Sepsis and shock

What is shock

tissue perfusion is inadequate to deliver oxygen and nutrients to support cellular function

three physiologic responses that are common to all types of shock

• Hypoperfusion of tissues

• Hypermetabolism

• Activation of the inflammatory response

Hypovolemic shock

Loss of plasma or blood volume of at least 15% to 30%.

What can lead to hypovolemic shock?

Excessive fluid loss from diuresis, vomiting, or diarrhea;

Blood loss secondary to surgery, trauma, childbirth, burns, and diabetic ketoacidosis.

Older adult clients are more prone to dehydration

Cardiogenic shock

Cardiac pump failure due to a direct cardiac cause

What can lead to cardiogenic shock

MI, heart failure, cardiomyopathy, dysrhythmias

Older adult clients are at increased risk for MI and cardiomyopathy.

Obstructive shock

Cardiac pump failure due to an indirect cardiac factor

What can lead to obstructive shock

blockage of great vessels, pulmonary artery stenosis, pulmonary embolism, cardiac tamponade, tension pneumothorax, and aortic dissection.

Septic shock

Toxins and bacteria causing an inflammatory response and subsequent massive vasodilation

Neurogenic shock

Head trauma, spinal cord injury, and epidural anesthesia are among the causes.

Distributive shock

vasodilation

3 types of distributive shock

• Septic: resulting from acute infection causing relative vasodilation

• Neurogenic: resulting from loss of sympathetic tone causing relative vasodilation

• Anaphylactic: resulting from severe allergic reaction producing acute systemic vasodilation

4 stages of shock

• Initial (early) ***

• Compensatory

• Progressive

• Irreversible (Refractory) 

Initial stage of shock (what is it and what are some s/s)

Decrease in MAP, but BP remains normal 

Small increase in HR. Otherwise little to no symptoms

Compensatory stage of shock (what is it and what are some s/s)

Lower BP but still WNL, Increased HR to compensate and increase cardiac output to restore tissue perfusion and oxygenation.

• High RR d/t acidosis. May cause compensatory respirtroy alkalosis

• Cold/clammy skin r/t blood shunting to vital organs. Leads to UO decreasing

• PTs can start to get confused/agitated

• SNS causes vasoconstriction, increased HR, increased heart contractility to maintain BP, CO

• Perfusion of tissues is inadequate

• Acidosis occurs from anaerobic metabolism

• Confusion, agitation may occur

Progressive stage of shock (what is it and what are some s/s)

Compensatory mechanisms begin to fail. Severely hypotensive, decreased MAP

Rapid RR, crackles, hypoxia, Severely tachycardic, Decreased LOC, decreased UO

• HR still high but BP and MAP decrease

• All organs suffer from hypoperfusion (due to poor CO!)

• Lungs begin to fail, alveoli collapse, pulmonary edema occurs

• Inadequate perfusion of heart leads to dysrhythmias, ischemia

• As MAP falls below 70, GFR cannot be maintained

  • Acute kidney injury may occur

• Disseminated intravascular coagulation (DIC) may occur as cause or complication of shock

• Metabolic acidosis from lactic acid build up 

• Hypotension SBP <90, MAP <65 = NOT GOOD PERFUSION

• Skin starts to mottle

• Pt now lethargic

Irreversible stage of shock (what is it and what are some s/s)

Organ damage so severe that the patient does not respond to treatment and cannot survive.

• BP unresponsive to measures to increase

• Renal, liver failure

• Anaerobic metabolism worsens acidosis

• Multiple organ dysfunction progresses to complete organ failure

• Pt needs intubation

• unresponsive to vasopressors and fluids

• Skin is jaundiced r/t liver failure

• No urine output r/t kidney failure

• Pt unconscious

procalcitonin and CRP are

inflammatory markers

ABG lab results for someone in shock

acidosis

serum lactic acid lab results for someone in shock

Increases due to anaerobic metabolism

prolactin lab results for someone in shock

elevated

CRP lab results for someone in shock

elevated

serum glucose lab results for someone in shock

elevated

electrolytes lab results for someone in shock

elevated

cardiac enzymes (Creatine phosphokinase, troponin, etc) lab results for someone in shock

increased

Hgb and Hct lab results for someone in shock

Decreased with hemorrhage, increased with dehydration

what cultures should you collect from a pt in shock

blood, urine, wound

what are some diagnostics you should run for a pt in shock

• hemodynamic monitoring

• EKG

• echo

• CT

• CXR

• EGD/colonoscopy

general shock management strategies

Fluid replacement to restore intravascular volume

Vasoactive medications to restore vasomotor tone, improve cardiac function

Nutritional support to address metabolic requirements (not immediate)

nursing interventions for pt in shock

• monitor VS frequently 

• keep pt warm

• I&O’s

• O2 therapy 

• shock position 

• frequent VS

• telemetry monitoring 

• LOC

• cap refil

• call rapid response if signs of worsening

what is the shock position

The shock position (passive leg raise)  flat on their back while their legs are passively raised to a 45 degree angle. Purpose = elevate the legs so that blood can flow from the lower body to the heart.

