Shock: Renee Smith RN, DNP, Edd (C), MSN, Cen, PHN, Acnp, TCRN

Shock
Renee Smith
RN, DNP, EdD(c), MSN, CEN, PHN, ACNP, TCRN
Trauma Program Manager
St. Francis Medical Center
Lynwood, CA
CDU Faculty
Shock Objectives
 Define Shock
 Describe four types of shock
 Discuss the nursing assessment of
patient in shock
 Delineate appropriate nursing
interventions in shock
 Evaluate outcomes for patient in shock
Shock
 Shock is a syndrome resulting from
inadequate perfusion of tissues
 Decreased supply of oxygen & nutrients to
meet metabolic demands of cell
(ENA, 2001)
 Shock is systemic response to clinical insult
(illness or injury) resulting in inadequate
perfusion
(ENA, 2007)
Shock
 Regardless of precipitating cause, shock leads

to mean arterial blood pressure inadequate to
meet the needs of the tissues
 Initially compensation mechanism to improve
perfusion
 When compensation fails cascade of cellular
abnormalities end organ dysfunction and
death
Shock
 Early symptoms of shock often subtle &

require vigilance by health care team -
nursing to avoid them being overlooked
Shock 3 Stages
 Compensated (Nonprogressive)
 Uncompensated (Progressive)
 Irreversible (Refractory)
Compensated (Nonprogressive)
 Receptors sense drop in systemic

pressure
 SNS activated to restore adequate
tissue perfusion
 Vital organ function preserved: Heart &
Brain
 Cell converts from aerobic to anaerobic
respiration
Compensated (Nonprogressive)
 Resulting lactic acidemia causes cellular

damage
 Preexisting medical history & age cause
additional stressors
Compensated Shock Signs!
 Tachycardia, Rising DBP, reduced PP(S-D)

 Weak pulse, Cool periphery, increase CRF>2
 Low, concentrated UOP
 Increased RR
 Nausea
 Diaphoresis, Increased Blood Sugar
 Confusion, Anxiety, Restlessness
Uncompensated (Progressive)
 Compensation mechanisms begin to fail to

maintain perfusion to vital organs
 Mechanisms initially helpful become
ineffective & cause further tissue damage
 Cellular derangement & death within all organ
systems
 Severe lactic acidemia, inflammation, immune
system activation
Uncompensated (Progressive)
 Multisystem deterioration or failure

 Even if oxygen is sufficient, some cells
damage & not able to use it
Irreversible (Refractory)
 Final stage of shock critical point no

treatment can reverse process
 Cellular destruction so severe death
inevitable
 Specific causes of shock
indistinguishable
Irreversible (Refractory)
Each patients shock state can be unique,

clinical progression may be altered by
several factors:
 Cause of shock
 Patient age
 Severity
 Duration of hypoperfusion
 Presence of comorbidities
Shock Etiologies
(ATLS, 2012)
 Hypovolemia (volume loss)
 Cardiogenic (broken pump)
 Obstructive (obstruction to flow)
 Distributive (have volume - in wrong place)
Hypovolemic
 Etiology: hemorrhage, burns, vomiting

 Underlying pathology: whole blood loss,
plasma loss
 Most common shock state
 Classified into 4 groups
4 Classes
 Class I: up to 15% loss

 Class II: 15-30% loss
 Class III: 30-40% loss
 Class IV: >40% loss
(ENA, 2002)
Shock Class
Cardiogenic
 Inadequate perfusion from inadequate

contractility
 Etiology:Blunt cardiac injury,
dysrhythmias, cardiac failure, cardiac
tamponade, myocardial infarction
 Pathology: loss of cardiac contractility,
reduced cardiac output
Cardiogenic Shock
 Left ventricular rupture

