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  • Good work mate. Just a suggestion
    Types of shock can perhaps be better classified as
    hypovolaemic
    cardiogenic
    distributive (septic,anaphylactic & neurogenic)
    restrictive &
    obstructive.
    These will encompass everything
    Eg of restrictive shock is tamponade/tension pneumo/haemothorax etc and obstructive shock is pulmonary embolism for eg
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  • 1. Shock
    Dr. Tanuj Paul Bhatia
  • 2. Definition
    Inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function.
  • 3. DISTRIBUTION OF BODY FLUIDS
  • 4.
  • 5.
  • 6. TYPES OF SHOCK
    Hypovolemic shock
    Septic shock
    Cardiogenic shock
    Neurogenic shock
    Anaphylactic shock
  • 7. Hypovolaemic shock
    Most common form seen clinically.
    Results from depletion of circulating blood volume.
    This may result from
    Hemorrhage
    Plasma loss eg. Burns
    Loss of ECF eg.
    Intestinal fistulas,
    Vomiting
    Diarrhoea
  • 8. Pathophysiology
  • 9. Autoregulation
  • 10. Other mechanisms
    Renin from JGA,
    Angiotensin ,
    Aldosterone from adrenal cortex,
    Anti-diuretic hormone from pituitary
  • 11.
    • Despite these adjustments cells become starved.
    Anerobic metabolism and lactic acidosis.
    Sustained hypoxia.
    “Sick cell syndrome”
  • 12. Clinical picture
  • 13. Mild hypovolaemia
    Deficit <20% of blood volume.
    Cool, damp extremities.
    Patient is thirsty.
    Maybe chilly.
    UOP and BP are normal in supine position but BP may fall on standing.
  • 14. Moderate hypovolemia
    Deficit of 20%-40% of blood volume.
    Cold extremities.
    Thirst.
    Chills.
    Moderate tachycardia.
    Decreased urine output.
    BP falls in standing position but may be normal in supine position.
  • 15. Severe hypovolaemia
    Deficit >40% of blood volume.
    All above signs.
    Decreased urinary output.
    Rapid, thready pulse.
    Low BP.
    Restlessness and agitation due to decreased cerebral perfusion.
  • 16. Parameters α competence of circulation
    Level of cerebral activity.
    Hourly urine output (normal = 30-50ml/hr in adults).
    Central venous pressure.
    Normal range of CVP is 3-5 cm of H2O above the manubriosternal angle.
  • 17. Investigations
    Baseline investigations.
    ABG = arterial blood gases (pH,pO2,pCO2)
    ECG monitoring.
    Serum electrolytes.
  • 18. Management
    Aim – to increase cardiac output and tissue perfusion.
    Plan :
    1. Tackle the primary problem eg. Hemorrhage.
    2. Adequate fluid replacement.
    3. Improving cardiac function with inotropic drugs.
    4. Correcting acid base disturbance and electrolyte abnormalities.
  • 19. Outline of treatment
    Resuscitation = A + B
    Fluid replacement
    • Crystalloid solution used for initial resuscitation.
    • 20. Glucose should not be used as it may cause diuresis and further depletion of circulating volume.
    • 21. 2 litres of crystalloid are given as fast as possible in sever shock.
    • 22. Severity of shock determines the rate of fluid.
    • 23. CVP acts as a guideline.
    3. Positioning: elevation of both legs.
  • 24. Classification of hypovolemicShock
    Class EBLTreatment
    I <15% (<750ml) Fluids
    II 15-30% (750-1.5L) Fluids
    III 30-40% (1.5L-2.0L) Fluids + Blood
    IV >40% (>2.0L) Fluids + Blood
  • 25. Vasopressor drugs
    Use of vasopressor drugs not recommended in routine.
    They raise blood pressure by increasing peripheral vascular resistance  decreasing tissue perfusion.
    Inotropic drugs like Dopamine and Dobutamine may need to be used to improve cardiac action.
  • 26. Indicators of successful resuscitation
    Warm skin.
    Well perfused skin.
    Urine output 30-60 ml/hr.
    Alert sensorium.
  • 27. Venous access
    Peripheral line
    Central line
  • Parenteral fluid therapy
    Crystalloids
    Isotonic
    Hypertonic
    Hypotonic
    Colloids
    Albumin preperations
    Dextran
    Hydroxyethyl starch
  • 30. Crystalloids
    Crystalloids are solutions that contain sodium as the major osmotically active particle.
    Relatively inexpensive
    Readily available
    Useful for :
    - volume expansion
    - maintenance infusion
    - correction of electrolyte disorders
  • 31. Isotonic crystalloids
    E.g.. Lactated ringer’s solution(RL), 0.9% NaCl(normal saline)
    Distribute uniformly throughout the ECF.
    RL mimics ECF and is considered a BALANCED SALT SOLUTION.
    RL preferred for replacing GI losses and extracellular fluid volume losses.
    Normal Saline preferred in the presence of hyperkalemia, hypercalcemia, hyponatremia, hypochloremia, or metabolic alkalosis.
  • 32. Other crystalloids
    Hypertonic saline solutions(e.g. 10%NaCl) : can be used for resuscitation in combination with colloids.
