T3 Shock Flashcards

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1
Q

Any problem impairing oxygen delivery* to tissues and organs can precipitate _____??

Widespread abnormal cellular metabolism
Oxygenation and tissue perfusion needs not met*

“Whole-body” response; “syndrome”
Lead to life-threatening emergency

All organs, tissues and cells need a continuous supply of oxygen

Lungs first bring oxygen into the body through ventilation and gas exchange. Cardiovascular system delivers oxygen by perfusion to tissues.

It is a condition and not a disease, it is a whole body response that occurs when too little oxygen is delivered.

All body organs are affected and either work harder to adapt and compensate or fail to function. Syndrome because it happens in a predictable sequence.

Any problem that impairs perfusion and gas exchange to tissues can start the syndrome of _____ and lead to life threatening emergency.

A

Shock

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2
Q

Perfusion measured by mean arterial pressure (MAP)*

Factors that influence MAP:

A

total blood volume, cardiac output, size and integrity of vascular bed
Vasodilation
Vasoconstriction

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3
Q

Types of shock

A
Hypovolemic
Cardiogenic
Distributive 
Includes septic shock, neurogenic shock, capillary leak syndrome, and anaphylactic shock)
Obstructive

Table 37-1 causes and types of shock

More than one type of shock can be present at the same time: trauma + myocardial infarction

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4
Q

Shock is classified by ?

Most signs and symptoms of shock are similar regardless of what starts the process or which tissues are affected first. Symptoms result from ??

A

Shock is classified by type of impairment causing it

Most signs and symptoms of shock are similar regardless of what starts the process or which tissues are affected first.

Symptoms result from compensatory mechanisms in an attempt to maintain perfusion.

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5
Q

Low circulating blood volume*
-Causes mean arterial pressure (MAP) decrease; inadequate total body oxygenation

Commonly caused* by hemorrhage (external or internal), dehydration
-Other causes: trauma, ulcers, inadequate clotting, dehydration, vomiting, diarrhea

Total body fluid decreases*

A

Hypovolemic shock

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6
Q

Direct pump failure (fluid volume is not effected)*

Causes are directly related to the heart

  • MI
  • Cardiac arrest
  • Dysrhythmias
A

Cardiogenic shock

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7
Q

Fluid is shifted from central -vascular space*

Total body fluid is normal or slightly increased

Includes septic shock, neurogenic shock, capillary leak and anaphylactic shock*

Other causes:
-Pain, stress, capillary leak, burns

A

Distributive shock

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8
Q

?? is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs.

?? is the loss of MAP that occurs when sympathetic nerve impulses are decreased and blood vessels smooth muscles relax causing vasodilation

??is an extreme type of allergic reaction. It begins within seconds to minutes after exposure to a specific allergen in a susceptible adult. The result is widespread loss of blood vessel tone, with decreased blood pressure and cardiac output.

??is a widespread infection that triggers whole-body inflammation. It leads to distributive shock when infectious microorganisms are present in the blood and is most commonly called_________?. A complete discussion of the pathophysiology, prevention, and care for the patient with sepsis and septic shock begins with theIMMUNITYconcept exemplar.

???is the response of capillaries to the presence of histamine and other chemicals that enlarge capillary pores and allow fluid to shift from the capillaries into the interstitial tissues. These fluids are stagnant, and noGAS EXCHANGEoccurs. Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, large wounds, kidney disease, hypoproteinemia, and trauma

A

Blood volume

Neural induced distributive shock

Anaphylaxis

Sepsis

septic shock

Capillary leak syndrome

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9
Q

Cardiac function is decreased by a noncardiac factor.
Total body fluid is not effected but central volume is decreased

Causes:*
Cardiac tamponade
Arterial stenosis
Pulmonary embolism
Tension pneumothorax
A

Obstructive shock

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10
Q

S/s of shock

A

Similar regardless of type

Symptoms result from compensatory mechanisms*

I’m Chart 37-1

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11
Q

Stages of shock

A

Initial
Nonprogressive
Progressive
Refractory

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12
Q

Which stage?

