Unit 1: Sepsis/Septic Shock Flashcards

1
Q

Sepsis

A

life-threatening organ dysfunction caused by a deregulated host response to infection

  • start of the infection and can lead to septic shock w/ tissue damage, organ failure, and death
  • this occurs when the inflammatory response is no longer localized and there is an uncontrolled physiologic response
  • organ dysfunction and hypoperfusion in the presence of an infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Septic Shock

A

sepsis w/ underlying circulatory and cellular/metabolic abnormalities profound enough to substantially increase mortality

  • occurs when circulatory and metabolic abnormalities are profound; increased mortality
  • circulatory system is unable to supply adequate amounts of oxygen to the tissues
  • decreased cardiac output
  • decreased oxygen delivery
  • decreased oxygen consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cardiac Output

A

amount of blood ejected by the heart each minute

  • affected by contractility which is the force of the mechanical contraction
  • poor contractility decreased stroke volume thus decreasing cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Oxygen Delivery (DO2)

A

amount of oxygen delivered to the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Oxygen Consumption (VO2)

A

reflects the amount of oxygen extracted from the blood at the tissue level
-can be measured through evaluation of a blood sample, a mixed venous oxygen saturation (SvO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type of Shock: Distributive Shock

A

is the result of disease states such as sepsis, anaphylaxis, or neurogenic or spinal shock that cause poor vascular tone and vasodilation resulting in increased vascular capacity and venous pooling
-in this form of shock, blood volume is adequate, but a state of hypovolemia exists b/c of venous pooling and decreased venous return to the right heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathophysiology

A
  • invasion of a pathogen initiates a series of complex responses by the hosts immune system
  • the initial, immediate response is the activation of the innate immune response; nonspecific to any antigen

> Innate Immune response Involves:

  • mobilization of macrophages and neutrophils to the area
  • activation of pro-inflammatory cytokines or signaling molecules
  • activation of complement proteins, proteins that immobilize and breakdown pathogens
  • activation of coagulation system; activated coagulation produces a fibrin mesh to help localize the invading organism and activates bradykinin which dilates vessels and increases capillary permeability
  • local blood vessels dilate, increasing circulation to the involved area, allows influx of immune cells; local redness, warmth and edema; done in effort to kill invading organism and keep response localized
  • sepsis occurs when the inflammatory response is no longer localized
  • response becomes amplified and uncontrolled
  • the normal deactivation process, which decreases the production of pro-inflammatory cytokines and produces anti-inflammatory cytokines, is impaired
  • the excessive release of proinflammatory cytokines = damage to the endothelial cells lining the blood vessels producing vasodilation, decreased vasomotor tone, and increasing capillary permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How Sepsis and Septic Shock become a Result

A

result when pro-inflammatory cytokines overpower anti-inflammatory cytokines

  • results in excessive systemic inflammation, massive peripheral vasodilation, and increased capillary permeability
  • endotoxins released by gram-negative bacteria and exotoxins produced by gram-positive bacteria add to the pro-inflammatory effect
  • excessive inflammation = enhanced coagulation = widespread fibrin deposits and excessive clotting throughout vascular system; also results in decreased fibrinolysis (breakdown of clots)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Decreased Fibrinolysis

A

breakdown of clots becomes decreased
-occurs d/t decreased levels of activated protein C and antithrombin III seen in septic patients
>Protein C: modulates production of thrombin and promote fibrinolysis
>Thrombin: modulate the conversion of fibrinogen to fibrin clots
>Antithrombin III: deactivates thrombin

-decreased levels of both protein C and antithrombin III = enhanced thrombin formation = clot formation and impaired fibrinolysis = impaired blood flow d/t microvascular clots and organ dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Clinical Manifestations of Septic Shock

A

reflect the poor vascular tone and vasodilation that results in increased vascular capacity and blood pooling in the venous system

  • adequate blood volume, but relative hypovolemia exists b/c of decreased venous return to the right heart
  • invasion of a pathogen initiates a series of complex immune system responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Risk Factors for Septic Shock

A
  • 10-52% of ICU patients w/ sepsis die from septic shock
  • age
  • comorbidities
  • invasive lines/monitoring devices
  • chemotherapy
  • immunosuppressive drugs
  • antibiotic resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Early Stages of Septic Shock/Sepsis

