Introduction to Shock States

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  1. Types of shock
    • Hypovolemic
    • Transport
    • Obstuctive
    • Cardiogenic
  2. 3 Physiologic issues w/ Hypovolemic shock
    • Volume decrease
    • Intravascular compartment increased (vessel size)
    • Reduced ventricular filling pressure, SV, CO, and BP
  3. Causes of volume loss
    • Hemorrhage
    • Dehydration
    • Burns
    • Vomiting: losing fluid and decreased intake bc vomiting
    • Diarrhea
    • 3rd spacing
  4. Causes of increased intravascular compartment
    • Vasodilation: neurogenic shock, spinal cord injury, anaphylactic shock (allergic rx), septic shock (dilated and fluid in 3rd spaces)
    • Paraplegics' legs do not get signal to vasocontrict
  5. Sepsis
    • Must meet 2 criteria
    • Temp: >100.4 or <96.8
    • HR: >90
    • RR: >20
    • WBC: >1200, <4000, or >10% band cells
    • BP is not an indicator!
  6. Severe Sepsis
    • Sepsis PLUS at least one criteria
    • Acute Organ dysfunction: at least one
    • Hypoperfusion
    • Hypotension: lactic acidosis, oliguria
    • Acute LOC alteration
  7. Septic Shock
    • Persistent Sepsis-Induced hypotension: despite adequate fluids
    • MODS
    • Persistent shock state
  8. Transport shock causes
    • Hemorrhage
    • Anemia
    • Carbon monoxide toxicity: has greater affinity than O2
  9. Obstructive shock causes
    • PE: V/Q perfusion mismatch, increased pulmonary vascular resistance
    • Tension pneumothorax: impedes venous return
    • Cardiac tamponade: impairs ventricular filling and decreases CO
  10. Cardigenic Shock: R vs. L
    • Right: ventricle fails to pump necessary volume
    • Left: ventricle fails to pump oxygenated volume
  11. Cardiogenic Shock causes
    • Massive MI (#1)
    • Acute Mitral Valve regurgitation
    • Cardiomyopathy: so large that beomces ineffective, can't squeeze well
  12. Cardiogenic Shock at risk populations
    • Elderly
    • Diabetic
    • Anterior MI
    • Previous MI
  13. 4 Stages of shock
    • Initial
    • Compensatory
    • Progressive
    • Refractory
  14. Initial Stage of Progression
    • Decreased O2 delivery leads to anaerobic metabolism and lactic acidosis
    • Want to catch here
  15. Compensatory Stage of Progression
    • Neuroendocrine reponses are activated and clinical s/s can be seen
    • Kidneys retain, HR increases, CO increases, LOC changes
    • Looks for trends
  16. Progressive Stage of Progression
  17. Refractory Stage of Progression
    • Cell destruction and death
    • Resistance to conventional therapy
  18. Clinical findings in shock
    • BP, HR, UOP, RR (compensatory)
    • Lactate levels: measure of impaired O2 and hypoperfusion
    • Base Deficit: the amt. of bicarb/base the body needs to raise one liter of blood to normal pH
  19. Clinicals Signs in hypovolemic shock
    • VS: decreased BP (orthostatic), increased HR, decreased UOP
    • Hemodynamics: decreased PAP PAQP and CO, increased SVR (compensation vasocontriction)
    • Skin: cool, poor cap refill
  20. Clinical signs in neurogenic shock
    • VS: decreased HR
    • Hemodynamics: decreased SVR, CO, RAP, PAP, PAWP
    • Skin: warm, no sweating below level of spinal cord injury
  21. Clincal signs of anaphylatic shock
    • Erythema
    • Urticaria
    • Pruritis
    • Angioedema
    • Dyspnea
    • Wheezing
    • Feeling warm
    • Laryngeal edema
    • Severe bronchoconstriction w/ stridor
    • Decreased LOC
    • Common, develops w/in 5-30mins but can take as long as 6-12hrs
  22. Early/Late S/S of septic shock
    • Early: Changes in LOC, increased RR, fever or hypothermia
    • Progressive: fluid shifts (3rd spacing and edema), increased WBCs, positive blood cultures, pulmonary infiltrates, normal or increased CO/CI, decreased bowel sounds (perfusion issue, protects heart and lungs first), ischemia/necrosis of extremities (fibrinolytic response), coagulopathy (bleeding from insertion sites, prolonged bleeding time, altered platelet count; compromised liver)
  23. Clinical signs of transport shock
    • Low HCT
    • Low to normal RAP and PAWP: depends of body's ability to compensate
  24. Transport shock: carbon Monoxide s/s
    • HA
    • Malaise
    • Nausea
    • Memory loss
    • Personality changes
    • Neurologic dysfunction
  25. Clinical signs of Obstructive shock
    Pulsus Paradoxus: a decrease of >10mmHg of the SBP during inspiration
  26. ABGs for shock
    will see metabolic acidosis initially because of lactic acid
  27. Treatment: Optimize O2 delivery
    • Supplemental O2
    • IV fluids: LR, blood for low HCT, albumin for normal HCT
    • Inotropic med: dopamine, dobutamine, milrinone; use w/ caution, can exacerbate problem if valuves aren't working or demand is too high
    • Vasocontrictors: epinephrine, norephinephrine (levophed), vasopressin
    • Vasodilators: nitroprusside, nitroglycerin; decreases afterload
  28. Treatment: Minimize O2 Consumption
    • Decrease total body work
    • Decrease pain
    • Decrease anxiety
    • Decrease temp
  29. Treatment: Specific Options
    • Treat hypersensitivity rx: antihistamines (Benadryl), Bronchodilators (albuterol)
    • Low-Dose Steroids: body needs this to help drive compensatory mechanisms
    • Restore balance b/t coag and fibrinolysis: Xigris (extreme cases)
Card Set
Introduction to Shock States
Shock States
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