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8. shock

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superficial introduction to the topic for bachelor level

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8. shock

  1. 1. Dr. Saugat Chapagain SHOCK
  2. 2. WHAT IS IT??? Life threatening clinical syndrome of cardiovascular collapse characterised by: • An acute reduction of effective circulating blood volume (hypotension) • An inadequate perfusion of cells and tissues (hypoperfusion)
  3. 3. AETIOLOGICAL CLASSIFICATION • Hypovolemic shock • Cardiogenic shock (normovolemia) • Septic shock – gram negative (endotoxic) or gram positive (exotoxic) • Neurogenic shock • Anaphylactic shock
  4. 4. PATHOGENESIS • Reduced effective circulating blood volume. • Reduced supply of oxygen to the cells and tissues with resultant anoxia. • Inflammatory mediators and toxins released from shock-induced cellular injury.
  5. 5. COMPENSATED SHOCK • Non-progressive, initial, reversible • In early stage, body acts to provide supply to the vital organs (brain and heart) • Peripheral vasoconstriction (widespread) and kidneys retain fluid. • After prompt management, body’s homestasis may be returned easily
  6. 6. PROGRESSIVE DECOMPENSATED SHOCK Usu. a/w pre existing co-morbidity. Persistence of shock + progressive deterioration. Circulatory and metabolic imbalance (incl. met acidosis) Effects: • Pulmonary hypoperfusion • Tissue ischemia
  7. 7. IRREVERSAL/ DECOMPENSATED • Severe shock. • Recovery poor or absent despite compensatory mechanism as well as therapy. • MODS common.
  8. 8. MORPHOLOGY IN SHOCK Brain Gross – • Area supplied by the most distal branches of cerebral arteries suffer from severe ischemic necrosis. Microscopic – • Changes are prominent if ischemia lasts for 12-24 hrs at least. • Cytoplasm of affected neurons are intensely eosinophilic and nucleus is small and pyknotic. • Dead neurons replaced by gliosis.
  9. 9. Heart 2 types of changes: • Haemorrhages and necrosis – • Zonal lesions – Lung More prominenet changes in septic shock Not much effect in hypovolemic shock Gross – • Heavy and wet Microscopic – • ARDS changes seen • Congestion, interstitial and alveolar oedema, interstitial lymphocytic infiltrate, alveolar hyaline membranes, etc.
  10. 10. Kidney End result is almost always anuria and death. Gross – • Soft and swollen • Section shows blurred margins Microscopic – • Tubular lesions seen at all levels of nephron (ATN) Adrenals • Show stress response • Release of aldosterone in response to hypoxic kidney, release of glucocorticoid (from cortex) • Release of adrenaline from medulla. • Acute adrenal haemorrhagic necrosis may occur in serious conditions.
  11. 11. GIT – • May show mucosal haemorrhage and necrosis. Liver – • May show fatty changes and central necrosis.
  12. 12. CLINICAL FEATURES • Very low pressure. • Subnormal temperature. • Feeble and irregular pulse. • Shallow and sighing respiration. • Other features: • Pale face, sunken eyes, weakness, cold and clammy skin.
  13. 13. CLINICAL FEATURES Symptoms: • Restlessness • Sweating, coldness • Rapidly shallow breathing Signs: • Altered level of consciousness, rapid and weak pulse • Hypotention, oliguria, anxiety • Cold clammy skin.
  14. 14. SPECIFIC FEATURES In septic shock: • Fever • Skin – pink and well perfused In cardiogenic shock: • Raised CVP/ JVP • Lungs – b/l basal crepts + • Liver – enlarged d/t decreased pumping of the venous return. In anaphylactic shock: • Rashes. • Vomiting. • SoB. • Headache, body ache.
  15. 15. COMPLICATIONS • Acute Respiratory Distress Syndrome. • Disseminated Intravascular coagulation. • Acute renal failure • Multiple organ dysfunction syndrome • Stupor, coma and death.
  16. 16. • Septic shock • Neurogenic shock PATHOPHYSIOLOGY Tissue death/ necrosis Tissue Hypoperfusion Vasodialation and hypotention Production of cytokines Release of bacterial endotoxins Unconsciousness (hypoxia/ ischemia) Reduced supply to the brain Decreased cardiac output Hypotension and decreased heart rate Decreased sympathetic activity controling vascular tone Anaesthesia, brain or spinal injury
  17. 17. • Type I hypersensitivity reaction • IgE mediated rxn. • Systemic vasodilation and increased vascular permeability ANAPHYLACTIC SHOCK a/w bronchoconstriction and skin rashes Venous pooling of blood and hpotension. Vasodilation Systemic release of mediators (histamine/ bradykinin) Allergic substance enters circulation/ organism
  18. 18. MANAGEMENT Principles • Clinical monitoring • Maintenance of ABC • Clearing the Airway • Maintenance of Respiration • Maintenance of Circulation • Prevention of Renal Shut down • Correction of Acid base balance • Treatment of underlying cause
  19. 19. CLINICAL MONITORING • History • Vitals • Pulse • Pressure • Temperature • Respiration rate • CVP • Urinary output
  20. 20. MAINTENANCE OF RESPIRATION • Keep patient in well ventilated room. • Extend neck and support jaw • Place in left lateral position • Airway in mouth to prevent fallback of tongue • Supplement of nasal O2 • ET intubation and ventilation (if needed)
  21. 21. MAINTENANCE OF CIRCULATION • Control of bleeding (hemorrhagic shock) • IV access and start suitable IV fluid (RL, NS, DNS, 5-D, dextran, hemacele) • Necessary investigation incl. blood grouping and cross matching • Blood transfusion if needed.
  22. 22. SUPPORTIVE CARE • Prevention of renal shut down (AKI/ MODS) • Foley’s catheterization • I/O charting strictly • Correction of acid base balance • Identification and treatment of underlying cause • Septic shock- • Broad spectrum antibiotics • TT prophylaxis • Excision of source of sepsis
  23. 23. CARE OF ANAPHYLACTIC SHOCK • Stop drug/ agent causing anaphylaxis • Clear the airway • IV antihistamine (phenargan, promethazine, avil, meperamine) • IV steroid (hydrocort) • IV adrenaline 0.5ml or SC 1:1000
  24. 24. THANK YOU
  • RiaPandhi

    Apr. 7, 2021

superficial introduction to the topic for bachelor level

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