A

“hyperdynamic or warm” sepsis
>reflect the initial inflammatory response
-tachycardic
-bounding pulses
-warm, flushed skin
-febrile
-BP normal as a result of compensatory responses
-initial signs of decreased organ perfusion may be present; confusion, decreased urine output
-increased cardiac output as long as there is adequate fluid resuscitation
-filling pressures low (CVP and PAOP) b/c of increased cardiac output
-systemic vascular resistance (SVR) low b/c of systemic vasodilation
-venous oxygen levels temporarily increase d/t increase in cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Late Stages of Sepsis/Septic Shock

A

“hypodynamic or cold” shock

  • cool, pale skin; cyanotic and mottled
  • weak and thready pulses
  • hypothermia
  • tachycardia persists (trying to compensate)
  • BP remains low
  • signs of end-organ hypoperfusion; lethargy, or coma, and anuria
  • decreased cardiac output w/ variable filling pressures depending on fluid resuscitation
  • systemic vascular resistance (SVR) remains low
  • venous oxygen levels decrease
  • decreased/absent urine output/bowel sounds (organs shutting down)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diagnosing Sepsis

A

> Identification of infection through evaluation of indicators of infection

  • fever
  • increased WBC
  • changes in BP, HR, and RR

> Signs of specific infection

  • lung consolidation
  • frequent or painful urination
  • peritonitis

> Laboratory Tests

  • CBC
  • Metabolic Profiles
  • Urine testing
  • cultures

> Imaging

  • General radiographs
  • CT scans
  • MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sequential Organ Failure Assessment (SOFA)

A

guides assessment of sepsis

  • higher the score = higher mortality (0-4)
  • evaluation begins w/ a quick SOFA (qSOFA); evaluates for increased respiratory rate, decreased BP, and altered mentation
  • if indicated, continue w/ SOFA (ICU)
  • SOFA used in critical care to describe organ dysfunction or failure and describes the severity of the organ failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nursing Assessment: qSOFA score

A

the presence of 2 of any of these criteria prompts further evaluation of organ dysfunction:
>Any change in mental status
>Systolic BP <100 mmHg
>Respiratory rate >22 breaths/min

  • pts assigned one point for each abnormal parameter
  • non-ICU patients w/ a total score of 2 or 3 are considered at elevated risk for an extended ICU stay or death and should be assessed for evidence of organ dysfunction using the SOFA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The qSOFA score

A

developed to be easily and quickly implemented in clinical settings outside the ICU w/ technology or lab tests

  • qSOFA is a predictor of mortality risk and not a defining characteristic of sepsis; used to identify patients who require further assessment for organ failure
  • consists of patients Glasgow Coma Scale (GCS), systolic BP, and respiratory rate
  • patients w/ a suspected infection and qSOFA score of 2 or greater have a greater risk for morbidity d/t sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Systemic Inflammatory Response Syndrome (SIRS) Criteria

A
  • Temp: <96.8 or >100
  • HR >90 (except A. fib)
  • RR >20
  • WBC <4, >12, or 10% BANDS (immature neutrophils signaling infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Abnormal SOFA Parameters

A

> Respiratory:
-PaO2:FiO2 <300 mmHg / respiratory failure requiring need for mechanical support

> Coagulation
-Platelets <100,000, INR >1.5, or PTT >60 seconds

> Hepatic:
-Bilirubin >2 mg/dL

> Cardiovascular:
-hypotension requiring vasopressor support/ SBP <90

> Neurologic:
-GCS <12

> Renal: Creatinine >2 mg/dL, or urine output <5 ml/kg/hr. x 2 hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Medical Management

A

First line therapy: PREVENTION

  • handwashing
  • meticulous aseptic technique for invasive procedures
  • elimination of invasive therapies when possible
  • aggressive mouthcare (brushing teeth w/ chlorhexidine products) may prevent ventilator-associated pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bundle of Care Campaign

A

developed to help standardize the complex treatment need in pts w/ severe sepsis
-includes activities that need to be completed within 1 hour after identifying sepsis; should begin immediately

