Uploaded by Roman Zapotny

Septic Shock

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Septic Shock:
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Septic shock occurs due to sepsis and leads to major decrease in tissue
perfusion
o Bacteria (main cause of sepsis)
 Gram + or –
o Fungus, virus or parasite
Sepsis: body’s amplified response to infection
o Think of septic shock being the END RESULT of sepsis
Characteristics of septic shock:
o Persistent hypotension (SBP <90)
 EVEN WITH LARGE AMOUNTS OF FLUID REPLACEMENT
o Needs vasopressors (ex: norepinephrine) in order to keep MAP:
NORMAL 70-100
 Less than 65 MAP means were not perfusing well
 MAP: how well the vital organs are being perfused
o >2 mmol/L serum lactate
 When cells are struggling and not receiving enough oxygen
they will switch from aerobic metabolism to anaerobic
metabolism (no oxygen, so they’re going to metabolize
without it) which then produces lactic acid
 ALTERED TISSUE PERFUSION!!!
Septic shock is a distributive form of shock
o There is issues with small vessels being able to distribute blood flow
to those cells, so they cant get oxygen
 DUE TO A DECREASE SVR ISSUE (MAJOR VASODILATION)
occurring in the body throughout the body in these vessels
 VESSEL WIDENS (VASODILATION) = DECREASE IN SVR
 Early stages of septic shock have a high or normal
cardiac output
o Microorganism has invaded the body, the immune system in sepsis
has responded in EXAGGERATED WAY (makes things worse) leading
to septic shock.
 Microorganism damages the surrounding tissues and the
immune system responds, releasing cytokines and proinflammatory mediators (MAKING SEPSIS WORSE)
 Vasodilation: widening the vessels, DECREASE in SVR,
and DECREASE in blood flow
 INCREASED vessel permeability leading them to LEAK
o Moves to interstitial tissue leading to relative
hypovolemia
 Limiting blood flow and oxygen
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Later on: decrease myocardial function
o TNF and Interleukin-1 (IL-1)
 Decreases the ejection fraction: the
percentage of blood ejected by your
heart with each contraction
Septic Shock Risk Factors
o S: suppressed immune system
 Examples: HIV, AIDs, immunosuppressive therapy, steroids,
chemo, altered nutrition
o E: extreme age (infant/elderly)
o P: people who have received an organ transplant
o S: surgical procedure: anything invasive
o I: indwelling devices
 Example: foley, central line, trach etc.
o S: sickness (chronic)
 Examples: DM, alcoholism, renal failure, liver failure
Common sites of Sepsis:
o GI (abdomen)
o Respiratory (lungs)
o GU (urinary tract)
S/S of Septic Shock
o Early Signs:
 “WARM” = compensated
 Hyperdynamic: vasodilation
o Warm/flushed skin, DECREASED BP, INCREASED
HR, INCREASED RR, INCREASED TEMP, INCREASED
CO, restless, anxiety (HOPE TO TURN THAT PATIENT
AROUND AT THIS POINT)
o Late Signs:
 “COLD” = uncompensated
 Hypodynamic: vasoconstriction
o Cold/clammy skin, severe hypotension,
tachycardia, tachypnea, oliguria, coma,
hypothermia, & DECREASED CO (MORE SEVERE)
Interventions:
o Increase perfusion
 Fluid bolus
 Vasopressors to constrict the blood vessels instead of having
major vasodilation
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Clots:
o Platelet aggregation (Platelet aggregating
factor)
 Use our clotting factor up
o Increase oxygenation
 Keep oxygen saturation > 95%
 Though they are at risk for developing respiratory failure due
to acute respiratory distress syndrome (increased capillary
permeability going on, the fluid goes into the aveoli sacs and
causes them to collapse leading to respiratory failure
 Intubation and mechanical ventilation is needed
o Fight microorganism
 Obtain cultures ASAP and start antibiotic therapy if this is a
bacteria so we can get rid of it
o Decrease inflammation
 Low dose corticosteroids or activated protein-C
 Has anti-inflammatory and anti-thrombotic effects
o CLOT ISSUES
o Nutrition
 Get early nutrition, decreased tissue perfusion can lead to
altered gut integrity so we can start nutrition early through
feedings and prevent stress ulcers and improve outcomes
o Control Blood Glucose
 Hyperglycemia alters the way that the immune system can
work
 Insulin drip
SEPTIC SHOCK
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S  Start Antibiotics
o Administer within 1st hour…improves patient outcomes
 Broad-spectrum is used until microorganism can be identified
o Cultures needed BEFORE antibiotic administration… however don’t
delay antibiotic therapy
E  Enteral Nutrition
o Early: helps with GI Integrity
o Nutrition plays an important role with immune health, healing, and
helps with stress ulcer prevention
 GI drugs may be ordered (Ex: Famotidine) to help with ulcer
prevention
P  Protein Activated C
o Has anti-inflammatory & anti-thrombotic effect
 Most effective if started within 24-48 hours… WATCH FOR
BLEEDING!
