- Occurs d/t sepsis & leads to a major decrease in tissue perfusion to organs & tissues
- Shock occurs b/c of an invasion by a microorganism
What is sepsis?
- The body’s response to infection
- In sepsis, the response to the infection is amplified & a system-wide inflammatory response is activated
- Unfortunately, what occurs throughout the small vessels in the body during sepsis is what leads to the dec in blood flow (hence tissue perfusion) to organs/tissues
! Therefore, septic shock is really the end result of sepsis if it’s not treated promptly & effectively
Next, how you can know if pt w/sepsis is entering into shock territory…
☆ Persistent hypotension (<90 SBP) that doesn’t respond to IV fluids
☆ Needs vasopressors (e.g., norepinephrine) to maintain perfusion (a MAP >65 mmHg)
> Tells us how well vital organs are being perfused
☆ Serum lactate > ___ mmol/L
When cells start to struggle (hence not receiving enough O2 d/t a dec in tissue perfusion) they will switch from aerobic to anaerobic metabolism
Result of anaerobic metabolism is the build-up of lactic acid in the blood
D/t a dec in tissue perfusion, serum lactate will be elevated
2
- In septic shock, hypotension is NOT occurring d/t a low CO like w/some of the other types of shock (cardiogenic)
- It’s occurring d/t a drastic dec in systemic vascular resistance d/t the vasodilation occurring in the small vessels along w/an incr in capillary permeability & micro-clot formation in the vessels
- These phenomena are occurring d/t the body’s exaggerated response to the infection present in the body
! Remember, septic shock is a ___ form of shock; anaphylactic & neurogenic are 2 other types
distributive
What does this mean?
That there’s an issue w/the distribution of blood flow in the small blood vessels of the body; the alteration in how blood is distributed leads to a limited supply of blood (hence O2) to the body’s tissues & organs
- It’s much diff than cardiogenic shock b/c w/this type of shock, the heart’s CO decr
> CO is how much blood the heart is actually able to pump per min - If it can’t pump enough blood per min, the amt of blood flowing to the cell’s organs & tissues falls; the cells can experience hypoxic inj & die
In septic shock, there’s a different reason for this DECREASE in tissue perfusion & drop in BP, stemming from how the systemic vascular resistance is greatly diminished d/t…
MAJOR vasodilation that’s altering tissue perfusion
- vessels become so large that blood is pooling & not flowing to tissues/organs
Hypovolemia (relative)
- d/t leaking vessels & this causes incr capillary permeability
> fluid moves from the intravascular space to the interstitial space, so there’s a decr in circulating blood vol
Clot formation in microcirculation
- this blocks blood flow throughout the vessels so blood can’t flow to the tissues, hence decr tissue perfusion
All of this together majorly diminishes tissue perfusion (hence the development of shock & organ death)
Let’s look @ how this happens…
- A microorganism enters the pt’s body; it can be a bacteria (most common cause of sepsis & it can be either gram positive or negative), virus, parasite, or fungus
- This invasion can cause sepsis - sepsis leads to an amplified activation of the body’s systemic inflammatory response system to fight that infection & this is SYSTEM-WIDE!
- In sepsis, the body thinks it’s helping to attack the microorganism that has entered the body, but really it’s failing & causing dysfunction to organs, which leads to septic shock
- During this process, chemicals are released by the microorganism & immune cells that will lead to vasodilation, incr capillary permeability, clot formation, & decr myocardial function
Okay, how?
