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Shock

Shock. Nasman Puar, dr.SpAn Bagian Anestesiologi Fakultas Kedokteran Unand/ RSUP Dr. M. Djamil Padang. What is Shock?. = hypotension ? = low blood pressure ? = haemorrhage ? = unconscious ?. Shock =. Clinical syndrome

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Shock

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  1. Shock Nasman Puar, dr.SpAn Bagian Anestesiologi Fakultas Kedokteran Unand/ RSUP Dr. M. Djamil Padang

  2. What is Shock? = hypotension ? = low blood pressure ? = haemorrhage ? = unconscious ?

  3. Shock = • Clinical syndrome • Associated with signs of hypoperfusion: mental status change, oliguria, acidosis, etc • May be associated with hypotension • Inadequate organ perfusion and tissue oxygenation to meet tissue oxygen demand

  4. Physiological response to shock • Normally the body can compensate for some decreased tissue perfusion through a variety of mechanisms • When compensation fails, shock develops and if uncorrected becomes irreversible

  5. Physiological response to shock • Sympathetic Nervous System – Adrenal response (neuro-humoral) • Systemic response • Progressive vasoconstriction • Increased blood flow to major organs • Increased cardiac output • Increased respiratory rate and volume • Decreased urine output (water retention) • Decreased gastric activity

  6. Pathophysiology • Initially, neurohumoral compensatory mechanisms maintain perfusion to vital organs • If appropriate treatment is not promptly instituted, these compensatory mechanisms are overwhelmed, producing ischemia, cellular damage, multiple organ failure and death

  7. Shock at the cellular level • Decreased blood flow to the tissues causes cellular hypoxia • Anaerobic metabolism begins • Cell swelling, mitochondrial disruption, and eventual cell death; tissues die; organs fail; organ systems fail • If Low Perfusion States persists  compensatory response fail Irreversible  Death imminent!!

  8. Venous Return Cardiac Output A V VR CO 4800 = 60 x 80 cc Perfusion VR equals CO CO = Heart Rate x Stroke Volume SV = f . EDV. C. TPR Normal Hemodynamic

  9. Reaksi kompensasi

  10. Pathophysiology • Imbalance between organ perfusion & oxygen demand • DO2 = Oxygen content x Cardiac output • Oxygen content depends on Hb & SaO2 • SaO2 depends on Airway & Breathing • Cardiac Output & Hb are parts of Circulation matters

  11. Volume (preload) SVR (afterload) Rate (f) CO Pump (contractility) CO = HR x SV Contractility Preload Afterload

  12. Common features of shock Mentation change Heart rate  Blood pressure  Pulse pressure  Arterial pH  Shock Respiratory rate  Urine output  - Neonate < 2 ml/kg/hour - Infant < 1,5 ml - Pre school age < 1 ml - Adult < 0,5 ml Peripheral perfusion - cold, pale , clammy

  13. Shock Categories • Hypovolemic : haemorrarghic, dehydration • Blood volume problem • Cardiogenic : AMI, severe dysrhytmia, pericardial tamponade • Blood pump and/or rate problem

  14. Shock Categories • Distributive: septic shock, anaphylaxis, neurogenic shock • Blood vessel problem • Obstructive: aortic stenosis, massive pulmonary embolus • Blood flow problem

  15. Rapid formulation of working Dx Defining features of shock • Heart rate  • Respiratory rate  • Mentation changes • Blood pressure  • Urine output  • Arterial pH 

  16. Rapid formulation of working Dx • Defining features in compensatory shock • Can be difficult to detect with subtle indicators • Tachycardia • Decreased skin perfusion • Alterations in mental status • Some condition such as medications, age, pregnancy can hide signs and symptoms

  17. Rapid formulation of working Dx Is cardiac output reduced?

  18. Rapid formulation of working Dx Is the heart too full?

  19. Rapid formulation of working Dx What does not fit? Overlapping etiologies (septic-cardiogenic, septic-hypovolemic, cardiogenic-hypovolemic) Other etiologies Get more information Echocardiography, CVP, Swan-ganz catheterization, etc

  20. ABC resusitasi Shock management • Recognize inadequate organ perfusion • Identify the cause (working diagnosis) • Hypovolemic • Cardiogenic • Distributive • Obstructive • Restore the organ perfusion and tissue oxygenation • Oxygen and ventilatory support • Fluid therapy • Inotrope or vasoactive drugs • Treat the cause

  21. Goals of Respiratory Management • To protect the airway • To correct inadequate oxygenation and ventilation • To rest the respiratory muscle • Caution in cervical trauma! A - B

