http://webcache.googleusercontent.com/search?

q=cache:DZ3B2mmeqhMJ:www.austincc.edu/adnlev4/rnsg2331online/module15/53-RNSG%25202432-online
%2520Mod_15%2520Notes%2520Su07.doc+&cd=2&hl=en&ct=clnk&gl=us

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 topre-hospital) a clients stay in the ED.organizational flow of
events involves triage (prioritization), in-depth nursing assessment of the client,
diagnostic testing, formulation of diagnoses, outcome management, evaluation,
disposition, and documentation.

RNSG 2432 87
 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

88 RNSG 2432
Types of trauma
5) Blunt: no communication between damaged tissue and outside environment;
injuries internal...can be minor to lethal

6) 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

7) Often combination of blunt and penetrating

8) 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

RNSG 2432 89
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 ERestimates 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)

90 RNSG 2432
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!

RNSG 2432 91
 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 badpriority is ABCs
(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: ? clients 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. 159understand rationale) See below
also.

92 RNSG 2432
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
(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)

RNSG 2432 93
 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

Crystalloids (first line treatment) inexpensive; **initial treatment-usually 1-2

L bolus of crystalloids (NS or RL); rapid based upon clients needs; (more than 4-
5 L causes internal and external edema, does not provide RBCs) (FYIrecall
colloids-albumin for volume expansion)

What are nursing implications re use of plasma expanders such as albumin &
dextran? (p. 157)

*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%.)
3) 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)
4) Hypovolemic shock-volume loading (blood & fluid) > major intervention; drug
therapy- last choice!
5) Pain control; opiates, however, cautiously as will altered LOC
6) Tetanus immunization, if indicated & potential for gas gangrene later and tetanus!
What organism causes this?
7) Blood Transfusions (Blood type O-Universal donor) (Use NS only when adm
blood-review transfusions)
8) Emergency surgery (determined by injury)

e. Organ Donation *not tested with this unitread, 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-
94 RNSG 2432
 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
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 >life-threatening 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
RNSG 2432 95
 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

* 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

96 RNSG 2432
 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
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 MODSmultiple 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
RNSG 2432 97
 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 RBCs
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 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.
d. 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
e. Renal: Dec. kidney perfusion > to oliguria (urine output < 20 ml/o) ; develop ATN
(can recover function if basement membrane intact; epithelial cells regenerate)
f. Skin, temperature, thirst; Skin: cool, pale, hypothermic due to vasoconstriction

98 RNSG 2432
 g. 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!
h. 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

b. Cardiogenic (See p. 155, Box 6-3 Assessment Findings in Clients in Cardiogenic

Shock) (review from heart failure)

RNSG 2432 99
 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

100 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 pathogens 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)

RNSG 2432 101

 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.

102 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!)

RNSG 2432 103

 3. Life Span and Effects of Shock

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)

104 RNSG 2432

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..
d. Dec. in B/P by 20 and Inc. HR by 20 = shock
e. Oliguria
f. Tachycardia
g. Decreased level of Consciousness
h. 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)
RNSG 2432 105
 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)
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

106 RNSG 2432