Ch20

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Author:
wvuong
ID:
298652
Filename:
Ch20
Updated:
2015-03-18 04:32:32
Tags:
Shock
Folders:
patho
Description:
shock
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  1. Common factor among all types of shock are...
    hypoperfusion and impaired cellular oxygen utilization
  2. Inadequate cellular oxygenation may result from:
    • decreased cardiac output 
    • maldistribution of blood flow 
    • reduced blood oxygen content
  3. Impaired tissue oxygenation results in
    • anaerobic metabolism 
    • free radiation production 
    • macrophage function
  4. Failure of microcirculation to autoregulate blood flow leads to?
    activation of coagulation
  5. Describe the triangle
    Coagulopathy (lactic acidosis) --> metabolic acidosis (decreased mycardial performance) ---> Hypothermia (Halt coagulation cascade) ---> coagulopathy
  6. What are the compensatory mechanisms and the stages of shock
    compensatory stage: homeostatic mechanisms are sufficient to maintain adequate tissue perfusion despite a reduction in CO 

    SNS activation attempts to maintain bp even tho CO has fallen
  7. Progressive stage of shock is?
    marked by hypotension and tissue hypoxia
  8. progressive stage includes...
    • lactate production = ^ anaerobic metabolism 
    • lack of ATP = cellular swelling, dysfunction, and deaht 
    • cellular and organ dysfuction result from oxygen free radicals, release of inflammatory cytokines, and activation of the clotting cascade
  9. Cardiogenic shock
    result of severe ventricular dysfunction associated with MI
  10. features of Cardiogenic shock
    • decreased CO 
    • elevated L ventricular end diastolic pressure 
    • S3 heart sounds 
    • pulmonary edema
  11. Cardiogenic shock
    [patho]
    [treatment]
    • low CO = reduced oxygen delivery to tissues = higher oxygen extraction = low SvO2
    • therapy aimed at improving CO and mycardial oxygen delivery, preload reducing, afterload reducing agents 
    • intraaortic balloon counterpulsation, ventricular assist devices, heart transplantation
  12. obstructive shock
    results from mechanical obstructions that prevent effective cardiac filling and stroke volume
  13. obstructive shock 
    [common cause]
    pulmonary embolism, cardiac tamponade, and tension pneumothorax
  14. obstructive shock 
    [treatment]
    rapid management of underlying obstruction is required to prevent cardiovascular collapse
  15. Hypovolemic shock
    results from inadequate circulation blood volume precipitated by hemorrhage, burns, dehydration, or leakage of fluid into interstitial spaces 

    low CO and intracardiac pressures lead to SNS activation = elevated HR, vasoconstriction, increased contractility
  16. Hemorrhagic shock
    correlates with amt of blood loss
  17. Hemorrhagic shock 
    [treatment]
    therapy aimed at fluid replacement and control of the source of volume loss 

    colloids, crystalloids, and blood products used for fluid replacement
  18. Distributive shock
    characterized by excessive vasodilation and peripheral pooling of blood 

    CO inadequate due to reduced preload
  19. Anaphylactic shock
    • excessive mast cell degranulation mediated by IgE antibodies in response to antigen 
    • mast cells release vasodilatory mediators resulting in severe hypotension
  20. Anaphylactic shock 
    [symptoms]
    • urticaria
    • bronchoconstriction
    • stridor
    • wheezng 
    • itching
  21. anaphylactic shock 
    [treatment]
    maintenance of airway patency, use of epinephrine, antihistamines, vasopressors, and fluids
  22. Neurogenic shock
    results from loss of sympathetic activation of arteriolar smooth muscle
  23. Neurogenic shock 
    [causes include]
    medullary depression (brain injury, drug overdose) or lesions of sympathetic nerve fibers (spinal cord injury)
  24. Neurogenic shock 
    [treatment]
    vasopressors, fluids
  25. Septic shock
    results from severe systemic inflammatory response to infection

    characterized by release of immune mediators results in widespread inflammation

    initially characterized by high CO due to sympathetic activation of the heart
  26. septic shock 
    [common causes]
    • g(-) and g(+) bacteria, fungal infections 
    • g(-) shock: endotoxins in bacterial cell walls stimulation massive immune system activation
  27. Septic shock 
    [patho]
    • clotting cascade, complement system, and kinin system activated 
    • widespread inflammation leads to profound peripheral vasodilation with hypotension, maldistribution of blood flow with cellular hypoxia, and increased capillary permeability with edema formation
  28. Septic Shock 
    What is present
    • CO is high, cellular hypoxia still remains 
    • reduced cellular oxygen utilization is manifested as high SvO2
  29. Septic shock 
    [treatments]
    • therapy aimed @improving distribution of blood flow and manage infection with antibiotics 
    • adm of fluids and drugs to improve cardiac and vascular performance to improve distribution of blood flow
  30. Arterial oxygen content 
    low CO results in?
    maldistribution of flow?
    greater O2 extraction and lower ScO2

    less O2 extraction and higher SvO2
  31. Hemodynamic monitoring
    • pumonary artery catheter insert via jugular/subclavian veinsmeasures: CO and SvO2
    • R atrial pressure used to manage blood vol. 
    • pulmonary press. used to detect pumonary complications 
    • pulmonary artery diastolic press. reflects L preload 
    • pulmonary capillary occlusion press is direct measure of L atrial pressure
  32. Complications of shock
    • results in reduced/inadequate cellular O2 consumption and may affect all organs and systems 
    • complications are inflammatory; inflammed triggered by hypoxic injury to cells by antigen/endotoxin 
    • excessive immune response leads to leaking capillaries, damage from proteolytic enzymes and systemic activation of clotting, complement, and kinin systems
  33. Types of complications of shock
    • ARDS- common assoc. with septic shock
    • DIC
    • ARF
    • MODS
  34. ARDS - acute respiratory distress syndrome
    • development of refractory hypoxemia, decreased pulmonary compliance, and radiographic evidence of pulmonary edema 
    • neutrophils release proteolytic enzymes, produce O2 free radicals, and secrete inflammatory chemicals that make pulmonary capillaries leaky
  35. DIC - disseminated intravascular coagulopathy
    • immune activation of the clotting cascade 
    • microcirculation obstructions lead to ischemic tissue damage 
    • widespread clot formation consumes platelets and clotting factors 
    • platelet count and fibrinogen lvls are low; fibrin degradation products are elevated
  36. ARF - acute renal failure
    • Kidneys undergo long time of hypoperfusions 
    • vasoconstriction causes decreased glomerular blood flow [reduced hydrostatic pressure and filtration rates]
    • acute tubular necrosis (ATN) assoc. with decreased urinary excretion of waste produts (creatinine and urea)
  37. MODS - multiple organ dysfuction syndrome
    • most common causes: sepsis and septic shock 
    • initiated by immune mechanisms that are overactive and destructive 
    • cytokines affect endothelium, recruit neutrophils, and activate inflammation in vascular beds leading to tissue destruction and organ dysfunction

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