1. Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240
SHOCK:
Ruth M. Kolk, RN,MS,CEN
Joy Borrero, RN, MSN
NUR240

2. Overview of Shock
Definition: Shock can be defined as a clinical clinical syndrome of decreased blood flow to body tissues resulting in cellular dysfunction and eventual organ failure.
Tissue perfusion in shock is inadequate to supply to oxygen and nutrients to cells. Although shock begins as a cellular phenomenon, it is a dynamic process which has been described as a final pathway to death.
Risk Factors
MAP: a change in sympathetic tone by dilation or constriction of blood vessels will affect MAP
MAP= 2D+S 3

3. CLASSIFICATION OF SHOCK
Hypovolemic: decreased intravascular volume-dehydration or hemorrhage
Cardiogenic : inability of the heart to pump blood-MI,valve disorders,dysrhythmias,arrest
Distributive or vasogenic: abnormality in the vascular system that produces a maldistribution of blood volume –neurogenic anaphylactic, septic, capillary leak
Obstructive –tension pneumo, pulmonary embolism, pulmonary HTN

4. Hypovolemic shock characterized by decreased intravascular volume
Hypovolemic shock characterized by decreased intravascular volume. Inadequate fluid volume in the intravascular compartments results in decreased blood flow and reduced tissue perfusion
Excessive fluid loss
Causes: internal fluid shifts
external fluid loss

5. Hypovolemia
Decrease in circulating volume – hemorrhage, plasma volume loss
Untreated will lead to hypovolemic shock –causes profound alteration in tissue perfusion . Cellular O2 demand exceeds available supply

6. Stages of Hypovolemic shock
1. Initial – MAP decreased less than 10mm Hg. Compensation is effective. No visible changes
2. Compensatory –body’s primary goal is to maintain blood flow to heart & brain through vasoconstriction ( epinephrine ) & shunting to vital organs. Anaerobic metabolism occurs.

7. Compensatory continued
Decreased peripheral blood flow
Tachycardia to maintain C.O.
Pulse pressure narrows
Initially BP may be “ normal “
Urine output decreases
Early s/s of shock : thirst, restless/anxiety , AMS

8. Shock : late signs & symptoms Progressive and Refractory Stages
Tachypnea & tachycardia
Weak pulse
Narrow pulse pressure
Flat neck veins
Pale , cool ,clammy skin
Hypotension
Oliguria

9. Progressive (intermediate )
Vital organs develop hypoxia
Significant changes occur at cellular level which makes resuscitation difficult
Cardiac dysrhythmias due to inadequate oxygenation
Microclotting :DIC begins

10. Refractory ( irreversible )
Tissue perfusion is negligible
Acidosis is prevalent
Cellular necrosis occurs due to lack of oxygen
Massive DIC
Multi system organ failure

11. Interventions for shock- GOALS?
Position patient – supine vs semifowlers
Large bore vascular access
Oxygen
Crystalloid infusions
Blood transfusions
Vasopressors
Prevent heat loss ( warmed IV fluids) , heating blankets

12. Cardiogenic Shock
Caused by decreased cardiac output that results from impaired heart function. Impaired heart function can be classified as systolic or diastolic.

13. Pathophysiology of Cardiogenic Shock
When LV cannot propel blood forward, two problems occur:
Decreased stroke with resultant declines in CO, BP & tissue perfusion.
As BP decreases perfusion to coronary muscles also decreases potentiating myocardial ischemia & predisposing the patient to further muscle damage.

14. Classic cardiogenic shock is secondary to systolic dysfunction
Classic cardiogenic shock is secondary to systolic dysfunction. (the ability of the heart to pump blood forward). The left ventricle has a greater workload and metabolic demand than the right ventricle. Left ventricular dysfunction affects forward flow of blood into systemic circulation.

15. Death of the heart (MI) places the patient at risk of developing cardiogenic shock.
Necrotic heart muscle does not contract normally leading to decreased CO and inadequate tissue perfusion.

