Sepsis Flashcards
what is the sepsis continuum
infection -> SIRS -> Sepsis -> septic shock -> MODS
what kind of a response is sepsis
dysregulated widespread systemic response to infection that injures own tissues/organs
What is SIRS
systemic inflammatory response
what can trigger sirs
infectious or non-infectious insult such as trauam, thermal injury, massive blood replacement, pancreatitis
How is SIRS defined
2+ of the following criteria Temp >39 or <36 HR > 90 RR >20 or PaCO2 <32 WBC >12 or <4
What is the term for a subset of sepsis where circulatory, cellular and metabolic alterations are associated with a higher mortality rate
septic shock
what are 4 criteria of septic shock
fulfills sepsis definition
persistent hypotension despite adequate fluid replacement
lactate >2
requires pressers to maintain MAP >65
when does MODS occur
if dysregulation worsens and organ dysfxn increases
inadequate cellular oxygenation results in organ dysfunction
can MODS occur in result to a non-infectious insult
yes
In MODS what 2 systems do we most often see dysfunction
resp and renal
What is the acronym VIPP for and what does it stand for
acronym for normal inflammatory response Vascular response Immune Response Platelet-related actions Plasma protein response
what 5 things occur in the vascular response
increased permeability and vasodilation
release of histamine, bradykinin and prostaglandins
What Factor is activated when it comes in contact with collagen
Hageman Factor XII
Where is the Hageman Factor produced
liver
Haveman Factor stimulates what to produce what
Prekallkrien System to release Bradykinin
What does Bradykinin do
Potent vasodilator
Increases permeability
increases pain
what are the two things that can stimulate Prekallkrien system
Hageman Factor XII
Complement System
what is activated by damaged endoethelium
Hageman Factor XII
What type of cells does bradykinin stimulate
Mast cells
What 4 things are involved in the immune response portion of VIPP
neutrophils
monocytes/macrophages
antibodies
antigen
what are the of Platelet-related actions
coagulation and fibrinolysis
traps exudate, microorganisms and foreign bodies
what is the plasma protein repsonse
complement system
what does the complement system do
vasodilation
promote leukocyte chemotaxis and augments phagocytosis
what 3 cells are attracted to an area of cellular injury by chemical messengers
mast cells
neutrophils
monocytes
what do neutrophils do (3)
provide first wave of attack on invading organisms
phagocytosis
move out of vascular space and attack foreign organisms (extravasation/ emigration)
what do monocytes do
ass through membrane into tissues where they grow into macrophages
attach to certain tissue and destroy bacteria
phagocytosis
When cellular injury occurs what 3 things occur
mast cells, neutrophils and monocytes are attracted to area by chem messengers
release more chem mediators to call for help
increased cellular activity at area
what are the 3 complement pathways
classical
alternative
lectin
the three complement pathways activate what
C3
What are three cell derived mediators
(ways cells can call for more help)
histamine
cytokines
arachidonic acid pathways
what is histamine released from and what does it do
released from degranulated mast cells
promotes vasodilation and capillary permeability
what are cytokines and give 3 examples
chemical messengers
interleukins, tumor necrosis factor, interferons
T or F cytokines play a role in acquired immunity
true
what are the two components or arachidonic acid pathway
prostaglandins and leukotrienes
what does the bradkykinin cascade do
increase capillary permeability
stimulate pain receptors
what is the responsibility of the clotting cascade
tissue repair, platelet aggregation, clot formation
what is a main function of the complement system
opsonization
where do B and T lymphocytes originate from
stem cells in bone marrow
which cells produce antibodies
B-cells
What does the acronym ABCCs of sepsis stand for
Arachidonic Acid (AA)
Bradykinin
Coagulation
Complement
What does Arachidonic acid do
creates initial vasoconstriction around injury to keep localized then vasoidlation to increase bloodflow to area to bring inflammatory cells
how does arachidonic acid exert its affects
prostoglandins - inc vasodilation and permeability
thromboxanes - promote platelet aggregation
What are the systemic effects of AA (2)
vasoconstriction/vasodilation - maldistribution of blood
decreased afterload
widespread permeability - fluid shifts (edema)
decreased preload
What activates the release of bradykinin
tissue injury
what does bradykinin do (3)
vasodilation and increased permeability
stimulates mast cells to release histamine causing vasodilation
stimulates AA, coag cascade and complement cascade
what are the systemic effects of bradykinin
profound vasodilation and widespread permeability - maldistribution of blood flow and fluid shifts
decreased preload and afterload
what are the two pathways in the coagulation cascade and what are each of them triggered by
extrinsic - tissue factor from damaged tissues
intrinsic - proenzymes secreted in blood
T or F the intrinsic and extrinsic pathway meet up at the main pathway in the coagulation cascade
False
commmon pathway
what occurs in the common pathway of the clotting cascade
prothrombin is converted to thrombin
thrombin helps convert fibrinogen to fibrin
Fibrin forms mesh for platelets to adhere to forming a clot
what does widespread permeability from AA cause in the lungs
fluid shifts into lungs - increased AC membrane thickness, decreased lung compliance and impaired ventilation and gas exchange
what occurs in the vascular response
and what is it caused by
