SHOCK
SHOCK
            Dr Iram Khurshid
               MBBS, FCPS
             (Histopathology)
        Assistant professor, CKMC
                                    1
SHOCK
                  SHOCK
  OUTLINE
  DEFINITION
  TYPES OF SHOCK
  CLINICAL FEATURES OF SHOCK
  HYPOVOLAEMIC SHOCK
  CARDIOGENIC SHOCK
  SEPTIC SHOCK
  ANAPHYLACTIC SHOCK
  MISCELLANEOUS
                               4
SHOCK
    DEFINITION
Shock is a state in
which diminished
cardiac output or
reduced effective
circulating blood
volume impairs tissue
perfusion and leads to
cellular hypoxia.        5
SHOCK
        Shock: Aetiology
  ❖ Reduction in
    blood volume
  ❖ Reduction in
   cardiac output
  ❖ Redistribution of
   blood
SHOCK
    TYPES OF SHOCK
   1) Cardiogenic
   2) Hypovolemic
   3) Septic
   4) Anaphylactic
   5) Miscellaneous
   •    Neurogenic
                      5
SHOCK
        7
    SHOCK
       CLINICAL FEATURES OF SHOCK
    In acute circulatory failure the
    patient typically
                             Restless, confused
    shows the following: Pale cold sweaty
                              Peripheral cyanosis
                              Rapid weak pulse
                              Low blood pressure
                              Drowsiness, coma
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SHOCK
        1. HYPOVOLEMIC SHOCK
• CAUSES:
 • Blood loss                              120
                                           100
 •   hemorrhage                            80
                                           60
 •
                                           40
     Body water loss.                      20
 •   Burns (>10% surface area                    Normal   10%      25%
                                                           BLOOD LOSS
                                                                         50%
 •   Vomiting/ Diarrhea/ Dehydration.
 • EFFECTS:
 • Loss 10%: No effect
 • Loss 25%: Hypovolemic symptoms 36 hrs
 • Loss 50%: Coma → death.
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SHOCK
             Hypovolemic Shock:
                   Mechanism
Haemorrhage or fluid loss        Inadequate blood volume
Decreased cardiac output        Hypotension       Impaired
tissue perfusion            Cellular hypoxia        Shock
SHOCK
    LOSS OF BLOOD VOLUME
 EARLY COMPENSATORY CHANGES                 120
 When blood is lost the body reacts         100
                                            80
 specifically to preserve blood supply to   60
                                            40
 the brain and heart.                       20
                                             0
                                                  Normal   10%      25%   50%
 The adrenal gland secretes                                 BLOOD LOSS
 catecholamines which increase peripheral
 resistance (raising the blood pressure).
 The kidneys secrete renin which retains
 sodium and thus water by the renin-
 angiotensin system
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SHOCK
        LOSS OF BLOOD VOLUME:
           MANAGEMENT                    120
                                         100
  These early compensatory            80
  changes suffice if <25%             60
                                      40
  blood volume lost.                  20
  If >25% blood volume lost then       0
  transfusion is required as there       Normal 10%      25%
                                                 BLOOD LOSS
                                                               50%
  is a risk of shock, dependent
  upon the age and health of the
  patient.
     Transfusion is ideally done with cross-matched
     whole blood.
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 SHOCK
    HYPOVOLEMIC SHOCK LATE
      EFFECTS
If blood volume is not restored, the     120
                                         100
following events take place, resulting    80
in a critically ill patient:              60
                                          40
                                          20
Widespread ischaemic damage occurs        0
                                               Normal   10%      25%        50%
                                                         BLOOD LOSS
Brain:  Neuronal necrosis
Kidney: Acute tubular necrosis
Heart:  Infarction/ coagulative
        necrosis
                                                                       15
SHOCK
          2. Septic Shock
• 25-50% mortality
• Common cause of death in ICU
• Caused by bacterial endotoxins or exotoxins in the
  blood.
• The toxins can be released, from bacteria in a focus
  of sepsis (abscess), septicaemia ( meningococcal)
  Infected burns.
• Instrumentation e.g. Urogenital
• Immunosuppression
    SHOCK
                SEPTIC SHOCK:
            ENDOTOXIC and EXOTOXIC
The diagram shows production of
exotoxins by bacteria which
remain intact (left).
 This contrasts with endotoxic
shock where the whole bacteria
break up and cell wall
lipopolysaccarides activate the
complement and coagulation cascades.
.
