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Diagnosis and Management of shock

Diagnosis and Management of shock

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Diagnosis and Management of shock

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  1. Diagnosis and Management of shock Dr.Hossam Hassan Consultant and Assistant prof D.E.M

  2. Objectives Identify the 4 main catigories of shock Discuss the goals of resuscitation in shock Summarize the general principles of shock management Describe the physiologic effects of vasopressors and inotropic agents

  3. CASE STUDY A25 Years old lady with no prior history of any chronic disease presented to the emergency departement complaining of a productive cough of greenish yellow sputum.

  4. VITAL SIGNS Temp.38.8 Ht.Rate 129/Min R.R 27/Min BP 112/68

  5. Where do you triage this Pt.? What information do you need to determine if this Pt. is in shock? What initial interventions are needed to stabilize that Pt.?

  6. Shock is a syndrome of impaired tissue oxygenation and perfusion due to a variety of etiologies If left untreated Irreversible injury ,Organ dysfunction And finally death

  7. Clinical ulterations in shock The presentation of patients with shock may be Subtle(mild confusion,tachycardia) Or easily identifiable(profound hypotesion.anuria)

  8. The clinical manifestation of shock result from 1- inadequate tissue perfusion and oxygenation 2- Compansatory responses 3- The specific etiology

  9. Clasification of shock 1-hypovolemic a-Hemorrhagic b-nonhemorrhagic 2-Cardiogenic Ischemic Myopathy Mechanical Arrhythmia

  10. 3- Distributive Septic Adrenal crises Neurogenic (spinal shock) Anaphylactic

  11. 4- Obstructive Massive Pulmonary embolism Tension pneumothorax Cardiac tamponade Constrictive pericarditis

  12. HYPOVOLEMIC SHOCK It occure when the intra vascular volume is depleted relative to the vascular capacity as a result of 1- Hge. 2- G.I.T loss 3-urinary loss 4-dehydration

  13. HYPOVOLAEMIC SHOCK Management The goal is to restore the fluid lost Vasopressors are used only as a temporary method to restore B.P untill fluid resuscitation take place

  14. Hypovolaemic shock The commonest cause of acute hypovolaemic shock in surgical practice is bleeding due to trauma, ruptured aortic aneurysm, gastrointestinal and obstetric haemorrhage.

  15. Hypovolaemic shock normal adult blood volume is about 7% of body weight, with a 70kg man having an estimated blood volume (EBV)of around 5000ml.

  16. Hypovolaemic shock The severity of haemorrhagic shock is frequently classified according to percentage of EBV lost where class I (< 15%) represents a compensated state (as may occur following the donation of a unit of blood) and class IV(> 40%) is immediately life threatening.

  17. Hypovolaemic shock Arrest of haemorrhage and intravascular fluid resuscitation should occur concurrently; there is little role for inotropes or vasopressors in the treatment of a hypotensive hypovolaemic patient.

  18. Hypovolaemic shock In the emergency situation, before bleeding has been controlled, a systolic blood pressure of 80-90 mmHg is increasingly used as a resuscitation target (permissive hypotension) as it is thought less likely to dislodge clot and lead to dilutional coagulopathy.

  19. Hypovolaemic shock Once active bleeding has been stopped, resuscitation can be shifted to optimize organ perfusion and tissue oxygen delivery .

  20. Hypovolaemic shock It remains unclear whether permissive hypotension is appro­priate for all cases of haemorrhagic shock but it appears to improve outcomes following penetrating trauma and ruptured aortic aneurysm.

  21. Hypovolaemic shock Rapid fluid resuscitation requires secure vascular access and this is best achieved through two wide-bore (14- or 16-gauge) peripheral intravenous cannulae; cannulation of a central vein provides an alternative means.

  22. Hypovolaemic shock the type of fluid used (crystalloid or colloid ) is probably less important than the adequate restoration of circulating volume itself.

  23. Hypovolaemic shock In the case of Iife-threatening or continued haemorrhage, blood will be required early in the resuscitation. ldeally, fully cross-matched packed red blood cells (PRBCs) should be administered, but type­ specific or O Rhesus-negative blood may be used until it becomes available.

  24. Hypovolaemic shock Massive transfusion can lead to hypothermia, hypocalcaemia, hyper- or hypokalaemia and coagulopathy. The acute coagulopathy of trauma (ACOT) is well recognized and multifactorial.

