NOTES Mod #15 Trauma/Shock cmj
Module #15: Nursing Care of the Individual Requiring Critical Care: Trauma,
Shock, Emergency and Critical Care Nursing
Trauma/Triage
(click here-two separate sites)
A. Etiology/Pathophysiology etc
1. Definition: *Regarding Emergency Care: there may appear to be “chaos” in
the ED, however there is an inherent order in the timing and choice of
interventions performed throughout (and prior to…pre-hospital) a client’s stay
in the ED….organizational flow of events involves triage (prioritization), indepth nursing assessment of the client, diagnostic testing, formulation of
diagnoses, outcome management, evaluation, disposition, and
documentation.
2. Trauma: Sudden accidents or purposeful acts leading to injury, disability or
death
a. Impact: initial physical injuries and long term effects; rehabilitation and
psychosocial effects on clients and family members
b. Components of Traumas
1) Host: person or group at risk of injury
2) Mechanism: source of energy that causes trauma
*Most common: mechanical energy from motor vehicles in accidents
3) Intention: deliberate or unintentional
4) Environment: location and under what circumstances
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c. Types of trauma
1) Blunt: no communication between damaged tissue and outside
environment; injuries internal...can be minor to lethal
2) Penetrating: actual tissue damage to body structures, obvious from
outside; result of foreign objects set in motion; affect internal organs;
ex gun shot wounds, stab wounds common
3) Often combination of blunt and penetrating
4) Pathophysiology/manifestations determined by location and extent of
injury
B. Common Manifestation/Complications
* Determined by location/extent of injury; psychosocial impact also
What potential “problems” do these photos suggest?
C. Therapeutic Interventions/Collaborative Care
1. Goals of Collaborative Care: stabilization and appropriate intervention
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Pre-hospital Care
a. Injury identification
1) Require rapid comprehensive trauma assessment (use different
systems) *Glasco Coma scale is one aspect: See text p. 140 Table
6-2 Champion Revised Trauma Scoring Scale * modifications of
this used in ER…estimates chance of survival...higher the score, the
better the chance. (*know how to use this)
2) Determines need for trauma center and rapid transport
3) *Airway, Breathing, Circulation
4) Level of consciousness
5) Spinal cord injuries with deficit
6) Any obvious injuries (penetrating injuries to abdomen, chest, pelvis,
neck head)
7) Evaluate crush injuries
8) Major burns
b. Critical interventions
1) Life support
2) Immobilize cervical spine
3) Airway management (intubation); breathing
4) Treat hemorrhage and shock
5) Apply direct pressure over wounds
c. Rapid Transport ASAP to regional trauma center!
2. Hospital Care: Emergency Department Care
a. Support above critical interventions
1) In ER > triaged as to severity of problem
2) Triage categories include: Emergent (client must be treated
immediately; otherwise life/limb /vision threaten); Urgent (client
requires treatment, but life/limb/vision not threatened if care cannot
be provided within 1-2 hours); Non-urgent (client requires
evaluation and possible treatment, but time is not critical factor)
b. Assessment to determine of injuries/plan of treatment
1) A- airway obstruction- blood, teeth tongue or vomiting (may required
immediate intubation)
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2) B-breathing-? pneumothorax and tension pneumothorax (mediastinal
shift to unaffected side) and require chest tube; may have cardiac
contusion with cardiac tamponade; require open thoracotomy What
is a pneumothorax, hemothorax??
3) C- circulation-? signs of hemorrhage (external and internal) and
hypovolemic shock
Abd. Trauma-bleeding into abd. Cavity
Blunt abdominal trauma;
distended Why is abd
distended?
Pelvic fracture-bleed into retroperitoneal space; major blood loss!
346  RNSG 2432
4) Physical Examination of Trauma requires:
a) Inspect, palpate each body area > identify obvious evidence
of injury (DCAP-BTLS) such as below: (mnemonic helps you
remember!)
