Shock

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    UNDER CONSTRUCTION

     

    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.
    • ShockChart.png
    • 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

     

    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/mwithout 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:
      • VasoactiveCardiogenicShock.png
    • 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.
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