- Microorganism releases toxic substances that’ll damage the surrounding tissues
- Presence of these substances leads the body to release cytokines & pro-inflammatory mediators to fight & clean up this mess from the microorganism, making sepsis worse
- Substances will cause following effects throughout the WHOLE body…
- Chemicals will lead to changes in capillary permeability (blood vessels will leak), vessels will widen (vasodilate), & coag issues will occur (clots will form within vessels & clotting factors will be depleted)
- Also, to be released d/t this process will be platelet-activating factor (PAF)
> Leads to platelet aggregation, which will lead to clot formation in the microcirculation
> Remember, these vessels are damaged & this is SYSTEM-WIDE, so many small clots will form throughout the vessels, further blocking blood flow & lead to a further decr in tissue perfusion
- Problem w/this is that it’ll use up clotting factors & DIC can occur (watch for oozing of blood out of body orifices)
- Also, the heart’s function will become depressed d/t the presence of these cytokines in the body, esp TNF & IL-1
> Heart will have a decr EF (the % of blood leaving the heart w/each contraction)
! D/t all of this, organs will have difficulty functioning b/c their blood supply will be limited
Risk Factors: Septic Shock - “sepsis” mnemonic
Suppressed immune system: AIDS/HIV, immunosuppressive therapy, steroids, chemo, pregnancy, malnutrition
Extreme age: infants & elderly
People who’ve received an organ transplant
Surgical procedures (anything invasive)
Indwelling devices: Foley, central lines, trachs, etc.
Sickness (chronic cond): diabetes, hepatitis, alcoholism, renal insufficiency
What are 3 of the most common sites of sepsis?
GI (abdomen)
respiratory (lungs)
GU (urinary tract)
s/s Septic Shock
Early stages - “warm phase” (pt hyperdynamic & compensation occurring)
→ warm/flushed skin d/t vasodilation (cool/clammy in late stage)
→ decr BP
→ hyperthermia
→ high CO (to help maintain tissue perfusion & compensation… remember, it’s not a CO problem so heart can pump @ this point but will fail later on)
→ decr SVR d/t massive vasodilation
→ tachycardia
→ Incr RR
→ lethargic/anxiety
Late stage - “cold phase” (pt is hypodynamic & decompensation is occurring)
→ skin pale, cold, clammy
→ severe hypotension
→ incr HR
→ hypothermia
→ depressed heart function results in low CO & incr SVR (vasoconstriction)
→ oliguria (<30 mL/hr of urine)
→ coma
! When a pt is having persistent hypotension that isn’t responding to fluid, needs vasopressors to maintain MAP >65, & lactate >2 mmol/L & altered tissue perfusion is occurring, the pt is in septic shock!
Nursing Interventions & Treatment for Septic Shock, Goal Summary
✔ Incr tissue perfusion (fluid replacement & then vasopressors if not working)
✔ Oxygenate (>95%: tissues need O2 & resp failure occurs d/t ARDS, which will require mech vent)
✔ Fight infection (cultures, abx)
✔ Decr inflammation (some pts are candidates for drotrecogin alfa & corticosteroids)
✔ Nutrition (helps body fight infection, prevent stress ulcers, & heal)
✔ Control glucose (this helps body fight infection… hyperglycemia leads to the altered function in the immune system)
Remember, “Septic Shock” mnemonic
Start abx - need to be started within the 1st hrs of septic shock
- broad-spectrum used until microorganism identified; CULTURES 1st but don’t delay abx
Enteral nutrition - early
- this helps maintain gut integrity, helps w/healing/fighting infection & prevent stress ulcers (may need prophylactic rx’s like famotidine as well)
Protein activated C - Drotrecogin alfa
- has anti-inflammatory, anti-thrombotic, & profibrinolytic effects
> needs to be started within the 1st 24-48 hrs… watch for BLEEDING
! NOTE: “Xigris” is no longer on the market & used in the treatment of septic shock
Titrate vasopressors to keep MAP >65 mmHg: norepinephrine (1st choice)
- causes vasoconstriction, which incr SVR (this is majorly needed d/t the vasodilation occurring in septic shock)
- USED WHEN fluid replacements are not helping (! fluid replacement is first)
- MAP is the amt of pressure in the arteries during 1 cardiac cycle & shows how well the vital organs are being perfused (if less <65, organs aren’t being perfused very well)