22
Q

Bundle of Care Criteria

A

(Within 3 hours of suspected sepsis)

  • Measure Lactate (lactic acid) level; repeat if >2
  • Obtain blood cultures (prior to antibiotics)
  • Administer broad spectrum antibiotics within 1 hr.
  • Fluid resuscitation: 30 ml/kg of crystalloid (normal saline or lactated ringers) for hypotension or lactate level 4 or greater, or if there are 2 SBP <90

(Within 6 hours)
-Vasopressors if BP is unresponsive during or after fluid resuscitation; maintain mean arterial pressure (MAP) at 65 mmHg or above

23
Q

Lactate Levels

A
  • used as a marker of tissue hypoxia d/t inadequate oxygen delivery in sepsis
  • cannot be used in isolation as a “test” for sepsis; adjunctive assessment tool
  • elevated levels can be attributed to lactic acidosis from tissue hypoxia or from a nontissue hypoxic state
  • high = not enough oxygen to tissues
24
Q

Complications of Sepsis

A
  • Disseminated Intravascular Coagulopathy (DIC)

- Multiple Organ Dysfunction Syndrome (MODS)

25
Complications: DIC and what it does
- hematological disorder; enhanced coagulation - occurs b/c of enhanced coagulation from the release of procoagulant factors as part of the inflammatory response associated w/ sepsis - clotting/thrombic phase and a bleeding phase >Initial Thrombotic Stage: - last hours or several days - large amounts of thrombin are produced in response to decreased levels of protein C and antithrombin III = excessive production of fibrin clots and consumption of clotting factors - excessive coagulation leads to clots lodging in the microvasculature = ischemia and necrosis - cyanosis and ischemia in the fingers and toes and tip of nose - organ ischemia may be present - risk for thrombophlebitis, PE, and stroke >Bleeding stage: - initiation of fibrinolysis - although impaired in sepsis, occurs in attempt to break down and remove the clot - the breakdown causes increased circulating fibrin degradation products, which are powerful anticoagulants; they impair the activity of thrombin resulting in a decreased ability to form a fibrin clot - combo of lack of available clotting factors and the anticoagulant properties of the fibrin degradation products = excessive bleeding d/t inability to form clots
26
Diagnosis of DIC
based on clinical picture w/ lab results - decreased fibrinogen - increased fibrin degradation products - increased D-Dimer (indication of clot breakdown) - decreased platelets - prolonged PT and PTT - decreased antithrombin III levels
27
Management of DIC
-vigorous tx of underlying disorders -treating the disorders caused by the excessive clotting and bleeding: >hypotension >hypoxemia >respiratory distress >metabolic acidosis associated w/ poor tissue perfusion >volume replacement w/ crystalloids >blood replacement >replacement of clotting factors w/ fresh frozen plasma and platelets
28
Complications: Multiple Organ Dysfunction Syndrome (MODS)
- result of the excessive inflammation - decreased O2 to the organ systems = impaired tissue perfusion - organs fail d/t poor oxygen utilization, microvascular dysfunction, maldistribution of blood flow, and metabolic acidosis - often lungs fail first (ARDS) followed by the renal system, hepatic system, and GI system - focus = support all body systems
29
Nursing Management: Assessment and Analysis
>Clinical manifestations r/t initial increase in cardiac output that occurs d/t the tachycardia and decreased systemic vascular resistance -presents as warm and flushed w/ bounding pulses >Later manifestations reflect the prolonged poor tissue perfusion -hypotension, tachycardia, hyperventilation, decreased LOC, weak pulses, cold cyanotic mottled skin -urine output and bowel sounds decreased or absent -w/o successful intervention = manifestations of enhanced coagulation (necrotic tissues in extremities) -later stages, excessive bleeding from any puncture wounds, IV sites, or wounds begin
30
Nursing Diagnoses
altered tissue perfusion r/t inadequate cardiac output
31
Nursing Assessments for Sepsis/Septic Shock
- Neurological Status - Vital Signs - Hemodynamic Parameter - Urine Output - Skin color and temperature - Bleeding - Laboratory Tests - Lactate/ Base Deficit - Clotting studies
32
Assessments: Neurological Status
-decreased LOC occurs as a result of decreased cardiac output and hyperventilation which = a decrease in cerebral blood flow