Deformities
Contusions (deep bruising)
Abrasions (scrapes)
Punctures or penetrations
Burns
Tenderness to palpation
Lacerations (cuts)
Swelling
b) Primary Survey >determine immediate needs (several evaluative
tools can be used); includes evaluation of LOC (A-alert, oriented
X3; V-verbal, responds to verbal stimuli; P-pain, responds to
painful stimuli; U- unresponsive) where does the client fall within
this category?
c) Secondary Assessment- Head to toe to determine extent of
injuries and includes:
(1) Integumentary- contusions, abrasions, punctures, lacerations
(Consider risk for infection)
(2) Abdominal-high risk for hemorrhage and peritonitis-(Bowel
ischemia and infarction; Rupture of large bowel-peritonitis)
(3) Musculoskeletal *High priority if threatens life or limb;
dislocated hip/joint; pulseless extremity; significant blood loss
from pelvic fracture (Note can look “bad”…priority is “ABC’s”
(4) Neurological- head and spinal cord injuries **Must
immobilize spinal cord…
(5) Psychological- sudden death or serious injury
c. Diagnostic Tests common to ER setting
1) Blood type and crossmatch: ? client’s blood type; ready donor blood
for transfusion (Review blood administration; universal blood donor,
etc, safety; autotransfusion)
Hypovolemic-due to hemorrhage> adm blood, blood products> keep
HCT 30-35% and HGB 12.5-14.5 g/100 ml. What blood products
usually given? (p. 159) what crystalloid solution and why? (p.
159…understand rationale) See below also.
2) Blood Alcohol level: alters level of consciousness and pain response
(20-50% of those injured are intoxicated!)
3) Urine Drug screen: alters level of consciousness and pain response
4) Pregnancy test for women of child-bearing age: treatment concerns
5) Diagnostic Peritoneal Lavage (click here for more): test presence
of free blood (or bile, or food, feces…) in peritoneal cavity; determines
if hemorrhaging, injury internally and need for exploratory laparotomy
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(Catheter placed in lower abdomen and aspiration for free blood;
infuse warm isotonic solution rapidly and drain by gravity; check for
presence of blood) (if blood, bile, feces, send to OR)
6) Computerized Tomography (CT Scan) special x-ray of body area in
layers with computerized views; brain, chest, abdomen and MRI;
critical to early identification of injury.
d. Medications/Treatment/Surgical Intervention
1) Most likely initiated at scene; oxygenation! Why important?
2) Intravenous access (2 large bore large bore IVs; NS (give with
blood); or Ringers Lactate) blood components (See text p. 143 & 159;
Table 6-3 Types of Blood components Used in Transfusion Therapy
348  RNSG 2432
Crystalloids (first line treatment) inexpensive; **initial
treatment-usually 1-2 L bolus of crystalloids (NS or RL); rapid
based upon client’s needs; (more than 4-5 L causes internal and
external edema, does not provide RBC’s) (FYI…recall colloidsalbumin for volume expansion)
What are nursing implications re use of plasma expanders such as
albumin & dextran? (p. 157)
3)
4)
5)
6)
7)
8)
*Hypovolemic shock with massive bleeding; rule –“3-1” replace blood loss with crystalloids; for every 1 ml of blood loss, 3 ml
crystalloids given; once blood loss = 1500cc; blood transfusion with
packed red blood given along with other blood products as FFP and
platelets to restore clotting factors. Transfusion recommended
when hemoglobulin = 7-8 g/dl and hematocrit - 21% to 24%.)
Cardiovascular support may require inotropic agents
(vasopressors) *If volume replacement does not adequately support
CO and MAP to ensure and maintain tissue perfusion; may need
vasopressors as dopamine (Inotropin) and norepinephrine
(Levophed) to support BP and increase cardiac contractility.
How does dopamine work? (p. 142, 880)
Hypovolemic shock-volume loading (blood & fluid) > major
intervention; drug therapy- last choice!
Pain control; opiates, however, cautiously as will altered LOC
Tetanus immunization, if indicated & potential for gas gangrene later
and tetanus! What organism causes this?