Obstructive
 Etiology: cardiac tamponade, tension

pneumothorax, tension hemothorax
 Pathology: compression of heart with
obstruction to atrial filling, mediastinal
shift with obstruction to atrial filling,
combination of both
Cardiac tamponade CXR
Distributive
 Etiology: neurogenic shock (SCI),

anaphylactic shock (allergic rxn), septic
shock (toxin released by bacteria)
 Pathology: venous pooling,
maldistribution of blood volume,
shunting in microcirculation, decrease
venous resistance, poor distribution of
blood flow
Distributive Shock
Nursing Assessment of Shock
Nursing Physical Assessment
 Determine LOC
 Assess breathing effectiveness, rate
 Identify bleeding sources
 Assess skin signs (ashen, pale, blue,
temperature? moisture?)
 Observe external jugular veins (flat,
distended (*hypovolemia may not be
distended)
Nursing Physical Assessment
 Obtain B/P (auscultate, doppler)

 Calculate pulse pressure (S-D)
 Auscultate heart: muffled sounds,
 Auscultate breath sounds: decreased,
absent,
 Auscultate bowel sounds: absent- intra
abdominal bleeding or profound shock
Diagnostics
 Radiological studies: CXR, pelvis, femur
 Spiral CT (Rapid Pan Scan)
 Angiography (Vascular injury Aortic/Pelvic)
 Labs: type & cross, UA, ABG, CBC, chem
panel, trauma panel (acidosis, hypoxia?)
*LACTATE <2 & BASE DEFICIT+/- 2
 The nurse assures the tests are performed
and communicates with the team, if patient
unstable nurse stays with the patient !
Aortic Angiography
Pelvic Angiography
Nursing Diagnosis
 Gas exchange, impaired r/t:

 Ineffective breathing, ineffective airway,
aspiration, altered blood flow, oxygen
carrying capacity
 Interventions: ABC’s, O2, blood,
 Outcomes: ABG (wnl), skins, LOC, resps,
bilateral breath sounds, heart sounds normal
(ENA, 2001)
Planning & Implementation
 Administer oxygen (NRBM, AMBU,ETT,Vent)- Oxygen
is essential for shock!
 Control any bleeding (direct pressure, Quik Clot
dressing, OR, meds factor VIII, TXA)
 IV Fluids LR, NS, Plasmalyte*
 IV Voluven
 Initiate blood replacement (O-, type specific) FFP,
Cryoprecipitate, Platelets, MTP
 Give blood through filter, use only NS! (Consider
autotransfusion as appropriate)
 Prepare for OR
Planning & Implementation
 Legs elevated
 Additional large bore IV’s needed? Or
Level I? IV Vasopressors?
 Insert NG or OG tube
 Place foley catheter
 Cardiac monitoring a must, rate, rhythm
 Pulse oximetry (good waveform must
be present)
NGT placement?
Ongoing Assessment &
Evaluation
 ABC’s (airway still okay?)
 Monitor urinary output (end organ perfusion)
 IV resuscitation, I&O’s
 Collaborate with team members
 Monitor temperature (hypothermia can cause
resuscitation problems or failures!),
 Monitor Labs: Serum Lactate, Base Deficit,
Lytes, H&H
 Recall the Triad: Hypothermia,
Coagulopathy, Acidosis
https://www.youtube.com/watch?v
=rPqhB0ScvIo&feature=player_det
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Shock: Renee Smith RN, DNP, Edd (C), MSN, Cen, PHN, Acnp, TCRN

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Shock

 Regardless of precipitating cause, shock leads

 Early symptoms of shock often subtle &

 Receptors sense drop in systemic

 Resulting lactic acidemia causes cellular

 Tachycardia, Rising DBP, reduced PP(S-D)

 Compensation mechanisms begin to fail to

 Multisystem deterioration or failure

 Final stage of shock critical point no

Each patients shock state can be unique,

 Etiology: hemorrhage, burns, vomiting

 Class I: up to 15% loss

 Inadequate perfusion from inadequate

 Left ventricular rupture

 Etiology: cardiac tamponade, tension

 Etiology: neurogenic shock (SCI),

 Obtain B/P (auscultate, doppler)

 Gas exchange, impaired r/t:

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