Septic Shock Flashcards

1
Q
  • 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
A

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
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2
Q

! Therefore, septic shock is really the end result of sepsis if it’s not treated promptly & effectively

A

Next, how you can know if pt w/sepsis is entering into shock territory…

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3
Q

☆ Persistent hypotension (<90 SBP) that doesn’t respond to IV fluids

A

☆ Needs vasopressors (e.g., norepinephrine) to maintain perfusion (a MAP >65 mmHg)
> Tells us how well vital organs are being perfused

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4
Q

☆ 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

A

2

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5
Q
  • In septic shock, hypotension is NOT occurring d/t a low CO like w/some of the other types of shock (cardiogenic)
A
  • 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
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6
Q

! Remember, septic shock is a ___ form of shock; anaphylactic & neurogenic are 2 other types

A

distributive

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7
Q

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

A
  • 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
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8
Q

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…

A

MAJOR vasodilation that’s altering tissue perfusion

  • vessels become so large that blood is pooling & not flowing to tissues/organs
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9
Q

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
A

Clot formation in microcirculation

  • this blocks blood flow throughout the vessels so blood can’t flow to the tissues, hence decr tissue perfusion
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10
Q

All of this together majorly diminishes tissue perfusion (hence the development of shock & organ death)

A

Let’s look @ how this happens…

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11
Q
  • 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!
A
  • 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
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12
Q

Okay, how?

A
  • 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…
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13
Q
  • 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)
A
  • 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

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14
Q
  • Problem w/this is that it’ll use up clotting factors & DIC can occur (watch for oozing of blood out of body orifices)
A
  • 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)
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15
Q

! D/t all of this, organs will have difficulty functioning b/c their blood supply will be limited

A
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16
Q

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

A

Surgical procedures (anything invasive)

Indwelling devices: Foley, central lines, trachs, etc.

Sickness (chronic cond): diabetes, hepatitis, alcoholism, renal insufficiency

17
Q

What are 3 of the most common sites of sepsis?

A

GI (abdomen)
respiratory (lungs)
GU (urinary tract)

18
Q

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

A

→ 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

19
Q

Late stage - “cold phase” (pt is hypodynamic & decompensation is occurring)

→ skin pale, cold, clammy

→ severe hypotension

→ incr HR

→ hypothermia

A

→ depressed heart function results in low CO & incr SVR (vasoconstriction)

→ oliguria (<30 mL/hr of urine)

→ coma

20
Q

! 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!

A
21
Q

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)

A

✔ Fight infection (cultures, abx)

✔ Decr inflammation (some pts are candidates for drotrecogin alfa & corticosteroids)

✔ Nutrition (helps body fight infection, prevent stress ulcers, & heal)

22
Q

✔ Control glucose (this helps body fight infection… hyperglycemia leads to the altered function in the immune system)

A

Remember, “Septic Shock” mnemonic

23
Q

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
A

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)
24
Q

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

A

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)
25
Q

Inotropics may be added w/the vasopressors (____), if there’s still low tissue perfusion

A

dobutamine

26
Q

Crystalloids or colloids fluids: FIRST, if not working then vasopressors

  • the large amts of fluid will fill those dilated vessels & refill the depletion of circ vol
  • needs @ least 2 IV sites… warm fluids to prevent hypothermia
A
  • successful: incr BP &/or incr CVP (8-12 mmHg)
  • Monitor u/o 30 mL/hr or greater…. needs a Foley
27
Q

Steroids low-dose (corticosteroids): used in SOME pts to help decr the amplified inflammation, esp if pt is not responding to vasopressors

A

Hemodynamic monitoring: central venous/arterial cath to assess tissue perfusion & filling pressures in the right side of the heart

  • right atrium: CVP
  • PAWP: filling pressure of left side of the heart
28
Q

Oxygenate: keep O2 sat >95%… tissues need O2

  • many pts will experience resp fail (ARDS) & will need intubation & mech vent
A

Cultures: blood, wound, urine, etc. obtain BEFORE abx

29
Q

Keep glucose < ___ mg/dL

  • may need insulin drip; the immune system is affected by hyperglycemia
A

180

30
Q

Other

! Check lactate lvls: if pt needs vasopressors to keep MAP >65 mmHg even though fluid replacement has been given & lactate lvl is >2 mmol/L, think SEPTIC SHOCK

A

Foley insertion: strict I&O

  • u/o will help you assess tissue perfusion & if kidneys are being perfused well; should be >30 mL/hr