Module E

Shock, MODS

Roy Model- Oxygenation-Perfusion

Required Readings (see syllabus for detailed reading)

Lewis, Heitkemper, & Dirksen, Medical-Surgical Nursing. (current ed)

a. Shock, systemic inflammatory response (SIRS), multiple organ dysfunction (MODS)

Recommended Readings

Pathophysiology book

Theory Objectives
Section 1- Shock
1. Define shock as a compromised process of oxygenation.
2. Differentiate among the three major classifications of shock in relationship to cause,
precipitating factors, stages, compensatory mechanisms and effect on major body
systems.
3. Discuss the pathophysiology, clinical manifestations and diagnostic evaluation of shock.
4. Discuss shock as a predisposing condition to disseminated intravascular coagulation
(DIC).
5. Identify first level assessment (behaviors) of a person in shock
6. Discuss goals of medical and drug therapy for the different types of shock.
7. Explain the nurse’s role in health promotion of shock.
8. Discuss the nurse’s role during each stage of shock.
9. Select and prioritize adaptation problems indicative of shock.
10. Discuss nursing interventions aimed at preventing serious side effects of shock.
11. Discuss the criteria to determine the effectiveness of nursing interventions.

Section 2- MODS, SIRS

1. Discuss the pathophysiology, clinical manifestations and diagnostic evaluation of
systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction
syndromes (MODS).
2. Discuss the goals of medical and drug therapy for SIRS and MODS.
3. Select and prioritize adaptation problems indicative of SIRS and/or MODS.
4. Discuss nursing interventions aimed at preventing serious side effects of SIRS or/
MODS.
5. Discuss the criteria to determine the effectiveness of nursing interventions

Clinical Component
Objectives
1. Student participation in the care of clients presenting to the emergency room.
 2. If possible, student to follow a trauma client, or a client in shock, through the emergency
room admission procedure.
3. Student to participate in the care of a client receiving a blood transfusion, fluid challenge,
or other hemodynamic challenge.
4. Student participation in the critical care or step down units.

Drugs
Fluid replacement options for the ED client (blood, isotonic fluids) and any emergency drugs
and/ or treatment of drug overdose’s (including illicit drugs and prescription drugs)

Diet
As it pertains to the level of the client

Laboratory
Specimens for data collection, emergency room panels

Critical Thinking Question

1. A 56 year old man admitted to the hospital three days ago, after being injured in an industrial
accident in which his right leg was crushed. Upon admission to the ED, he was hypovolemic
and was treated with intravenous fluids and blood transfusions. He underwent surgery the
day of the accident and has been recovering on a surgical unit in the hospital. He has been
stable since surgery and has had good pain control. At 2 am he puts on his call light and
summons the nurse. The client tells the nurse that he feels nervous inside and unsettled.
What should the nurse include in the assessment? What are the collaborative interventions to
stop the progression of shock? What type of shock is being described? What are the early
signs of shock described in the first scenario? What orders would you expect from the
physician? What diagnostic studies would you expect to be ordered?
2. A young man arrives at the ED by ambulance after a MVA. He is immobilized on a
backboard with a cervical collar. An oxygen mask is in place. You note shallow, slow
respiration and no movement of the left chest wall. His scalp is bleeding, and his left leg is
angulated. How would you prioritize the patient’s needs? Generate an assessment strategy
and describe the patient’s treatment needs.
3. A young woman with a toddler in her arms waits her turn in line at the triage desk of ED.
The child is crying and rubbing her eyes and face. You overhear the mother telling another
patient that the child has had an allergic reaction to her first soft-cooked egg, which the child
smeared on her face. Analyze the information and explain the conclusion you would draw
and why. Then describe the action you would take and the rationale for your decision.
 Module E- Emergency Care
Section 1- Shock
I. Definition and Pathophysiology
i. Definition
1. Clinical syndrome, systemic imbalance between oxygen supply and demand
2. Inadequate blood flow to body organs and tissue causing life-threatening
cellular dysfunction
ii. Pathophysiology
1. stimulus leads to alteration in hemodynamics
2. body responds by maintaining perfusion to vital organs, heart and brain
3. results in inadequate tissue and cellular perfusion
4. alterations result in drop in BP
II. Hemodynamic terms
i. Stroke volume- SV
ii. Cardiac output- CO
iii. Mean arterial pressure- MAP
III. Stages of Shock
i. Early reversible and compensatory shock
1. MAP drop 10-15 mm Hg
2. 25-35% decrease in circulating volume
3. sympathetic system activation
4. low BP = increase HR, contractility, peripheral vasoconstriction
5. temporary no harm to tissue r/t circulation maintained
6. determine underlying etiology
ii. Intermediate or progressive shock
1. 20% drop MAP
2. increase in fluid loss (1800 ml or more)
3. severe vasostriction- ? oxygen deficiency
4. body switch to anaerobic state
5. increased HR and vasoconstriction
6. ? hypoxic heart and brain
7. ischemic/ anoxic other tissues
8. acidosis, Hyperkalemia
9. needs rapid treatment
iii. Refractory or irreversible shock
1. anoxic tissues, cellular death spreading
2. extent of damage, difficulty to restore even is stable BP
3. cellular death leads to tissue death, vital organs fail
4. death
IV. Review the Effects of Shock on Body Systems-
System Cardio Resp GI/Liver Neuro Renal Skin

