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Overview of Shock

Lecturer: Michelle Hodgkiss
           2008
Aims of the Session
• Definition
• Classification
• Factors leading to the progression of shock
  and tissue hypoperfusion
• Description and discussion of the four
  stages of shock
• Assessment & systematic review
• Overview and treatment of Shock
Definition of Shock
     “Shock is a condition in which the
 cardiovascular system is no longer able to
   meet the body's metabolic and oxygen
  needs. Note that this definition does not
  include blood pressure limits. Although
many practitioners believe that shock exists
    when the systolic blood pressure falls
below 80 mmHg, some patients will still be
     able to maintain relatively normal
    metabolic function below this level.”
         Trauma Secrets 2nd ed 2003.
Shock

…Is potentially life threatening it can
   affect many organs and must be
reversed. Nurses need to be alerted to
 initial signs of shock to allow early
  intervention of treatment, prevent
         deterioration or death.
Events leading to inadequate
           tissue perfusion
•   Decreased cardiac output
•   Decreased blood volume
•   Pump failure
•   An increase in peripheral vasodilatation
•   Increased vascular permeability
Shock

                  Patient assessment



     Instigate
Immediate appropriate
      action
                                 Accurate interpretation
                                      of situation
Factors in the Progression of Shock
  Hypovolaemic Shock                             Cardiogenic Shock


                                                        MI
Endotoxaemia       Haemorrhage                       Myocarditis
   Burns            Diarrhoea                        Tamponade
  Trauma           Dehydration
 Anaphylaxis
                                                     Decreased CO
                  Decreased          Decreased
 Increased          Blood             Venous           Decreased
  Vascular         volume             Return            Tissue
permeability
                                                       Perfusion

                                                       Anoxic
                       Endothelial                      Cell
                        damage                         injury
Factors in the Progression of
              Shock Metabolic
                           acidosis

Decreased CO
                            Heart Failure


Decreased tissue                   Anaerobic
   perfusion                       Glycolysis in
                                   Muscle

  Anoxic cell
    injury         Renal Failure
Four Stages of Shock
•   Initial
•   Compensatory
•   Progressive
•   Refractory
Initial Phase
• Cardiac output , tissue perfusion ,
  oxygen delivery and nutrients to cells
  aerobic metabolism is and anaerobic
  metabolism begins to take over.
Compensatory Stage

     The body tries to overcome these
   effects with physiological adaptations




Neural            Hormonal           Chemical
Neural
• As C.O. & BP fall, Baroreceptors in the
  aorta & carotid arteries send a message to
  the medulla, stimulating the sympathetic
  nervous system, the adrenal medulla
  releases catecholamines – Adrenaline &
  noradrenaline.
• Increase in myocardial contractility, rate &
  vasoconstriction
Hormonal
• The sympathetic stimulation:
• Renal & spanchnic blood flow decreased
• Juxtaglomerular cells in nephron stimulated
  to release renin
• Renin-angiotensin-aldosterone system
  activated.
Chemical
• Increased production of aldosterone by the
  adrenal cortex
• Increased production of catecholamines by
  the adrenal medulla
• Increased production of ADH by the
  pituitary gland
• Effects of acidosis, oxygenation and carbon
  dioxide.
Progressive Stage
 Compensatory mechanisms begin to fail to perfuse
                      vital organs
• Reduced Cardiac Output
• Reduced coronary perfusion
• Decreased filling pressure
• Increased capillary permeability
• K+ leaks out of the cells
• Metabolic acidosis
Refractory Stage

Severe cell destruction
  Vital organs failed
   Death imminent
Assessing the Shocked Patient
•   Skin
•   Colour
•   Temperature
•   Conscious level
•   Respiratory rate & pattern
•   Heart rate & BP
•   Perfusion
•   Decreased urine output
Classification of Shock
•   Hypovolaemic
•   Cardiogenic
•   Anaphylactic Shock
•   Septic Shock
•   Neurogenic Shock
Classifications of Shock
Hypovolaemic
                    Cardiogenic



                    Septic
                      Neurogenic
     Distributive
                       Anaphylactic
Hypovolaemic Shock
• Causes
Commonly due to sudden blood loss –
Burns and Dehydration are the most common
  forms of shock
• Research of therapies vast
Clinical Findings Associated
        with Volume Loss
• < 500 mls = none
• 500 – 1000 mls = HR, BP, Urine, Resp,
  CO =, SVR
• 1000 – 2000 mls = As above & worsening, O2
  consumption , affected conscious level, skin
  perfusion, CO , SVR
• 2000 – 3000 mls = as above & worsening anuria,
  loss of consciousness, pulses, cold, pallor.
Management
•   Replace loss
•   ?Crystalloid vs Colloid vs Blood
•   O2 Therapy
•   Observations
•   Monitor blood results
Cardiogenic shock
                      Definition
  “…is the result of the loss of critical contractile
                 function of the heart”
               (Hudak & Gallo 1997)
Causes
• MI
• Tamponade
• Cardiomyopathy
• Ventricular septal rupture
Cardiogenic Shock