crystalloids used for fluid replacement

• Normal saline- usually start with this and then for large volumes switch to LR. can cause hypernatremia

• LR- better for large volume

colloids used in fluid replacement

• albumin- keep fluid in vasculature 

• dextran- may interfere with platelet aggregation

complications of fluid replacement

respiratory issues, electrolyte disturbances, hypothermia, FVO, pulmonary edema 

what should you do before administering fluids

warm the fluids to avoid hypothermia

when would you give vasoactive medications instead of fluids?

when Fluid may be contraindicated – such as in acute HF, decompensated HF, and chronic kidney failure. and use vasoactive meds if non responsive to other methods (fluid therapy or leg raise dont do anything)

intropic agents pros and cons

Improve contractility, increase stroke volume (volume ejected), increase cardiac output

Disadvantages 🡪 Increase oxygen demand of the heart, high risk for arrythmia 

intropic agents examples

dobutamine, dopamine, epinephrine, milrinone

vasodilators pros and cons

Reduce preload and afterload, reduce oxygen demand of heart

Disadvantages 🡪 Cause hypotension

vasodilators examples

nitroglycerine, nitroprusside, nicardipine, labetalol 

which two meds are BEST for cardiogenic shock/decompensated HF

Dobutamine and Milrinone = Great for cardiogenic shock/decompensated HF because they are INODILATORS

vasopressors pros and cons

Increase blood pressure by vasoconstriction, increase afterload 

Disadvantages 🡪 Increase afterload, thereby increasing cardiac workload; compromise perfusion to fingers, toes, skin, kidneys, lungs, gastrointestinal tract, can cause arrythmias 

vasporessros shunt blood to core so make sure to monitor distal extremities. check cap refil.

vasopressors examples

norepinephrine, dopamine, phenylephrine, vasopressin, epinephrine

arterial line care

• used to monitor MAP

• can be used for ABG and lab draws

• inserted by trained MD

• NO IV MEDICATIONS through this line.Tubing is usually streaked Red on the outside.

• IMC/ICU care required

Goal MAP

Goal MAP Above 65 for pressors 

Goal MAP Below 100 or 80 for conditions such as post op CABG, Aortic Dissection/Repair, Stroke 

normal CO

4-8 L/min

hallmark signs of cardiogenic/obstructive shock

Hallmark signs = Increased preload (CVP, PA, Wedge), Increased Afterload (SVR), Decreased Contractility  

Cold and Clammy – can also be hypotensive! (Good example of how BP does not always equal blood volume)

what is Pulmonary artery Catheter used for

Continuous monitoring of Preload (CVP, PA pressures, Can obtain Wedge pressure)

Can measure cardiac output in multiple ways , check invasive blood temperature monitoring

need CXR to confirm placement that the distal PA is in the right or left pulmonary artery

can draw mixed venous oxygen saturation (SVO2)

RN CAN NOT Reposition this catheter or Wedge

Mixed Venous Oxygen Saturation – SVO2 – Why Is this helpful? Where would we draw this from and why?

Indicator of oxygen delivery and oxygen consumption – helps differentiate cardiogenic from septic shock and to see improvements if therapy is working!

draw from pulmonary artery catheter

intra aortic balloon pump (IABP)

Helps with coronary perfusion, reduces afterload.  Risks include improper timing of balloon inflation and deflation, BEDREST if in femoral artery (can also be axillary)  Helps pre-CABG, Pre-Heart transplant .  

impella (percutaneous LVAD)

Guarantees a set amount of CO to assist the native heart. Offloads the LV. Helps assist in cath procedures, post MI, C shock, and Pre-transplant. Risk for bleeding, hemolysis, BEDREST if femoral artery. Can be axillary.