Baseline MAP decreased by <10 mm Hg*
-Total blood volume and cardiac output are directly related to MAP
-So increases or decreases directly effect MAP
Heart and respiratory rate increased from baseline, or slight increase in diastolic blood pressure*
-Adaptive responses of vascular constriction, increased heart rate*

MAP, mean arterial pressure.

A

Initial stage

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13
Q

Non progressive stage?

A

MAP decreases by 10 to 15 mm Hg*

Kidney and hormonal adaptive mechanisms activated*
-Ex: retain more fluid in hypovolemic

Tissue hypoxia in nonvital organs

  • Skin
  • GI tract

Acidosis and hyperkalemia

Stopping conditions that started shock and supportive interventions can prevent shock from progressing*

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14
Q

Progressive stage?

A

Sustained decrease in MAP of >20 mm Hg from baseline*

Compensatory mechanisms are
functioning but starting to fail*

Vital organs develop hypoxia*

  • Less vital organs become anoxic and ischemic
  • 5-20% drop in O2 sat

Life-threatening emergency

Conditions causing shock must be corrected within 1 hour of progressive stage onset*

Short phase

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15
Q

Refractory stage?

A

Too little oxygen reaches tissues; cell death and tissue damage result*

Body cannot respond effectively to interventions; shock continues

Rapid loss of consciousness, nonpalpable pulse, cold, dusky extremities; slow, shallow respirations; unmeasurable oxygen saturation*

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16
Q

Sequence of cell damage caused by massive release of toxic metabolites and enzymes*
Becomes a vicious cycle
-More dead cells release more metabolites
Microthrombi form
-Block tissue perfusion and damage even more cells
Occurs first in liver, heart, brain, kidney
Myocardial depressant factor from ischemic pancreas

A

Multiple organ dysfunction syndrome MODS

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17
Q

Risk factors and prevention of hypovolemic shock

A

Just being a patient is a risk factor

Can usually be prevented*

Avoid trauma and hemorrhage

  • Proper safety equipment
  • Seat belts
  • Awareness of hazards in home/workplace

Assess for dehydration*
Secondary prevention*
-Assess for early manifestations
Patient teaching

18
Q

Physical assessment of hypovolemic shock

Most symptoms we discuss are a result of ??

A
Cardiovascular
-
Decreased cardiac output
Increased pulse*
Decreased blood pressure*
Narrowed pulse pressure*
Postural hypotension
Low central venous pressure
Flat neck and hand veins in dependent positions
Slow capillary refill*
Diminished peripheral pulses*

??compensatory efforts

19
Q

Respiratory manifestations hypovolemic shock

A

Increased respiratory rate
Shallow depth of respirations
Increased Paco2
Decreased Pao2

Paco2, partial pressure of arterial carbon dioxide;

Pao2, partial pressure of arterial oxygen.

20
Q

Priority problems of hypovolemic shock

A

Hypoxia due to hypovolemia

Inadequate PERFUSION due to active fluid volume loss and hypotension

Anxiety due to potential for death and decreased cerebral PERFUSION

Decreased cognition due to decreased cerebral PERFUSION

21
Q

Priority interventions for hypovolemic shock

A

Focus on reversing the shock
-Restoring fluid volume

Ensure a patent airway

Insert/Maintain an IV

Administer oxygen*

Keep head flat or less than 30 degrees

Control bleeding*

22
Q

Tx for hypovolemic shock

A
Nonsurgical management
Oxygen
IV therapy
Drug therapy
Hemodynamic monitoring
23
Q

Pt education for hypovolemic shock

A

Hypovolemic shock is a complication of another condition and is resolved before patients are discharged from the acute care setting.

Teach patients and family members early indicators of shock

  • Increased thirst
  • Decreased urine output
  • Light-headedness
24
Q

Complex type of distributive shock*—bacterial/fungal infection progresses to dangerous condition within days

Disregulated response to infection

Infectious organisms have entered the bloodstream. As their numbers increase, widespread inflammation, known assystemicinflammatoryresponsesyndrome (SIRS), is triggered as a result of infection escaping local control.

???—a life-threatening organ dysfunction resulting from a dysregulated host response to infection*

Systemic Inflammatory Response Syndrome (SIRS)

A

Sepsis—a life-threatening organ dysfunction resulting from a dysregulated host response to infection* (Kleinpell et al., 2016)

Septic shock

25
Q

Septic shock progression stages?

