SUPP

• Shock

  Life-threatening, characterized by hypotension, which leads to insufficient delivery of oxygenated blood to cells/tissues
• Shock

  • Circulatory shock is not a PRIMARY disorder – it occurs as a consequence of a previous physiologic insult
  • Initial insults may include: infections {septic shock}, heart disease {cardiogenic shock}, trauma {hypovolemic/neurogenic}, blood loss {hypovolemic}, anaphylactic reactions
• Once circulatory shock develops, a similar cascade of events follows REGARDLESS of the primary insult
• Pathogenesis of Circulatory Shock

  Characterized by an imbalance between O2 supply & O2 requirements at the cellular level, leading to cellular hypoxia and potentially tissue/organ damage and death
• 4 Types of Circulatory Shock

  • Cardiogenic (i.e., pump failure)
  • Hypovolemic (i.e., fluid loss)
  • Obstructive (i.e., a blockage that decreases CO)
  • Distributive (i.e., inappropriate vasodilation r/i decreased CO)
• Cardiogenic Shock

  • AMI – most common cause (esp. w/ anterior wall), Valve disease, Ventricular rupture, Can also be secondary to mechanical (e.g. tamponade, mediastinal shifts, pericardial effusion, etc.)
• Hypovolemic Shock

  • Acute hemorrhage, Dehydration (e.g., vomiting/diarrhea, DKA, HHS), Overuse of diuretics, Loss of plasma proteins (i.e., burns, crush injuries)
• Obstructive Shock

  • Pulmonary embolism, Cardiac tamponade, Tension pneumothorax
• Distributive Shock

  • Central blood is distributed to peripheral beds, Anaphylaxis (aka anaphylactic shock), Neurotrauma (aka neurogenic shock), Spinal anesthesia, Sepsis (infection) (aka septic/toxic shock)
• Impaired Tissue Oxygenation

  Continuous supply of O2 is needed by all cells to make ATP, Less O2 = less aerobic metabolism, Cell relies on anaerobic metabolism, Leads to lactic acid production and metabolic acidosis
• Impaired Tissue Oxygenation

  1. Loss of Na/K pump

  2. Na enters cell

  3. Water follows passively (Hydropic swelling)

  4. Ca++ also enters cell

  5. Further disruption in ATP production

  6. Loss of membrane integrity

  7. Cell death can result in minutes to hours
• Reperfusion Injury

  When O2 is restored to a cell, there is an increase in the production of free radicals (superoxide, peroxide, hydroxyl radicals, singlet oxygen) which can attack membrane structure, denature proteins, and break apart DNA
• Chemical Mediators

  • TNF-α (Tumor Necrosis Factor)
  • Interleukin-1 (IL-1)
  • Nitric Oxide (NO)
  • Norepinephrine
  • Epinephrine
  • Leukotrienes
  • Histamine
• Chemical Mediators

  • TNF-α = inflammation & neutrophil activation, IL-1 = inflammation, vasodilation, vascular leakiness, NO = vasodilator
• Macrophages & tissue cells are stimulated to release inflammatory cytokines in response to hypoxic tissue injury
• A hallmark of septic shock & the late stages of other types of shock is the failure of the microcirculation to auto-regulate the blood flow (some areas will be over-perfused, other areas will be under-perfused)
• TNF-α & IL-1

  Induce cell to produce NO, which is a powerful vasodilator, but in excessive amounts it is detrimental
• Efforts to block TNF-α & IL-1 in patients with septic shock have not decreased mortality, suggesting that other mediators are involved
• The inflammatory response is what causes most of the complications associated with organ damage/failure in shock
• Stages / Compensatory Mechanisms of Shock

  • Compensated / Non-progressive Shock
  • Progressive / De-compensated Shock
  • Refractory / "Irreversible" Shock
• Compensated Shock

  • Narrow Pulse Pressure, tachycardia {>100 bpm}, tachypnea {fast & deep}, oliguria, cool, clammy skin, altered mentation {combative/agitation/restlessness}, thirst, dilated pupils
• In early stages of hypovolemia, BP is stable {d/t SNS responses}, when volume losses = 25% total blood loss → BP drops quickly
• At some point, the compensatory mechanisms can no longer sustain adequate perfusion to tissues, leading to hypoxic injury and the Progressive Stage of Shock
• Metabolic Acidosis

  Increases the burden on the Resp/Renal system, leads to electrolyte disturbances which can cause life-threatening arrhythmias, causes the release of myocardial depressant factor which worsens the shock
• Progressive Shock

  • hypotension < 90mmHg, narrowing pulse pressure, Tachycardia/tachypnea, ARF = acute renal failure {oliguria to anuria}, Decreased LOC {confused, lethargic, slurred speech}, metabolic & respiratory acidosis, loss of peripheral pulses, sluggish pupillary reactions
• Refractory/Irreversible Shock

  • S-C-D, bradycardia to asystole, loss of vasomotor tone {decreased DBP}, narrowing of pulse pressure… to zero, respiratory arrest, ashen colour, dependent lividity {skin discoloration from venous congestion}, pupils fixed & dilated
• Complications of Shock

  • ARDS: Acute Respiratory Distress Syndrome
  • DIC: Disseminated intravascular coagulation
  • ARF: Acute Renal Failure
  • MODS: Multiple Organ Dysfunction Syndrome
• ARDS


  • a form of respiratory failure most commonly associated w/ septic shock, characterized by: refractory hypoxemia, ↓ pulmonary compliance, pulmonary edema {non-cardiogenic}, mortality in patients with shock complicated by ARDS = 60-90%
• ARDS

  1. Tissue ischemia in the lungs leads to neutrophil migration to the pulmonary capillaries

  2. Neutrophils release destructive enzymes AND oxygen free radicals

  3. Neutrophils secrete chemical mediators which make the pulmonary capillaries "leaky" leading to pulmonary edema

  4. Inflammation damages Type II pneumocytes responsible for surfactant production

  5. Loss of surfactant ↑ surface tension in alveoli causing ↓ lung compliance and atelectasis
• DIC

  • Serious complication often of septic shock, characterized by abnormal clot formation in the microvascular beds, leading to ischemic tissue damage, consumption of clotting factors, and increased risk of major bleeding
• ARF

  • In shock, kidneys undergo prolonged hypoperfusion, causing vasoconstriction, ↓ GHP and ↓ GFR, leading to acute tubular necrosis, ↓ urine output, and ↑ BUN and creatinine
• Approximately 50% of all trauma deaths are immediate, 30% are due to Multiple Organ Dysfunction Syndrome (MODS)
• Spontaneous intracranial hemorrhage

  Particularly disastrous as a sequelae of DIC
• Tx for DIC is complex & generally unsatisfactory
• Acute renal failure (ARF)

  In shock, the kidneys undergo prolonged periods of hypoperfusion
• Vasoconstriction of the afferent arterioles

  Decreases GHP and GFR
• Hypoxic cellular damage occurs after 15-20 minutes of acute ischemia
• Acute tubular necrosis (ATN)

  Decrease of excretion & wastes in the blood, causing a measurable increase in BUN & creatinine
• Urine output

  Quickly falls to zero (oliguria to anuria)
• The kidneys do NOT respond to fluid replacement & diuretics in ATN