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    Shock

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    shibilahamza2001

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    Shock

    Uploaded by

    shibilahamza2001
    4 views35 pages

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    Copyright:

    © All Rights Reserved
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    Download as pptx, pdf, or txt
    4 views35 pages

    Shock

    Uploaded by

    shibilahamza2001

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 35

    SHOCK

    Shibila.V.P
    Final year MBBS
    Introduction
    Types and Causes
    Pathogenesis
    Stages of shock
    Clinical features
    Management
    What is shock ?
    “Shock is a state in which
    diminished cardiac output
    or reduced effective
    circulating blood volume
    impairs tissue perfusion and
    leads to cellular hypoxia.”
    • Acute circulatory failure
    • Life threatening clinical syndrome of cardiovascular
    collapse
    • Hypotension and Hypoperfusion
    • First reversible damage
    • Prolonged shock - irreversible cell injury and death.
    Cardiogenic primary pump failure
    shock
    Hypovolemic Low blood volume
    shock

    SHOCK
    Peripheral
    vasodilation

    Distributive
    Types
    shock
    Septic
    Anaphylactic
    Neurogenic

    Obstructive Obstruction to blood


    shock flow
    Type of Causes Principal Mechanism
    Shock
    Cardiogenic Myocardial infarction Decreased cardiac output due to
    Ventricular arrhythmias Failure of myocardial pump resulting
    shock Myocarditis from intrinsic myocardial damage,
    Aortic stenosis extrinsic compression, or obstruction
    Mitral regurgitation to flow.

    Hypovolemic Fluid loss Decreased cardiac output due to


    (Hemorrhage, vomiting, diarrhea, inadequate blood or plasma volume
    shock burns etc. )

    Distributive Overwhelming microbial infections, Widespread vasodilation leading to


    Trauma, Pancreatitis, IgE mediated reduced systemic vascular
    shock hypersensitivity reactions, Anesthetic resistance and hypotension
    accidents, brain or a spinal injury,
    Obstructive shock
     Due to extracardiac obstruction to blood flow
     Heart pumps well, but due to obstruction cardiac output is
    reduced.
     Cardiac tamponade, pulmonary embolism, pericardial
    effusion, tension pneumothorax
    PATHOPHYSIOLOGY
     Inadequate perfusion.
     Compensatory mechanism, Catecholamines.
     Effective only in early stages.
     Tissue hypoxia
     Anaerobic metabolism, Lactic acid accumulation
     Cell membrane dysfunction
    PATHOPHYSIOLOGY
     Release of toxic substances and proteolytic enzymes
     Toxic substances enter circulation
     Endothelial damage
     Activation of inflammatory and coagulation cascade
     Vasodilator substance, Hypotension
     SIRS, MODS, Death
    PATHOGENESIS OF
    DIFFERENT TYPES
    OF SHOCK
    STAGES OF SHOCK Initial
    Deterioration of circulation is a
    progressive and continuous phenomenon,
    compensatory mechanism will eventually Compensatory
    become less effective.

     Initial stage ( insult )


    Progressive
     Compensatory shock ( Preshock )
     Progressive stage ( Shock )
     Refractory stage ( End-organ Refractory
    Dysfunction)
    Hypovolemic shock
     Most common form of shock
     MC cause of death following fractures of major bones.
     Pelvis and Femur
     Hemorrhagic or non-hemorrhagic
     External or internal hemorrhage
     Pelvis – 1500-2000 mL
     Femur – 1000-1500 mL
    CLINICAL FEATURES OF SHOCK
     Fast and feeble peripheral pulse
     Hand and feet- pale, cool, and clammy.
     Decreased urine output
     Lethargy, confusion, restlessness and somnolence common
     Tachypnoea, Tachycardia
     Cyanosis may be present
     Low BP
    CLINICAL FEATURES OF SHOCK
     Septic shock- Skin may be warm, or fever may be
    present
     Cardiogenic shock- May have chest pain, Dyspnoea
     Anaphylactic shock- May have angioedema, urticaria,
    Wheezing
    Effects of SHOCK
     Heart – Decreased CO, Tachycardia, Hypotension
     Respiratory – Interstitial oedema, Decreased gas exchange,
    ARDS and Pulmonary oedema.
     Renal – Decreased GFR, tubular reabsorption of salt and water
    increases for compensatory response. But in severe case
    Tubular necrosis
     Hepatic – Raised liver enzymes, Failure to metabolize waste
    products, Jaundice
     CNS – Hypoperfusion leads to drowsiness. ( Brain is the last
    organ to get under perfused )
     Endocrine – ADH , Increased reabsorption of water.
     Metabolic – Lactic acidosis
     Cellular changes – Due to release of lysosomal enzymes which
    alters the cell membrane permeability, sickle cell syndrome
     Blood – Alteration in cellular components, Coagulation
    abnormalities ( DIC )
     GIT – Mucosal ischemia, Bleeding from GIT, Malena and
    hematemesis.
    MANAGEMENT

