Shock

Definition

  • Inadequate tissue perfusion relative to tissue demands = insufficient delivery of oxygen and metabolic substrates
  • End organ dysfunction requiring support (pressors, ventilation, renal replacement, etc.)

Pathophysiology

Cellular Hypoxia → ↓ ATP, cell death
Hormonal Hypothalamic - ACTH - adrenal activation, catecholamines, hyperglycemia
Inflammatory ↑ vascular permeability, vasodilation, platelet aggregation
Followed by later anti-inflammatory peak → immunosuppression
Cardiac Increased cardiac workload → ischemia, cardiomyopathy (Takotsubo) 
Pulmonary Hypoxemia → compensatory respiratory acidosis, tachypnea; leaky vessels →pulmonary edema; ARDS 
Renal  Decreased perfusion → AKI, ATN, ↓ UOP, RAA axis activation
GI Mucosal breakdown, ulcers, bacterial translocation across impaired cellular membranes, transaminitis, cholecystitis, pancreatitis
Heme  Platelet activation/aggregation → thrombocytopenia, DIC
Neuro  Brain will preserve perfusion at all costs with cerebral autoregulation. Delirium, myopathy, neuropathy


Types of shock

  Pathophys Etiologies
Hypovolemic ↓ intravascular volume hemorrhage, burns, 3rd-spacing
Cardiogenic pump failure MI, arrhythmia
Obstructive blockage of flow PE, tamponade, tension PTX
Distributive ↓ systemic vascular resistance septic, neurogenic, anaphylaxis

Hypovolemic shock

  • Have lost ~ 2 L of blood by the time BP is affected
  Class I Class II Class III Class IV
Blood loss < 15% (750 ml) 15-30% (750 cc - 1.5 L) 30-40% (1.5 - 2 L) > 40% (> 2 L)
Vitals Normal HR 100-120
↑ Pulse pressure
RR 20-30		 HR 120-140
Hypotensive
RR 30-40		 HR > 140
Marked hypotension
RR > 35
UOP (cc/hr) > 30  20-30  5-20  Negligible 
Mental status Slightly anxious  Mod. anxious  Anxious, confused Confused, lethargic 

Neurogenic shock

  • Systemic hypotension, bradycardia
  • Loss of regulation of cardiovascular tone → unopposed vagal input
  • Risk with cervical, high thoracic injury

Septic shock

  • Sepsis = SIRS + infection (organ dysfunction in response to infection)
  • Septic shock = persistent hypotension requiring pressors for MAP > 65; lactate > 2 despite adequate volume resuscitation
    • Most common causes: pneumonia (> 50%), abdominal infection, UTI
    • 20-30% mortality
  • Criteria
    • SIRS: 2 or more of:
      • T > 38 or < 36
      • HR > 90
      • RR > 20 or PaCO2 < 32
      • WBC > 12 or < 4, or > 10% immature bands
      • (blood pressure not mentioned)
    • qSOFA (Sequential Organ Failure Assessment) score screens for higher mortality
      • ≥ 2/3 of: GCS ≤ 13, SBP ≤ 100, RR ≥ 22 
    • Lactate ≥ 4 ~ severe sepsis
      • More specific sepsis biomarkers exist (e.g. procalcitonin)
  • CBC/coags - hemorrhage, infection, coagulopathy
  • BMP/Cr, LFTs - end organ damage
  • ABG, lactate - tissue perfusion
    • Lactate is not a direct measure of tissue perfusion - useful for observing downtrend/clearance with early therapy, but not as useful after perfusion has been restored
    • Lactate clearance also ↓ with liver failure
  • ScvO2 - central venous oxygen saturation (measured through central line); usual goal > 70%
  • Should start arterial line for BP monitoring; central line for pressors
  • Suspected type of shock
    • Septic - cultures
    • Cardiogenic - troponin, echo
    • Obstructive - CT/PE protocol, echo (tamponade)

Phases of managing shock

  1. Maintain blood pressure (fluids, pressors), correct underlying cause
  2. Provide oxygen availability, optimize cardiac output, SvO2, lactate
  3. Provide organ support, minimize complications
  4. Wean pressors, achieve negative fluid balance

Hypovolemic shock

Cardiogenic shock

  • Diuresis
  • Inotropes + vasopressors
  • Intra-aortic balloon pump, LVAD, ECMO

Obstructive shock

  • Fix the underlying cause - anticoagulate PE, or drain the tamponade

Septic shock

  • Early treatment saves lives (abx in < 1 hr)
    • Poor consensus on current guidelines for fluid resuscitation (IV crystalloid, 30 ml/kg over 1st 3 hrs)
    • MAP goal ≥ 65 mmHg
    • Blood Cx + other relevant cultures (urine, resp, CSF) 
      • 2 sets of BCx will detect 90% of bloodstream infxns
      • Don't delay abx therapy
    • Broad spectrum abx STAT, narrow as soon as appropriate; duration x 7-10 days
    • Source identification and control (e.g. remove lines from outside hospitals)
    • ?Steroids - Annane (benefit to steroids), CORTICUS (no benefit to steroids), ADRENAL (2017) - no change in mortality, but slightly shortened duration of shock, vent, etc. 
      • Use if unable to wean off pressors
      • IV hydrocortisone 200 mg/day
  • Fluid responsiveness - add more here___
    • Use dynamic over static variables to predict fluid responsiveness, e.g. PPV > CVP
    • PPV - (life in the fast lane)
      • pt should be sedated, mechanically ventilated, a-line for this to be accurate but can look at through pulse-ox when awake (lower sens/spec)
author: admin | last edited: June 13, 2018, 3:51 p.m. | pk: 90 | unpublished