  A decrease in CO leads to compensatory
 measures to restore function. Cardiogenic
shock is a result of the cycle of progressive
  deterioration. A reduced cardiac output
 leads to tissue hypoperfusion & increased
    myocardial workload leads to lactic
    acidosis then worsening contractility
Management
•   Myocardial and tissue oxygenation
•   Increase contractility
•   Minimise risk of extension to injury
•   Reduce afterload
•   Possible surgery
Septic Shock
• Development of septicaemia usually bacterial,
  occasionally viral
• Immune and inflammatory response causing
  vasodilatation, reduced venous return, reduced
  cardiac output.
• Increased O2 requirements from anaerobic
  metabolism
• Cell damage as a result of released endotoxins –
  capillary permeability
Clinical Presentation
• Initially – may be pyrexial, flushed,
  tachycardic, tachypnoeic, ? Normal BP or
  slightly reduced, urine output.
• Cold, clammy, pallid, altered level of
  consciousness, cyanosed, hypoxic, acidotic,
  hypotensive, tachycardic,
  tachypnoeic/reparatory failure, oliguric,
  anuric
Anaphylactic Shock
      An allergic reaction to an allergen.
• Hypersensitivity leading to histamine
  released causing to increased capillary
  permeability.
• Severe onslaught
• Vasodilatation & reduced cardiac output.
Management
•   Hydrocortisone
•   Adrenaline
•   Treat cause
•   Inotropes, fluids, etc
Neurogenic Shock
• Due to lack of neural control
• Vasodilatation
• As a result of loss of parasympathetic &
  sympathetic nervous control
Causes
•   Head injury
•   Spinal injury/shock
•   Iatrogenic
•   Pain
•   Stress/pain
Further reading
• Daily, E. K, & Schroeder,J.S. Techniques in
  Bedside Hemodynamic Monitoring. 5th Edition.
  1994. Mosby
• Gideon P. Naude, et al (2003) Trauma Secrets 2nd
  Edition. Handley Belfus. Philadelphia.
• Hudak & Gallo. CM (1994) Critical Care Nursing:
  A Holistic Approach Lippincott Philadelphia
Any questions

