Download Shock

Chapter 54:
Shock, Systemic Inflammatory
Response Syndrome, and
Multiple Organ Dysfunction
Syndrome
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Shock
• Complex syndrome
• Alteration in compensatory mechanisms that results in:
– Circulatory underperfusion
– Respiratory underperfusion
– Increased coagulation
– Stimulation of the inflammatory responses leading
to:
• Multiple organs failing
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The Delicate Balance
• Tissue oxygenation and perfusion
–
Cells usually take up 25% of oxygen delivered.
–
This oxygen consumption is referred to as VO2.
–
Delivery of oxygen to the cellular tissue is the DaO2.
–
In stress VO2 depends upon DaO2.
–
Compensatory mechanisms ensure this takes place.
–
When cells can’t extract enough oxygen, the body turns to
anaerobic metabolism, which can lead to lactic acidosis.
–
Cellular death can occur if this process isn’t reversed.
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Compensatory Mechanisms: Autonomic
Nervous System
See Figure 54-1.
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Question
The nurse suspects that a patient injured in a motor vehicle
accident is going into hypovolemic shock. Which of the
following compensatory mechanisms will help maintain a
patient’s blood pressure?
A. Increased urinary output
B. Decreased respiratory effort
C. Decreased preload
D. Increase in systemic vascular resistance (SVR)
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Answer
D. Increase in systemic vascular resistance (SVR)
Rationale: The release of catecholamines causes a
peripheral vasoconstriction and therefore an increase in
the systemic vascular resistance (SVR) as well as venous
vasoconstriction, which increases the preload.
Respirations increase to supply more oxygen to the
tissues. Urinary output decreases to conserve sodium
and water under the influence of ADA.
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Compensatory Mechanisms in Shock
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Shock Stages: A Progressive Downward
Spiral
Vital signs
Cerebral
perfusion
Reversible
STAGE I
Nonprogressive
stage
Relatively normal
Intact
Yes
STAGE II
Progressive stage
Noticeable
changes;
tachycardia and
tachypnea
Change in LOC
Yes, if recognized
and treated
appropriately
STAGE III
Irreversible
Temp down
Pulse down
Respirations down
Hypotensive
Profound decrease
in cerebral
perfusion
No
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Classifications of Shock
• Hypovolemic
– Burns
– Hemorrhage
• Cardiogenic
– Pump failure
• Distributive
– Spinal cord injury
– Sepsis
– Anaphylaxis
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Hypovolemic Shock
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Pathophysiology
• Decreased circulating volume stimulates SNS and
hormonal responses.
• Blood is shunted to the heart and brain at the expense of
the kidney, liver, and gut.
• If volume isn’t restored and compensatory mechanisms
fail, the SNS increases myocardial demand and oxygen
consumption (MvO2).
• End-organ failure can result.
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Signs/Symptoms Depend on the Volume
Lost
ASSESSMENT DATA
LAB DATA
• Change in LOC
• Serum lactate
• Tachypnea
• Serial ABGs
• Cool clammy skin
• Hemoglobin and hematocrit
• Tachycardia
• Coagulation profiles
• Hypotension (with >30%
blood loss)
• Decreased urinary output
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Treatment: Fluid Resuscitation
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Nursing Management During Fluid
Resuscitation
• Deliver warmed fluids through large-bore IVs
• Monitor for pulmonary edema, which can occur if fluids are
given too quickly
• Elevate lower extremities
• Monitoring
– Vital signs
– Oxygen saturation
– Mentation (LOC)
– Urinary output and labs
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Cardiogenic Shock
• Decrease in oxygenation to the tissues from decreased
heart pumping
• Most significant cause is myocardial infarction
– 40% of left ventricular mass infarction
• Often occurs at home
• Other causes include ruptured papillary muscle,
ventricular septal defect/rupture, cardiomyopathy,
valvular disease, and dsyrhythmias
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Pathophysiology of Cardiogenic Shock
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Question
Decreased cardiac output from cardiogenic shock leads to
an increase in sodium and water retention, further
leading to a downward spiral unless reversed.
A. True
B. False
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ANSWER
A. True
Rationale: When the cardiac output drops, renin and
angiotensin are secreted. Their ultimate response is
to hold on to sodium and water. In hypovolemic and
distributive shock, this is a beneficial mechanism
because it helps keep water in the tubes. In
cardiogenic shock, however, this increases edema,
which puts more stress on the heart.
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Signs/Symptoms
ASSESSMENTS
LABS/DIAGNOSTICS
• Identify who is at high risk
–
MI
• Elevated cardiac enzymes
(troponin, CPK-MB)
–
Ejection fraction <35%
• BNP
–
Diabetes mellitus
• ECG changes
–
Elderly
• Echocardiography
• Pulmonary artery pressures
• Chest pain
• Thready rapid pulses
• Distended neck veins
• Pulmonary congestion
(crackles, gurgles,
hemoptysis)
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Treatment and Nursing Care
• Judicious fluids with diuretics and nitrates
• Monitor and replace electrolytes, especially K+, Ca, Mg
• Narcotic analgesics, but watch the SaO2
• Treat rhythm disturbances
• Possible cardioversion and pacing
• Pulmonary artery pressure monitoring
• Left ventricular assistive devices: IABP, LVA
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Medications
• Medication administration (beta-blockers, dopamine,
dobutamine, etc.)
