Seminar on shock

Seminar on shock

1. SEMINAR Dr. Faria Yasmin Resident : phase - A Neonatology Dr. Farzana Azma Azad Resident: Phase- B General Pediatrics BSMMU

2. SHOCK

3. Objective Definition Types with causes Pathophysiology of shock Stages of shock General management of shock Management of shock according to types

4. Definition Shock is an acute process characterized by the body’s inability to deliver adequate oxygen to meet the metabolic demands of vital organs and tissue.

5. Types 5 major types of shock: Hypovolemic Cardiogenic Obstructive Distributive Septic

6. Causes of shock according to types Hypovolemic Shock: (↓ preload secondary to internal or external losses) Blood loss: hemorrhage Plasma loss: burns, nephrotic syndrome Water and electrolyte loss: vomiting, diarrhea. Inadequate fluid intake Osmotic diuresis (DKA) Third space loss

7. Cardiogenic shock: ( cardiac pump failure secondary to poor myocardial function) Congenital heart disease Cardiomyopathies – infectious or acquired, dilated or restrictive Ischemia Arrhythmias

8. Septic shock: ( multiple forms of shock Hypovolemic , distributive, cardiogenic ) Bacterial, viral, fungus Distributive shock: ( Abnormalities of vasomotor tone due to loss of venous and arterial capacitance) Anaphylaxis Neurogenic Drugs

9. Obstructive shock : ( ↓ CO secondary to direct impediment to right or left heart outflow or restriction to all cardiac chambers) Tension pneumothorax Pericardial temponade Pulmonary embolism Anterior mediastinal mass Ductal dependent congenital heart lesions (Critical coarctation of the aorta)

10. Pathophysiology of shock

11. 1. Extracorporeal fluid loss Hypovolemic shock may be due to direct blood loss through hemorrhage or abnormal loss of body fluids 2. Lowering plasma oncotic forces Hypovolemic shock may also result from hypoprotinaemia 3. Abnormal vasodilatation Distributive shock occurs when there is loss of vascular tone ( venous, arterial or both)

12. 4. Increased vascular permeability Sepsis may change vascular permeability in the absence of any change in capillary hydrostatic pressure( endotoxin from sepsis, histamine release in anaphylaxis) 5. Cardiac dysfunction Peripheral hypoperfusion may result from any condition that affects hearts pumping action (ischemia, acidosis, drugs, sepsis, constrictive pericarditis )

13. PATHOPHYSIOLOGY

14. Stages of Shock Compensated Stage Decompensated stage Irreversible stage

15. Compensatory physiological mechanism 1 Activation of sympathetic nervous system & neurohormonal response 3. Renal excreation of H + to maintain normal body P H 2. ↑RR with greater CO2 elimination 4. Maintenance of intravascular volume through Renin-angiotensin-aldosterone , Cortisol Catecholamine synthesis & release Antidiuretic hormone secretion

16. Events in non progressive stage Widespread tissue hypoxia Anaerobic glycolysis with excessive production of lactic acid Latic acidosis ↓ tissue pH & blunts vasomotor response Arteriols dilatation causes peripheral pooling of blood Decreased CO Endothelial injury with subsequent DIC

17. Clinical manifestation

18. Initial manifestation : Tachycardia or tachypnea Progression leads to decreased urine output Poor peripheral perfusion, low BP Respiratory distress or failure Alteration of mental status Tachycardia, with or without tachypnea , may be the first or only sign of early compensated shock

19. Late signs of shock Bradycardia Altered mental status (lethargy, coma) Hypotonia Cheyne-stokes breathing Hypotension is a very late sign

20. Regardless of etiology, uncompensated shock Hypotension, high systemic vascular resistance, ↓ CO, respiratory failure, and Oliguria , occurs late in the progression of disease

21. Type of shock CO systemic vascular resistance MAP capillary wedge pressure CVP Hypovolemic ↓ ↑ ↔ or ↓ ↓↓↓ ↓↓↓ Cardiogenic            Systolic ↓↓ ↑↑↑ ↔ or ↓ ↑↑ ↑↑  Diastolic ↔ ↑↑ ↔ ↑↑ ↑ Obstructive ↓ ↑ ↔ or ↓ ↑↑ ↑↑ Distributive ↑↑ ↓↓↓ ↔ or ↓ ↔ or ↓ ↔ or ↓ Septic:            Early ↑↑↑ ↓↓↓ ↔ or ↓ ↓ ↓  Late ↓↓ ↓↓ ↓↓ ↑ ↑ or ↔ Hemodynamic Variables in different shock states

22. Management of shock

23. General management of Shock Positioning Airway and breathing Vascular access Fluid resuscitation Monitoring Frequent reassessment Laboratory studies Medication therapy

24. Positioning: If hemodynamically stable , allow the child remain in most comfortable position. If the child is hypotensive and breathing is compromised : Trendelenburg position. Airway and Breathing: High concentration of O2 supplementation has to be given to all patients with shock. If respiration is ineffective, mental status is impaired or work of breathing is significantly increased => need O2 with ventilation.

