Septic Shock NCLEX Review
It means there is an issue with
Septic shock occurs due to sepsis and leads to a major
decrease in tissue perfusion to organs and tissues.
So, in other words, shock (which is where cells are
deprived of oxygen due to the lack of perfusion) occurs
because of an invasion by a microorganism (septic).
According to CDC.gov, “1 in 3 patients who die in a
hospital have sepsis.” This is a very alarming statistic!
Therefore, as nurses, we must be able to recognize
the early signs and symptoms of this condition and
know what patients are at risk for developing it.
What is sepsis? It’s the body’s response to infection. In
sepsis, the response to the infection is amplified and a
system-wide inflammatory response is activated.
Unfortunately, what occurs throughout the small vessels
in the body during sepsis is what leads to the decrease in
blood flow (hence tissue perfusion) to organs/tissues.
Therefore, septic shock is the result of sepsis if it’s not
treated promptly and effectively.
Septic shock is characterized by the following (this is
how you can know if your patient with sepsis is entering
into shock territory):
 Persistent hypotension (<90 SBP) that doesn’t
respond to IV fluids
 Needs vasopressors (example Norepinephrine) to
maintain perfusion (a MAP >65 mmHg)
 MAP (mean arterial pressure): this number tells us
how well vital organs are being perfused. If it’s lower
than 65 mmHg, the organs aren’t being perfused very
well.
 Serum Lactate >2 mmol/
 Remember from our video on “stages of shock” we
talked about how when cells start to struggle (hence
not receiving enough oxygen due to a decrease in
tissue perfusion) they will switch from aerobic to
anaerobic metabolism. The result of anaerobic
metabolism is the buildup of lactic acid in the blood.
Therefore, due to a decrease in tissue perfusion the
serum lactate will be elevated.
In septic shock, hypotension is NOT occurring due to a
low cardiac output like with some of the other types of
shock (ex: cardiogenic shock). It’s occurring due to a
drastic decrease in systemic vascular resistance due to
the vasodilation occurring in the small vessels along
with an increase in capillary permeability and micro-clot
formation in the vessels. These phenomena are occurring
due to the body’s exaggerated response to the infection
present in the body.
Now, let’s talk about the specifics of why we have
persistent hypotension, a decrease in system vascular
resistance, vasodilation, increased capillary
permeability, micro-clot formation, etc.
First, it’s important to know that a septic shock is
a distributive form of
shock. Anaphylactic and neurogenic shock are the other
two types of distributive shock.
What does this mean?
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 oxygen) to the
body’s tissues and organs.
It’s much different from cardiogenic shock because with
this type of shock the heart’s cardiac output decreases.
Cardiac output is how much blood the heart can pump
per minute. If it can’t pump enough blood per minute,
the amount of blood flowing to the cell’s organs and
tissue falls. The cells can experience hypoxic injury and
die.
But here in septic shock there is a different reason for
this DECREASE in tissue perfusion and drop in blood
pressure: It stems from how the systemic vascular
resistance is greatly diminished due to:
MAJOR vasodilation that is altering tissue perfusion
Vessels become so large that blood is pooling and not
flowing to tissues/organs
Hypovolemia (relative): due to leaking vessels and this
causes increased capillary permeability
Fluid moves from the intravascular space to the
interstitial space, so there is a decrease in circulating
blood volume
Clot formation in microcirculation: this blocks blood
flow throughout the vessels so blood can’t flow to the
tissues, hence decreasing tissue perfusion.
All of this together majorly diminishes tissue perfusion
(hence the development of shock and organ death).
Let’s analyze how this happens:
A microorganism enters the patient’s body. It can be a
bacteria (the most common cause of sepsis and 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 and
this is SYSTEM-WIDE!
In sepsis, the body thinks it is helping to attack the
microorganism that has entered the body, but it’s failing
and causing dysfunction in organs, which leads to septic
shock.
During this process, chemicals are released by the
microorganism and immune cells that will lead to
vasodilation, increase capillary permeability, clot
formation, and decreased myocardial function.
How?
The microorganism releases toxic substances that will
damage the surrounding tissues. The presence of these
substances leads the body to release cytokines and pro-
inflammatory mediators to fight and clean up this mess
from the microorganism, which makes sepsis worst.
These substances will cause the following effects Signs and Symptoms of Septic Shock
throughout the WHOLE body:
Early stages “warm phase” (patient is hyperdynamic
The chemicals will lead to changes in capillary and compensation is occurring):
permeability (blood vessels will leak), vessels will widen
(vasodilate), and coagulation issues will occur (clots will  warm/flushed skin due to vasodilation (cool/clammy
form within vessels and clotting factors will be in late stage)
depleted).  decreased blood pressure
 hyperthermia
Also to be released due to this process taking place will  high cardiac output (to help maintain tissue
be the “platelet-activating factor”. PAF leads to platelet perfusion and compensation…. remember it’s not a
aggregation, which will lead to clot formation in the CO problem so the heart can pump at this point but
microcirculation. Remember these vessels are damaged it will fail later on)
and this is SYSTEM-WIDE, so many small clots will  decreased systemic vascular resistance due to
form throughout the vessels. This will further block massive vasodilation
blood flow and lead to a further decrease in tissue  tachycardia
perfusion.  increased respirations
 lethargic/anxiety
The problem with this is that it will use up clotting Late stage “cold phase” (patient is hyperdynamic and
factors and DIC (disseminated intravascular coagulation) decompensation is occurring):
can occur. Watch for oozing of blood out of body  skin pale, cold, clammy
orifices.  severe hypotension
 increased heart rate
And if it can’t get any worst the heart’s function will  hypothermia
become depressed due to the presence of these cytokines  depressed heart function results in low cardiac
in the body, especially tumor necrosis factor and output and increases systemic vascular resistance
interleukin-1. The heart will have a decreased ejection (vasoconstriction)
fraction (this is the percentage of blood leaving the heart  oliguria (less than 30 mL/hr of urine)
with each contraction).  coma
When a patient is having persistent hypotension that
Due to all of this, organs will have difficulty functioning isn’t responding to fluid, needs vasopressors to maintain
because their blood supply will be limited. MAP >65, lactate >2 mmol/L, and altered tissue
perfusion is occurring, the patient is in septic shock!
Risk Factors for developing Septic Shock
Nursing Interventions and Treatment for Septic
Shock