    17
 In practice, endotoxic and septic
       shock are often used
          synonymously
SHOCK
              SEPTIC SHOCK ETIOLOGY
ENDOTOXIC
GRAM NEGATIVE ENDOTOXINS
CELL WALL LIPOPOLYSACCARIDES
   E. coli, Proteus Klebsiella, Bacteroides,
   Pseudomonas (burns),Meningococci Most      commonly
EXOTOXIC                               triggered by gram+ve
GRAM POSITIVE EXOTOXINS                bacilli, followed by
Examples: Staph aureus skin
infection,streptococci, pneumococci,   gram –ve bacilli and
clostridium
 19          etc                       fungi.
SHOCK
Pathogenesis of Septic shock
 Substances from these
 microorganisms activate
 Macrophages , neutrophils,
 endothelial cells,
 complements which results
 in INFLAMMATORY &
 COUNTER INFLAMMATORY
 RESPONSE leading to Septic
 shock
20
 Inflammatory mediators are
 increased, which results in arterial
 vasodilation, vascular leakage, and
 venous blood pooling thereby
 causing Tissue hypoperfusion, cellular
 hypoxia, and metabolic derangements
 which finally leads to multi organ
 failure and death
SHOCK
  SEPTIC
  SHOCK:
  EXAMPLE
  The brain is
  covered in
  purulent
  exudate: this
  is
  meningococc
  al meningitis
 23
SHOCK
 3. CARDIOGENIC SHOCK: CAUSES
Myocardial infarction and its
complications, for example ruptured
papillary muscle, result in
ACUTE PUMP FAILURE
Mortality is high (at least 80%).
The effects are similar to
hypovolaemic shock, but of
course management is different as
there is no urgent requirement for
fluid.
SHOCK
        4.ANAPHYLACTIC SHOCK:
           ETIOLOGY
         ❑Drugs
         e.g.penicillin
         ❑Stings
         ❑Foods e.g. Shellfish,
         Peanuts
   Histamine release from blood
   basophils →
   Vasodilatation - blood
   pressure drops
SHOCK
ANAPHYLACTIC SHOCK:
MECHANISM
Antigen, for example wasp venom
accesses specific IgE on blood
basophils. IgE dimerises at the
cell surface and the basophil
releases histamine by
degranulation → vasodilatation
causes the blood pressure to
drop.
Clinical features of shock develop
rapidly.
                                     24
SHOCK
        ANAPHYLACTIC SHOCK: MECHANISM
SHOCK
  ANAPHYLACTIC
  SHOCK: TREATMENT
 Adrenaline(vasoconstrictor,
 bronchodilator) and
 hydrocortisone are given in
 the acute phase.
 The patient may recover
 without further specific
 treatment.
 If not, full support in an intensive
 care unit will be required.
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SHOCK
      5. MISCELLANEOUS CAUSES OF
      SHOCK
       Neurogenic:
      e.g. severe head or spinal cord injury.
      characterized by organ tissue hypoperfusion due to
      disruption of normal sympathetic control over
      vascular tone.
      This critical condition often arises from spinal cord
      injuries and frequently occurs in the cervical and upper
      thoracic spinal cord, especially those above the T6 level .
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SHOCK
SHOCK
        Stages of shock
        1.Non-progressive stage
        2.Progressive stage
        3.Irreversible stage
SHOCK
         Stages of shock
        1.Non-progressive stage:
                             By the action of
            There is          baroreceptors,
         compensation        catecholamines,      Tachycardia,
                           Renin-angiotensin-      peripheral
         and perfusion                          vasoconstriction
         of vital organs   aldosterone system
SHOCK
             Stages of shock
        2. Progressive stage:
          Characterized by tissue hypoperfusion
          and onset of worsening circulatory and
          metabolic imbalances.
        a. Tissue hypoxia
        b. Anaerobic glycolysis
        c. Lactic acidosis
        d. Arteriolar dilatation
SHOCK
           Stages of shock
    3.3.Irreversible stage: Severe
        cellular and tissue injury which is irreversible
        a.Tissue injury, necrosis,
        infarction
        b.Common organs affected:
          heart, kidney, brain, lungs, adrenal and
          GIT
SHOCK
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SHOCK
        What is the primary cause of
        septic shock?
           A.Bleeding
           B.Medication Allergy
           C.Infection
           D.Poison
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SHOCK
      A 20-year-old man is brought to the
      emergency room after rupturing his spleen
      in a motorcycle accident. His blood
      pressure on admission is 80/60 mm Hg.This
      patient is most likely suffering from which of
      the following conditions?
                (A)Acute pancreatitis
                (B)Cardiogenic shock
                (C)Hypersplenism
                (D)Hypovolemic shock
 38             (E)Septic shock
SHOCK
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