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  2. 2. DEFINATIONShock give rise to systemic hypoperfusion caused by reduction either in cardiac output or in effective circulatory blood volume. End results are : Hypotension Tissue hypoperfusion Cellular hypoxia Reversible injury Irreversible injury with persistent of shock End organ dysfunction Death
  3. 3. TYPES OF SHOCK Hypovolumic shock Cardiogenic shock Septic shock Anaphylactic shock Neurogenic shock
  4. 4. HYPOVOLUMIC SHOCK Hypovolumic shock occurs due to rapid reduction in blood volume or plasma volume. Causes of hypovlumic shock : 1. Hemorrhage 2. Severe dehydration-severe vomiting, severe diarrhea 3. Severe burn 4. Abdominal ascities 5. Acute pancreatitis 6. Diabetes mellitus 7. Over use of Diuretics
  5. 5. HYPOVOLUMIC SHOCK  Pathophysiology of hypovolumic shock : Dehydration, Hemorrhage Reduction in intravascular blood volume Decreased pre-load Decreased stroke volume & CO Systemic hypoperfusion Compensatory vasoconstriction Tissue ischemia, hypoxia Cellular & organ dysfunction
  6. 6. CARDIOGENIC SHOCK Cardiogenic shock is characterized by reduced pumping ability of heart due to intrinsic myocardial damage or extrinsic or obstruction to out flow. It is most commonly occurs in association with and as a direct result of acute myocardial ischemia. Incidence: -Cardiogenic shock occurs in 8.6% of patient with ST segment elevation. -Myocardial ischemia with 29% of those presenting to the hospital already in shock. -2% of non ST segment elevation MI.
  7. 7. CARDIOGENIC SHOCK Risk factor : -Pre existing myocardial damage -Diabetes Mellitus -Advanced age -Previous MI -Dysarythmia
  8. 8. CARDIOGENIC SHOCK Causes of Cardiogenic shock : MI Vulvular regurgitation Acute myocarditis Cardiomyopathy Cardiac tamponade Pulmonary embolism Acute vulvular dysfunction Cardiac dysarythmia Rupture ventricular aneurysm Beta-blocker overdose Ca-channel blocker overdose
  9. 9. CARDIOGENIC SHOCK Pathophysiology of cardiogenic shock : Myocardial Infraction Myocardial ischemia or injury Myocardial dysfunction Systemic inflammatory response Decreased CO & stroke volume Increased NO synthesis Systemic hypoperfusion Hypotension Vasodilatation Decreased coronary perfusion Compensatory vasoconstriction Cardiac & other end organ damage Progressive myocardial dysfunction Death
  10. 10. SEPTIC SHOCK Sepsis is a clinical state that accompanies infection either confined to a local site from which toxin are absored or associated with invasion of organism in to the blood stream. Causes of septic shock: -Overhelming microbial infection -Gram +ve septicemia -Endotoxic shock (Gram –ve septicemia) -Fungal sepsis -Super antigen
  11. 11. SEPTIC SHOCK
  12. 12. SEPTIC SHOCK Microbiology : Gm + Staphylococcus Streptococcus Gm - E.Coli Klebsiella Proteus Other Fungi
  13. 13. SEPTIC SHOCK Pathophysiology of septic shock : Bacterial infection Endotxin ( LPS ) & other microbial products Binds to LPS binding protein in serum Binds to CD14 receptors on mononeuclear cells CD14 binds to TLR4 Release of chemical mediators
  14. 14. SEPTIC SHOCK Pathophysiology of septic shock :
  15. 15. SEPTIC SHOCK Patho-physiology of septic shock : In septic shock systemic vasodilatation and pooling of blood in the periphery leads to tissue hypo perfusion and though the cardiac out put is preserved this is accompanying widespread endothelial cell activation and often leads to hablypercoagulable state that can manifest DIC.Septic shock is associated with change in metabolism that can directly suppress cellular function. The net effect is hypo perfusion and dysfunction of multi-organ.
