Pathophysiology of shock

1. PATHOPHYSIOLOGY OF SHOCK

2. CIRCULATORY SHOCK Definition :- shock is a syndrome in which there is inadequate tissue perfusion associated with reduction of cardiac output (absolute or relative )

3. Definition of Shock Inadequate perfusion and oxygenation and supply of nutrients to cells vital organs Cellular dysfunction and damage Organ dysfunction and damage High mortality - 20-90% Early intervention reduces mortality

4. Pathophysiology: Overview Tissue perfusion is determined by Mean Arterial Pressure (MAP) MAP = CO x SVR Heart rate Stroke Volume

5. Classification Four categories depending on cause of reduced CO Hypovolaemic shock Cardiogenic shock Distributive shock Obstructive shock

6. Hypovolaemic Shock Reduced CO is due to low blood volume AKA cold shock Causes Hemorrhagic shock Surgical shock Burns shock Dehydration shock Traumatic shock

7. Distributive Shock Excessive vasodilatation due to toxic substances or neural regulation Increased in capacitance of vessels CO decreases in spite of normal blood volume AKA warm shock

8. Distributive Shock four types:- Neurogenic shock Anaphylactic shock Septicaemic shock Endotoxic shock

9. Neurogenic shock Causes :-two types Marked reduction in sympathetic vasomotor tone Deep general anesthesia Spinal anesthesia Brain damage Increased vagal tone :- vasovagal syncope , emotional fainting

10. Anaphylactic Shock Acute allergic reaction Large quantities of histamine Widespread vasodilatation Reducing peripheral resistance Increased capillary permeability Reduction in blood volume Leading to shock

11. Septicaemic Shock Septicaemia ? Bowel perforation , peritonitis Toxins produced by bacteria

12. Endotoxic Shock

13. Cardiogenic Shock Heart’s pumping ability is reduced Severe systolic dysfunction Venous return is not pumped out So reduced CO Congestion of lungs and vicera AKA congested shock

14. Causes Myocardial infarction Cardiac arrhythmias Congestive heart failure

15. Obstructive Shock External pressure on the heart which reduces CO Reduces ventricular filling Pericardial tamponade Tension pneumothorax Constrictive pericarditis

16. Stages And Clinical Features Of Shock Non –progressive shock Progressive shock Refractory shock

17. Non-progressive stage AKA compensated shock Moderate reduction in CO Occurs after loss of 10-15% of blood vol Leading to compensatory mechanisms Immediate compensatory mechanisms Long term compensatory mechanisms

18. Rapid Compensatory Mechanism (Neural) Includes three nervous reflexes Baroreceptor reflex Chemoreceptor reflex CNS ischemic response Others responses

19. Mechanoreceptors Baroreceptors – stretch receptors which sense change in pressure Chemoreceptor – detects change in chemical composition of blood

20. Location of receptors Carotid body (chemoreceptor ) Carotid sinus ( baroreceptor ) Aortic arch contains both baro & chemoreceptor

21. Receptors

22. Innervation Carotid sinus – glossopharyngeal nerve corotid body Aortic arch – vagus nerve Aaorti sinus

23. Baroreceptor Reflex

24. Baroreceptor Reflex When the BP falls Barorecptors gets inactivated They reduce their inhibitory effect on VMC so increase in BP and HR

25. Chemoreceptor Reflex Due to hypoxia When the blood pressure fall below 70mm/hg

26. CNS Ischemic Response When the BP falls below 40mm/hg Ischemia of VMC Activation of VMC Increases symp dischrage Increases BP , HR , CO

27. Tachycardia

28. Vasoconstriction Occurs in all vessels except cerebral and coronary vessels So it increases venous return In turn increases CO Skin becomes pale and cold Vasoconstriction of kidney reduces gfr Vasoconstriction of skeletal muscle So bypassing of blood to vital organs

29. Increased RR Due to chemoreceptor reflex Also because of hypoxia And by increasing thoracic pumping action Increases CO

