Shock Flashcards

1
Q

Shock (defined)

A

1st slide

Medically, shock is defined as a
condition where the tissues in the
body don’t receive enough oxygen
and nutrients to allow the cells to
function. This ultimately leads to
cellular death, progressing to organ
failure, and finally, if untreated, whole
body failure and death.

2nd slide:

  • Cells need two things to function: oxygen and glucose
  • If cells are deprived of oxygen, instead of using aerobic (with oxygen) metabolism to function, the cells use the anaerobic (without oxygen) pathway to produce energy.
  • Lactic acid is formed as a by product of anaerobic metabolism.
  • This acid changes the acid-base balance in the blood, making it more acidic

3rd slide:

  • Widespread impaired cellular dysfunction in response to decreased tissue perfusion and oxygenation
  • Imbalance in supply and demand for O2 and nutrients
  • “Whole-Body” response
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2
Q

Impacts of Shock Early–>Late to:

  1. Blood Pressure
  2. Pulse
  3. Skin Color
  4. Skin Temp
  5. Alertness
  6. Respiration
A
  1. Blood Pressure: Normal –> Systolic<90mmHg
  2. Pulse: Increase rate–>Increase rate+weak
  3. Skin Color: Normal–>Pale
  4. Skin Temp: Cool/moist–>Cold
  5. Alertness: Anxious–>Coma
  6. Respiration: Increase rate/Increase depth–> Increase rate/shallow

(Slide 5)

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3
Q

Initial Stage of Shock

A
  • Changes occur at cellular level
  • Metabolism changes to anaerobic
    • Lactic acid accumulation causes cell damage
  • Baseline MAP decreases by < 10 mm Hg
  • Adaptive responses effective in keeping MAP & CO within the normal range
  • What changes in VS if any might you expect to see?
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4
Q

Nonprogressive (Compensatory)
Stage of Shock

A
  • Neural, hormonal & biochemical compensatory mechanisms respond to anaerobic metabolism
  • Baseline MAP decreases 10-15 mm Hg
  • Decreased perfusion activates SNS
    • ↓ renal perfusion activates RAAS
    • Vasoconstriction maintains vital organ perfusion
    • Tissue hypoxia in nonvital organs
    • Cool, clammy skin (warm & flushed with septic)
  • Blood shunted from lungs
    • ↓ PaO2 levels from V/Q/ mismatch
    • Increase in rate/depth of respirations
  • SNS stimulation ↑ myocardium O2
    demands
  • Impaired GI motility – risk for paralytic ileus
  • Correction of causes of shock can prevent shock from progressing
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5
Q

Progressive (Uncompensated)
Stage of Shock

A
  • Sustained drop of baseline MAP > 20 mm Hg
  • Vital organs develop life-threatening hypoxia
  • Decreased cellular perfusion and altered capillary permeability
    • Leakage of protein into interstitial space
    • ↑ Interstitial edema (anasarca)
  • Organ failure
    • Neurological
    • Pulmonary (ARDS)
    • Renal
    • Liver/GI (ischemic gut)
  • Lungs: Fluid moves into alveoli
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6
Q

Refractory Stage of Shock

A
  • Extensive cell death & tissue damage result from too little oxygen reaching the tissues
  • Body respond ineffectively to interventions, and shock continues
    • Profound hypotension and hypoxemia
    • Tachycardia worsens
    • Decreased coronary blood flow
    • Cerebral ischemia
    • Failure of one organ system affects others
  • Recovery unlikely
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7
Q

What changes in do we expect in early sepsis/SIRS, late sepsis, and septic shock (MODS)?:

  1. cardiac output
  2. stroke volume
  3. serum lactate (arterial)
  4. blood glucose
  5. oxygen saturation
  6. serum creatinine
  7. segmented neutrophils
  8. band neutrophils
A

Page 3

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