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 Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic

5. Types of Shock Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic 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? 1.Insufficient delivery of oxygen & nutrients to cells and tissues. 2.Inadequate clearance of metabolites.

10. Outcomes of cellular hypoxia 1.Shift from aerobic to anaerobic metabolism. 2.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. Cellular Response to Shock  Tissue perfusion perfusion  Na + Pump Function Function  ATP synthesis synthesis AnaerobicmetabolismAnaerobicmetabolism  Cellular edema  Vascular volume  Cellular edema  Vascular volume Impaired cellular metabolism metabolism  O 2 use use Intracellular Na +  Intracellular Na + & water Intracellular Na +  Intracellular Na + & water ImpairedglucoseusageImpairedglucoseusage Stimulation of clotting cascade & inflammatoryresponse Stimulation of clotting cascade & inflammatoryresponse

13. Hypovolemic Shock Decreased intravascular volume Causes: –Diarrhoea –Prolonged & excessive vomiting –Massive haemorrhage –Burns 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 1.Pump failure:  Ejection fraction < 20%  Associated with myocardial infarction  Associated with Conduction disturbances ( heart block or arrhythmias) 2.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. Cardiogenic Shock  CO R.A.S.ActivationR.A.S.Activation  Dyspnea  O 2 supply supply  Volume/ Preload Preload  SVR  Peripheral & pulmonary edema  Peripheral & pulmonary edema Impaired myocardial function Impaired  Myocardial O 2 demand  Myocardial O 2 demand  Catecholamine Release Release

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

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

30. Effects of cytokine release

31. Effects Of Lipopolysaccharide (LPS) And Secondarily Induced Effector Molecules

32. MODS= Multiple organ dysfunction syndrome

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

35. Stages of Shock Compensated Uncompensated Irreversible Compensated Uncompensated Irreversible

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

37. 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

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

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

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

45. Symptoms of Shock 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) General SymptomsSpecific Symptoms

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

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

48. 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

49. 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

50. 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)

51. Morphology of Shock Hypoxic injury to multiple organs Kidneys –medulla and tubules most affected –acute tubular necrosis Gastrointestinal tract –mucosa most sensitive to hypoxia Brain Heart –subendocardial necrosis of myocardium Lungs –resistant to hypoxia but involved with septic shock

52. Kidney in shock:Coagulation necrosis of tubules

53. Renal Biopsy in DIC Capillary loops of glomeruli occluded by fibrin thrombi. H&E stain on left and MSB (Martius scarlet blue) for fibrin on the right

54. Myocardial necrosis(coagulation necrosis)

55. Adult respiratory syndrome (ARDS) Synonyms: –Shock lung –Diffuse alveolar damage –Acute alveolar injury –Traumatic wet lungs These are descriptive terms for a syndrome caused by diffuse alveolar capillary damage.

56. Clinically characterized by: Rapid onset of severe life-threatening respiratory insufficiency Cyanosis Severe arterial hypoxemia that is refractory to oxygen therapy Frequently progresses to extrapulmonary multisystem organ failure.

57. Some causes of ARDS: Shock Sepsis Extensive surface burns Massive fractures & other trauma

58. Morphology: In the acute edematous stage, the lungs are heavy, firm & boggy due to congestion, edema & inflammation.

59. Markedly congested & heavy lung

60. Microscopy Alveoli are lined by waxy hyaline membranes.

61. This is followed by: Proliferation of type II pneumocytes. However resolution does not usually occur. More commonly, there is organization of the fibrin exudate, with resultant intra-alveolar fibrosis. There is marked thickening of the alveolar septae.

62. Mortality rate of ARDS is high (60%).

63. Approach to study: 1.Definition of shock 2.Classification of shock 3.Causes of shock 4.Pathogenesis of cardiac, neurogenic, septic & anaphylactic shock 5.Stages of shock including compensatory mechanisms 6.Clinical features of shock (at each stage) 7.Morphology of various organs & tissues in shock

65. Thank you