Sepsis 1 Flashcards
describe fever stages and when it should be treated
- natural response to infection
- treated if >100.7 -101
- fever at 103= Rigers (shaking motion, body attempts to cool off)
- fever at 106= will start to kill you
- fever at 107= brain damage
process of sepsis
1) infection (fever, chills, D, malaise)
2) SIRS (systemic infmallatory response, all over generlized complaints)
3) shock (decreased BP, tachypenea, tachycardia)
4) MODS
5) death
what is septic shock broken down into
warm (DIC)
cold (ARDS)
sepsis protocol
- catch early
- temp increases
- lactic acid is produced (elevated lactate levels)
- BP decreases
why does lactate increase during septic shock
d/t anaerobic environment
-goes off the normal pyruvate cycle which causes an increase in lactate
what is a normal and problematic lactate level
normal should be <1
problem is >2
describe SIRS
- releases products (histamines and natural killer cells) that inflame body
- start to dilate everything
- vessels open up so products can be released (increase in vascular bed)
- BP begins to decrease
s/s of SIRS
hypotension tachycardia tachypnea oliguria hypoxia hypercapnia seizures/coma
what do kinins do
immune cells that kill other cells
what do free radicals do
oxygen that has no where to go, builds up
what do macrophages do
clean up act as trash can
envelope bacteria and release lysosomes
describe distributive shock
- caused by increase in permeability
- loss of sympathetic tone
- two types:neural and chemical
sepsis vs anaphylaxis
sepsis: caused by toxins released by organisms invading the body and causes SIRS
anaphylaxis: type 1 allergic reaction, antigen antibody reaction, IgE, basophils, and mast cells
describe anaphylaxis
- immediate allergic reaction to allergen (peanuts, bee stings, meds, shellfish)
- rapid release of products
- causes similar shock like s/s
- anoxic period
- releases same factors as shock and shuts of bronchial tubes
- results from type 1 allergic reaction
what can anaphylaxis lead to
decreased cardiac conduction, dysrthytmias, bronchial edema, hypoxia, death
what does SIRS leads to
DIC (disseminated intravascular coagulation)
what is DIC
- *small clots form d/t toxins and inflammation in order to stop infectious process (kidneys and gut get clotted off)
- causes platelets to be used up, pt can have massive bleeding (bleeding under skin/bruising)
what happens as DIC continues
as inflammation continues, capillaries leak, fluid shifts from vessels to interstitial space and BP drops which leads to SHOCK
what are the first signs of DIC
1) BP drops dramatically (want clotting cascade back to normal so give HEPARIN)
2) start to see things bleed (ie/ IV site, nose)
what is important to do at the start of DIC
*intubate before they go into shock to protect the airway
how long does sepsis take to develop
3 days
ie/ will NOT see infection hrs after surgery
what drugs are given for DIC
- norepinephrine to vasoconstrict and increase HR and BP
- vasopressin to hold in fluid, clamps off bleeding
why give heparin for DIC if already bleeding??
to go back to normal clotting cascade
if heparin doesnt work, give platelets and clotting factors (FFP, 6 pack of platelets, factor 7 or 10)
what is important to remember about DIC
it is difficult to get someone out of DIC
supplement and let body heal on own
what is the process of septic shock
1) inflammation (vasodilation)- phase 1
2) tissue damage (ishemia & DIC)- phase 1
3) ARDS- phase 2
4) MODS- phase 2
5) death- phase 2
describe phase one of septic shock
AKA WARM
- Alkalodic (d/t breathing off CO2 rapidly)
- HYPER- everything is rapid, body is attempting good circulation
- temp is elevated, HR is elevated (hyperdynamic, but cannot maintain this forever)
- bounding pulse, increased RR
what occurs inside the body during phase 1 of septic shock
- immature WBC: blast cells fight infection
- decreased platelets and c-reactive proteins
- increased d dimers
why do platelets decrease during phase 1
released during sepsis to fight infection
sign that there is inflammation
SIRS starts
why do d dimers increased during phase 1
tells you clotting factors and fibrin split factors
a lot of clots are being broken up rapidly so d dimer will be elevated
how long does phase 1 last
hrs- days
manage before gets worse