LVAD (left ventricular asssit device)

Durable – can go home with this.  Connected to drive line, power cables.  Can not swim.  Must have batteries charged if traveling.  Risks include driveline infections, risk of bleeding, risk of clots/stroke.  CAN NOT TURN OFF – FATAL.  Surgically sewn into LV and Aorta.  CPR precautions – Avoid CPR when able – can dislodge LVAD

ECMO (Extracorporeal Membranous Oxygenation)

bypass machine to allow for out of body oxygenation and circulation. Mechanical circulatory support. Greatest amount of support – high mortality.

s/s of neurogenic shock

Evidenced by signs of parasympathetic stimulation

• Hypotension

• Bradycardia

• Temperature dysregulation

neurogenic shock treatment

• stabilize spinal cord injury 

• discontinue spinal anesthesia

• prevention- proper positioning with spinal/epidural 

• vasporessors, atropine, inotropic agents

s/s of anaphylactic shock

• Acute onset of symptoms

• Presence of 2 or more symptoms - respiratory  and/or cardiac compromise, reduced BP, GI distress, and skin or mucosal tissue irritation

• headache, lightheadedness, nausea, vomiting, acute abdominal pain, feeling of impending doom.

anaphylactic shock treatment

• vasopressors

• histamine blockers

• bronchodilators 

• corticosteroids 

MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)

Presence of altered function of two or more organs in an acutely ill patient such that interventions are necessary to support continued organ function

Shock untreated = MODS

treatment/management of MODS

• dialysis 

• surgery for obstructions 

• intubation

• ECMO

• Promoting adequate organ perfusion

• Providing nutritional support

nutritional therapy should also administer what to increase survival rates

Glutamine increases survival rates -> restores cell energy that is lost during shock

H2 blockers prevent excess acid production during times of stress

what is sepsis?

• Life-threatening organ dysfunction caused by a dysregulated host response to infection

what are some things that can increase risk for sepsis

surgery, central lines, catheters, double rooms, intubation, immunosuppression, prosthetic materials (ex valves and joints), chemo

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS) criteria

you have two or more of the following:

• Temperature of 101F OR less than 96.8F

• Heart rate >90/min

• RR of 20 or PaCO2<32

• WBC count >12 or <4, or >10% bands

sepsis criteria

SIRS plus evidence of infection (known or suspected)

Lactic > 2

severe sepsis criteria

SEPSIS PLUS ORGAN DYSFUNCTION, HYPOTENSION, OR HYPOPERFUSION

• (LACTIC ACID >4

• SBP <90 OR MAP <65

• DECREASED URINE OUTPUT)

septic shock criteria

HYPOTENSION (DESPITE FLUID RESUSCITATION) PLUS HYPOPERFUSION ABNORMALITIES

major difference between severe sepsis and septic shock

if you tried and intervention and it did not work it is shocxk

why measure lactate?

Marker of hypoperfusion and ischemia = inadequate oxygen delivery

normal lactate level

Normal level: 0.5-1

lactate level where you should suspect sepsis

lactate greater than 2

lactate level in severe sepsis

lactate greater than 4

how often do you need to check lactate?

Half life is 20 minutes. Check serially to assess response to intervention. at least every 4hrs

progression of sepsis

body over responding to bacteria in sepsis. inflammtory response activates clotting cascade 

causes widespread systemic response and low perfusion causing tissue injury 

common to see DIC with severe sepsis 

Primary bacteremia =

unknown source of infection

bacteremia means bacteria in bloodstream 

bacteremia does not always equal sepsis

sepsis bundle

• 1) Measure lactate level*
  2) Obtain blood cultures prior to administration of antibiotics
  3) Administer broad spectrum antibiotics
  4) Begin rapid administration of  30 ml/kg crystalloid for hypotension or lactate ≥4mmol/L

    5) Apply vasopressors if hypotensive during or after fluid resuscitation to maintain a MAP >65

*Remeasure lactate if initial lactate elevated (>2)

MANAGEMENT OF THE PATIENT WITH SEPSIS

Monitor access sites, monitor MAP, monitor BP, VS at least Q2H x 6 hrs and after every fluid bolus, call provider if urine output less than 0.5 ml/kg/hr, strict I and O, fluid challenges as specified, initiation of antibiotics, trend lactic acid level, neuro checks, telemetry monitoring, 

lactate clearance that can assess response to fluid resuscitation

Lactate clearance of at least 10% at a minimum of 2 hours after resuscitation initiation is a valid way to assess initial response to resuscitation in severe sepsis.