Sepsis, MODS Flashcards
Shock
Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
Imbalance in supply/demand for O2 and nutrients
Shocks Causes
Acute widespread reduction in affective tissue perfusion
- Anaerobic metabolism
- Lactic acidosis
- Organ Dysfunction
- Metabolic abnormalities
- Irreversible organ damage and death
Classification of Shock
Cardiogenic: Decrease in heart pumping capacity
Hypovolemic: Decreased intravascular volume
- Absolute (Blood Loss)
- Relative (Third spacing)
Distributive: MAJOR vasodilation
- Neurogenic
- Anaphylactic
- Septic
Obstructive: Heart cant move blood forward
Stages of Shock
1) Initial
2) Compensatory
3) Progressive
4) Refractory
Initial Stage
- usually not clinically apparent
- metabolism changes at cellular level from aerobic to anaerobic
Lactic acid builds up and must be removed by liver
Process requires O2, unavailable due to decreased tissue perfusion
(Anyone lying down with a HR over 100..something is wrong)
Compensatory Stage
Body tries to overcome consequences of anaerobic metabolism and maintain homeostasis
- Baroreceptors in carotid and aortic bodies activate SNS in response to decreased BP
- SNS stimulation increases myocardial O2 demands
- Vasoconstriction while blood to vital organs maintained
- impaired GI motility
- slowed peristalsis
- risk for paralytic ileum (dead, sleepy, bowel)
Cool, clammy skin EXCEPT septic patient who is warm and flushed
- decreased blood to kidneys activates renin-angiotensin system
- angiotensin 1 converted to angiotensin 2 causing vasoconstriction
* Prepare for vasoconstriction need to return blood flow back to important organs
Compensatory Stage
Body is able to compensate for changes in tissue perfusion
If cause of shock is corrected, patient recovers with little or no residual effects
If cause of shock is not corrected, patient enters progressive stage
Catch this early for your patient
If not recovering, move the patient to ICU
Progressive Stage: Pulmonary Affects
Fluid moves into alveoli
- edema
- dec surfactant
- worsening V/Q mismatch
- tachypnea
- crackles
- inc work of breathing
Progressive Stage
Begins when compensatory mechanisms fail
- leakage of protein into interstitial space
- inc systemic interstitial edema
- Anasarca (edema everywhere)
Progressive stage (change in mental status, fluid shift)
Distinguishing features of dec cellular perfusion and altered capillary permeability
- leakage of protein into interstitial space
- inc of systemic interstitial edema
- pulmonary edema
Cardiac output begins to dec, resulting in a dec in BP
Sustained hypoerfusion
- weak peripheral pulses
- ischemia of distal extremities
- dysrhytmias and cardiac ischemia (MI)
Progressive Shock
Mucosal barrier of GI system becomes ischemic
- ulcers, GI bleeding, dec ability to absorb nutrients.
Hypo perfusion leads to renal tubular ischemia
- may result in AKI, elevated BUN and Crt, metabolic acidosis
Liver fails to metabolize drugs and waste
- jaundice, elevated enzymes, risk for DIC and bleeding
Refractory Stage
Exacerbation of anaerobic metabolism
Accumulation of lactic acid and waste products
Increased capillary per ability
Profound hypotension and hypoxemia
Tachycardia worsens
Failure of one organ system affects others
Recovery unlikely
Septic Shock
A distributive shock
Sepsis: systemic inflammatory response to documented or suspected infection
Severe sepsis: sepsis complicated by organ dysfunction (#1 kidney)
Presence of sepsis with hypotension despite fluid resuscitation
Presence of inadequate tissue perfusion resulting in hypoxia
Compensated: organ function is maintained
Uncompensated: end-organ dysfunction
Irreversible: end-organ cell death
Compensated: tachycardia, RR, BP normal
Uncompensated: Super-tachy, BP low, Tachypnea
Irreversible: Bradycardia, BP low, apnea, confusion
Who is more susceptible for septic shock
Older patients (dec immune response)
Those who are immunocompromised
Those with chronic illness
Surgery or trauma patients
