Shock

Shock

Types
1. Cardiogenic
  1. Failure of the heart to pump properly
    1. Causes:
      1. Death of Cardiac muscle
        Ex. Disease of blood vessels
        Thrombosis
      2. Arrhythmia
      3. Obstruction of blood flow leaving heart
        Ex. PTE (Pulmonary thromboembolism)
      4. Primary Cardiac Disease
        Ex. DCM, HCM
        DCM: Dogs
        HCM: Cats
        Cardiomegaly
        Tricuspid valve dysplasia
        Myocardial fibrosis
    2. Decrease in SV & CO
2. Hypovolemic
  1. Shock due to reduced circulating blood volume
    1. Causes:
      1. Blood Loss
        Haemorrhage
        Blood volume = 7% of BW
        Ex. 5kg Cat: 5 *.07 = 0.35L = 350mL blood
      2. Fluid loss
        Vomiting, Diarrhea, Burns
    2. Hypotension & Hypoperfusion
    3. Recovery possible under certain circumstances
      1. If caught early => Fluid Therapy
      2. Can lose 10% of fluid volume
3. Blood Maldistribution
  1. Blood pools in peripheral tissues due to a decrease in peripheral resistance in blood vessels
    1. Blood volume is unchanged, but the VASCULAR SPACE increases so that effective circulating blood volume decreases
    2. Types:
      1. Neurogenic Shock
        Damage to CNS (usually spinal cord)
        Loss of autonomic signals to smooth muscle in blood vessel walls
        Vasodilation
        Blood pooling in veins
        Need resistance to keep blood flowing
      2. Anaphylactic Shock
        Food
        Pollen
        Bee stings
        Mast cell degranulation
        Histamine
        Leaky dilated blood vessels
        Drop in BP & Reduced perfusion
        Hypovolemia & Hypoperfusion
        Oedema
      3. Septic Shock
        Most common form of maldistributive shock
        Mediated by vascular & inflammatory mediators in response to bacterial & fungal infection
        Trigger: Gram -ve Bacteria => LPS (Endotoxin)
        Binds TLR4 & CD14 (Monocyte derived cells: Dendritic cells & Macrophages)
        Cytokine release: IL-1 & IL -6
        Factor XII
        Coagulation
        Thrombosis +
        Low Dose:
        Activation of Macrophages, Endothelial cells & Complement
        Medium Dose:
        Raised TNF & IL-1 => Pyrexia
        High Dose:
        Vasodilation, Hypotension, Reduced myocardial contractility (Reduced CO) & Hypoperfusion
        BV injury (release of too many cytokines)
        => DIC
  2. Pooling, stagnation, Hypoxia
Stages
1. 1) Compensated
  1. Increase in CO & Vasoconstriction to maintain BP & tissue oxygenation
    1. Tachycardia
    2. Via Stimulation of SNS
      1. Adrenaline
  2. Control of H2O balance
    1. GRF drops => Increase H2O absorption
      1. RAAS
        ADH
2. 2) Progressive
  1. Compensatory Mechanisms cannot cope with prolonged or severe drop in blood volume
    1. Hypoperfusion & Cell injury
      1. Low O2 => Cell metabolism shifts to Anaerobic respiration
        Lactic Acid production & reduced ATP
        Cell membrane damage, Lysosomal enzyme release
        => Tissue Necrosis
        ATP needed to maintain cellular membranes
3. 3) Irreversible
  1. Mechanisms aimed at Vasoconstriction are overwhemled
    1. Widespread Vasodilation & Organ failure
Clincal Features
1. Hypotension
2. Weak pulse & Tachycardia
3. Hyperventilation
4. Decreased urine production
5. Peripheral vasoconstriction (During compensation)
6. Lesions
  1. Congestion & pooling of blood
  2. Oedema & Haemorrhage
    1. Petechial
    2. Ecchymotic
  3. Thromobosis (Microscopic)
    1. Coagulation cascade
  4. Cellular Necrosis (Microscopic)
    1. Ex. Myocardial cells, Neurons, Hepatocytes, Renal Tubules

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Cardiomegaly (image/png)

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