Blood Transfusions (Blood type O-Universal donor) (Use NS only
when adm blood-review “transfusions”)
Emergency surgery (determined by injury)
e. Organ Donation *not tested with this unit…read, cover in Mod 13
1) What are brain death criteria? (p. 145-box 6-1) & below
2) Uniform Anatomical Gift Act (1968, 1987)
3) Care given to maintain circulation and perfuse organs if organs to be
donated *Note; hepatitis, even HIV not absolute contraindications for
organ donation any longer; nurses and physicians MUST call the
Donor Referral Line (1-800-275-1744) in event of potential donor;
nurses and physicians are NOT to communicate information about
donor request etc (contrary to text)
4) Supportive care to family member; assist with grief
5) Brain Death Criteria:
a) Irreversible condition
b) Apnea with PACO2 >60
c) No response to deep stimuli
d) No spontaneous movement
e) No gag or corneal reflex
f) No oculocephalic or oculovestibular reflex
g) Absence of toxic or metabolic disorders.
f.
Forensic Considerations
1) Trauma due to illegal activity
2) Determine if client under influence of alcohol, illegal drugs
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3) Maintain chain of custody, i.e. preserve, label, document, and dispose
evidence (Important!)
3. Common Nursing Diagnoses for Trauma Clients (p. 146-148)
a. Ineffective Airway Clearance (assess airway, check O2 sats, LOC)
b. Risk for Infection
c. Impaired Physical Mobility
d. Spiritual Distress: Client and Family
e. Risk for Post-Trauma Syndrome
1) Intense emotional response to disastrous event
2) Impaired coping mechanisms
3) Nurses assist client and family to express feelings
4) Referrals for counseling, support groups
f. Teaching Need: Prevention of Trauma: educate the public about trauma
prevention and safety e.g. seatbelts, bicycle helmets
*Read carefully-recognize priority nsg problem/dx and intervention
Shock
(Click here-article- hypovolemic shock)
A. Etiology/Pathophysiology etc
1. Definition: Clinical syndrome, systemic imbalance between oxygen supply
and demand; Inadequate blood flow to body organs and tissue >lifethreatening cellular dysfunction resulting in: *inadequate tissue perfusion
and *decreased O2 at cellular level
2. Pathophysiology: Shock triggered by a stimulus (**drop in the MAP) >
leads to alteration in hemodynamics within body
a. Body responds by maintaining perfusion to vital organs, heart and
brain
b. Results in inadequate tissue and cellular perfusion; if not reversed,
body develops acidosis; if untreated, progresses to organ hypoxia,
ischemia and death
c. Alteration in hemodynamics results in drop in arterial blood pressure
by one of these mechanisms
1) Decrease in cardiac output (ability of heart to supply adequate
circulation)
2) Decrease in circulating blood volume
3) Increase in size of vascular bed
d. Terms: pathophysiology of shock (review only): Stroke Volume
(SV): amount of blood pumped into aorta by contraction of left ventricle;
Cardiac Output (CO): amount of blood pumped into aorta by contraction
of left ventricle in one minute; Systemic Vascular Resistance (SVR):
amount of resistance provided by vascular bed against flow of blood being
ejected from left ventricle (vasoconstriction increases SVR); and Mean
arterial pressure (MAP): product of cardiac output and systemic vascular
resistance * Review Class Lab#4 Hemodynamic Monitoring and Mod #4
Heart Failure
MAP = systolic BP + 2 (Diastolic BP)
3
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* Remember MAP of 60 or greater needed to maintain tissue
perfusion and oxygenation!
Regardless of cause- reaction and symptoms typically follow same
course-differentiate stages/type of shock/ underlying cause
* Important to understand this concept
e. Stages of Shock/type of shock!