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Overview of Shock

  • 1. Overview of Shock Lecturer: Michelle Hodgkiss 2008
  • 2. Aims of the Session • Definition • Classification • Factors leading to the progression of shock and tissue hypoperfusion • Description and discussion of the four stages of shock • Assessment & systematic review • Overview and treatment of Shock
  • 3. Definition of Shock “Shock is a condition in which the cardiovascular system is no longer able to meet the body's metabolic and oxygen needs. Note that this definition does not include blood pressure limits. Although many practitioners believe that shock exists when the systolic blood pressure falls below 80 mmHg, some patients will still be able to maintain relatively normal metabolic function below this level.” Trauma Secrets 2nd ed 2003.
  • 4. Shock …Is potentially life threatening it can affect many organs and must be reversed. Nurses need to be alerted to initial signs of shock to allow early intervention of treatment, prevent deterioration or death.
  • 5. Events leading to inadequate tissue perfusion • Decreased cardiac output • Decreased blood volume • Pump failure • An increase in peripheral vasodilatation • Increased vascular permeability
  • 6. Shock Patient assessment Instigate Immediate appropriate action Accurate interpretation of situation
  • 7. Factors in the Progression of Shock Hypovolaemic Shock Cardiogenic Shock MI Endotoxaemia Haemorrhage Myocarditis Burns Diarrhoea Tamponade Trauma Dehydration Anaphylaxis Decreased CO Decreased Decreased Increased Blood Venous Decreased Vascular volume Return Tissue permeability Perfusion Anoxic Endothelial Cell damage injury
  • 8. Factors in the Progression of Shock Metabolic acidosis Decreased CO Heart Failure Decreased tissue Anaerobic perfusion Glycolysis in Muscle Anoxic cell injury Renal Failure
  • 9. Four Stages of Shock • Initial • Compensatory • Progressive • Refractory
  • 10. Initial Phase • Cardiac output , tissue perfusion , oxygen delivery and nutrients to cells aerobic metabolism is and anaerobic metabolism begins to take over.
  • 11. Compensatory Stage The body tries to overcome these effects with physiological adaptations Neural Hormonal Chemical
  • 12. Neural • As C.O. & BP fall, Baroreceptors in the aorta & carotid arteries send a message to the medulla, stimulating the sympathetic nervous system, the adrenal medulla releases catecholamines – Adrenaline & noradrenaline. • Increase in myocardial contractility, rate & vasoconstriction
  • 13. Hormonal • The sympathetic stimulation: • Renal & spanchnic blood flow decreased • Juxtaglomerular cells in nephron stimulated to release renin • Renin-angiotensin-aldosterone system activated.
  • 14. Chemical • Increased production of aldosterone by the adrenal cortex • Increased production of catecholamines by the adrenal medulla • Increased production of ADH by the pituitary gland • Effects of acidosis, oxygenation and carbon dioxide.
  • 15. Progressive Stage Compensatory mechanisms begin to fail to perfuse vital organs • Reduced Cardiac Output • Reduced coronary perfusion • Decreased filling pressure • Increased capillary permeability • K+ leaks out of the cells • Metabolic acidosis
  • 16. Refractory Stage Severe cell destruction Vital organs failed Death imminent
  • 17. Assessing the Shocked Patient • Skin • Colour • Temperature • Conscious level • Respiratory rate & pattern • Heart rate & BP • Perfusion • Decreased urine output
  • 18. Classification of Shock • Hypovolaemic • Cardiogenic • Anaphylactic Shock • Septic Shock • Neurogenic Shock
  • 19. Classifications of Shock Hypovolaemic Cardiogenic Septic Neurogenic Distributive Anaphylactic
  • 20. Hypovolaemic Shock • Causes Commonly due to sudden blood loss – Burns and Dehydration are the most common forms of shock • Research of therapies vast
  • 21. Clinical Findings Associated with Volume Loss • < 500 mls = none • 500 – 1000 mls = HR, BP, Urine, Resp, CO =, SVR • 1000 – 2000 mls = As above & worsening, O2 consumption , affected conscious level, skin perfusion, CO , SVR • 2000 – 3000 mls = as above & worsening anuria, loss of consciousness, pulses, cold, pallor.
  • 22. Management • Replace loss • ?Crystalloid vs Colloid vs Blood • O2 Therapy • Observations • Monitor blood results
  • 23. Cardiogenic shock Definition “…is the result of the loss of critical contractile function of the heart” (Hudak & Gallo 1997) Causes • MI • Tamponade • Cardiomyopathy • Ventricular septal rupture
  • 24. Cardiogenic Shock A decrease in CO leads to compensatory measures to restore function. Cardiogenic shock is a result of the cycle of progressive deterioration. A reduced cardiac output leads to tissue hypoperfusion & increased myocardial workload leads to lactic acidosis then worsening contractility
  • 25. Management • Myocardial and tissue oxygenation • Increase contractility • Minimise risk of extension to injury • Reduce afterload • Possible surgery
  • 26. Septic Shock • Development of septicaemia usually bacterial, occasionally viral • Immune and inflammatory response causing vasodilatation, reduced venous return, reduced cardiac output. • Increased O2 requirements from anaerobic metabolism • Cell damage as a result of released endotoxins – capillary permeability
  • 27. Clinical Presentation • Initially – may be pyrexial, flushed, tachycardic, tachypnoeic, ? Normal BP or slightly reduced, urine output. • Cold, clammy, pallid, altered level of consciousness, cyanosed, hypoxic, acidotic, hypotensive, tachycardic, tachypnoeic/reparatory failure, oliguric, anuric
  • 28. Anaphylactic Shock An allergic reaction to an allergen. • Hypersensitivity leading to histamine released causing to increased capillary permeability. • Severe onslaught • Vasodilatation & reduced cardiac output.
  • 29. Management • Hydrocortisone • Adrenaline • Treat cause • Inotropes, fluids, etc
  • 30. Neurogenic Shock • Due to lack of neural control • Vasodilatation • As a result of loss of parasympathetic & sympathetic nervous control
  • 31. Causes • Head injury • Spinal injury/shock • Iatrogenic • Pain • Stress/pain
  • 32. Further reading • Daily, E. K, & Schroeder,J.S. Techniques in Bedside Hemodynamic Monitoring. 5th Edition. 1994. Mosby • Gideon P. Naude, et al (2003) Trauma Secrets 2nd Edition. Handley Belfus. Philadelphia. • Hudak & Gallo. CM (1994) Critical Care Nursing: A Holistic Approach Lippincott Philadelphia