A

Local infection

Systemic infection

SIRS (systemic inflammatory response syndrome)

Organ failure (sepsis)

MODS (multiple organ dysfunction syndrome) (septic shock)

Death

26
Q

Form of distributive shock

Stage of sepsis and SIRS—multiple organ failure evident; uncontrolled bleeding occurs*

Capillary leak occurs: plasma leaks into tissues at this time*

Death rate for patients in this stage is very high

A

Septic shock

27
Q

Complications of sepsis

A

SIRS

DIC: Inappropriate clotting, microthrombi, causes hypoxia and bleeding

Microthrombi formation is widespread, with clots forming where they are not needed. This process uses up (consumes) many of the available platelets and clotting factors, a condition known asdisseminated intravascular coagulation (DIC).Damage to endothelial cells reduces anticlotting actions and triggers the formation of even more small clots, increasing DIC

28
Q

Health promotion and maintenance for sepsis

A

Prevention is the best management strategy

Evaluate risk

Use aseptic technique

Early detection of sepsis*

29
Q

Assessment for septic shock

A

History:
Age*
Recent illness
Recent trauma

Sepsis develops easily among older adults and those with decreased immunity

30
Q

S/s of septic shock

A

Low BP, high HR

Decrease O2 saturation

ARDS

Skin is warm in initial stages then clammy and pale with mottling

Petechiae, brusing, bleeding (DIC)

Low U/O

31
Q

Labs to dx septic shock

A

CBC
Cultures
Lactate/procalcitonin*
Coag panel

32
Q

Interventions for septic shock

A

Table 37-5*

Oxygen therapy*

Drug therapy

The most common causative agents are gram-negative bacteria*

Multiple antibiotics*

Vasoconstrictors*

Agents to enhance myocardial perfusion and contractility

Blood replacement therapy

33
Q

A 59-year-old male is 3 days postoperative after a colon resection. The nurse has delegated to the unlicensed assistive personnel (UAP) to take his morning vital signs. At 8:00 AM the NA reports that the patient’s oral temperature is 101.6º F.

What is the nurse’s priority action?

A

ANS: When the patient’s elevated temperature is reported by the nursing assistant, it is the nurse’s responsibility to determine what action should be taken. The nurse should proceed to his room to perform a complete assessment.

34
Q

Upon assessment, the nurse notes that the patient is flushed and slightly diaphoretic. He appears lethargic, but responds to simple questions. His vital signs are now BP 90/40, HR 134, RR 26 and deep, and his temperature has risen to 102.8º F. Lungs are clear throughout. His abdominal wound has a dressing that is moist with a moderate amount of purulent drainage.

What is the nurse’s interpretation of this data?

A

ANS: The development of infection should be considered based on the patient’s operative history and vital signs. He has tachycardia and increased respirations, as well as a moderate amount of purulent drainage at the abdominal dressing site. Surgical dressings should not contain purulent drainage.

35
Q

Twenty minutes later, the nurse calls the health care provider to report the abnormal findings. The provider orders
Tylenol 650 mg PO prn q6h for temp above 101º F
Blood cultures × 2, 5 minutes apart
C&S of abdominal wound drainage
Vancomycin 750 mg IVPB over 1 hour every 24 hour

In what order should the nurse implement these interventions?

A

ANS: C, B, D, A

Based on the findings, this patient is possibly developing sepsis. The wound should be cultured immediately and the nurse should notify the laboratory that blood cultures must be obtained. All cultures must be drawn before administering the antibiotics. The first anti-infective should be started within 1 hour after the blood and wound cultures are obtained. The nurse may then give the patient Tylenol for his fever.

36
Q

Over the next hour, the patient continues to decline with a decreased level of consciousness and a temperature of 103.8º F. BP is 80/40, HR is 134, and RR is 34. The nurse calls the provider to report these findings and obtain orders for the patient to be transferred to the ICU. When preparing for this transfer, the nurse notes that the O2 saturation is 87% on room air.

What is the priority nursing action?