16. This type of shock is the leading cause of in-hospital death
Those at the greatest risk are patients who have lost a large portion of Left ventricular muscle mass (anterior wall)

17. Noncoronary Causes
Valvular defects, such as stenosis or regurgitation.
Stenosis refers to incomplete opening of the valve (impedes blood flow )
Decreased stroke volume
Decreased cardiac output
cardiomyopathy

18. Pathophysiology Cardiogenic Shock
Impaired Function of LV
Inadequate systolic emptying
LV filling pressures
Stroke volume
LA pressures CO
Pulmonary congestion
Tissue perfusion
Pulmonary capillary
pressures
Pulmonary
Interstitial edema
Intra-alveolar edema

19. Distributive Shock Types: Neurogenic
Vasogenic ( anaphylactic, septic, endotoxins)
Septic

20. Sepsis-Induced Distributive Shock

21. Neurogenic Shock
Massive vasodilatation secondary to loss of sympathetic tone.
Cause is usually spinal cord injury or head injury
Rare and usually transitory

22. Neurogenic Pathophysiology
Massive Vasodilatation
Venous Dilation
Arterial Dilation
Venous return
Peripheral vascular
Ventricular filling
resistance
Stroke volume CO
Blood Pressure
Tissue Perfusion

23. Anaphylactic Shock
Characterized by massive dilatation and increased capillary permeability. Potentially life threatening.
Causes: Antigen – Antibody Reaction

24. Anaphylactic Shock Patho
Antibody
Antigen Antibody Reaction
Histamine
Release of Vasoactive Mediators
Prosglandin
Serotonin
Massive Vasodilatation
Capillary Refill
Veins
Arteries
Venous
return
SVR
Blood Pressure CO
Tissue Perfusion

25. Septic Shock Severe overwhelming infection.
It develops as a result of invasion of foreign microorganisms and subsequent over- activity & dysfunction of body’s defense system.
Septic shock & its sequelue are described as part of a clinical continuum.

26. Septic Shock Continuum
At one end of the continuum is infection.
Presence of microorganisms stimulate the body to activate the inflammatory response.
As inflammatory response becomes more widespread, SIR (Systemic Inflammatory Response) develops.

27. Sepsis can then progress to severe sepsis, in which the inflammatory response, initiated to help the body, begins to have harmful effects.
Imbalance between coagulation & fibrinolysis

28. Pathophysiology of sepsis
Severe sepsis, organ dysfunction hypoperfusion begins
Hypotension despite adequate fluid resuscitation
Lactic acidosis
MODS
Most common cause of ICU death

29. NCLEX time
In planning an in-service for a group of health care providers employed in an assisted-living facility, the nurse identifies which of the following as risk factors for sepsis? (Choose all that apply.
A.Cardiomyopathy
B.Low serum albumin level
C.History of anaphylaxis
D.Prolonged use of corticosteroids
E.Age older than 85
F.Chemotherapy treatment for cancer
abdf

30. NCLEX TIME
The nurse monitors the client for which clinical manifestation as a compensatory mechanism to the initial stage of shock?
A.Vascular vasodilation
B.Increased heart rate
C.Decreased mean arterial pressure
D.Elevated body temperature a

31. NCLEX Time
The nurse recognizes the client with which disorder is at greatest risk for hypovolemic shock?
A.Myopathies
B.Sepsis
C.Pericarditis
D.Burns d

32. NCLEX TIME
The nurse understands that the rationale for the administration of positive inotropic medications to the client in shock is to :
A.Increase heart rate
B.Increase cardiac contractility
C.Increase cellular metabolism
D.Increase oxygen consumption b

33. Critical Thinking Challenge
Your client is a 33-year-old woman who is returned to your outpatient unit after having a surgical tubal ligation by colposcopy. After moving her from the stretcher to her bed, you take her vital signs. Her pulse is 110 and thready, blood pressure is 90/72, respiratory rate is 28, and pulse oximetry is 89%. When you shake her shoulder, she opens her eyes but does not answer any questions.
What should you do first?
What other assessment data should you obtain?
Given the type of surgery, where would you expect bleeding to occur and what manifestations would you expect to find?
She still has an IV in her left hand infusing dextrose 5% in 0.45% saline. The postsurgical orders indicate that it should be removed when she is stable. Should you remove it now? Why or why not?

34. NCLEX Time
Which blood product is indicated for the client with hypovolemic shock secondary to large blood loss?
A.Packed red blood cells
B.Fresh frozen plasma
C.Platelets
D.Whole blood d

35. NCLEX Time
Which clinical finding does the nurse look for in the client responding effectively to treatment for the initial stage of shock?
A.Increased urine output
B.Increased heart rate
C.Decreased bowel sounds
D.Decreased blood pressure a

36. NCLEX Time
Which of the following clinical manifestations would indicate a worsening in the condition of a client in the late stage of septic shock?
A.Warm, flushed skin
B.Bleeding, oozing from intravenous sites
C.Increasing body temperature
D.Urine output of 20 mL/hr b

37. Your client who had tubal ligation by colposcopy has no external bleeding, but her abdomen is enlarging and you observe skin discoloration on her lower back.
Is O2 an appropriate tx for her?
Should you apply pressure to the abd area? Why or why not?
What type(s) of IV fluid would be indicated for her? Why?