Overview of Shock

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Overview of Shock

  1. 1. Overview of Shock Lecturer: Michelle Hodgkiss 2008
  2. 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. 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. 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. 5. Events leading to inadequate tissue perfusion • Decreased cardiac output • Decreased blood volume • Pump failure • An increase in peripheral vasodilatation • Increased vascular permeability
  6. 6. Shock Patient assessment Instigate Immediate appropriate action Accurate interpretation of situation
  7. 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. 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. 9. Four Stages of Shock • Initial • Compensatory • Progressive • Refractory
  10. 10. Initial Phase • Cardiac output , tissue perfusion , oxygen delivery and nutrients to cells aerobic metabolism is and anaerobic metabolism begins to take over.
  11. 11. Compensatory Stage The body tries to overcome these effects with physiological adaptations Neural Hormonal Chemical
  12. 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. 13. Hormonal • The sympathetic stimulation: • Renal & spanchnic blood flow decreased • Juxtaglomerular cells in nephron stimulated to release renin • Renin-angiotensin-aldosterone system activated.
  14. 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. 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. 16. Refractory Stage Severe cell destruction Vital organs failed Death imminent
  17. 17. Assessing the Shocked Patient • Skin • Colour • Temperature • Conscious level • Respiratory rate & pattern • Heart rate & BP • Perfusion • Decreased urine output
  18. 18. Classification of Shock • Hypovolaemic • Cardiogenic • Anaphylactic Shock • Septic Shock • Neurogenic Shock
  19. 19. Classifications of Shock Hypovolaemic Cardiogenic Septic Neurogenic Distributive Anaphylactic
  20. 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. 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. 22. Management • Replace loss • ?Crystalloid vs Colloid vs Blood • O2 Therapy • Observations • Monitor blood results
  23. 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. 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. 25. Management • Myocardial and tissue oxygenation • Increase contractility • Minimise risk of extension to injury • Reduce afterload • Possible surgery
  26. 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. 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. 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. 29. Management • Hydrocortisone • Adrenaline • Treat cause • Inotropes, fluids, etc
  30. 30. Neurogenic Shock • Due to lack of neural control • Vasodilatation • As a result of loss of parasympathetic & sympathetic nervous control
  31. 31. Causes • Head injury • Spinal injury/shock • Iatrogenic • Pain • Stress/pain
  32. 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
  33. 33. Any questions

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