  22. Goals Therapy of Shock • Reverse the pathophysiologic abnormalities • Avoid adverse consequences of excessive therapy • Titration: “too little vs too much” • Test  Response • Maintain body temperature! C-E

  23. Shock management Heart full Inotrope Vasoactive drugs Volume expansion

  24. Fluid challenge • Fluid deficit may exist in all kinds of shock • Is the heart too full? • No : • Crystalloid 1 – 2 L (20 ml/kg) fast • Not too full (cardiogenic shock without obvious fluid overload) • Crystalloid 250 ml in 20 minute • Yes : • No fluid challenge

  25. Fluid challenge • Assess patient response • Next therapeutic decision depend on patient response • Better : continue with fluid challenge • Transient : • Continue with fluid therapy • On going losses : find and fix • No response: • Severe hypovolemia • Other etiologies

  26. Fluid management in traumatic/haemorrargic shock Shock Fluid Loading 1000-2000 ml Warm fluid!! Good response Transient response No response Mild Blood loss Moderate loss On going losses Severe Blood loss Shock Non-hypovolemic Re-evaluate Maintenance Fluid/blood Fluid/blood Surgical consultation Surgical consultation Surgical resuscitation Get more information

  27. Re-assess Organ Perfusion Monitor • Vital signs • CNS state • Peripheral perfusion • Pulse oximetry • Urine output

  28. Vasoactive & Inotropic agents • Use after fluid resuscitation failed (normovolemia) • More efficacious if normovolemia • May obscure hypovolemia mmHg systolic 70 100 • epinephrine • norepinephrine • dopamin • nitroglycerin (ischemia) • nitropruside • dopamin (shock) • norepinephrine (+dopamin) • dobutamin (shock -)

  29. Vasoactive & Inotropic agents • After fluid resuscitation !! • Elevate MAP to 60-65 mmHg • Watch out: Excessive vasoconstriction  monitor lactate! • Ischemia • Contractility 

  30. Anaphylactic shock • Severe systemic hypersensitivity reaction • Characterized by: hypotension & airway compromise • Potentially life threatening • Classic tipe I hypersensitivity reaction (mediated by IgE) • Watch out: mild allergic reaction may progress to severe anaphylaxis

  31. Anaphylactic shock • Inadequate perfusion of tissues through maldistribution of blood flow • Intravascular volume is maldistributed because of alterations in blood vessels • Cardiac pump & blood volume are normal but blood is not reaching the tissues

  32. Anaphylactic shock • History & physical examination • Clinical signs of systemic allergic: urticaria, angioedema, abdominal pain, nausea & vomiting, bronchospasm, rhinorrhea, cutaneus flushing, etc • + Hypotension & airway compromise !! • Begin: within first hour - 8 hours after exposure • The faster onset, the more severe

  33. Anaphylactic shock Therapy: • ABC resuscitation first !!! • Drug: Epinephrine • adult: 0,3 - 0,5 mg SC or IM (1:1000) 0,1 mg IV (1:100.000) • children: 0,01mg/kg SC or IM (1:1000) only given after ABC resusitasion, no cardiac arrest, in severe hypotension may be repeated after 10 - 20 mnt.

  34. Anaphylactic shock Subsequent management • Give antihistamines ( chlorpheniramine 10-20 mg slowly IV ) • Give corticosteroids (200mg hydrocortisone IV ) • Bronchodilators ( salbutamol 250ugIV or 2.5-5mg by nebulizer, aminophylline 250mg up to 5mg/kg by slow IV) • Refer to ICU

  35. Shock Shock Hypoxic Cellular Priming Ischemic Cellular Damage Reperfusion Injury Inflammation Organ Failure Cellular Damage Death Multiple Organ Failure Death Old and New Paradigm of Shock

  36. Hemorrhage Trauma Hypoxia Prime insult Cellular ischemia Resuscitation Reperfusion injury Vasoconstriction Microcirculatory thrombosis Leukocyte/platelet/RBC aggregation Primary perpetuators Microcirculatory flow maldistribution Leukocyte-mediated cell injury Cytokine and other mediator effects, locally and systemically Secondary perpetuators Gut translocation Sepsis Tertiary perpetuators

  37. Haldane Hypoxia not only stops the machine It wrecks the machine! Time saving is life saving!

  38. Summary • Early recognition of shock state • Oxygenation and ventilation • Restore organ perfusion • Monitor patient response • Titrate therapy • Prompt and appropriate action

  39. Thank U 4 your attention!

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