FLuids Flashcards
Reason for Fluid Resuscitation
- Restore volume lost to sustain critical organ perfusion
- Maintain oxygen carrying capacity for adequate cellular oxygen delivery
- Correct derangements in coagulation
Types of Fluids Used (primary volume expanders)
Crystalloid
Emergency release blood (O Neg)
Pts blood type
Lethal Triad
Hypothermia
Acidosis
Coagulopathy
why’do we care about fluid rescuitation
transportation of gases nutrients and wastes
generation of electrical activity for body function and health
volume loss patho
decreased volume causes stimulation of cardiac stretch and baroreceptors = lowered BP and venous return = decreased SV
stimulation of sympathetic NS = increased HR, vasoconstriction, ventricular contraction
kidneys: activate RAAS and ADH (water retention and increased thirst)
volume loss 2/2 hemorrhage causes
activation of coagulation system
platelet deposition and local medaiteors in effort o seal injury site and prevent further blood loss
electrolytes in intracellular space
potassium
magnesium
no Ca, little NA, Cl
extraceullar space elexttrolyes
Na, Cl
ECF composed of
20% of all TBW
interstitial, vascular, transcelluar
interstitial space
transport mediator
vascular compartment with cells
vascular compartment
blood
essential for transport of electrolytes, gasses, nutrients, wastes
interstitial fluid
transport vessel for electrolytes and gases, nutrients, wastes between cellular and vascular compartments
serves as reservoir
interstitial fluid as a reservoir
mucopolysaccharide gel
aids body in times of hemorrhagic and volume loss
helps try to maintain
transcellular compartment
separation of thin membrane material
fluid accumulates here when theird spacing
not available for exchange
4 forces of fluid transfer
- capillary filtration pressure
- capillary colloid osmotic pressure
- interstitial fluid pressure
- tissue colloid osmotic pressure
these forces oppose each other so that there is little fluid left in interstitial space
capillary filtration pressure
mechanical force
forces water out of capillaries and into intersitium
capillary colloid osmotic pressure
pulls water back into capillary
[osmotic pressure
generated by plasma proteins
interstitial fluid pressure
opposes movement of water OUT of capillary
tissue colloid osmotic pressure
pulls water from capillary to interstitial space
electrolytes
substance that dissociate in solution to form charged particles
non electrolytes
dont dissociate
glucose and urea
hypovolemia
any condition of EC volume reduction that causes reduction in tissue perfusion
absolute hypovolemia
volume has LEFT the body
hemorrhage, burns, vomiting, polyuria, evaporation
reactive hypovolemia
fluid is still within the body but not available
capillary leak, ascites, effusion, vasodilation
sensible loss
early measured or quantified by individual or clinician
insensible loss
volume loss that is not easily measured or quantified
classic signs of hypovolemia
tachycardia
HoTN
poor peripheral perfusion (weak pulse, prolonged refills)
AMs or ACS 2/2 poor global perfusion
outliers of hypovolemia s/s
intraabdominal bleed MAY cause paradoxical vagal stimulation THEREFORE present with bradycardia
Cushing reflex
intracranial bleed causes HTN and bradycardia (as opposed to normal hypovolemia signs)
IV access
large bore (NST 18 or less)
2 sites
rate of infusion size and pressure matter
can alter diameter and gravity
options other than peripheral lines
central lines (fem line) IO placement saphenous vein cut down
2 components of fluid therapy
replacement therapy
maintenance therapy
replacement fluid therapy
corrects exiting water and electrolyte deficits
GI/GU dz, bleeding, thrid spacing
maintenance fluid thearpy
replace ongoing losses of water and electrolytes under what would be considered NORMAL conditions
I.e. post op
crystalloid or colloid?
there is no clinical difference in survival BUT crystalloid is recommend
preferred agent of fluid replacement
crystalloid
crystalloid
low onchotic pressure = does not last
substantial shift between vascular space and cellular space
3:1 rule
3:1 rule crystalloid
for every 1 L of fluid loss, 3L of fluid replaced
lactated ringer
buffering of academia
increase of cytokine release
hyperkalemia is a risk (caution in renal pts)
increased electrolytes, lactic acidosis risk
normal saline
slightly hyperosmolar
risk of causing hyperchloremic metabolic acidosis if gibing large volumes
crystalloid (LR or NS) can induce
neutrophil activation
MC colloid used
ALBUMIN
osmotic pressure
unable to go into extravascular space BUT NOT substitute for blood
cons of colloid
no evidence of improved outcomes compared to crystalloid
more expensive
if HEMORRHAGIC or SEPTIC vessels become so permeable that heven this high load is not able to stay in vessel
fresh frozen plasma
liquid portion of blood
unconcentrated source of clotting factors
independent of platelets
plamsa contains
albumin fibrinogen globulins glucose lytes hormones and CO2
universal donor of FFP
AB
when do we use FFP?
correction of bleeding that is secondary to a factor deficiency
urgent reversal of Coumadin (Vitamin K takes too long)
when do you transfuse blood?
following rapid transfusion of 2-3 L of crystalloid that had modest improvement in hemodynamics
pts who initially improved then deteroiated
hemodynamic instability from gross blood loss
goal of transfusion
PERFUSION
do not transfuse just to appease lab criteria, transfuse patients that need it
emergency release
4:4:6
PRBCs:FFP:PLT
NOT whole blood
massive transfusion
need of >10 u blood in 24 hrs
massive hemorrhage (FFP and PLT needed)
1:1:1
massive transfusion in trauma bay uses this system
Belmont
allows for rapid transfusion, warming
no risk of air emboli
can be loaded and ready in 1 minute
universal blood donor
O neg
universal platelet donor
NONE
crucial value of low platelet
< 50,000
1 unit of platelet = 10,000 increase in concentration
when do you give platelets?
part of Er or massive protocol
prevention of bleeding in those with known thrombocytopenia (<10K)
when would you use hypertonic saline?
- head trauma
2. hyponatremia
head trauma and hypertonic saline
intracranial hemorrhage
minimized risk of cerebral edema
NEVER used as a volume expander
3% MC used
hyponatremia and hypertonic saline
3%
nephrology management
if pt is hyponatremic and seizing, load them with tis
ocygen carrying rescucitation
synthetic blood that was proposed to be used to increse O2 delivery
studies showed that O2 doesnt last, causes more issues (I.e. ischemia)
when would you increase infusion flow rate?
burns
dehydration
shock
DKA
when would you decrease infusion flow rate
CHF
Kidney disease
elderly patient
permissive HoTN
theory that you leave some HoTN to prevent hypercoaguability and allow for stronger clot formation at a lower BP
main takeaway of TRICC trial
do NOT transfuse someone based on H and H values
instead transfuse based on those who NEED