1) Stage 1-Early reversible and Compensatory Shock (p. 150)
*Initial stage: MAP dec. to less than 10 mmHg; circulating blood
volume usually less than 500 mL; SNS inc. HR and force contraction >
CO; peripheral vasoconstriction, inc. SVR and yields inc. arterial
pressure; individual does not note symptoms unless progressive insult
a) MAP 10 -15 mm Hg below normal levels
b) Decrease in circulating blood volume (25-35% less) loss of
1000 mL or more
c) Sympathetic nervous system stimulated; release
catecholamines (epinephrines and norepinephrines);
bronchodilation and increased cardiac output occurs due to beta
receptor stimulation
d) 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
e) Renin-angiotensin-release of aldosterone to reabsorb H2O and
sodium; loose potassium (increase fluid volume to compensate for
decreased renal perfusion)
f) Posterior pituitary releases ADH (antidiuretic hormone, also called
vasopressin) to increase intravascular fluid volume)
g) Get fluid shift from interstitial to capillaries due to decrease in
hydrostatic pressure in capillaries
h) Circulation maintained, but only sustained short time without
harm to tissues; must treat underlying cause of shock; will
progress to next stage
***Preserve perfusion of heart and brain!
2) Stage II- Intermediate or progressive shock (severe or
decompensated)
a) Further drop in MAP (20 mm below normal values) * As
shock continues to progress, compensatory mechanisms from the
previous phase continue unchecked, worsening the status!
b) Increase in fluid loss of 35-50% (1800 – 2500 ml) due to
hemorrhage or fluid leakage
c) Vasoconstriction continues; cells become more O2 deficient>start
anaerobic metabolism )
d) **Body switches to anaerobic metabolism > lactic acid as a
waste product.
e) Body inc. heart rate and vasoconstriction.
f) Heart and brain cells become hypoxic
g) More severe effects on other tissues > become ischemic and anoxic
RNSG 2432  351
h) Fluid shifts into interstitial space; proteins shift into interstitial
space; fluid follows! * As cells die due to hypoxic state, > release
destructive enzymes and proteins into surrounding tissues >inc.
oncotic pressure into interstitial space (third-spacing) >,circulating
volume is further decreased
i) Metabolic acidosis with hyperkalemia develops
j) Needs rapid treatment; poor survival rate!
3) Stage III-Refractory or irreversible shock (also called
MODS…multiple organ dysfunction> death)
a) Tissues anoxic, cellular death widespread
b) Even with restoration of blood pressure and fluid volume > too
much damage to restore homeostasis of tissues
c) Cellular death leads > tissue death > vital organs fail and death
occurs
*Know understand these stages
B. Common Manifestation/Complications
1. Effects of Shock on Body Systems (See text p. 152 Multsystem effects of
Shock)
a. 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
4) DIC [disseminated intravascular coagulation); late effect of
hypoxia; slow-moving acid blood - hypercoagulable, does not
coagulate unless clot-initiating factor present
a) Factors= bacterial endotoxins and thromboplastin of RBCs;
hemolysis (destruction of RBC’s
b) Massive crush injury occurs
c) Stagnant acidic blood
b. Respiratory
1) Initially: inc. respiratory rate (chemoreceptors sense dec. pH, depth of
respiration inc. to “blow-off” CO2 to compensate for metabolic
acidosis; cellular hypoxia not caused by inadequate ventilation but by
inadequate tissue perfusion > inc. respiratory effort does not correct
the problem > lactic acid accumulates> becomes more acidic >
blood pH and bicarbonate levels dec.
a) Gas exchange impaired >leads to anaerobic metabolism
b) Leads to acidosis (metabolic and respiratory)
2) Acute Respiratory Distress Syndrome (ARDS): complication of
decreased lung perfusion (Review Mod 1 ARDS)
c. Gastrointestinal and Hepatic
1) GI organs > ischemic, with blood circulation shunted to heart and
brain > Stress Ulcers (GI mucosa > ischemic, prone to rapid
ulceration) and Paralytic Ileus (dec. gastrointestinal motility with
decreased blood flow)
2) Altered liver metabolism: initially glucose made available, then
hypoglycemia, fat breakdown leads to ketones and metabolic
352  RNSG 2432
d.
e.
f.
g.
h.
acidosis; toxicity and bleeding (Liver- impaired circulation and may be
source of toxic materials; anoxic liver does not detoxify; may release
vasoactive substances; bacterial invasion from intestines.