 Ex: Drotrecogin Alpha
T  Titrate Vasopressors (MAP > 65mmHg)
o Example: Norepinephrine
o Used when fluid replacement is unsuccessful
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o Causes vasoconstriction and increases SVR
I  Inotropics
o Example: Dobutamine
o May be added if there is still low tissue perfusion along with the
vasopressors
o Helps increase the strength of the heart’s contractions
C  Crystalloids or colloid Solutions
o Used as first INITIAL treatment… if not working then vasopressors are
added to the treatment
o Successful if increasing BP (SBP >90 mmHg) ad CVP within normal
range (8-12 mmHg)
o Unsuccessful if persistent hypotension and CVP is less than 8 mmHg
S  Steroids (corticosteroids… low-dose)
o Used in some patients to help decrease the amplified inflammation
by the immune system, especially if the patient isn’t responding to
vasopressors
H  Hemodynamic Monitoring
o Treated in the ICU
o Will have a central venous/arterial catheter (A-line) to help assess
tissue perfusion and filling pressures in the heart
O  Oxygenate
o Keep O2 >95% (tissues need oxygen)
o At risk for ARDS most patients need intubation with mechanical
ventilation
C  Cultures
o Collect BEFORE antibiotics
o Help identify microorganism causing the infection so appropriate
antibiotics can be ordered
K  Keep glucose <180 mg/dL
o Prevent hyperglycemia… this affects the immune system and
healing
o Star on an insulin drip to control
OTHER INTERVENTIONS:
o Monitor serum lactate levels: > 2-4 mmol/L abnormal… shows cells
are struggling for oxygen and have switched to anaerobic
metabolism
o Monitor UOP (Foley insertion): >30 mL/hr… if low kidneys are failing
due to decreased tissue perfusion
What is the most common infection?
o Bacterial most common is Gram + BUT can be both
With septic shock the cause is infection
Anaphylactic, neurogenic and septic  distributive shock
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o What you have in your vascular system distributes where it SHOULD
NOT be
o SNS gets out of sync
o With sepsis, the body MASSIVELY vasodilates
 Body is releasing nitric oxide and that is a natural vasodilator
 Global vasodilation
 They dilate and then start to leak
 Capillary permeability leakage and is going interstitial
SIRS: Systemic Inflammatory Response Syndrome
o Prevent this from going to MODS (Multiple Organ Dysfunction
Syndrome)
SNS does a great job at our blood vessels keeping the way they should
o Dilate and constrict on their own
When the BP is too low, indicative of perfusion or lack there of  organs
start to die and then going into MODS
CVP: amount of blood in the heart in the right atrium SPECIFICALLY
o Normal 2-8
o Septic patients should have a CVP of 8-12****
o
The larger the bore IV, we get the fluids in quicker (Goal is 2)
Anticipate giving IV fluids (CRYTALLOIDS  Multiple liters in a short amount
of time)
Intravascular volume is getting depleted (vessels are leaking)
Must replace this to help with cardiac output
Get cultures
THEN START ANTIBIOTIC
Check BP first, biggest thing to see if they are responding the therapy
If monitoring intake, ALWAYS monitor the output
How much blood is being pumped out of the heart per minute (Cardiac
Output)
At the beginning of sepsis cardiac output will be HIGH OR NORMAL
BECAUSE BODY IS RECOGNIZING AN ISSUE AND THEN IT WILL FALL
If youre patients BP does not come back over SBP >100 after all the IV fluid
they are in septic shock
Then vasopressors will be needed to bring the BP back up to increase the
SVR and vasoconstrict the vessels
Kidneys get hit first
Oliguria or anuric could be happening first
Band cells are immature WBC’s
