Shock and its management

for surgical post graduate students
by
Dr. Nabarun Biswas

1. SHOCK DR. NABARUN BISWAS REGISTRAR SURGERY MMCH

2. Out line Definition of shock Pathophysiology Classification Pitfalls Resuscitation Monitoring

3. Definition of Shock Shock is a systemic state of low tissue perfusion which is inadequate for normal cellular respiration . With insufficient delivery of glucose and oxygen, cells switch from aerobic to anaerobic metabolism. If perfusion is not restored cell death ensues.

4. Pathophysiology of shock Cellular effect Microvascular effect Systemic effect

5. Cellular effect = a. Metabolic Acidosis b. ↑ K + ↓perfusion to tissue  O 2 deprivation cells switch aerobic to anerobic metabolism lactic acid formation = Metabolic acidosis Anerobic respiration intracellular glucose exhausted anerobic respiration stopped Na + - K + pump fails in intracellular organelles  Lysosomes disrupt  enzyme released  cell lysis  K + released into blood = Hyperkalaemia .

6. Microvascular effect = 1. Tissue Oedema 2. More Cellular Hypoxia Tissue ischemia  Hypoxia + Acidosis  compliment activation & priming of Neutrophil  produces O 2 free radicals & cytokines  injury to endothelium  leaky endothelium = Tissue oedema & more hypoxia.

7. Systemic Effect Cardio-vascular  Tachycardia & vasoconstriction Respiratory  Respiratory Alkalosis Renal  Oliguria Endocrine  Na + , H 2 O retention & Vasoconstriction

8. 1.Cardio-vascular effect ↓ preload & afterload  stimulates Baroreceptor mechanism  ↑ sympathetic activity catecholamine secretion = Tachycardia & Vasoconstriction

9. 2.Respiratory systemic effect Metabolic acidosis + catecholamine  ↑ respiratory rate & minute ventilation  ↑ CO 2 excretion = Compensatory respiratory Alkalosis

10. 3.Renal systemic effect ↓ renal perfusion pressure  ↓GFR = Oliguria ↓ renal perfusion pressure  stimulates Renin-Angiotensin- Aldosterone Axis  Na + , H 2 O retention & Vasoconstriction = Oliguria

11. 4.Endocrine effect Posterior pituitary : ↓ preload  stimulates hypothalamic osmoreceptor  stimulates posterior pituitary  ADH secretion  = Na + , H 2 O retention & Vasoconstriction Kidney: ↓ preload  ↓ renal perfusion pressure  stimulates Renin -Angiotensin mechanism = Na + , H 2 O retention & Vasoconstriction Adrenal : sympathetic activation  stimulates adrenal cortex  cortisol release = Na + , H 2 O retention

12. Pathophysiological Classification of shock [ H-CODE ] Hypovolemic shock Cardiogenic shock Obstructive shock Distributive shock Endocrine shock

13. Hypovolemic shock Reduced circulating volume Haemorrhagic Nonhaemorrhagic Vomiting Diarrhoea Less intake Urinary loss Evaporation Third space loss

14. Cardiogenic shock Failure pumping action of Heart Cardiac MI Dysrhythmia Valvular heart disease Cardiomyopathy Myocardial injury Non-cardiac Endogenous – bacterial endocarditis or humoral agent Exogenous - Drugs

15. Obstructive Shock Reduction in preload due to mechanical obstruction in cardiac filling Cardiac tamponade Tension pneumothorax Massive pulmonary embolism Air embolism  Mechanical obstruction of right/left heart filling  ↓ preload  Obstructive Shock

16. Distributive shock Vascular dilation Low systemic vascular resistance Inadequate afterload Resulting abnormally high cardiac output Hypotension = distributive shock

17. Distributive shock Types: Septic shock Anaphylactic shock Neurogenic shock

18. Pathophysiology of septic shock 2 stage ; early stage or warm shock & late stage or cold shock Hypotension occurs due to effect of Endotoxin Endotoxin acts by 3 mechanism Direct damage of endothelium Activation of complement system (Humoral) Activation of immune system (Cellular)

19. Events in early stage of septic shock Cutaneous vasodilation  Warm Shock Vasodilation  ↓ systemic vascular resistance  ↓ BP As BP = CO + SVR, so to compensate low BP, CO increases  Hyper dynamic state Vascular damage  coagulation system activation  Coagulopathy Leaky vasculature  fluid in tissue space  Tissue oedema Vascular damage occurs in multi organs  MODS Maldistribution of blood flow @ microvascular level & A-V shunting Dysfunction of cellular utilization of O 2

20. Late phase of Septic shock If septic shock untreated/ maltreated following physiological changes occur All immune mediators are cardio-depressant + persistent leaky endothelium+ vasodilation  decreases CO  BP falls severely = Hypodynamic stage. If patient in shock for long enough  sympathetic system tries to constrict peripheral vessel  Skin become Cool (late sign of septic shock) Fluid loss in interstitial space  Hypovolemia

21. Distributive shock … cont Anaphylactic shock Histamine release  vasodilation  ↓ preload shock Neurogenic shock Spinal cord injury sympathetic failure  vascular tone lost  peripheral pooling  Shock

22. Endocrine shock It is the combination of – Distributive shock  problem in vessel  pooling Cardiogenic shock  problem in heart Hypovolemic shock  ↓ blood vol. To remember DCH

23. Endocrine shock Hypothyroidism Hyperthyroidism Adrenal insufficiency

24. 1.In hypothyroidism D. SHOCK

25. Endocrine shock In Hyperthyroidism: High output Cardiac failure  Cardiogenic shock In Adrenal insufficiency: Low level of gluco -corticoid hypovolemia + poor response to circulating & exogenous catecholamines  H. SHOCK

26. Clinical classification of shoch (according to severity) Compensated Decompensated Mild Moderate Severe

27. Compensated shock Loss of blood volume < 15% ↓ blood flow to nonessential organs Preserve flow to brain, lungs, kidneys Only sign is tachycardia and cool periphery Occult hypoperfusion going on to skin, gut & mucosa If occult hypoperfusion prolonged then “Ischemia reperfusion syndrome” may occur.