25. Fluid resuscitation: Infusion of 20ml/kg bolus isotonic crystalloid solution over 5-20 min → can be given upto 3 bolus at a time over 60 min (In all types of shock except cardiogenic and obstructive shock) In cardiogenic shock: Infusion of 5- 10ml /kg bolus isotonic crystalloid solution over 10-20min → given to maintain initial CO but if patient is deteriorating ,stop infusion immediately and manage accordingly.

26. In obstructive shock 10-20ml/kg isotonic crystalloid fluid may initially given to maintain CO but rapid identification is needed for effective management.

27. Monitoring: Heart rate Blood pressure Temperature Respiratory rate O2 saturation by pulse oxymetry Mental status Urine output

28. CBC Hb %- ↓ TC -WBC: ↑ or ↓ (ominous sign of sepsis) DC-WBC: Neutrophil - shifted to left ( immature form ↑ - bands, myelocyte , promyelocyte ). Neutrophil ↓ (ominous sign) ESR - ↑ CRP: ↑ Platelet count: ↓ Investigation

29. PBF : WBC- immature neutrophil , vacuolation , toxic granules Prothrombin Time: ↑ , APTT :↑ Serum albumin: ↓ Serum fibrinogen: ↓ FDP : ↑ RBS : ↑ /↓

30. Serum electrolyte: Imbalance. Serum Calcium: ↓ ABG : metabolic acidosis (pH↓), high anion gap. - PaO 2 ↓ Serum lactate: ↑ Renal Function Test: Serum Creatinine - N/ ↑ X-ray chest P/A view: ARDS Need to exclude pneumothorax , pericardia effusion

31. Cardiovascular Drug treatment of Shock

32. Medication Therapy DRUGS INDICATION DOPAMINE Given in all types of shock Preferred fluid refractory septic shock as a vasoactive agent DOBUTAMINE Given with dopamine if only dopamine use is not beneficial Typically used in cardiogenic shock, septic shock ADRENALINE Preferred vasoactive agent in “cold shock” as it increases stroke volume Treatment of choice for anaphylactic shock NORADRENALINE Combination with dobutamine may be used in septic shock;

33. Drug Effect Dosing range Comment Dopamine ↑ Cardiac contractility 3-20 µg/kg/min ↑ Risk of arrhythmias at high doses Significant peripheral vasoconstriction at >10 µg/kg/min     Epinephrine ↑ Heart rate and ↑ cardiac contractility 0.05-3.0 µg/kg/min May ↓ renal perfusion at high doses Potent vasoconstrictor ↑ Myocardial O 2  consumption Risk of arrhythmia at high doses

34. Drug Effect(s) Dosing range Comment(s) Dobutamine ↑ Cardiac contractility 1-10 µg/kg/min — Peripheral vasodilator Norepinephrine Potent vasoconstriction 0.05-1.5 µg/kg/min ↑ Blood pressure secondary to ↑ systemic vascular resistance No significant effect on cardiac contractility ↑ Left ventricular afterload Phenylephrine Potent vasoconstriction 0.5-2.0 µg/kg/min Can cause sudden hypertension ↑ O 2  consumption

35. HYPOVOLEMIC SHOCK

36. Management of Hypovolemic Shock Mainstay of Management - Fluid resuscitation Identification of type of volume loss (non-hemorrhagic /hemorrhagic) Replacement of volume deficit Prevention and replacement of ongoing loss Restoration acid –base balance Correction of metabolic derangement

37. Stepwise management of Hypovolemic Shock Infusion of 20ml/kg bolus isotonic crystalloid solution with in 20 min → can be given upto 3 bolus at a time over 1 hour If there is hemorrhage 3 bolus of crystalloid solution 20ml/kg is needed and for blood replacement 10ml/kg PRBC or 20ml/kg whole blood (transfusion given in significant blood loss and crystalloid refractory hemorrhagic shock).

38. Medication Therapy: Vasoactive agents are not routinely indicated for hypovolemic shock management. Given in case of - Morbid child with profound hypovolemic shock -Hypotension Inj. Dopamine >10µgm/kg/min Acid- Base balance: Both respiratory alkalosis and metabolic acidosis occur in hypovolemic shock. But alkalosis couldn’t completely compensate. Bicarbonate is indicated if there is significant loss of HCO 3 -.