  16. 16. SEPTIC SHOCK Major factors contributing to the pathophysiology of septic shock are following. Inflammatory mediators; Various microbial cell wall contains lipopolysaccaride are released when the cell wall are degraded. Free LPS bind to circulatory LPS.This complex then binds to a cell surface receptor CD14 on macrophage, mononuclear paghocytic cell, endothelial cell.CD14 binds to the signal transducing protein TLR-4.Upon activation cascade of cytokines mediators TNF,TL-1,IL-8,INF- .The compliment cascade are activated directly or through proteolytic activity of plasmin resulting in production of anaphylotoxins C3a&C5a,chemotatctic factor C5a causes vasodilatation & increases vascular permeability.Activated endothelial cell and macrophage release NO contribute to pro-inflammatory state.
  17. 17. SEPTIC SHOCK Endothelial cell activation and injury: Endothelial cell activation by microbial products or inflammatory mediators produced by leukocytes. Has 3 major sequele-thrombosis,increase vascular permiability,vasodilation Pro-inflammatory cytokines result in increased tissue factor production by endothelial cell and monocyte.The production of endothelial anti-coagulant factor-tissue factor pathway inhibator,thrombomodulin and protein-C reduced.Reduced blood flow at the level of small vessels' produce stasis that reduce the wash out of activated coagulation factor results in deposition of fibrin rich thrombi in small vessels, that lead to tissue hypoperfusion..
  18. 18. In DIC increase consumption of coagulation factor & platelet leads to bleeding & hage. Increase vascular permiability leads exudation of fluid in to interstitum causing oedema. Endothelium increase the relase of NO.
  19. 19. SEPTIC SHOCK Metabolic abnormalities:Septis patient exhibit insulin resistance and hypoglycemia. Cytokines such as TNF & IL-1,stress induced hormone(glucagon,catecholamines)all drive gluconeogenesis.At the same time the pro- inflammatory cytokines suppress insulin release while simultaneously promoting insulin resistance in the liver & other tissue, by surface expression of glucose transporter. Hyperglycemia reduced neutrophil function & bactericidal activity. Sepsis also related with adrenal insufficiency & factional deficency of glucocortcoid.
  20. 20. SEPTIC SHOCK Immuno suppression: hyper inflammatory state activate immuno- suprssion mechanism which involve both innate & adaptive immunity by production of anti- inflammatory mediators(soluable TNF receptors,IL- recepor antagonist& IL-10). Organ dysfunction: Systemic hypotension, interstitial edema, small vessels thrombosis reduce the delivery of oxygen &to the tissue.
  21. 21. SEPTIC SHOCK High level of cytokines, secondary mediators reduces myocardial contractility & CO. Increase vascular permeability & endothelial injury acute respiratory distress syndrome ultimately cause multiple organ failure.
  22. 22.  Toxic shock syndrome: Toxic shock syndrome is a potentially fatal illness caused by bacterial toxin(super antigen) released by – Staphylococcus aureus & Streptococcus pyogens. Streptococcal TSS associated with recent soft tissue injury like surgery,pharyngitis,NSAID drug use. Staphylococcal TSS observe mostly among menstruating women, but also associated with cutaneous infection, post-partum & C/S wound infection & focal staphylococcal infection like abscess,empyma,pneumonia.
  23. 23. NEUROGENIC SHOCK Neurogenic shock occurs in the setting of anesthetic accident or spinal cord injury causes loss of vascular tone and peripheral pulling of blood.
  24. 24. ANAPHYLACTIC SHOCK In Anaphylactic shock,decreased systemic vascular resistance due primarily to massive histamine release from mast cell after activation of IgE mediated hypersensitivity reaction as well as increase synthesis of prostaglandin. That leads to vasodilatation and increase vascular permiability.Ultimate results are systemic hypotension, tissue perfusion and cellular anoxia.
  25. 25. ANAPHYLACTIC SHOCK Causes of anaphylactic shock: 1.Iatrogenic( drug) 2.Accidental exposure to an allergen and co-exiting respiratory complaints(wheezing & dyspnea)& or purities. Systemic inflammatory response in anaphylactic shock: Respiratory distress Wheezing Urticarial rash Angioedema.
