MS5 Shock and MODS

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MS5 Shock and MODS
2013-03-15 02:30:54
Multisystem diesase

Shock and MODS
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  1. Shock
    State in which organ damage is caused by decreased perfusion, or the tissue responds as if there is decreased perfusion

    • -Most types of shock cause low BP
    • -V= I*R
    • -ΔP (MAP-CVP) = CO*SVR
    • -low BP from low CO, or low SVR
  2. Causes of low cardiac output (CO)
    • Low venous filling:
    • -"dehydration" = ↓ ECV
    • -blood loss
    • -Loss of fluid from vasculature: "3rd spacing" (capillary leak)

    • Cardiac dysfunction:
    • -heart failure
  3. Low CO Symptoms
    low venous fillinng vs cardiac dysfunction
    • Low venous filling:
    • -Low skin turgor
    • -Flat neck veins
    • -Lungs clear

    • Cardiac dysfunction:
    • -Skin edema
    • -Distended neck veins
    • -Lungs edematous
  4. Low Systemic Vascular Resistance (SVR)
    • Vasodilation:
    • -unusual to happen alone (e.g. nitroglycerine, nifedipine overdose)
    • -Large part of sepsis
  5. Shock signs and sx
    Low CO vs Low SVR
    • Low CO:
    • -Cold extremities
    • -Pale skin
    • -Slow nail bed refill
    • -Compensation:
    •      1. Increased SVR - preferential flow to vital organs
    •      2. Attempt to increase CO - tachycardia, increase stroke volume (?)

    • Low SVR:
    • -Warm extremities
    • -Normal or pink skin
    • -Brisk nail bed refill
    • -Compensation:
    •      1. Attempt to increase SVR - preferential flow to vital organs
    •      2. Increased CO - tachycardia, stroke volume
  6. Complications of shock
    • Hemodynamic compromise: hypoperfusion
    • Systemic inflammatory response
  7. Hypoperfusion
    What's the problem?
    • Oxygen is required for electron tranport chain to function: generation of 36 ATP vs 2 ATP
    • -Recycles NADH → NAD+
    • -Recycles FADH2 → FADH

    *Krebs cycle does NOT require oxygen
  8. Signs of decreased perfusion
    • Brain → confusion
    • Heart → Tachycardia, low stroke volume
    • Kidney → Low urine output
    • Intestine → Low peristalsis
    • Skin → Pallor, diaphoresis
    • Respiratory → Tachypnea
    • Cellular metabolism → Lactic acid cycle supplements aerobic metabolism
  9. Lactic acidosis
    • Lactate itself can lower blood pH
    • -Acidosis → cardiac dysfunction
    • -some drugs (vasopressors) won't work as well

    • Strong evidence that cells are starving
    • -cellular death
    • -organ damage
  10. Systemic inflammatory response
    • Elevated levels of circulating proinflammatory mediators:
    • -TNF α
    • -Interleukins
    • -Prostaglandins
    • -Other

    • Activation of endothelial cells and leukocytes:
    • -Activated endothelial cells produce nitric oxide (vasodilator)
    • -Intracellular adhesion molecules; leukocytes express corresponding ligands
    • -Leukocytes collect in the capillaries and postcapillary venules; invade lung and systemic tissues
    • -Endothelial and parenchymal cells make chemotactic cytokines
  11. Endothelial-Leukocyte interactions

    • -Activated leukocytes release oxygen free radicals
    • -Complement and coagulation pathways activated → Damaged RBCs, WBCs, fibrin, platelets accumulate in capillaries, impairing O2 delivery
  12. Disseminated intravascular coagulation (DIC)
    definition and sx
    • -Extreme, widespread coagulation in capillaries
    • -Body attempts to remove clots via fibrinolysis
    • -Coagulation factors get used faster than they are made
    • -Risk of bleeding and of capillary thrombosis

    • Effects on tissue:
    • -Direct damage via leukocyte action
    • -Perfusion problems due to microvascular clot and debris
    • -Capillary leak → tissue edema; lowers intravascular volume and cardiac output
    • -Organs become very unhappy
  13. Vasodilation
    • Activated vascular endothelial cells produce nitric oxide (a vasodilator)
    • Prostaglandin I2 (PGI2) causes vasodilation of the systemic vasculature (low SVR)
    • Thromboxane A2 causes vasoconstriction of pulmonary arteries and pulmonary hypertension
  14. Sepsis → shock
    • Endotoxins and other mediators cause:
    • 1. Cellular poisoning that mimics hypoperfusion:
    • -similar effect of cyanide poisoning: uncoupling of the H+-ATPase
    • -Anaerobic metabolism → lactic acidosis

