5 shock and SIRS Flashcards
what is shock?
inadequate cellular energy production caused either by poor oxygen delivery or increased cellular oxygen consumption
what fraction of body water is intracellular? how easily accessible is this fluid?
2/3
NOT easily accessible
give rehydration fluids fast or slow? why?
slow
to give fluids time to get into cells
give fluids to fix plasma volume fast or slow?
fast - to rapidly expand fluid volulme
what fraction of body water is extracellular?
how is this extracellular fluid divided up?
1/3 is ECV
1/4 of this is plasma volume
and 3/4 of this is interstitial volume
dehydration is a lack of intra or extra cellular fluid volume?
which is hypovolemia?
deh = lack in intra cellular fluid volume
hypovolemia = lack of extra cell fluid volume
dec 02 delivery (DO2) is what?
diminished tissue perfusion
GDV, CHF, massive hemorrhage, anaphylaxis
inc o2 consumption is what?
inc cell metabolism
heat stroke, sepsis, seizures, tremors, etc
why does energy prod dec?
No o2 = shift to anaerobic metabolism
which is more efficient: aerobic metabolism or anaerobic metabolism?
aerobic metabolism MUCH MORE efficient
{36 ATP vs 2 ATP per cycle}
determinants of DO2?
- CO
- CaO2
what is CO?
SV x HR
what is CaO2?
Hgb, SaO2, PaO2
classifications of shock?
cardiogenic
hypovolemic
obstructive
distributive / vasogenic
Call Help Or Die
PaO2 is a measure of?
amount o2 dissolved in blood
SaO2 is a measure of?
saturation of Hb
dehydration assessed based on what standard?
% loss of body weight
ciln signs of dehydration?
drastic change in body weight
skin turgor
mucus membrane turgor
cells lack fluid - extravascular loss
cardiogenic shock etiology?
how common is it?
2* to any severe cardiac dz
not common - MC heart problem in dogs is mitral valve insufficiency, which does not lead to shock
Tx cardiogenic shock?
pos ionotrope or chornotrope
NO fluids
hypovolemic shock can be further classified into 2 categories. what are they? and what are examples w/in each category?
- absolute hypovolemia -
hemorrhage - internal / external blood loss of whole blood from intravasclar space - relative hypovolemia - loss of plasma volume -
severe deh, burns, cavitary effusions, anaphylaxis, snake bite
obstructive shock is?
ex?
obstruction of blood flow, px normal global tissue perfusion
GDV, caval syndrome, pericardial effusion, pulm thromboembolism
initial and long term Tx of obstructive shock?
initial - fluids
long term - Sx to correct underlying issue
distributive shock is?
ex?
maldistribution of blood flow
severe systemic vasodilation -> pooling of blood in peripheral capillary beds b/c sys vasc cannot constrict and respond appropriately
SIRS, sepsis, endotoxemia, anaphylaxis, trauma
clinical stages of shock are:
compensatory
early decompensatory
decompensatory
signs of compensatory shock?
neurohumoral response
hyperdynamic
early decompensatory signs of shock?
flow redistributes to heart and brain
Vo2 dependent on Do2
anaerobic shoft
decompensatory or terminal stage of shock:
autoregulation fails
sympathetic control lost
how do cats differ?
cats often skip the decompensatory stage: bradycardia hypothermia hypoglycemia hypotension
smaller blood volume than dog
overall approach to shock?
must ID and Tx underlying cause, support patient to treat or px SIRS / other complicatons
overall general signs of shock?
- pallor
- tachycardia
- dull mentation
- cool extremities
- poor pulse quality
use of pressors?
inc SVR
use of chronotropes?
inc HR
use of fluids?
inc preload
correct hypovolemia
correct hemoconcentration
reverse/maintain hydration
use of vasodilators?
reduce afterload
use of contractility?
inc strength of contraction
RBC transfusion?
inc Hb (o2 carrying capacity)
o2 therapy?
inc dissolved o2
monitor parameters for shock: in order of clinical applicability?
mentation MM color CRT HR pulse quality blood pressure urine output CVP acid-base
upper limit for shock dose of crystalloid?
purpose?
dogs: 80-90 mL/kg
cats: 50-60 mL/kg
give in 20 mL/kg aliquots
70% of amt given will move into interstitum w/in 1 hour of giving - makes blood hyperosmolar so fluid shifts from blood and into interstitum/tissue, where it is needed
upper limit for colloid?
purpose?
up to 20 mL/kg
5 mL/kg aliquots (less in cats)
maintain fluid volume - volume expansion b/c inc oncotic pressure in vasculature
minimal change to osmolarity
hypertonic saline upper limit dose?
4 mL/kg bolus
uncommon to use
when to give crystalloid?
dehydrated
has kidney fxn
intact brain, lungs
when to give colloid?
normal hydration
less volume desired
hypoproteinemic
major drugs for ionotropic and pressor support?
what is route of administration?
dobutabmine: ionotrope
dopamine: low dose is ionotrope
high dose is pressor
IV CRI administration
what is SIRS?
local problem causes systemic inflammation - an over correction to inflammation
2* to endogenous inflammatory mediators or bacT toxins
can cause shock or result from shock
major cytokines in SIRS?
IL 1 IL 6 IL 8 TNF a platelet activating factor
what end points should you give fluids to?
- blood pressure
- urine output
- CVP
- acid base parameters (base deficit, lactate)
how is MODS caused?
animals w SIRS have damage to vascular endothelium from activation of coagulation, complement pathways, PGs and LTs
which are the target cells for SIRS?
WBC
platelet
endothelial cells
define MODS?
severe, acquired dysfunction of 2 or more organ systems for over 24-48 hours NOT due to 1* illness
what are SIRS criteria?
- hyper or hypothermia
- tachycardia
- tachypnea
- respiratory alkalosis (low PaCo2)
- leukocytosis or leukopenia (left shift)
SIRS tx?
- abx
- GI protectants and nutrition [avoid break down]
- positive pressure ventilation (ARDS)
- anticipate and avoid complications
- critically ill - req 24 hour care facility and monitoring
when giving crystalloid and colloid solution at the same time, what adjustment needs to be made?
dec crystalloid dose by half the normal dose
some etiology of infectious SIRS?
pyometra prostatitis pyelonephritis peritonitis pneumonia pancreatitis
some non infectious etiology of SIRS?
neoplasia heat stroke severe burns severe trauma snake envenomation
steps to SIRS:
1 - local inflammation
2 - inflammatory mediators travel
3 - distant vascular endothelial effects
4 - MODS
