HYPOVOLEMIC SHOCK

I. Pathophysiology:

  1. Pathophysiology:
  2. Diminished cardiac output because of diminished intravascular vol.
  3. Decreased systemic art. pressure leads to increased carotid sinus sympathetic activity, constriction of arterioles & venules, tachycardia, contractility, hyperglycemia, etc.
  4. ADH, renin-angiotensin-aldosterone
  5. Cardiac output is redistributed ( flow to skin, muscle, mesentery, renal cortex)
  6. Anaerobic metabolism; lactic acidosis
  7. O2 delivery is decreased by
  1. venous return CO
  2. O2 carrying capacity

II. Dx.

  1. Look for source of blood loss
  2. Require >500ml for systemic signs except in elderly/anemics
  3. BP less sens. than HR, esp. if loss is slow (may require a 30% loss of intravasc. vol. before 's occur)
  4. Orthostatic vital sign changes
    1. Systolic BP drop >10mm suggests >20% blood loss
    2. Pulse increase of > 30/min is seen in 2-4% of normal, euvolemic adults; systolic BP drop > 10mm Hg occurs in 10% of euvolemic adults < 65yo and 11-30% of euvolemic adults > 65yo (JAMA 281:1022, 1999--AFP)
  5. General status, LOC
  6. Syncope, lightheadedness, nau, diaph., thirst, pallor, hypotn = >40% blood loss
  7. Skin turgor & temperature, capillary refill
  8. Air hunger
  9. Urine output

III. Labs.

  1. ABG : look for metabolic acidosis
  2. Lytes : anion gap, BUN/Cr, establish baseline early

IV. Tx.

  1. Restore volume
  1. Crystalloid (NS or LR) vs. colloid (e.g. blood, FFP, albumin)--no advantage to colloid in one meta-analysis of 19 randomized trials (in fact, sig. higher risk of death in pts randomized to colloid!) (BMJ 316:961, 1998--JW; BMJ 317:235, 1998--AFP)
  1. Control bleeding : pressure dressings, drugs, surgery
  2. Supplemental O2
  3. Foley to monitor u/o