PHRD5015 Lecture 24 - Sepsis

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daynuhmay
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252549
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PHRD5015 Lecture 24 - Sepsis
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2013-12-11 05:55:30
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Sepsis
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Sepsis
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Sepsis
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  1. evolution of sepsis
    • 1) infection
    • 2) toxin release
    • 3) inflammatory cytokines
    • 4) activated neutrophils
    • 5) endothelial injury/microclots
    • 6) hypoperfusion/ischemia
    • 7) organ dysfunction (severe sepsis)
    • 8) death
  2. 2 things that combine to set off immune response leading to sepsis
    • pathogen factors (infection)
    • host factors (environment, genetics, age, etc)
  3. 3 outcomes of sepsis
    • 1) inflammation
    • 2) coagulation
    • 3) reduced fibrinolysis
  4. protein that is depleted in sepsis
    thrombomodulin (normally binds to thrombin to activate anti-coag molecules like Protein C & S)
  5. unbound thrombin
    acts as pro-coagulant/pro-inflammatory mediator
  6. neurohormonal response to sepsis (3)
    • 1) ACh suppresses cytokine response
    • 2) N/E & Epi released to increase BP, but are also pro-inflammatory
    • 3) increased ACTH -> increased cortisol
  7. what causes organ failure in sepsis? (3)
    • 1) decreased BP
    • 2) NET (neutrophil endothelial thrombosis)
    • 3) 1+2=tissue hypoperfusion & decreased tissue oxygenation
  8. SVR (systemic vascular resistance)
    • blood flow resistance of all systemic vasculature (except pulmonary vasculature) 
    • *how vasoconstricted someone is
  9. volume of blood the left ventricle sees to pump
    preload
  10. amount of blood the left ventricle pumps in 1 min
    cardiac output (CO)
  11. S(c)VO2
    central venous oxygen saturation
  12. what oxygen delivery is measured by (2)
    • 1) lactate
    • 2) S(c)VO2
  13. to treat shock syndrome (3)
    • 1) give blood
    • 2) put on ventilator
    • 3) give drugs to drive up CO
  14. not enough blood volume due to trauma (dec. preload, vasoconstriction)
    hypovolemic shock
  15. heart is not working due to failure, arrythmia, MI, valvular dysfunction (vasoconstriction, inc. SVR, dec. CO)
    cardiogenic shock
  16. more space to distribute volume due to sepsis, liver failure, etc (vasodilation, dec. SVR, dec. preload)
    distributive shock
  17. 3 main objectives of "early goal directed therapy"
    • 1) increase blood vol w/ fluid replacement
    • 2) increase BP w/ vasoconstrictors
    • 3) put on ventilator/give blood to ensure O2 delivery
  18. for trauma, it is almost statistically significant to give ____.
    normal saline (NS)
  19. for sepsis, it is almost statistically significant to give _____.
    albumin
  20. agent has a lot of 1 effects ->
    stim heart and cause arrhythmia & tachycardia 

    *dobutamine, dopamine, epi
  21. agent has a lot of 1 effects ->
    systemic vasoconstriction

    *N/E, phenylephrine, epinephrine
  22. drug hits 1/2, or dopa receptors ->
    primarily cAMP mediator -> PKA activation -> inc. heart rate & vasodilation
  23. drug hits 1 or vasopressin receptors ->
    primarily IP3 -> calcium/calmodulin release -> vasoconstriction
  24. preferred initial vasopressor
    norepinephrine
  25. when dopamine should be used as a vasopressor
    only if CO or heart rate are low to do increased effect on 1 receptors
  26. when dobutamine can be used as vasopressor
    can be used for myocardial dysfunction
  27. rationale for vasopressin
    vascular V1 receptors enhance Ca2+ release from SR to vasoconstrict
  28. rationale for corticosteroid use
    • reverse adrenal insufficiency
    • directly & indirectly inhibit Nf-kB
    • reduce production of direct vasodilators

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