Neurologic
1) Develops cerebral hypoxia (cerebral edema due to hypoxia)
2) Restlessness initially > altered level of consciousness, lethargy, coma;
have emboli
3) Circulatory collapse- sympathetic stimulation lost > bradycardia >
death
Renal: Dec. kidney perfusion > to oliguria (urine output < 20 ml/o) ;
develop ATN (can recover function if basement membrane intact;
epithelial cells regenerate)
Skin, temperature, thirst; Skin: cool, pale, hypothermic due to
vasoconstriction
Immune System: All forms of shock severely deplete macrophages
(found in blood cells and tissues) > cannot remove bacteria and
endotoxins from the blood stream > increased chance for sepsis!
MODS (multiple organ dysfunction)- Ultimately all body systems fail and
death.
2. Types of Shock (categorized according to underlying causes)
a. Hypovolemic; loss of intravascular volume > 15-25% (See p. 154,
Box 6-2, Assessment Findings in Clients in Hypovolemic Shock)
1) Most common: occurs with other types of shock
2) Common stimuli/causes hemorrhage, burns, severe dehydration, third
spacing such as bowel obstruction, burns, liver
3) Progresses through stages of shock unless restoration of fluid volume
RNSG 2432  353
b. Cardiogenic (See p. 155, Box 6-3 Assessment Findings in Clients in
Cardiogenic Shock) (review from heart failure)
May lead to
cadiogenic shock
1) Pumping ability of heart compromised to degree that cannot maintain
cardiac output (CO) and adequate tissue perfusion (pump failure);
2) Common causes: MI, cardiomyopathy, arrhythmia, cardiac
tamponade; cardiac arrest
3) Leads to left and right sided heart failure; decreased CO and
MAP; increased LVEDP (*decreased MAP stimulates sympathetic
system; beta receptors stimulated; increases O2 needs; cardiac
stress!)
4) Cyanosis common
c. Obstructive (hard to diagnose)***
1) Heart or great vessels obstructed; venous return or cardiac pumping
action impeded; cardiac preload dec./severely compromised; inc.
pressure on right side of heart and an inadequate blood return
(different from cardiogenic shock- heart itself has adequate pumping
abilities and is not necessarily diseased)
2) Common cause: *pulmonary embolism, pneumothorax
d. Distributive (Vasogenic); includes several types of shock-result in
widespread vasodilatation and dec. peripheral resistance; *blood volume
does not change, have relative hypvolemia! (need to understand
this concept!)
1) Septic Shock (Toxic shock (click here to learn more) found in
menstruating women who use tampons) (See text p. 156, Box 6-4
Assessment Findings in Clients with Septic Shock)
a) Leading cause of death in intensive care units
b) Common stimuli: Gram negative bacterial most often causative
agent; others (pseudomonas, E coli); Gram positive bacterial
infections (staphylococcus and streptococcus) 60% mortality rate
despite treatment
354  RNSG 2432
46-year-old man presented with nonnecrotizing cellulitis and
streptococcal toxic shock syndrome. The leg was incised to exclude
underlying necrotizing infection. Courtesy of Rob Green, MD.
Patient in septic shock can exhibit
can exhibit skin lesions; most
often on lower extremities;
associated with development of
DIC;
c) Increased risk: clients with chronic illness, poor nutritional status,
invasive procedure or tubes, as central lines, foley catheters
d) Course: Septicemia (bacteremia initially) develops> pathogens
and their toxins in 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
(*understand this concept)
e) Phases Septic Shock (SIRS) systemic inflammatory response
syndrome: (1) Warm Phase (early); skin flushed, warm due to
vasodilatation; (2) Cold Phase (late): skin cool due to fluid deficit
with shock. Have deep respirations, lethargic, coma
f) CO high and SVR low (warm phase)
g) DIC high risk with septic shock
h) Priority: early recognition; tachycardia, hyperthermia (or
hypothermia) and hypotension due to decreased SVR; blood
volume adequate, but misplaced
i) Interventions: Some controversy over management and treatment
(not in text)
(1) Maintain airway -adequate cardiac output; oxygen, IV access,
hemodynamic monitoring, BP support with fluids and
medications, cultures and appropriate antibiotics; treat elevated
temperature (some controversy) but inc. temperature inc.
