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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
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2 things that combine to set off immune response leading to sepsis
- pathogen factors (infection)
- host factors (environment, genetics, age, etc)
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3 outcomes of sepsis
- 1) inflammation
- 2) coagulation
- 3) reduced fibrinolysis
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protein that is depleted in sepsis
thrombomodulin (normally binds to thrombin to activate anti-coag molecules like Protein C & S)
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unbound thrombin
acts as pro-coagulant/pro-inflammatory mediator
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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
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what causes organ failure in sepsis? (3)
- 1) decreased BP
- 2) NET (neutrophil endothelial thrombosis)
- 3) 1+2=tissue hypoperfusion & decreased tissue oxygenation
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SVR (systemic vascular resistance)
- blood flow resistance of all systemic vasculature (except pulmonary vasculature)
- *how vasoconstricted someone is
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volume of blood the left ventricle sees to pump
preload
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amount of blood the left ventricle pumps in 1 min
cardiac output (CO)
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S(c)VO2
central venous oxygen saturation
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what oxygen delivery is measured by (2)
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to treat shock syndrome (3)
- 1) give blood
- 2) put on ventilator
- 3) give drugs to drive up CO
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not enough blood volume due to trauma (dec. preload, vasoconstriction)
hypovolemic shock
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heart is not working due to failure, arrythmia, MI, valvular dysfunction (vasoconstriction, inc. SVR, dec. CO)
cardiogenic shock
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more space to distribute volume due to sepsis, liver failure, etc (vasodilation, dec. SVR, dec. preload)
distributive shock
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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
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for trauma, it is almost statistically significant to give ____.
normal saline (NS)
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for sepsis, it is almost statistically significant to give _____.
albumin
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agent has a lot of 1 effects ->
stim heart and cause arrhythmia & tachycardia
*dobutamine, dopamine, epi
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agent has a lot of 1 effects ->
systemic vasoconstriction
*N/E, phenylephrine, epinephrine
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drug hits 1/2, or dopa receptors ->
primarily cAMP mediator -> PKA activation -> inc. heart rate & vasodilation
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drug hits 1 or vasopressin receptors ->
primarily IP3 -> calcium/calmodulin release -> vasoconstriction
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preferred initial vasopressor
norepinephrine
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when dopamine should be used as a vasopressor
only if CO or heart rate are low to do increased effect on 1 receptors
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when dobutamine can be used as vasopressor
can be used for myocardial dysfunction
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rationale for vasopressin
vascular V1 receptors enhance Ca2+ release from SR to vasoconstrict
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rationale for corticosteroid use
- reverse adrenal insufficiency
- directly & indirectly inhibit Nf-kB
- reduce production of direct vasodilators
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