  25. Hypovolaemic shock Dilution of clotting factors and platelets as a result of fluid resuscitation, combined with their consumption at the point of bleeding, results in clotting factor deficiency, thrombocytopaenia and coagulopa­thy.

  26. Hypovolaemic shock Hypothermia, metabolic acidosis and hypocalcaemia also significantly impair normal coagulation.

  27. Hypovolaemic shock Resuscitation strategies aggressively targeting the 'lethal triad' of hypthermia, acidosis and coagulopathy appear to significantly improve outcome following military trauma and observational studies support the immediate use of measures to prevent hypothermia, early correction of severe metabolic acidosis (pH < 7.1), maintenance of ionized calcium> l.o mmol and the earl y empirical use of clotting factors and platelets.

  28. Hypovolaemic shock Where possible, correction of coagulopathy should be guided by laboratory results (platelet count, prothrombin tme, activated partial thromboplastin time and fibrinogen concentration).

  29. Hypovolaemic shock Clotting factor deficiency is normally treated by the administration of fresh frozen plasma (FFP) (10-15mljkg), thrombo cytopaenia or platelet dysfunction by the administration of platelets .

  30. Hypovolaemic shock Fibrinogen deficiency (< l.0 g/L) is best treated with fresh frozen plasma or cryo­precipitate (usually 10 units). The antifibrinolytic, tranexamic acid, can be used to inhibit fibrinolysis and has been shown to reduce mortality from bleeding when used early (< 3 hours) and following major trauma.

  31. Hypovolaemic shock Early administration is important for its beneficial effect. ln the case of rapid haemorrhage, it is often not possible to use traditional laboratory results to guide the correction of coagulopathy because of the time delay in obtaining these results.

  32. Hypovolaemic shock This has led to a formula-driven approach to the use of PRBC, FFP and platelets targeting the early empirical treatment of coagulopathy.

  33. Hypovolaemic shock Although t he evidence for these strategies is still emerging, current military guidelines advocate the administration of warmed PRBC and fresh frozen plasma (FFP) in a 1:1 ratio as soon as possible in the resuscitation of major haemorrhage following trauma in conjunction with platelet transfusions to maintain platelets> 100 .

  34. Distributive shock It is characterized by loss of vascular tone The most common form of distributive shock is septic shock The hemodynamic profile of septic shock include

  35. Cardiac output normal or increased Ventricular filing pressure normal or low SVR low Diastolic pressure low Pulse pressure wide

  36. Management of septic shock The initial approach to the patient with septic shock is the restoration and maintenance of adequate intravascular volume Prompt institution of appropriate antibiotic

  37. CARDIOGENIC SHOCK Forward flow of blood is inadequate bec. Of pump failure due to loss of functional myocardium It is the most severe form of heart failure and it is distinguished from chronic heart failure by the presence of hypotension,hypoperfusion and the need for different therapuetic inteventions

  38. Hemodynamic chracteristics Cardiac output low Ventricular filing pressure high SVR High Mixed venous o2 sat low

  39. MANAGEMENT OF CARDIOGENIC SHOCK The main goal is to improve myocardial function Arrhythmia should be treated Reperfusion PCI is the treatment of choice in ACS Inotropes and vasopresor

  40. Obstructive shock Obstruction to the outflow due to impaired cardiac filling and excessive after load Cardiac tamponade and constrictive pericarditis impair diastolic filling of the Rt.ventricle Tension pneumothorax limit Rt.ventricular filing by obstruction of venous return Massive pulmonary embolism increase Rt.ventricular afterload

  41. Hemodynamic profile in obst. Shock Cardiac output low Afterload high Lt.Vent.filling pressure variable Pulsus paradoxicus in Tamponade Distended Jugular viens

  42. Management Of Obstructive Shock Directed Mainly to Management of the cause

  43. GENERAL Principles of shock management The overall goal of shock management is to improve oxygen delivery or utilization in order to prevent cellular and organ injury Effective therapy requires treatment of the underlying etiology

  44. Restoration of adequate perfusion, monitoring and comperhensive supportive care Interventions to restore perfusion center on achieving an adequate B.P, increasing cardiac output and optimizing oxygen content of the blood

  45. Oxygen demand should also be reduced