30. Increased Skeletal Muscle Activity Person becomes restless Increases pumping Increases venous return

31. Increased Secretion Of Catecholamines From adrenal medulla Increases symp drive i.e. vasoconstriction and increased HR Stimulates RAS

32. Increase Secretion Of Vasopressin ADH from posterior pituitary Increases water absorption Pressor action of vessels

33. Increases Secretion Of Cortisol Increased glucocortioids Increases sensitivity of vessels to catecholamines

34. Intermediate Compensatory Mechanisms RAAS Reverse stress relaxation Capillary fluid shift mechanism

35. Long Term Compensatory Mechanisms Restoration of plasma volume and proteins Plasma volume by 12 – 72 hours Proteins by 3-4 days by liver Restoration of red cell mass – will occur within 10 days and fully restored by 4-8 wks

36. Progressive Shock Occurs after 15-25% loss of blood volume Compensatory mechanisms are not effective Despite Intense vasoconstriction Not able to maintain BP , CO CVS begins to deteriorate Due to positive feedback cycles Timely intervention is needed Or will progress to refractory shock

37. Positive Feedback Cycles Cardiac failure Due to severe dec in BP Diastolic BP falls Blood supply to heart falls Weakens myocardium Leading to heart failure Acts as positive cycle

38. Vasomotor Failure There occurs a point where body fails to circulate the vital organs Failure of VMC will produce widespread vasodilatation So CO and BP are further decreased

39. Peripheral Circulatory Failure Due to hypoxia and metabolites accumulation vasodilatation occurs Capillary permeability increases Pooling and sluggish blood flow Intravascular clotting occurs

40. Septicemia And Toxemia Hypoxia in GIT Damage to mucosal barrier Leading to entry of bacteria thro’ portal circulation Damage liver and reaches systemic circulation Systemic toxemia and septicemia Leading to irreversible shock

41. Effect On Tissue Level Widespread tissue damage Liver (first) , heart , lung Failure of Na-K pump Reduced mitochondrial activity Activation of lysosomes Depleted nutrients (glucose mainly) Depleted action of hormones (insulin) Hypoxia – anaerobic metabolism – lactic acid accumulation – Pco2 increase –acidosis – vasodilatation (vicious cycle )

42. Refractory Shock Therapeutic interventions are ineffective and patient dies eventually Point of no return – severe depletion of ATP Leading to necrosis (death of tissues ) Multi-organ failure Death

43. Treatment Of Shock Correcting a cause & helping physiological compensatory mechanisms General measures Prevent sweating Trendelenburg position

44. Replacement Therapy Transfusion of whole blood Plasma Dextran Ringer lactate Normal saline

45. Sympathomimetic drugs Adrenaline Nor-adrenalin Dapamine Oxygen therapy Gluocorticoids

46. Splanchnic Circulation Intestinal circulation Hepatic circulation Splenic circulation

47. Intestinal Circulation Normal intestinal blood flow is 20% of CO Which increases to 50 during digestion 60 – 70 % of blood flow is to mucosa Countercurrent exchanger system in villi noted Supply of oxygen to tip of the villi is reduced i.e. intestinal necrosis is common in shock

48. Normal Blood Flow Gastric – 40ml/100g/min Intestinal – 60ml/100g/min Pancreatic – 80ml/100g/min

49. Regulation Neural Autoregulation Metabolic regulation Adenosine Osmolarity Potassium By GI activity – functional hyperemia Due to gastric hormones

50. Hepatic Circulation 28% of cardiac output Blood derived from two sources Portal – 75% (less oxygen content) Hepatic artery – 25% (rich in 02) 1500ml/min or 58ml/100g/min

51. Regulation Of Hepatic Blood Flow Hepatic arterial buffer response Neural Metabolic Autoregulation Regulation by intestinal activity

52. Importance Filters blood Detoxification Metabolism and storage Reservoir of blood Contribute 60% of blood during shock Hepatomegaly Portal hypertension and ascitis

53. Splenic Circulation Splenic artery Sympathetic vasoconstrictor fibers Splenic capsule contraction