39. Obstructive shock Treatment of underlying cause -pericardial drain, chest tube, surgical intervention -if the patient is a neonate with a ductal dependent lesion then give PGE Further evaluation, invasive monitoring, pharmacologic therapy, appropriate consultation to be done according to cause.

40. CARDIOGENIC SHOCK

41. TREATMENT Treatment is aimed at reinstitution of adequate cardiac output and peripheral perfusion Sl ow adminstration (10-20 min) fluid bolus (5-10 ml/kg bolus ) with careful monitoring for response. Management of underlying cause.

42. Administration of ionotropes Dopamine is the 1 st line agent. Milrinone improves systolic function and decreases SVR without a significant increase in heart rate. Also causes diastolic relaxation. Dobutamine & other vesodilator may be considered. Epinephrine - in pt with persistant , profound hypotension.

43. Cont... Pt with deteriorating cardiogenic shock may get benefit from -Left ventricular assist device( LVAD ) - Right and left ventricular assist device( BiVAD ) - Extracorporeal membrane oxygenation( ECMO )

44. Distributive Shock It is characterized by high CO and low SVR (opposite of hypovolemic , cardiogenic , and obstructive) Maldistribution of blood flow causing inadequate tissue perfusion Due to release of endotoxin , vasoactive substances, complement cascade activation, and microcirculation thrombosis Early septic shock is the most common form

45. Management of Anaphylactic Shock Specific treatment: Inj.Adrenaline I/M 0.01mg/kg repeat the second dose after 10 to 15 minutes in severe anaphylaxis Salbutamol nebulization for bronchospasm Antihistamines: Diphenhydramine I/V Corticosteroid

46. Management of Neurogenic Shock Treatment- initial fluid therapy. Phenylephrine and vasopressin causes vasoconstriction and may be considered in the treatment for pt with spinal cord injury

47. SEPTIC SHOCK Septic shock is most common and caused by infectious organism or their by-product (eg, endotoxin).

48. Septic shock Hypovolumic shock Cardiogenic shock Distributive shock Intravascular fluid losses through capillary leaks Myocardial depressant effects of sepsis ↓ systemic vascular resistance Alteration of preload, afterload & myocardial contractility

49. CAUSATIVE ORGANISM In neonate -- Group B strept Escherichia coli Listeria monocytogenes enterovirus herpes simplex virus In older children Streptococcus pneumoniae Neisseria meningitidis Staph aureus ( methicillin sens or resistant) In immunocompromised and hospitalized pt- Escherichia coli, pseudomonas klebsiella , Acinetobacter Enterobacter Serratia

50. PATHOPHYSIOLOGY OF SEPTIC PROCESS

51. Focus of infection Superantigens and endotoxin Activated inflammatory cell Activation of host defence Endogenous mediator release Pro-inflammatory cytokines Anti-inflammatory cytokines Platelet activating factors Arachidonic acid metabolite Myocardial depressant substance Endogenous opiates Activation of coagulation system Activation of complement system Activated endothelium -increased expression of endo derived adhesion molecule Decreased thrombomodulin , increased plasminogen activator inhibitor Thrombosis and antifibrinolysis Hypovolemia , cardiac and vascular failure, capillary leak, ARDS, DIC, decreased steroid synthesis SHOCK MODS DEATH

52. Septic shock has 2 phases: Early or Warm shock- occurs in some patients with - increased hyperdynamic cardiac output and - decreased systemic vascular resistance. - manifested by bounding pulse, widened pulse pressure Late or Cold shock- occurs in other patients with -decreased cardiac output -elevated systemic vascular resistance. -manifested by poor peripheral perfusion(prolonged capillary refill) In both cases ,perfusion to major organ systems may be compromised.

53. Antibiotic therapy Anemia should be treated in the setting of septic shock to improve delivery of oxygen to the tissues. Most experts recommend maintaining a hemoglobin level 10 g/ dL ( hematocrit of 0.30 [30%]) in the setting of septic shock. Treatment of hypoglycaemia and hypocalcemia Identification and correction of metabolic derangement.

54. Treatment outline Proper counselling . ABC management. Fluid therapy. Use of vasoactive drugs. Correction of metabolic abnormality. Use of antibiotics. Adjuvent therapy. Treatment of cause. Follow up and monitoring.

55. TAKE HOME MESSAGE Goal of therapy is identification, evaluation, and treatment of shock in its earliest stage Initial priorities are for the ABC’s Fluid resuscitation begins with 20cc/kg of crystalloid or 10cc/kg of colloid Subsequent treatment depends on the etiology of shock and the patient’s hemodynamic condition Successful resuscitation depends on early and judicious intervention Aggressive resuscitation except if cardiogenic

56. TH 58 THANK YOU…