ventilation, DIC should be treated appropriately [e.g., blood
products], renal failure may require dialysis).
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