Initial s/sx
Progressive s/sx

Complications

V. Types of Shock
i. Hypovolemic
1. decrease in intravascular volume >15%
2. most common: occurs w/ other types of shock
3. etiology: hemorrhage, burns, severe dehydration, 3rd spacing
4. progresses through stages of shock without restoration of fluid volume
ii. Cardiogenic
1. pump compromised, cannot maintain cardiac output
2. etiology: AMI, cardiac arrest
3. develops left and right sided heart failure
4. cyanosis occurs with this type of shock
iii. Septic Shock
1. leading cause of death in ICU
2. etiology: gram negative bacteria, gram positive bacteria
3. at risk: chronic illness, poor nutrition, invasive procedures or tubes
4. course
a. septicemia develops
b. endotoxins disrupt circulation
c. normal coagulation mechanisms
d. inflammatory response triggered
e. phases
i. early- warm: skin flushed due to vasodilation
ii. late- cold: skin cool due to fluid deficit
iv. Neurogenic Shock
1. imbalance between parasympathetic and sympathetic stimulation of vascular
smooth muscle, resulting in sustained vasodilation
2. etiology: head injury, spinal cord trauma, insulin reactions, anesthesia
v. Anaphylactic Shock
1. result in widespread hypersensitivity
2. vasodilation occurs leading to hypovolemia and altered cellular metabolism
3. sensitized in past, re-contact
4. allergic reaction w/ large amounts of histamine released
5. histamine leads to increased capillary permeability and massive vasodilation
6. develops respiratory distress w/ bronchospasm and laryngospasm

VI. Nursing Diagnosis

i. Decreased cardiac output
ii. Altered tissue perfusion
iii. anxiety
VII. Interventions (AIDC)

i.
Focus on treating the etiology to stop progression
ii.
Rapid identification, rapid diagnosis, rapid aggressive treatment
iii.
Goal: improve arterial oxygenation and tissue perfusion
iv.Determine type of shock
v.Diagnostic tests
1. H/H- ?hypovolemic
2. ABG- compensatory mechanisms
3. Electrolytes
4. BUN/ Creat: ?renal function
5. WBC, Bld cultures: septic shock, causative agent
6. Cardiac enzymes: cardiogenic shock
vi. Medications
1. Inotropic agents: improve cardiac contractility
2. vasoactive agents: cause vasoconstriction or vasodilation according to client’s
symptoms
3. Other- antibiotic, steriods
vii. Oxygen therapy
1. patent airway, oxygenation
2. monitor ABG’s, pulse ox (more accurate in early stage)
3. mechanical ventilation, trach
viii. Fluid replacement
1. essential in hypovolemic shock
2. Crystalloids
a. Dextrose or electrolyte solutions
b. Increase intravascular and interstitial fluid vol
c. I.e.: Isotonic (0.9 %NaCl, LR), hypotonic (D5 ½ NS)
3. Colloids
a. Do not diffuse easily through capillary walls
b. Fluids stay in vascular compartment; increase osmotic pressure
c. I.e.: albumin, hetastarch, plasma protein fraction, dextran
4. Blood and Blood prod
a. Treatment of hemorrhage
b. Restore coagulation properties
Nursing: assess the situation; notify the MD in early phase of shock, transfer to critical unit, and
supportive care to the pt/ family

