Unit 1: Sepsis/Septic Shock Flashcards
Sepsis
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
Septic Shock
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
Cardiac Output
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
Oxygen Delivery (DO2)
amount of oxygen delivered to the tissues
Oxygen Consumption (VO2)
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)
Type of Shock: Distributive Shock
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
Pathophysiology
- 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 Sepsis and Septic Shock become a Result
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)
Decreased Fibrinolysis
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
Clinical Manifestations of Septic Shock
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
Risk Factors for Septic Shock
- 10-52% of ICU patients w/ sepsis die from septic shock
- age
- comorbidities
- invasive lines/monitoring devices
- chemotherapy
- immunosuppressive drugs
- antibiotic resistance
Early Stages of Septic Shock/Sepsis
“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
Late Stages of Sepsis/Septic Shock
“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)
Diagnosing Sepsis
> 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
Sequential Organ Failure Assessment (SOFA)
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
Nursing Assessment: qSOFA score
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
The qSOFA score
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
Systemic Inflammatory Response Syndrome (SIRS) Criteria
- Temp: <96.8 or >100
- HR >90 (except A. fib)
- RR >20
- WBC <4, >12, or 10% BANDS (immature neutrophils signaling infection)
Abnormal SOFA Parameters
> 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.
Medical Management
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