Goal Summary: increase tissue perfusion (fluid

replacement and then vasopressors if not working),
oxygenate (>95%: tissues need oxygen and respiratory
failure occurs due to ARDS, which will require
mechanical ventilation), fight infection (cultures,
antibiotics), decrease inflammation (some patients are
candidates for Drotrecogin Alpha and corticosteroids),
nutrition (helps body fight infection, prevent stress
ulcers and heals), control glucose (this helps body fight
infection…hyperglycemia leads to the altered function in
“Sepsis” the immune system)

Suppressed immune system: AIDS/HIV, To help us remember all the treatment goals and nursing
immunosuppressive therapy, steroids, chemo, interventions remember:
pregnancy, malnutrition
“Septic Shock”
Extreme age (infants and elderly)
Start antibiotics: need to be started within the 1st hours of
People who’ve received an organ transplant septic shock….broad-spectrum used until
microorganism is identified….CULTURES first but
Surgical procedures (anything invasive) don’t delay antibiotics

Indwelling devices: Foley, central lines, tracks, etc. Enteral Nutrition: early…this helps maintain gut
integrity, helps with healing/fighting infection, and
Sickness (chronic conditions): diabetes, hepatitis, prevents stress ulcers (may need prophylactic drugs like
alcoholism, renal insufficiency Famotidine as well)

*** Most common sites of sepsis: GI (abdomen), Protein activated C: “Drotrecogin alpha”: has anti-
respiratory (lungs), GU (urinary tract) inflammatory and antithrombotic effects….needs to be
started within the first 24-48 hours….watch for
BLEEDING (NOTE: Drotrecogin alpha “Xigris” is no
longer on the market and used in the treatment of
Septic Shock)

Titrate Vasopressors to keep MAP >65 mmHg:

Norepinephrine (1st choice)

 Causes vasoconstriction, which INCREASES

systemic vascular resistance (this is majorly needed
due to the vasodilation occurring in septic shock)
 USED when fluid replacements are not helping
(fluids replacement is first).
 The mean arterial pressure is the amount of pressure
in the arteries during one cardiac cycle and shows
how well vital organs are being perfused (if it is less
than 65…organs are not being perfused very well).
Neotropics may be added with the vasopressors
(Dobutamine) if there is still low tissue perfusion

Crystalloids or Colloids fluids: FIRST, if not working

then vasopressors

 The large amounts of fluid will fill those dilated

vessels and refill the depletion of circulating
volume.
 Needs at least 2 IV sites…warm fluids to prevent
hypothermia
 Successful:  increased blood pressure and/or
increasing CVP (8-12 mmHg)
 Monitor urinary output 30 mL/hr or greater…needs
a Foley!
Steroids low dose (corticosteroids): used
in SOME patients to help decrease the amplified
inflammation, especially if the patient is not responding
to vasopressors

Hemodynamic monitoring: central venous/arterial cath

to assess tissue perfusion and filling pressures in the
right side of the heart (right atrium: CVP), (PAWP:
filling pressure of left side of the heart)

Oxygenate: keep oxygen saturation >95%…tissues need

oxygen. Many patients will experience respiratory
failure (ARDS) and will need intubation with
mechanical ventilation.

Cultures: blood, wound, urine, etc.

obtain BEFORE antibiotics

Keep glucose <180 mg/dL….may need insulin drip…the

immune system is affected by hyperglycemia

Other: Check lactate levels: if the patient needs

vasopressors to keep MAP >65 mmHg even though fluid
replacement has been given and lactate level is >2
mmol/L think SEPTIC SHOCK!

Foley insertion: strict intake and output. UOP will help

you assess tissue perfusion and if kidneys are being
perfused well…. UOP should be > 30 mL/hr