3 Shock, Sepsis, MODS & DIC (part 2) Flashcards
1 hour sepsis bundle (4)
Goal
-Lactate level (re measure if over 2)
-Blood cultures prior to admin of abx
—broad spectrum abx given
-Rapid admin of 30ml/kg crystalloid
(For HOTN or lactate over 4)
-Vasopressors
(If HOTN after fluid resuscitation)
GOAL: MAP over 65
Sepsis
-what we want SBP and MAP
Assess for what?
SBP over 90
MAP over 65
Assess for organ dysfunction:
UOP
Creatinine >2
Sepsis:
S/s
—hyperdynamic warm phase
—hyperdynamic cold phase
WARM:
—increased HR
—increased temp
—low BP
—hyperthermia
COLD:
—decreased LOC
—hypothermia
—skin cool and pale
Shock
Cardiac assessment
-changes in baseline
-compensatory changes
-CVP what shock increases vs decreases
-JVD in which one
Changes from baseline:
SBP below 90 or Decreased by 40 below baseline
Compensatory:
Increased HR
Decreased CO
CVP:
-increase in cardiogenic
-decreased in hypovolemic
JVD in cardiogenic
Fluid challenge in shock
-what gauge IV
-how to evaluate fluids working
18G
UOP/BP/CVP
Septic shock tx:
Colloids (what are they, what they do, example)
Dont use colloids in what type of patient and why
Contain proteins
—increase osmotic pressure
Ex: albumin
Dont use if increased capillary permeability:
—septic, anaphylactic, burn, increased edema, 3rd spacing
shock
Resp/renal assessment
Resp:
-increased RR d/t metabolic acidosis
Renal:
-oliguria from hypoperfusion
—once compensation fails = anuria
(AKI = increased potassium)
shock
GI assessment
-hypoperfussion leads to what
-prolonged leads to what
Hypoperfusion of liver does what
Hypoperfusion = slowed intestines =
—paralytic ileus
Prolonged = risk for infection
Liver:
-infection
-bleeding and clotting
shock
hematologic/skin assessment
Hematologic:
-decreased plts/clotting factors
-petechiae and ecchymosis
Skin:
-pale/clammy and cold (hypovolemic shock)
-red/warm and flushed (anaphylactic shock)
Fluid shifts from IV to in cell (edema)
Replacing blood loss
-3 products
-size of IV
-what 3 things to check
-how do we know their effective
PRBC/FFP/PLTs
18G
BP/HR/Temp
Know if effective by:
-Hgb/Hct
-Pt/Ptt
-Plts
shock:
Why we use oxygen and vents on these patients
What does sedation do
Target a tidal volume of what in ARDS pts?
Reduce workload on lungs
Correct acid/base balance
Sedation:
Decreases oxygen consumption
Target tidal volume:
6ml/kg
Goal directed resuscitation:
-3 things were trying to improve
Tx goals: 4 values we want
Preload
Afterload
Contractility
Tx goals:
ScvO2: 70-90
MAP: 65-90
CVP: 8-12 (different for fluid resuscitation)
UOP: >0.5/kg/hr
What meds increase BP
What meds decrease BP
Norepinephrine
Epinephrine
Phenylephrine
Dobutamine
Dopamiune
Vasopressin
Nitroglycerin
Nitroprusside
Shock hemodynamics
Preload (CVP/RAP/PAOP)
-what 3 shocks are we looking at and some txs
Hypovolemic or distributive shock:
—fluid resuscitation
Cardiogenic:
—diuretics, vasodilators
Shock hemodynamics
Decreased afterload:
-what 2 shocks and txs
Distributive:
-increase vascular tone
Hypovolemic:
-replace volume before vasopressor
Shock hemodynamics:
Increased afterload:
-1 shock and 2 txs
Cardiogenic:
-vasodialtors
-IABP
What do we want to do with cardiogenic shocks contractility?
Tx of cardiogenic shock
Want to increase it
Has lots of tx due to it affective everything:
—insulin, corticosteroids, abx, VTE prophylaxis, SUP
Shock management of temps
Hypo vs hyper (what does either affect)
Hypo:
Decreases contractility
—(decreases CO/O2 delivery)
Hyper:
—increases O2 demand
Shock nutrition:
Enteral feeding
TPN/lipids if unable to feed enteral feeding
MODS
Definition
Primary
Secondary
Mutisystem organ dysfunction syndrome
Primary: direct injury to an organ from shock
Secondary: dysfunction of other organs not involved in primary injury
MODS what organs can be affected
Respiratory
Hematological (liver)
—bleeding/clotting
Renal/intestines
—(increased BUN/Creat/metabolic acidosis)
Goals of care for MODS (4)
Control infection
Tissue oxygenation:
—SpO2: 88-92%
—Hgb 7-9
—SvO2 >70%
Restore IV volume
Support for each organ involved
DIC
Definition/ main thing
Disseminated intravascular coagulation
—microvascular coagulation
—depletion of clot factors and bleeding
DIC clot factor issue
-what is happening
—leads to what
clotting factors released:
—thrombin produced
—fibrin deposited in microvascular spaces
Leads to:
—tissue necrosis
—organ ischemia
