Shock

Introduction

• State of decreased tissue perfusion, resulting in poor oxygen delivery causing tissue ischemia.
  • Can cause organ dysfunction.
• Shock develops when one or more of key hemodynamic parameters contribute to perfusion.
• 

• Common Clinical Features of Shock

  Hypotension
  SBP <90 mm Hg
  MAP <60 mm Hg
  Acute decrease in SBP of >40 mm Hg
  Lack of MAP response to initial fluid challenge
  End-Organ Dysfunction Due to Hypoperfusion
  Decreased urine output
  Change in mental status
  Increased serum lactic acid level

• Three main types of shock:
  • Cardiogenic
    • Decreased cardiac output (i.e heart failure, massive PE, etc..)
  • Distributive
    • Deceased SVR (i.e. sepsis, anaphylaxis)
  • Hypovolemic
    • Decreased preload (i.e. hemorrhage, dehydration)

General Management Principles​

• 1. Restore perfusion!!!
  • Often fluids can help perfusion.
  • Vasopressors
  • Inotropes
• 2. Reverse the cause. (i.e. lysis of PE, treatment of infection).

• Often requires understanding which hemodynamic parameter is affected.
  • Swan Ganz Catheter has been used to differentiate shock states, but outcomes shown to be same (use vs. no use).
    • No longer recommended.

Fluid​s

• No conclusive evidence exist favour colloid vs. crystalloids (crystalloids b/c cheaper).
• Aggressive volume expansion = good outcomes in hypovolemic and septic shock.
• NOTE: Low albumin states: initially use crystalloid, but can third space, and often providers start using colloids (albumin).  Text book answer: no evidence to support colloids.
• NOTE: Concern about precipitating heart failure should not stop large bolus of fluids.

Vasopressors

• Contract smooth muscles at arterial walls, increase SVR, some also improve cardiac contractility.
• Nearly all have side-effects:
  • Cardiac arrhythmias, extremities or mesentery ischemia. (response to pressors can vary).
• See Vasopressor Section

Septic Shock

• See Infectious Diseases > Septis

Cardiogenic Shock

• Systemic hypotension and evidence of end-organ hypoperfusion (poor cardiac output).
  • Examples:
    • AKI
    • Aminotransferases
    • Hyperbilirubinemia
    • Cool extremities
    • Decreased mental status
• Definition of cardiogenic shock
  •  Cardiogenic shock is defined by persistent hypotension (sBP <80-90 mm Hg or MAP 30 mm Hg lower than baseline) with severe reduction in cardiac index (<1.8 L/min/m² without hemodynamic support or <2.0-2.2 L/min/m² with support) and adequate or elevated filling pressure (for example, left ventricular end-diastolic pressure >18 mm Hg or right ventricular end-diastolic pressure >10-15 mm Hg).
• Use IV vasoactive medications and device-based hemodynamic support.
• Identify treatable causes
  • MI (reperfusion) - free wall rupture, papillary muscle rupture (require urgery surgery).
• Medications:
  • 
• Main idea: many vasodilatory to reduce afterload in cardiogenic shock or increase cardiac output/index (inotropic).
• Dopamine and vasopressin for BP support rather than inotropy.
• If systemic BP is acceptable, can add IV vasodilator (i.e. nitroprusside) to help decrease cardiac output (drop afterload) 
  • But careful because: Dobutamine and Milirinone associated with higher risk of arrhythmias.
• IF vasoactive medications are not helpful, can use mechanical support:
  • Intra-aortic balloon pump
    • During diastole improves coronary and systemic perfusion
    • During systole deflates, reducing LV afterload.
  • Ventricular Assist Devices

Notes

• EARLY treatment of shock always has a survival benefit.
• Studies showing pre-hospital initiation of shock treatment or pre-ICU treatment by ward personnel improve outcomes.