    2. Low venous filling → decreased CO

    3. Systemic vasodilation

    4. Cardiac dysfunction
  15. Sepsis
    what to look for
    • Signs of shock
    • Signs of infection
    • Warm extremities
    • Unexplained organ dysfunction
  16. Multiple organ dysfunction syndrome (MODS)
    • Complication of shock manifested by damage to and dysfunction of several organ systems
    • Type and severity of damage is related to severity and duration of the shock
  17. MODS
    Brain injury
    • Mild confusion is very common
    • Coma can even occur
    • Brain is locked in skull 
    • Brain has difficulty autoregulating flow when mean arterial pressure is low
    • High pCO2 or low pO2 can dilate cerebral vessels,  further disrupting autoregulation
  18. MODS
    • Poor contractility due to impaired O2 extraction weakens force of systole
    • Incomplete relaxation due to injury reduces ventricular filling during diastole
    • Circulating catecholamines can cause vasoconstriction of the coronary arteries and their branches
    • Increased demand combined with impaired blood supply and O2 utilization can cause ischemia
    • Lactica acidosis in the myocardium is common
  19. MODS
    • The most commonly damaged organ in MODS
    • Acute Respiratory Distress Syndrome "ARDS"
    • The lung has massive surface area and exposure to endothelium
    • Survival depends on gas-blood interactions
    • Inflammatory edema with extravasation of blood proteins into the alveoli → surfactant function is markedly compromised
    • Pulmonary capillary bed gets obstructed with active debris
    • Inflammatory mediators and activated cells from everywhere all end up passing through the lung, where they get trapped
    • Deadly gas exchange abnormalities → ventilation perfusion mismatching
  20. MODS
    • Centrilobar hepatic necrosis
    • Leakage of transaminases (ALT, AST)
    • Liver synthetic function declines
    • -Bilirubin increases
    • -Coagulation factors and albumin can decrease
    • Decrease phagocytosis
    • Hypoglycemia (severe dysfunction)
    • Decreased clearance of toxic substances (drugs, metabolites can damage other organs)
  21. MODS
    GI system
    • Intestinal dysfunction is very common
    • Edema of the mucosa
    • Necrosis of the intestinal villa
    • Submucosal hemorrhage
    • End stage: hemorrhagic necrosis of the gut
    • **Gut ischemia/damage might be involved in the escalation of MODS
    • →Breakdown of mucosal barrier between gut
    • →translocation of bacteria and/or toxins into the blood and lymphatics
    • →Ineffective clearance by the compromised liver
  22. MODS
    • Renal function is a good indicator of a person's tolerance  of MODS (urine continuously)
    • Glomerular filtration rate can dramatically decrease
    • →decreased renal blood flow
    • →vasoconstriction of the arteries
    • Ischemia can cause renal tubules to necrose
    • Cellular debris can clog tubule lumen
    • The medulla can't stay hypertonic, which impairs countercurrent function
  23. MODS
    Blood and endocrine
    • Blood
    • -Decreased hematopoiesis
    • -Impaired immune cell function
    • -Thrombocytopenia
    • -Coagulopathy, including disseminated intravascular coagulation

    • Endocrine
    • -Insulin derangements
    • -Adrenal dysfunction
  24. MODS
    probability of death
    • Infection (no SIRS): ~20%
    • Sepsis: ~20%
    • Severe sepsis: ~35%
    • Sepsis with MODS: ~50%
  25. Sepsis
    • Cellular poisoning → Treat infection rapidly
    • Low venous filling/decreased cardiac output → Administer large volumes of fluid
    • Systemic vasodilation → Administer vasopressors
    • Cardiac dysfunction → possibly administer inotropic agents
  26. MODS
    • Prevent organ ischemia early
    • Support organ function: mechanical ventilation, dialysis
    • Find/remove source of MODS: abx, surgery
    • Await development of future therapies
    • For now...
    • -Early goal directed therapy: fluid management