  26. 26. STAGES OF SHOCK 1.An initial non progressive phage 2.A progressive stage 3.An irreversible stage
  27. 27. An initial non progressive phage: In this phage a varieties of neuro-hormonal & haemostatic mechanism helps to maintain cardiac out-put & blood pressure. These includes: - Baro-receptor reflex mechanism - Release of catecholamine's - Activation of Renin-angiotension axis - Anti-diuretic hormone release -Generalized sympathetic activation
  28. 28. Net effects are- 1.Tachycardia 2.Peripheral vasoconstriction 3.Renal conservation of fluid Resulting in restoration of circulation and tissue perfusion.
  29. 29. Progressive phase: If the compensatory mechanism fails to restore circulation, vital organ shows the effects of hypoxia.Persistant oxygen deficiency leads to intra cellular anaerobic glycolysis with lactic acidosis,thus reduce tissue pH and vasomotor response. Resulting reduce cardiac output and anoxic injury to endothelial cell leads to DIC.
  30. 30. Irreversible stage: When there is failure to restore circulation either by compensatory mechanism or by therapeutic intervention,the process of shock enters the irreversible stage. Wide spread cell injury is reflected in lysosomal enzyme lekage,nitric oxide reduced myocardial contractility,acute tubular necrosis ultimately death.
  31. 31. MORPHOLOGY OF SHOCK Since shock is characterized by failure of multi-organ systems, the cellular changes may appear in any tissue. Brain: ischemic encephalopathy. Heart: coagulative necrosis or subendocardial hemorrhage or contraction band necrosis. Kidney: acute tubular necrosis. Lung: diffuse alveolar damage develop shock lung. Gastrointestinal tract: Hemorrhagic enteropathy. Adrenal gland: cortical cell lipid depletion may occur. Liver: fatty change, central hemorrhagic necrosis.
  32. 32. CLINICAL PRESENTATION OF SHOCK Altered mental status- Restless,confusion,stupor,coma,agitation Patient may unconscious or semi-conscious Pallor Increase sweating Cold clammy skin. Warm in septic shock  Pulse-Tachycardia, rapid weak thready pulse  Respiration-Tachypnia, slow and regular Blood pressure-low blood pressure Temperature may or may not be raised Dehydration Reduce urine output
  33. 33. DIAGNOSIS OF SHOCK History taking General and physical examination Vital sign assessment
  34. 34. LAB DIAGNOSIS  CBC Biochemical test-serum electrolyte,ramdom blood sugar,s.creatinine ECG Chest x-ray Blood culture, urine R/M/E & C/S,sputum for gram stain & C/S Blood grouping & Cross matching Cardiac enzyme Arterial blood gas analysis
  35. 35. MANAGEMAENT OF SHOCK Admitted in intensive care unit Ensure ABC Clear airway, adequate breathing, assessment of circulation- pulse,BP,urine volume. Position of the patient Trendelenburg or supine position to increase cerebral blood flow. Oxygenation-High flow oxygen should be delivered. Establish IV access Restore circulatory blood volume-blood in case of bleeding,crystalioid(n/s,ringer’ s lactate ) cont..
  36. 36. Vasoactive drugs Dopamine with or with out dobutamine provide ionotropic support increasing perfusion of the ischemic myocardium &all body tissue. Surgical intervention if needed. Insulin therapy in case of hyperglycemia Treatment of underlying cause: Broad spectrum antibiotic coverage in case of infection. Cardiogenic shock-treatment according to cause such as MI or left ventricular failure. Hypovolumic shock-adrenalin I/m Hydrocortisone
  37. 37. In acute adrenal insufficiency-Corticosteroid use as life saving drug. Activated protein-C can be use in severe sepsis.
  38. 38. The prognosis varies with the origin of shock and its duration. 80%-90% of young with hypovolumic shock survive with appropiate management. Cardiogenic shock associated with extensive myocardial infraction mortality rate up to 75% Septic shock -mortality rate up to 75% PROGNOSIS OF SHOCK