28. Decompensated shock Progressive blood loss > 15% Progressive decompensation of renal, respiratory & CVS BP going to fall when blood loss > 30-40% 3 types Mild shock: Blood loss > 15% Tachycardia Tachypnoea Mild ↓ Urine output BP maintained but ↓pulse pressure Cool sweaty periphery Prolong capillary feeling time Mild anxiety

29. Decompensated shock Moderate shock Blood loss  30-40% Renal compensation fails & urine O/P falls < 0.5 ml /Kg/ Hr Further tachycardia BP starts to fall Drowsy & mildly confused

30. Decompensated shock Severe shock Blood loss > 40% Profound tachycardia Hypotension Urine O/P falls to “0” Unconscious Labored respiration

31. Pitfalls of shock Blood pressure Fit young adult & children can maintain BP up to end stage Elderly hypertensive patient shows normal Bp while in shock Tachycardia β blocker user/ pacemaker implanted patient may not show tachycardia Paradoxical bradycardia Capillary refilling Varies person to person Septic shock

32. Consequences of shock Irreversible shock / Refractory shock Last phase Despite restoring circulation there is progressive decline in BP & perfusion Progressive organ failure Cause: severity, delay, inadequate & inappropriate resuscitation

33. Consequences of shock 2 . Multi organ failure 2 or more organ fails to work Lungs  ARDS Kidney  ARF Clotting  Coagulopathy CVS  cardio-vascular failure

34. Management of shock Resuscitation of shocked patient should be carried out in 2 steps Initial resuscitation Continual resuscitation Fluid Vasopressor monitoring

35. Initial resuscitation Airway patency O 2 inhalation Ensure breathing & ventilation

36. Conduct / principle of resuscitation Rapid history & clinical examination to find Type of shock Timing of shock Severity of shock If doubt about type; assume hypovolemic shock  start fluid response If haemorrhagic shock  control & resuscitation side by side If non haemorrhagic shock  adequate resuscitation before any operation

37. Fluid therapy Principle: All shocked patient regardless type; fluid should be started Short wide bore cannula and start IV fluid Type of fluid: There is no ideal fluid Crystalloid (Hartman’s/ Ringer’s Lactate / NS) or colloid may be used In haemorrhagic shock  blood is ideal DA should never be used unless it’s Diabetes insipidus /Na + overload

38. Dynamic fluid response 250-500 ml fluid I/V over 5-10 min then see cardio-vascular status Heart rate BP CVP Responder Transient responder Non responder

39. Dynamic fluid response Responder Improved & sustained Not actively loosing fluid Continue fluid therapy in ward Transient responder Improved but revert over next 10-20 min Moderate ongoing fluid loss Send Patient for ICU support with fluid 3. Non responder Not improved Send patient OT for definitive treatment

40. Vasopressor & Inotrope support 2 nd line therapy Used in Distributive shock Agent : catecholamine & Vasopressin Vasopressin specially used in Adrenal insufficiency as there is catecholamine resistance Inotrope : Dobutamine, used in Cardiogenic shock Other drugs : Septic  vasopressin + Antibiotic Neurogenic  vasopressin + Prednisolone Anaphylactic  hydrocortisone + Adrenaline + Promethazine

41. Monitoring of shock Cardio-vascular monitoring a. Minimum [PUB-G] Pulse oximetry Urinary output BP ECG b. Additional [BCCB] Invasive BP CVP Cardiac Output Base deficit & S. lactate 2. Systemic & organ perfusion monitoring

42. Systemic & organ perfusion monitoring

43. CVP : After fluid challenge Normal: CVP rise 2-5 cm Gradually drift back over 10-20 min Decreased preload: No changes Require further fluids Cardiac insufficiency: High CVP

44. Cardiac output Measured by pulmonary artery catheter or Doppler USG Measure about Cardiac O/P Systemic vascular resistance Blood vol. End diastolic vol. Interpretation Hypovolemic S  ↓ blood vol. Cardiogenic S  ↓cardiac O/P Distributive S  ↓ vascular resistance & ↓ EDV

45. Base deficit Normal blood pH 7.4 In shock there is acidosis, so pH level become < 7.4 To normalize blood pH base need to added So “ the amount of base needed to make the pH 7.4 is called Base deficit” Base deficit measured by ABG

46. Serum lactate Normal  0.5 – 1 mmol/Li If <2  patient is resuscitated If >3  further resuscitation needed

47. Mixed venous O 2 saturation % saturation of O 2 returning to the heart Measured by CV line Interpretation: Normal  50-70% Hypovolemic/cardiogenic  <50% Septic/A-V fistula  >70%

48. End point of resuscitation Base deficit corrected S. lactate within normal range Mixed venous O2 saturation 50-70%