33
Assessment: Vital Signs
- Hypotension b/c of vasodilation; producing relative hypovolemia and decreased venous return - Tachycardia (compensatory mechanism) - Initially febrile, later hypothermia; bodys inability to continue adaptive response
34
Assessment: Hemodynamic Readings
- initially cardiac output is increased - as sepsis progresses, cardiac output decreases as a result of continued decreases in filling pressures (CVP and PAOP) - initially systemic vascular resistance (SVR) is low as a result of widespread vasodilation; can increase d/t compensation and vasopressor therapy
35
Assessment: Urine Output
decreased urine output as a result of decreased cardiac output and initiation of compensatory mechanisms
36
Assessment: Skin color and temperature
- initially skin flushed and warm b/c of increased cardiac output - later, cold skin and clammy = progression of shock - tissue necrosis in extremities may = the enhanced coagulation of DIH
37
Assessment: Bleeding
excessive bleeding from wounds and puncture sites b/c of consumption of clotting factors in DIC
38
Assessments: Laboratory Tests
>ABGs: initial may reflect a respiratory alkalosis d/t hyperventilation (excreting CO2 excessively) - hypercapnia (increased CO2) and hypoxia as respiratory failure worsens - later reveals metabolic acidosis d/t anaerobic metabolism >Venous Oxygen Saturation: - decreased SvO2 and ScvO2 = inadequate oxygen delivery - later may be increased d/t maldistribution of blood flow; not indicative of recovery >Metabolic Profile: -renal failure and liver failure e/b increased BUN and creatinine and liver function test results as a result of decreased organ perfusion
39
Assessment: Lactate/ Base deficit
-increased lactate and negative base deficit = poor perfusion at cellular level
40
Assessment: Clotting studies
indicative of progression to DIC - decreased levels of fibrinogen - increased fibrin degradation products - increased D-Dimer levels (indicator of clot breakdown) - decreased platelets - prolonged PT and aPTT - decreased antithrombin III levels
41
Nursing Actions for Sepsis/Septic Shock
- Meticulous hand washing + aseptic technique w/ all procedures - Administer Oxygen as ordered - Anticipate and Prepare for Intubation - Obtain Lactate level - Obtain 2 blood cultures from two different sites, obtain urine, sputum, and wound cultures - Administer antibiotics as ordered after cultures obtained - Administer fluid replacement as ordered - Administer vasoactive drips (norepinephrine) as ordered - Provide mouth care q 4 hours and PRN - Supportive care: nutrition, turning, DVT prophylaxis, ROM exercises, mobilize as tolerated
42
Nursing Actions: Administer oxygen as ordered
-maximizing oxygenation
43
Nursing Actions: Anticipate and Prepare for Intubation
to improve oxygenation or if respiratory failure ensues
44
Nursing Actions: Obtain Lactate level
- indicator of adequacy of perfusion | - increased levels signal presence of anaerobic (w/ O2) metabolism (>2)
45
Nursing Actions: Obtain 2 blood cultures from two different sites, obtain urine, sputum, and wound cultures
identify offending organism
46
Nursing Actions: Administer antibiotics as ordered after cultures obtained
antibiotics are first-line in attempt to control infection
47
Nursing Actions: Administer fluid replacement as ordered
aggressive fluid replacement is initial treatment to restore filling volumes (CVP and POAP/ preload) and blood pressure
48
Nursing Actions: Administer vasoactive drips as ordered
ex: norepinephrine, epinephrine, phenylephrine | - restore vascular tone if fluid replacement therapy is not effective at increasing blood pressure and cardiac output
49
Nursing Teachings
- cause of sepsis and importance of hand washing | - allow family member visitation during hospitalization
50
Evaluating Care Outcomes
- Interventions w/ antibiotics and fluids is essential in maintaining cardiac output - Vasoactive support if fluid replacement is not effective at maintaining BP - Hemodynamic monitoring and laboratory assessments help monitor effectiveness of treatment - Supportive care (mouth care, frequent turning, nutrition, DVT prophylaxis) - Successful treatment results in satisfactory blood pressure (BP) level and cardiac output, and adequate tissue perfusion