vasodilation - warmth capillary permeability - swelling histamine bradykinins prostaglandins causes pain and fever as well
what is involved in the immune response and what do we see
neutrophils
monocytes/macrophages (secrete cytokines)
anitbodies
antigens
seen as PUS
what is involved in the platelet phase what does it result in
coagulation cascade
fibrinolysis
results in clotting
what 2 things are involved in the plasma protein response and what does it do
complement and bradykinin
promotes inflammatory response
what releses histamine and what triggers it
released form MAST cells
triggered by phsyical injury, chemical agents and immunologic or infectius causes
what are 3 things histamine does
increases vessel dilation and permability
increased gastric acid secretion
increased airway mucous secretion
what are 2 important cytokines
what is another name for cytokines
leukocytes
interleukins & tumor necrosis factor
what do interleukins do (2)
type of cytokine cause fever (effects hypothalamus) recruits neutrophils and monocytes
what does TNF do and what is it
type of cytokine
causes widespread destruction
causes fever, hypotension, decreased organ perfusion and increased capillary permability
what are the two major branches of Arachidonic acid
lipoxygenase and clycloxygenase
what enzyme are we concerned about in the lipoxygenase branch of AA
leukotrienes
causes bronchoconstriction vasoconstriction and vascular permeability
what are the enzymes we are concerned about in the cycloxygenase pathway of AA
thromboxane and prostaglandins
what does thromboxane do
causes vasoconstriction and promotes platelet aggretagion
ASA works on this
what do prosglandins do in the AA pathway
vasodilation
permeability
pain
what is AAs major effects in sepsis (6)
vasodilation inc cap permeability edema pain fever maldsitribution of blood flow!
can AA cause fluid to shift into the lungs impairing gas exchange
yes
how is bradykinin released
hageman factor stimultes prekallkrien system to release bradykinin
what does bradykinin do
potent vasodilator
inc vascular permability
stimulates mast cells activating AA pathway
causes pain
T or F the prekallkrien system cannot be triggered by anthing other than hageman Facto
False can be triggered by the complement system
what is the hageman factor XII also invovled in? where is it produced and how is it activated
coagulation cascade
produced in the liver activates with tissue injury as it comes in contact with collagen
what are the major effects of bradykinin in sepsis
potent vasodilation
increased permeability
pain
what does bradykin do to afterload
decreased
what occurs at the common pathway in coagulation
prothrombin is converted to thrombin
firbinogen to fibrin
what are clots typically broken down by
plasmin
what happens with plasmin in sepsis
plasmin production is blocked by circulating cytokines which leads to increased clotting and less breakdown of clots
what happens in coagulation during sepsis
clotting and loss of clot breakdown leads to inappropriate blocking of blood flow in microvasculature contributing to maldistribution of blood flow leading to organ dysfunction
what are the 3 main pathways in complement system
classical
alterniative
lectin
what are the 3 outcomes of the complement pathways
opsonisation - stimulates phagocytosis
creation of MAC - pathogen destruction stimulating immune response
promotes inflammatory and immune response - histamine and chemotaxis
what do the 3 complement pathways activate
C3
what does C3 turn into and what does it do
C3B causes opsonization
what does C3B do
combines with C5 to make MAC
what is MAC
group of proteins that busts a hole through pathogens so water can rush in and cause pathogen to explode further triggering inflammation
what does C5 do
chemotaxsis
stimuates mast cells to release histamine
what is the major effect of complement in sepsis
intensifies inflammatory response
increased vasodilation and permeability cuases cell death
what produces MDF
ischemic pancreas
what does the acronym CHAOS stand for
pathogens trigger CHAOS C VS compromise Homeostasis Apoptosis Organ dysfunction Suppression of the immune system
what is the 2016 sepsis guideliens definition of sepsis
life threatening organ dysfunction caused by dysregulated host response to infection
what is septic shock defined as for 2016 sepsis guidelines
diagnosed with sepsis
required vasopressor therapy to maintain MAP >65
Lactate >2 despite fluid resus
what is a tool to identify pts outside the ICU with known or suspected infections at risk of sepsis
qSOFA
how is qSOFA scored
GCS <15
RR > 22
SBP < 100
need a score 2 or higher
what is a scoring system used to assess the severity of organ dysfunction in a pt with known sepsis
SOFA
Sepsis related Organ Failure Assesment
how is SOFE scored
infection + change in SOFA decreased PaO2 decrased GCS dec BP inc bili decreased platelts increased creatinien
what is the 1 hour bundle (5)
measure lactate
obtain blood cx prior to abx
adminster abx
initate crystalloid for hypotension or lactte
apply pressers if hypotensive after fluid resus
what is the 3 hour bundle
measure lactate
obtain blood cultures
administer Abx
initiate fluids
what is the 6 hour bundle
apply pressors for hypotension
remeasure lactate
if persistant hypotension measure CVP SCvO2, bedside US
passive leg raise or fluid challenge
ABCD’s for treatment of sepsis (O2 supply and demand
A - airway or abx
B - breathing mech vent
C - cardiac output
preload - fluids CVP 8-12
afterload - pressers MAP >65
contractility - inotrops ScvO2 >70
D -decrease demand or drugswhat other drugs might be necessary to decrease demand
glycemic control - insulin infusion
steroids - for pts in refractory shock
stress ulcer prophylaxis