metabolic demands. (High mortality rate)
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2) Neurogenic Shock See text. 156, Box 6-5 Assessment Findings in
clients in Neurogenic shock
a) Dec. sympathetic control of vasomotor responses; parasympathetic
stimulation unchecked > **sustained peripheral vasodilation
> dec. MAP
b) Common stimuli: head injury, spinal cord trauma, insulin reactions,
anesthesia (somewhat rare associated with significant spinal
trauma) R/O hypvolemic shock initially, NCS depressant drugs
c) Bradycardia due to parasympathetic influence early then
tachycardia
d) Decreased CO due to bradycardia; dec. PAP, pulmonary
capillary wedge pressure; dec. SVR due to vasodilation;
hypotension and hypothermia
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 cec. MAP; Late skin pale and
cool and heart rate inc.
f) Priority problem: maintain tissue perfusion
(1) Interventions- assessment and pulse oximetry; identify cause
and attempt to correct; maintain ABC; may involve infusing IV
fluids for volume replacement and initiating vasopressors to
control BP levels. If symptomatic bradycardia, use atropine,
maybe a transvenous pacemaker.
356  RNSG 2432
3) Anaphylactic Shock
(Click here for more)
See p. 157, Box 6-6 assessment Findings in Clients in Anaphylactic Shock
Urticaria
wheal
a) Result of widespread hypersensitivity (anaphylaxis); first
symptoms-dermatologic : pruritus, generalized erythemia, urticaria
usually on chest, then on face and angioedema
b) Vasodilation > hypovolemia and altered cellular metabolism
c) Sensitized in past, re-contact with the allergen (medication, bee
sting, food allergen)
d) Allergic reaction with large amounts of histamine released
e) Histamine > vasoconstriction of smooth muscles in bronchioles
(causes bronchospasm, laryngospasm), bladder, intestines > leads
to inc. permeability and massive vasodilatation (pooling of blood
in periphery)= hypovolemia
f) Serotonin- increases capillary permeability (can cause pulmonary)
g) Key manifestations: dyspnea, stridor, wheeze dec. BP, inc. heart
rate, dysrhythmias, laryngospasm/bronchospasm, warm,
edematous skin, restless to coma; oliguria to anuria
h) Priorities: Maintain airway
(1) Interventions: Find cause and remove!; administer
epinephrine (Adrenaline); provide oxygen, give
antihistamine; give corticosteroids
i) Need Medic Alert bracelet (teaching!)
3. Life Span and Effects of Shock
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The most common etiologies of shock in children are
hypovolemia and sepsis.
The major type of shock in pregnancy is hemorrhagic
(hypovolemic) and is the leading cause of maternal
death. Postpartum hemorrhage occurs most often in
the first hour following delivery (fundus and lochia
should be assessed every 15 minutes for the first hour
postpartum) but can occur up to a week following
childbirth.
Because the uterus is a nonessential body organ,
danger to the fetal blood supply occurs when the
woman's body begins to decrease blood flow to the
peripheral organs. (Pillitteri, 2003, p. 380)
Sepsis is a major cause of death in the elderly; shock
of any type is a strong predictor of mortality. Due to
the decrease in chronotropic response with aging,
tachycardia may not be present in the elderly
hypovolemic patient despite very low cardiac output.
Fluid resuscitation is best achieved with colloids such as
blood products as the elderly require higher
hemoglobin levels to facilitate oxygen delivery. Large
amounts of normal saline should be avoided; with
decreased renal function, metabolic acidosis may
result. Treatment is aimed not at normalizing
hemodynamic parameters, but at correcting any
oxygen deficit. (Fulmer, et al., 2001)
C. Therapeutic Interventions/Collaborative Care (summary all types)
1. Collaborative Care: focus on treating underlying cause to stop progress
through stages of shock; rapid shock identification; rapid diagnosis of cause;
rapid aggressive treatment: better outcome for client
2. Goal: improve arterial oxygenation and tissue perfusion; determine type of
shock
3. Assessment: **Keys:
a. Cool, clammy skin
b. Hypotension-widened pulse pressure
c. MAP<60 (need more than 60 for organs to be perfused)*Takes
40 minutes of MAP<60 to develop acute renal failure. *May see
slighly different values..