o >4000 WBC is most common of sepsis
Temp is low with sepsis
Sepsis  >90 HR, RR >20
My goal for my patient whether in SIRS, sepsis or in shock is to restore tissue
perfusion … they will lead to MODS if not and they will die
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Lactic acid = we do not want it to be 2 or above
o The higher the value to higher the mortality
o With an increase of lactic acid patient is in metabolic acidosis
 The body will try to compensate to try to blow off the CO2
 Could also be HYPERkalemic:
 intracellular = K+ extracellular = Na+ (due to the
sodium potassium pump)
 anytime I have a cell that breaks down, POTASSIUM
WILL LEAVE THE CELL AND GO TO THE EXTRACELLULAR
SPACE
 this happens due to the cell breaking down or its
coming out of the cell to help
initial stage – cardiac output will dip (warm and flushed)
compensation stage – increased cardiac output, with low SVR and
decreased CVP (worsening of symptoms) still in warm and flushed stage
o trying to kick out more blood to compensate
progressive stage - the compensatory mechanisms begin failing to meet
tissue metabolic needs, and the shock cycle is perpetuated.
refractory stage – they are in MODS, cool clammy, low BP, IRREVERSIBLE
QSOFA screening tool is what the hospitals go by  to kick in for sepsis
protocol
o SBP < or equal to 100
o RR, HR, BP
Early warning screening is failure to rescue & RRT
GCS for neuro function  check mentation
Nutritional supplementation and glucose control
o Cells go into metabolic hyperglycemic state
o O2 and glucose in the cells are being used up
o Critically ill people are hyper-metabolized
o On nutritional supplement within 24-48 hours (whether oral or tube
feed)
o Liver starts spitting out more glucose to compensate and become
insulin resistant
o Steroids increase blood sugar with COPDers
o Keep sugars between 140 and 180 is the goal
 Check sugars very frequently
Systemic inflammatory response due to microorganisms entering body
(know this)
Apoptosis : they pop
LOC  agitation, restless, anxiousness
Metabolic acidosis: lactic acid build up because cells changes from
aerobic to anaerobic
Metabolic support: medication or nutrition
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Priorities
o Early identification of sepsis syndrome
o Administering prescribed fluids, medications, and nutrition
o Providing comfort and emotional support
o Preventing and maintaining surveillance for complications
MODS
o Septic shock  refractory  MODS
o Failure of two or more separate organs
o Any critically ill patients will have GI issues and hydrochloric acid
becomes decreased and blood is diverted elsewhere and good
cells can die and sepsis can attack the gut in general
o PPI medications are used (Pepcid or Protonix) on IV drip
 To prevent these stress ulcers
 Bowel sounds, stools, distention
o Liver is a filter and when it doesn’t work
 LFT increased (AST/ALT)
 Bilirubin will be up
o Cardiovascular
 Arrhythmias
o Respiratory
 Lung sound changes, dyspnea, ABG
o Renal
 Low output, increased BUN
o Hematologic factors
 Coag factors are being used up
 Decreased
 Low platelet count: thrombocytopenia
 Normal range: 150,000-400,000
 As shock progresses
 DIC presents as red spots called petechia
 Used up platelets, thrombocytopenic, petechia
through the vascular space and lack of perfusion
o Neutrophils: WBC
o Leukocytes: low WBC
o Leukocytosis: increased WBC
o Neutropenic precautions: low immune system patients
o Erythrocytes: RBC
o Reticulocytes: immature RBC (not normal to see in general)
o Pancytopenia: all cells will be decreased
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