37
SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Embed Size (px)

Citation preview

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

SHOCK:

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

NUR240

Page 2: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

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

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 lossCauses: internal fluid shifts external fluid loss

Page 5: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Page 6: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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.

Page 7: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Page 8: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Shock : late signs & symptomsProgressive and Refractory Stages

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

Page 9: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Refractory ( irreversible )

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

of oxygen Massive DIC Multi system organ failure

Page 11: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Page 12: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Cardiogenic Shock

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

Page 13: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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.

Page 14: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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.

Page 15: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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.

Page 16: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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)

Page 17: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Page 18: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Pathophysiology Cardiogenic Shock

Impaired Function of LV

Stroke volume

CO

Tissue perfusion

LV filling pressures

LA pressures

Pulmonary congestion

Pulmonary capillarypressures

Pulmonary

Interstitial edema Intra-alveolar edema

Inadequate systolic emptying

Page 19: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Distributive Shock

Types: Neurogenic Vasogenic ( anaphylactic, septic,

endotoxins) Septic

Page 20: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Sepsis-Induced Distributive Shock

Page 21: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Neurogenic Shock

Massive vasodilatation secondary to loss of sympathetic tone.

Cause is usually spinal cord injury or head injury

Rare and usually transitory

Page 22: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Neurogenic Pathophysiology

Massive Vasodilatation

Venous Dilation

Venous return

CO

Ventricular filling

Stroke volume

Arterial Dilation

Peripheral vascular

resistance

Blood Pressure

Tissue Perfusion

Page 23: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Anaphylactic Shock

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

Causes: Antigen – Antibody Reaction

Page 24: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Anaphylactic Shock Patho

Antigen Antibody Reaction

Release of Vasoactive Mediators

Histamine

Prosglandin

Serotonin

Antibody

Massive VasodilatationCapillary Refill

Veins ArteriesSVRVenous

return

CO Blood PressureTissue Perfusion

Page 25: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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.

Page 26: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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.

Page 27: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Page 28: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

Pathophysiology of sepsis

Severe sepsis, organ dysfunction hypoperfusion begins

Hypotension despite adequate fluid resuscitation

Lactic acidosis MODS Most common cause of ICU death

Page 29: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

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

Page 31: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

Page 32: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

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?

Page 34: SHOCK: Ruth M. Kolk, RN,MS,CEN Joy Borrero, RN, MSN NUR240

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

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

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

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?