VIII. Blood Transfusions

i. Type and Crossmatch
1. Type A- A antigens
2. Type B- B antigens
3. Type O- no antigens (universal donor)
4. Type AB- A and B antigens (universal recipient)
ii. Blood transfusion reactions
Types of Reactions Febrile Hypersensitivity Hemolytic Volume Over
 Signs/ symptoms

Nursing Interventions

Section 2- MODS- multiple organ dysfunction syndrome

SIRS- systemic inflammatory response syndrome

DEFINE_
RISK FACTORS-

Pathophysiology
 Neuroendocrine activation
o Early responses trigger “stress hormones” aka “fight or flight”
 Inflammatory response
o Activation protects the pt from invading microorganisms, limit the extent of the injury,
and promote rapid healing. While the process is to protect, lack of appropriate regulation
lead to uncontrolled inflammation, dysfunction- DIC.
 Loss of endothelial integrity
o Endothelium is a single layer of protection. Damage results in increased permeability,
change in coagulation, and bld flow. Capillary leakage, edema, and DIC result.
 Maldistribution of volume
o Manifestation of generalized intracellular and extracellular edema, patchy areas of bld
flow, lack of oxygen and hypoxia
 Imbalance of oxygen supply/ demand
o Oxygen delivery is primarily by arterial, CO, hemoglobin level. Pt’s often suffer
ventilation/ perfusion, myocardial dys fx, and/ or hemorrhage.
 Alterations in metabolism
 During stress there is increased energy expenditure, hypermetabolism.
Gluconeogenesis increases, protein stores are depleted by catabolism. If
unattended than auto catabolism.

Assessment- clinical manifestations

 Cardiovascular
o Early signs- elevated CO and preload, decreased SVR/ venous return.
o Skin is warm, often flushed = false sense of security of adequate perfusion (vasodilation;
however, there are areas of vasoconstriction and hypoxia)
o Later- ectopy and decompensation
 Pulmonary
o Early- increased RR, resp alkalosis
 o Leaky pulm. Capillary membranes- ARDS, lung stiffening
 GI
o Hepatitic dys fx- coagulopathies, hepatic encephalophy, decreased synthesis of vital
proteins, poor drug clearance
o Increased pt/ PTT, disorientation, decreased albumin levels, increased toxic levels of
drugs
o Hypoperfusion of GI- Septicemia r/t translocation of gut bacteria
o Diarrhea, gross or occult bld stools, pain, distention, ileus
 CNS
o Restlessness, agitation, decrease LOC
 Renal
i. Acute tubular necrosis, decrease UA, increased BUN/ creat
 Hematologic system
o Initial- increased WBC
o Terminal stage- abnormal/ low WBC, decreased platelets
 Laboratory values
o Hyperglycemia = hyperdynamic state
o Terminal- hypoglycemia, accelerated coagulation, excessive fibrinolysis

Nursing Diagnosis
Anxiety r/t disease process, threat of death, possible role changes
Decreased cardiac output r/t oxygenation desaturation

Collaborative Care
 Controlling the initiation
 Prevention and early ID of infectious/ inflammatory process (culture everything, poss
early surgical debridement)
 Restoration of oxygen supply/ demand balance
 Provision of nutritional support and metabolic demands
 Individual organ support
 Psychologic support for the pt and family