Shock

Ken Tegtmeyer, MD
Pediatric Critical Care Medicine - University of Minnesota

Last Editied July 15, 1999
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Outline

  • Definition/Types of Shock
  • Compensatory/Decompensatory table
  • Compensatory Effects
  • Decompensatpry Effects
  • Recognition
  • Treatment
  • Monitoring
  • References
  •  

    Definition - a clinical state in which there is inadequate tissue perfusion to meet metabolic demands.

    Types of Shock

     Hypovolemic  Distributive  Cardiogenic  Miscellaneous
     dehydration  anaphylaxis  congenital heart disease  heat stroke
     gastroenteritis  neurogenic  ischemic heart disease  pulmonary embolus clot, fat or air
     deprivation  drug toxicity   anoxia pancreatitis
    heat stroke  septic shock*  Kawasaki's  drug overdose (barbiturates, b-agonists)
     hemorrhage    traumatic  
     burns    infectious cardiomyopathies  
         drug toxicity  
         tamponade  

    * Septic shock actually has components of several groups including distributive and cardiogenic.

     

    General Recognition:

    WHY is hypotension only seen as a late sign of shock?

     Compensatory mechanisms  Decompensatory effects
     Baroreceptors  Cardiac Failure
     Chemoreceptors  acidosis
     cerebral ischemia  CNS depression
     reabsorption of tissue fluids  Disseminated Intravascular Coagulation
     endogenous vasoconstrictors  depression of reticuloendothelial system
     Renal conservation of water  

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    Compensatory Mechanisms

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    Decompensatory Mechanisms

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    Recognition

    Again, blood pressure is not key to deciding whether or not someone is in shock, it does help decide whether they are in compensated or decompensated shock though.

    Lets think about Blood Pressure Control or production first, see the following diagram:

    Where:

    Recognition and Treatment of Shock Depends upon the Classification/Etiology of the Shock

    The commonly used analogy of the circulatory system includes three components, a pump (the Heart), plumbing (the vascular system) and Fluid (circulating blood volume). In order to assure adequate perfusion each of these systems needs to be functioning, otherwise Shock will ensue. Consequently the three main types of shock, plus septic shock are listed below.

    Hypovolemic Shock (problems with the fluid)

    Cardiogenic Shock (problems with the pump)

    Distributive Shock (problems with the plumbing)

    Septic shock (a combination)

    Treatment

    Always start with the ABC's

    1) Airway

    Needs will vary depending on etiology of shock, from no intervention to aggressive intervention (i.e. anaphylaxis)

    2) Breathing

    Patients need respiratory support and monitoring, consider O2 to help with oxygen delivery even though sats may be OK, patients may need intubation, or other respiratory support, particularly to help compensate for a profound metabolic acidosis.

    3) Circulation

    Read on.

    Treatment (after ABC's)

    Initial Treatment:

    Volume, Volume, Volume

    But after you have given volume, then what do you do? Or better yet, when is continuing to add volume not the right thing to do?

    Further Treatment:

    Volume (Preload)

     

    Contractility

    Drug
    Dosing Range
    Receptors
    Use
    Risk
    Dopamine
    2-20 mcg/kg/min
    alpha,beta, dopamine
    Renal Effects, early inotropy needs, septic shock
    Peripheral vasoconstriction
    Dobutamine
    3-20 mcg/kg/min
    beta-1 primarily
    Contractility
    Tachycardia, vasodilation
    Epinephrine
    0.01-2 mcg/kg/min
    beta>alpha,
    but both
    Contractility, vasoconstriction (higher doses)
    Tachycardia, vasoconstriction
    Milrinone
    0.3-0.7 mcg/kg/min
    Phosphodiesterase Inhibitor
    Inotropy, vasodilation
    Tachycardia, vasodilation

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    Afterload/Systemic Vascular Resistance

    The two tables below show first the vasoconstrictive agents, then the vasodilator agents

    Vasocontrictive Agents - also includes Dopamine from previous table
    Drug
    Dose Range
    Receptor Activity
    Use
    Risk
    Epinephrine
    0.01 - 2mcg/kg/min
    beta>alpha
    anaphylaxis,
    cardiogenic shock
    Ischemia, hypertension
    Norepinephrine
    0.05 - 1mcg/kg/min
    alpha>beta
    Severe vasodilation, hypotension
    Acidosis from poor perfusion, ischemic injury
    Phenylephrine
    0.1- 0.5 mcg/kg/min
    alpha selective
    Severe hypotension,
    Tet spells
    Acidosis, ischemic injury

    Vasodilator Agents
    Drug
    Dosing range
    Site of action
    Use
    Risk (similar for both)
    Nitroprusside
    0.3-7 mcg/kg/min
    Arteries > veins
    Afterload reduction
    Cyanide toxicity, hypotension
    Nitroglycerin
    0.5-5 mcg/kg/min
    Venodilation and coronaries, plus arteries
    Preload and afterload reduction, coronary vasospasm
    Hypotension, methemoglobinemia

     

    Summary of Treatment

    Hypovolemic Shock - a Preload issue, increase the Preload

    Cardiogenic Shock - a contractillity issue

    Distributive Shock - a systemic vascular resistance issue

    Septic Shock - a combination of the three

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    Monitoring

    Remember: Shock is not something that is broke that you fix and are done. It is an evolving process that is a symptom of something else going wrong with the patient, that left untreated can result in cardiopulmonary failure and death.

    Key items to monitor

     

    Electrolytes:

    Glucose

    Blood Gases

    Central Venous Pressure

     

    Hemodynamics

    Coagulation Status

     

    Urine Output

    Neurologic Status

     

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    References

    Rogers, MC Textbook of Pediatric Intensive Care. Chapter 15, p483-524. Williams and Wilkins, Baltimore, MD 1987.

    Berne RM and Levy MN. Physiology, 3rd edition. Chapter 32, pp 532-543. Mosby, St. Louis, 1993.

    De Bruin WJ et. al. "Fluid Resuscitation in Pediatrics." Critical Care Clinics 8(2): 423-438. April 1992

    Griffel MI and Kaufman BS "Pharmacology of Colloids and Crystalloids." Critical Care Clinics 8(2): 235-253. April 1992.

    Textbook of Pediatric Advanced Life Support. American Heart Association.


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    This page is meant for educational purposes only. Questions or comments regarding this page should be directed to the author at:

    tegtm001@tc.umn.edu

    This page last updated for content 7/14/1999
    This page last updated for format 7/14/1999