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SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN
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Page 1: Shock States Student Ppt

SHOCK:

Ruth M. Kolk, RN,MS,CENJoy Borrero, RN, MSN

Page 2: Shock States Student Ppt

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

Page 3: Shock States Student Ppt

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

Page 4: Shock States Student Ppt

Hypovolemic Shock Characterized by decreased intravascular

volume. Inadequate fluid volume in the intravascular compartments results in decreased blood flow and reduced tissue perfusion

Decrease in circulating volume – hemorrhage, plasma volume loss

Untreated hypovolemia will lead to hypovolemic shock –causes profound alteration in tissue perfusion. Cellular O2 demand exceeds available supply

Page 5: Shock States Student Ppt

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.

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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

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Shock: Progressive and Refractory Stages

Tachypnea & tachycardia Weak pulse Narrow pulse pressure Flat neck veins Pale , cool ,clammy skin Hypotension Oliguria

Page 8: Shock States Student Ppt

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

Page 9: Shock States Student Ppt

Refractory ( irreversible )

Tissue perfusion is negligible Acidosis is prevalent Cellular necrosis occurs due to lack

of oxygen Massive DIC Multi system organ failure

Page 10: Shock States Student Ppt

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

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Cardiogenic Shock

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

Page 12: Shock States Student Ppt

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.

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Cardiogenic Shock 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.

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.

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Other 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

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Distributive Shock

Types: Neurogenic Vasogenic ( anaphylactic, septic,

endotoxins) Septic

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Neurogenic Shock

Massive vasodilatation secondary to loss of sympathetic tone.

Cause is usually spinal cord injury or head injury

Rare and usually transitory

Page 17: Shock States Student Ppt

Anaphylactic Shock

Characterized by massive dilatation and increased capillary permeability. Potentially life threatening.

Causes: Antigen – Antibody Reaction

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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.

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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.

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Sepsis

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

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Pathophysiology of sepsis

Severe sepsis, organ dysfunction hypoperfusion begins

Hypotension despite adequate fluid resuscitation

Lactic acidosis MODS Most common cause of ICU death

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Sepsis treatment

Treatment is based on S/S Oxygen, IV fluidsBlood culturesConsider antibiotics Monitor VS Consider vasopressors

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Obstructive shock

Pulmonary emboli Cardiac tamponade Tension pneumothorax Pulmonary hypertension

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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.CardiomyopathyB.Low serum albumin levelC.History of anaphylaxisD.Prolonged use of corticosteroidsE.Age older than 85F.Chemotherapy treatment for cancer

Page 25: Shock States Student Ppt

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

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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

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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

Page 28: Shock States Student Ppt

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?

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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

Page 30: Shock States Student Ppt

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

Page 31: Shock States Student Ppt

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

Page 32: Shock States Student Ppt

Case study continues

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?