Module E Shock, MODS Roy Model-Oxygenation-Perfusion Required Readings (See Syllabus For Detailed Reading)
Module E Shock, MODS Roy Model-Oxygenation-Perfusion Required Readings (See Syllabus For Detailed Reading)
Module E Shock, MODS Roy Model-Oxygenation-Perfusion Required Readings (See Syllabus For Detailed Reading)
Shock, 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.
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
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
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
Nursing Interventions
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.
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