    Goals of management
     Treat reversible causes
     Improve cardiac function
     Improve tissue perfusion
    Laboratory investigations
    • Lactic acid
    • Complete blood count and differential
    • Renal function test
    • Liver function test
    • Urine analysis and urine sediment
    • Arterial blood gas
    • ECG, Echocardiography
    • PT, PTT
    MONITORING FOR PATIENTS IN SHOCK
    MINIMUM
     ECG
     Pulse oximetry
     Blood pressure
     Urine output
    ADDITIONAL MODALITIES
     Central venous pressure
     Invasive blood pressure
     Cardiac output
     Basic deficit and serum lactate
    General principles of management
     Preferably treated in ICU
     ECG monitoring
     Pulse oximetry
     Successful resuscitation-Reduction in serum lactate
    level.
    Resuscitation
    • Shouldn’t be delayed
    • If there is initial doubt – assume the cause is
    hypovolemia and start fluid resuscitation
    • IV fluid should be given through short, wide bore
    catheters
    • If blood is lost – ideal replacement is blood,
    crystalloid therapy required while awaiting for
    blood products
    INITIAL ASSSESMENT – ABC
    A – Airway
    GCS less than 8 – intubate
    Secure airway, if unable to maintain give oxygen
    Airway compromised in anaphylaxis
    B- Breathing
    If patient is conversing A and B are fine
    May need mechanical ventilation
    C- Circulation
    Restore perfusion.
    IV Fluids – continuous monitor
    • 2 large bore peripheral IV access – 18/16
    • Begin resuscitation with rapid infusion of 500mL-
    1L RL or isotonic NS
    • Continue resuscitation with IV fluids, blood
    products, or both
    • Hemorrhagic shock – After initial liter of IV fluid,
    PCV, Fresh frozen plasma, and platelets to
    replace lost blood
    • Type specific blood, in emergency O-ve packed
    cells can be given
    Fluid therapy
     Crystalloid solutions – Increase intravascular volume
    -Ringer lactate solution
    -Normal saline
    -Hartmann’s solution
     Colloid solutions – Pull fluid into the vascular spaces
    through osmosis
     Blood transfusions
     Cardiogenic – Inotropes, vasodilators, intra-aortic balloon pump.

     Obstructive jaundice – Urgent relief of obstruction

    Tension pneumothorax – needle thoracostomy

    Cardiac tamponade – pericardiocentesis

    Massive pulmonary embolism is difficult to treat.


     Neurogenic shock– High dose steroids, to decrease
    inflammation ,treat the symptoms
     Anaphylactic shock - Airway management
    epi 0.5-1mg IM or 50-100 microg IV
     Septic shock – Fluid administration
    Monitor VS
    Broad spectrum antibiotics
    Vasopressors
    Vasopressor and Inotropic support
     Vasopressor agents indicated in distributive shock
     phenylephrine, Dopamine, Noradrenaline
     Resistant to catecholamines, vasopressin can be
    used.
     Cardiogenic shock, inotropic therapy is required
    increase cardiac output
     DOC is Dobutamine
    End point resuscitation
    Heart rate < 100 / min
    Blood pressure of 90/60 mmHg
    Oxygen saturation of 93-95%

     As perfusion improves, aim is to normalize homeostasis


     Final end point of resuscitation – normal base deficit
    ( eliminate metabolic acidosis)
     Achieved within 12-24 hours of admission
     Hypovolemic shock -

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