    BUT, there is more danger of complications like hypernatremia, hyperchloremia, hypokalemia with rapid infusion.
    Hypotonic saline solutions (e.g. 0.45%NaCL):
    expand the intravascular compartment by as little as 10% of the volume infused.
    Not used for resuscitation for the same reason.
  • 33. Colloid solutions
    Contain high–molecular-weight substances that remain in the intravascular space.
    Lessens the total amount of fluid needed for resuscitation.
    Substantially more expensive than crystalloids .
    Indicated when crystalloids fail to sustain plasma volume because of low colloid osmotic pressure. E.g. Burns.
    E.g. Dextran, Albumin preperations, Hydroxyethyl starch.
  • 34. Maintenance fluids
    100 mL/kg per day for the first 10 kg.
    50 mL/kg per day for the second 10 kg.
    20 mL/kg per day for each subsequent 10 kg.
  • 35. THANK YOU
  • 36. Glasgow coma score
  • 37. SEPTIC SHOCK
  • 38. Septic shock
    Results either by gram +ve or gram –ve bacterial infection.
    Gram –ve sepsis is more dangerous, common scources of gram –ve organisms are:
    • Genitourinary tract
    • 39. Respiratory tract
    • 40. Intestines.
    • 41. Commonly involved gram –ve organisms are E. coli, Proteus, Klebsiella, P. aeruginosa.
  • Why is gram negative sepsis becoming more important?
    There is indiscriminate use of potent antibiotics now a days.
    Leads to development of virulent RESISTANT ORGANISMS.
    Hospitals are major reservoir of such infection.
    This can easily transmit from one patient to another.
  • 42. Pathophysiology of septic shock
    ‘ENDOTOXINS’
    Bacterial lipopolysaccharides.
    Part of bacterial cell wall.
    Released mainly when bacteria die.
  • 43. These lead to :-
    Activation of complement, fibrinolytic, kinin systems,
    Activation of platelets and neutrophils.
    Endovascular injury at microvascular level.
    Sudden release of vasoactive substances from injured endo. cells .
    Macrophage stimulation and release of mediators ( IL-6,TNF,Arachidonic acid metabolites)
    All these further lead to more endovascular damage.
  • 44.
  • 45. Risk factors for septic shock
    Liver failure,
    Immune deficiency,
    Diabetes,
    Malnutrition,
    Long term steroid administration,
    Cytotoxic drugs,
    Massive bacterial load. E.g. intestinal perforation.
  • 46. MOFS/MODS
    Multi organ failure/dysfunction syndrome.
    Mediators from neutrophils act in a non specific fashion, when activated systemically, can produce injury to normal micro-circulation.
    Features :
    Stress ulceration,
    Biochemical signs of liver failure,
    Lethargy,
    May progress to coma and later death.
  • 47. Clinical presentation of septic shock
    EARLY RECOGNITION IS VERY IMPORTANT
    Chills,
    Elevated temperature above 101 F,
    Hyperventilation,
    Oliguria,
    Altered sensorium,
    White blood cell count is raised.
  • 48. Management
    Shift to ICU,
    CVP monitoring,
    Urinary output monitoring,
    IV fluid infusion : RL@20ml/kg bolus..... further Mx according to CVP.
    Thorough search of the source of infection.
    Drain the infective process as soon and when possible.
  • 49. Pulmonary therapy
    Sepsis endothelial damage to pulmonary capillaries.
    Pronounced alveolar injury, interstitial oedema and hemorrhage.
    Treatment is by maintaining controlled airway and an assisted ventilation.
    Not needed if sepsis is controlled early.
  • 50. CARDIOGENIC SHOCK
  • 51. Etiology
    Massive myocardial infarction
    Severe valvular heart disease
    Arrhythmias
    Pulmonary embolism – right side of heart comes under sudden strain.
  • 52. Pathogenesis
  • 53. Diagnosis
    Previous history of cardiovascular disease,
    Distended neck veins,
    Low BP,
    Peripheral edema,
    Enlarged and tender liver,
    Rales on lung auscultation,
    ECG signs of ischaemia,
    Enlarged heart on X Ray.
  • 54. Treatment
    Opioids to relieve pain and provide sedation.
    Diuretics, decrease afterload ,alleviate peripheral and pulmonary edema.
    Inotropic drugs improve cardiac contractility. E.g. dopamine in low doses.
    Sometimes, Mechanical support to heart with an intra aortic balloon.
  • 55. NEUROGENIC SHOCK
  • 56. Neurogenic shock
  • 57. Pathogenesis
  • 58. Vasovagal or psychogenic shock
  • 59.
  • 60. Treatment of neurogenic shock
    Volume expansion with crystalloids,
    Vasoconstrictors are useful.
    Goal is to increase BP to sustain coronary perfusion.
    Trendelenburg’s position can be temporarily useful.
    Short term steroids may also be useful.
  • 61. Anaphylactic shock
    Known to follow penicillin injection or administration of serum.
  • 62. Treatment of anaphylactic shock
    Aqueous epinephrine 0.5-1 ml of 1:1000 solution given i.v.
    Repeat dose may be given in 5-10 minutes.
    Steroids.
    O2 administration.
    Volume expandors and pressor agents.
  • 63. THANK YOU