358  RNSG 2432
d.
e.
f.
g.
h.
Dec. in B/P by 20 and Inc. HR by 20 = shock
Oliguria
Tachycardia
Decreased level of Consciousness
Rales and edema-only in cardiogenic
4. Diagnostic tests for clients in shock
a. Blood hemoglobin and hematocrit: hypovolemic shock
b. Arterial Blood Gases: identify body compensatory mechanisms, such as
acidosis
c. Electrolytes (Na level decreases, K dec, later inc. K with cellular
breakdown
d. BUN and creatinine (renal failure), osmolality: renal function
e. Blood cultures: identify causative organism in septic shock; treat
f. White blood count and differential: septic shock
g. Cardiac enzymes: diagnosis of cardiogenic shock (Cardiac enzymes are:
lactate dehydrogenase (LDH); Creatine phosphokinase (CPK); serum
glutamic-oxaloacetic transaminase (SGOT):
h. CVP- Measures right heart pressure (Normal 4-10 cm H20 or 2-5 mmHg);
1) High reading means fluid overload
2) Low reading means fluid deficit
i. Swan Ganz or PA catheter for hemodynamic monitoring of left heart
pressures (Review values)
What do altered hemodynamic reading readings indicate
related to shock?
Low CVP?
High CO?
5. Medications/Treatment (depend upon cause of shock/trauma)
a. Oxygen Therapy: Patent airway and adequate oxygenation-critical!
Interventions; Monitor ABGs, pulse oximetry (more accurate in early
stage); Mechanical ventilation
b. Inotropic agents: improve cardiac contractility (dopamine, dobutamine)
c. Vasoactive agents according to symptoms: vasoconstrictors for
distributive shock (Levophed and epinephrine); vasodilator
(Nipride and Nitroglycerine) for cardiogenic shock
d. Other meds according to cause as antibiotics, steroids; diuretics, digoxin,
etc
e. Fluid Replacement: appropriate solutions-Types of Intravenous
Fluids
1) Crystalloid solutions: Dextrose or electrolyte solutions; inc.
intravascular and interstitial fluid volume; ex Isotonic (0.9% NaCl,
lactated Ringers) and hypotonic (5% dextrose in water, .45% NaCl)
2) Colloids: Do not diffuse easily through capillary walls; stay in vascular
compartment; increase osmotic pressure; ex: albumin, hetastarch,
plasma protein fraction, dextran.
3) Blood and Blood Products: treatment of hemorrhage; restore
coagulation properties
6. Nutrition : hypermetabolic state
a. Enteral feeding first choice (food in GI tract, dec risk GI bleed)
RNSG 2432  359
b. Early diet interventions dec. the risk of MODS
c. If cardiogenic- low Na and fluid restriction
d. High potassium if BUN and Creat OK
7. Surgery/Invasive
a. IABP for cardiogenic shock *review how they work!
b. VAD :BRIDGE TO HEART TRANSPLANT:USED IN PATIENTS WITH
CARDIOMYOPATHY
8. Other: Treat underlying cause
a. Positioning-flat with legs elevated
b. Assess for MODS
9. Nursing Process/Nursing Diagnosis
a. Nurse assess/analyze client situation and change in condition
b. Notify physician >early treatment before shock advanced and less
responsive to treatment
c. Care of client in shock: constant assessment /modify treatment
d. Transfer to intensive care unit for hemodynamic monitoring and
respiratory support
e. Complexities of changing status of fluid, acid-base, cardiovascular function
f. Support of client and family
10.Common Nursing Diagnoses
a. Decreased Cardiac Output
b. Altered Tissue Perfusion
c. Fluid volume deficit
d. Anxiety
360  RNSG 2432