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Shock

Shock. KVB. What is shock?. Shock is the clinical syndrome that results from inadequate tissue perfusion. Classification of shock. Cardiogenic , due to heart failure Hypovolemic (oligemic), due to fluid or blood loss Distributive (hypotensive) owing to peripheral vasodilation.

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Shock

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  1. Shock KVB

  2. What is shock? Shock is the clinical syndrome that results from inadequate tissue perfusion

  3. Classification of shock • Cardiogenic, due to heart failure • Hypovolemic (oligemic), due to fluid or blood loss • Distributive (hypotensive) owing to peripheral vasodilation

  4. Types of Shock • Hypovolemic • Cardiogenic • Neurogenic • Anaphylactic • Septic

  5. Types of Shock • Hypovolemic • Cardiogenic • Neurogenic • Anaphylactic • Septic Distributive shock

  6. Common types of shock: • Cardiogenic shock • Hypovolemic shock • Septic shock

  7. Less common types of shock • Neurogenic shock • Anaphylactic shock • Hypoadrenal shock

  8. Common factor • Circulatory collapse resulting from a disproportion between circulating blood volume & the vascular space that it has to fill. • The ensuing tissue hypoxia or anoxia leads to multiple organ failure.

  9. What happens with the perfusion deficit? • Insufficient delivery of oxygen & nutrients to cells and tissues. • Inadequate clearance of metabolites.

  10. Outcomes of cellular hypoxia • Shift from aerobic to anaerobic metabolism. • This results in increased lactate production and later on, lactic acidosis.

  11. The metabolic & hemodynamic derangements are correctible at the outset & are associated with reversible cell injury. • Persistence or worsening of the shock state leads to irreversible injury and death of cells and possibly , death of the patient.

  12. O2 use Impaired cellular metabolism Anaerobic metabolism Stimulation of clotting cascade & inflammatory response Impaired glucose usage • ATP synthesis  Intracellular Na+ & water • Cellular edema  Vascular volume • Na+ Pump Function Cellular Response to Shock • Tissue perfusion

  13. Hypovolemic Shock • Decreased intravascular volume • Causes: • Diarrhoea • Prolonged & excessive vomiting • Massive haemorrhage • Burns

  14. Hypovolemic Shock • Hemorrhage • external • internal • GI tract • hemothorax • peritoneal or retroperitoneal space • Loss of fluid into third space • burns • pancreatitis

  15. Causes of cardiogenic shock • Pump failure: • Ejection fraction < 20% • Associated with myocardial infarction • Associated with Conduction disturbances ( heart block or arrhythmias) • Obstructive heart failure • Caused by massive pulmonary emboli or valvular disease (Aortic stenosis)

  16. Cardiogenic Shock • Myocardial pump failure • myocardial infarction • myocardial rupture • cardiac arrhythmia • Extrinsic compression • cardiac tamponade • Outflow obstruction • pulmonary embolus

  17. Catecholamine Release R.A.S. Activation  SVR • Myocardial O2 demand • Volume/ Preload • O2 supply • Peripheral & pulmonary edema Impaired myocardial function  Dyspnea Cardiogenic Shock  CO

  18. Vascular Tone • Tissue perfusion Massive Vasodilation  Cardiac Output  SVR & Preload Neurogenic Shock Sympathetic Tone Or  Parasympathetic Tone

  19. Anaphylactic Shock • Massive & systemic allergic reaction • Large release of histamine • Increases membrane permeability & vasodilation

  20. Anaphylactic Shock Caused by a hypersensitivity reaction to an allergen in a previously sensitised patient

  21. Common allergens:

  22. Common Features • Angio-oedema • Bronchoconstriction • Vasodilatation and hypotension • Urticareal rash

  23. Angio-oedema Normal Oedematous glottis

  24. Septic Shock • “Circulatory failure” • Due to systemic infection

  25. Septic Shock • Leading cause of death in intensive care units • Most cases (70%) are caused by gram negative bacteria (LPS-lipopolysaccharide) • Also can occur with gram positive bacteria and fungal organisms

  26. Effects of cytokine release

  27. Effects OfLipopolysaccharide (LPS) And Secondarily Induced Effector Molecules

  28. MODS= Multiple organ dysfunction syndrome

  29. Multiple Organ Dysfunction System • Progressive dysfunction of two or more organ systems • Caused by uncontrolled inflammatory response to injury or illness • Typically sepsis

  30. Stages of Shock • Compensated • Uncompensated • Irreversible

  31. STAGES OF SHOCK • Initial stage (early compensation stage) • Nonprogressive stage (compensatory) • Progressive stage (intermediate) • Refractory stage (irreversible)

  32. Homeostatic Mechanisms in Shock • Baroreceptor reflexes and catecholamine release • maintain cerebral and cardiac perfusion • decrease perfusion to gut, skin and kidneys • Activation of renin-angiotensin system • angiotensin II constricts efferent arteriole of glomerulus to maintain GFR • aldosterone promotes sodium retention • Release of Arginine Vasopressin (ADH) • promotes renal conservation of water

  33. Kidney (juxtaglomerular apparatus) Detected by Releases Via ACE (Angiotensin Converting Enzyme) Renin Converts Angiotensin II… Angiotensinogen Angiotensin I… Renin-Angiotensin-Aldosterone • Plasma volume &/Or  [Na+]

  34. Uncompenstated Shock • Defense mechanisms begin to fail • Presentation • Hypotension • Marked increase in heart rate • Rapid, thready pulse • Agitation, restlessness, confusion

  35. Irreversible Shock • Complete failure of compensatory mechanisms • Death even in presence of resuscitation

  36. Anxiety /Nervousness Dizziness Weakness Nausea & Vomiting Thirst Confusion Decreased Urine Output History of Trauma / other illness Vomiting & Diarrhoea Chest Pain Fevers / Rigors Shortness of breath (stridor) Symptoms of Shock General Symptoms Specific Symptoms

  37. Signs of Shock • Pallor • Cold and clammy extremities • Sweating • Cyanosis • Tachypnoea • Tachycardia • Confusion & agitation • Stridor • Hypotension • Loss of consciousness

  38. Features of compensated shock • Tachycardia • Skin pallor due to constriction of arterioles • Reduced urine production

  39. Features of decompenstaed but still reversible shock • Hypotension • Dyspnoea & tachypnoea • Pulmonary oedema slowly develops, further worsening hypoxia • Oliguria (urine volume<500ml/24hr) • Acidosis due to anaerobic glycolysis

  40. Features of irreversible shock • Marked hypotension with extreme tachycardia (filiform pulse) • Respiratory distress which is not responsive to oxygen therapy & assisted ventilation • Loss of consciousness progressing to coma • Gastrointestinal bleeding • Anuria with elevated BUN & creatinine • Severe acidosis • Laboratory & clinical signs of DIC

  41. Clinical Course • Hypovolemic shock • If patient is young and healthy, most survive if resuscitation restores perfusion • Cardiogenic shock and septic shock • Up to 75% mortality even with best care • Patients succumb with multi-organ failure • Tubular necrosis of kidneys • Ischemic enteropathy • Disseminated intravascular coagulation • Acute respiratory distress syndrome (septic shock)

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