• Sodium nitroprusside, nitroglycerin
• ACE inhibitors
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Distributive Shock: Blood Shunted From
Core
• Anaphylaxis
– Allergens
• Neurogenic
– Loss of sympathetic tone from spinal cord injury
• Septic
– Sepsis
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Anaphylactic Shock
• Life-threatening response to an allergen
• Usually not with first exposure; antigens trigger a
response with second exposure
• Nurse should teach about prevention
• Mostly due to insect venom (injected)
– Drugs (injected or ingested) and foods are next most
common; ASA and NSAIDs are common
– Inhalation of antigens
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Antigen-Antibody Response
See Figure 54-8.
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Question
A patient presents to the Emergency Care Unit and is
thought to be having an anaphylactic reaction to a bee
sting. Which of the following symptoms might the patient
exhibit?
A. Crackles
B. Egophony
C. Stridor
D. Petechiae
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Answer
C. Stridor
Rationale: Patient with anaphylactic reactions can have
stridor due to bronchoconstriction from the allergen.
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Signs/Symptoms and Nursing Care
• SIGNS/SYMPTOMS
• NURSING CARE
–
Identify, remove offending
allergen
–
Oxygen and possible
intubation if not reversed
Dyspnea, wheezing; can
lead to stridor
–
Antihistamine such as
diphenhydramine
–
Severe respiratory distress
from laryngeal edema
–
Possible epinephrine
–
Hypotension and
circulatory collapse
–
Rapid infusion of NSS if
hypotensive
–
Circulatory support with
vasoconstrictors prn
–
Generalized erythema
–
Urticaria and pruritus
–
Anxiety and restlessness
–
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Septic Shock
• High mortality rates
• 1:4 patients in ICU will worsen from sepsis to septic shock
– Worse in first 10 days of diagnosis
• Initiated by an infection (gram – or + bacteria, fungi, etc.)
• Inflammatory response that kills organism causes an increased
permeability in the endothelial layer of the blood vessels. Fluid
moves into interstitial spaces.
• Stable fibrin clots form and adhere to the damaged
endothelium.
• Every organ system is affected.
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Organ Effects of Septic Shock
• CARDIOVASCULAR
• RESPIRATORY
–
Vasodilation in response to
nitric oxide release
–
Bronchoconstriction from
cytokine activity
–
Other mediators cause
vasoconstriction and
clotting in microcirculation
–
Interstitial edema from
inflammatory substances
–
Shunting
–
Impaired gas exchange
–
ARDS
–
Possible secondary
infection from
intubation/ventilation
–
Decreased CO, increased
SVR
–
Lactic acidosis, which
depresses myocardial
contraction
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Organ Effects of Septic Shock (cont.)
• HEMATOLOGICAL
CHANGES
– Platelet aggregation
• METABOLIC CHANGES
– Increased energy
consumption
– Obstructed flow
decreases tissue
metabolism
– Hyperglycemia
– Clotting factors depleted
– Mitochondrial and
cellular death
– Result: DIC
– Ketosis
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Findings and Treatment
• PHYSICAL FINDINGS
–
Changes in LOC
–
Tachypnea
–
Fever; hypothermia
–
Decreased urinary output
–
–
• TREATMENT
–
Antibiotics (“shotgun”
approach until causative
organism identified)
–
Restoring volume with
crystalloid/colloids
Decreased bowel sounds
–
Diminished peripheral
pulses
Monitoring for fluid
overload with PA catheter
–
Dopamine/Levophed/
vasopressin/dobutamine
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Question
A patient is suspected of having septic shock. Which of the
following medications improves outcomes in septic shock
by decreasing the imbalance of clotting in the
endothelium?
A. Drotrecogin alfa (activated) (Xigris)
B. Dobutamine
C. Epinephrine
D. Levophed
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Answer
A. Drotrecogin alfa (activated) (Xigris)
Rationale: Drotrecogin alfa (activated) (Xigris) decreases
the clotting in the microvasculature that increases
hypoxia in sepsis. Dobutamine, epinephrine, and
Levophed are used to help increase cardiac contractions
and improve vascular tone in septic shock.
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Nursing Care and Treatment
• Intubation and mechanical ventilation
– PEEP may be used if ARDS
• Drotrecogin alfa (activated) (Xigris)
– Reestablishes homeostasis of clotting system
• Nutritional support
– Enteral feedings
– TPN
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Systemic Inflammatory Response
Syndrome (SIRS)
• Should be suspected in any patient with shock or risk for
shock
• Inflammatory response that is systemic; microthrombic
in vessels
• Also caused by “leaky pipe syndrome” from released
vasodilator
• Management is similar to septic shock
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Multiorgan System Failure (MODS)
• Cause is unknown
• Inflammatory substances found in SIRS play a role in MODS
• Multiple organs fail; usually lungs, heart, kidney, and lastly
liver
– Pulmonary hypoventilation and hypoxia
– Decreased cardiac output; hypotension and dysrhythmias
– Increased risk of DIC
– Poor cerebral perfusion
– Liver failure
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Signs/Symptoms and Treatment
• Hypotension
• Tachycardia
• Tachypnea
• Hypo- or hyperthermia
• Treatment is supportive care and similar to septic shock
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