Draw an arterial blood gas sample.
Apply oxygen at 2 to 3 L per nasal cannula.
Administer acetaminophen 650 mg by mouth.
Place the patient on a cardiac telemetry monitor.

A

ANS: B

The patient is gravely ill. The first priority is his airway. He has a rapid respiratory rate and a low SaO2, so supplemental oxygen should be applied first. His elevated temperature should also be addressed. The nurse may choose to call the Rapid Response Team to help stabilize the patient, even though he is being transferred to the ICU.

37
Q

Your patient is a 42-year-old female that arrives in the ED with complaints of fever and not feeling well. She is currently undergoing chemotherapy for bladder cancer. She has an indwelling urinary catheter with scant amount of dark, foul smelling urine. She has a temperature of 102.2F, HR 136, BP 110/50 and RR 28. She is allergic to penicillin and Sulfa.
What type of shock is she experiencing?
What interventions do you anticipate the doctor will order?
What can you teach this patient about prevention of infection?
The doctor orders Bactrim. What should you be concern about? Why?

A

?

38
Q

Within 30 minutes of the patient’s transfer to the ICU, his condition continues to deteriorate. His SaO2 continues to fall, RR is 36/min, and the ICU nurse notes that there is blood oozing around his IV catheter sites. A Foley catheter is placed, and his urine output is minimal.
What is the nurse’s interpretation of these assessment findings?

A

The patient is going into severe sepsis. The main manifestations are low oxygen saturation, rapid respiratory rate, decreased to absent urine output, and changes in cognition. He is at risk for septic shock. The blood oozing around his IV catheters may indicate the presence of DIC.

39
Q

A 37-year-old male is admitted with a severely abscessed tooth, BP 90/42, HR 136, RR 28, Spo2 90% on room air, temperature 38.7º C. The nurse suspects that the patient has developed sepsis. What is the priority nursing intervention?

Insert an indwelling urinary catheter.
Initiate intravenous fluid resuscitation.
Obtain a complete chemistry for laboratory analysis.
Administer prescribed antibiotics prior to blood cultures.

A

ANS: B

Initiating IV fluids is the primary intervention, followed by obtaining laboratory values, blood cultures, and providing oxygen. Antibiotics should be started ASAP, however, after blood cultures are obtained. An indwelling urinary catheter is lower in the list of necessary priority interventions. The Surviving Sepsis Campaign and IHI Sepsis Bundle provide guidelines for interventions for early resuscitation and treatment of patients with sepsis. Once a patient is suspected of sepsis, the following items (initiated within 6 hours and completed within the first 24 hours) have been found to enhance survival: (1) Obtain, monitor, and treat serum lactate. (2) Obtain blood cultures prior to antibiotics. (3) Administer broad spectrum antibiotics as soon as possible. (4) Aggressively treat hypotension with IV fluids. (5) Apply vasopressor agents for hypotension that does not respond to fluids. (6) Assess and maximize tissue oxygenation (monitor SVO2). (See Table 37-5, p. 753.)

40
Q

When assessing a patient for shock, the nurse knows that which symptom is the earliest manifestation of shock?

Anuria
Increased heart rate
A decrease in respiratory rate and depth
A change in both systolic and diastolic blood pressure

A

ANS: B

The earliest clinical signs of hypovolemic shock are cardiovascular: increased heart rate and respiratory rate are the earliest manifestations of shock. Changes in systolic blood pressure are not always present in the initial stage of shock because of compensatory mechanisms and should not be used as the main indicator of shock presence or progression.

41
Q

Which clinical manifestations does the nurse recognize that indicates worsening in the condition of a patient in the refractory phase of shock?

Warm, flushed skin
Urine output of 20 mL/hr
Increasing respiratory rate
Bleeding, oozing from IV sites

A

ANS: D

The onset of disseminated intravascular coagulation (DIC) as evidenced by bleeding to include oozing from IV sites indicates a consumption of clotting factors that occurs in the refractory stage of shock. The refractory stage or irreversible stage of shock occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues. Vital organs have overwhelming damage. The body can no longer respond effectively to interventions and shock continues. The patient usually requires full system support (for example, mechanical ventilation, vasopressor agents, renal support [dialysis]), rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation.