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'Shock' in Dogs & Cats (Diagnosis (Perfusion parameters (HR…

- - - - Hypovolaemic shock
        
        Absolute (external blood loss) or relative (third space bleeding).
        
        Decrease circulating volume causes decreased venous return to the heart, which in turn decreases stroke volume. Decreased CO and blood delivery to tissues results.
        
        Blood loss most common cause (trauma, coagulopathy, ruptured neoplasm). Also caused by GIT/urinary losses and burns.
      - Obstructive shock
        
        Obstruction of blood flow to or from the heart. Examples include GDV (CVC obstruction), pneumothorax, pericardial tamponade, constrictive pericarditis, pulmonary thromboembolism (PTE).
      - Cardiogenic shock
        
        Primary cardiac dysfunction (DCM, HCM, valvular disease, severe dysrhythmia) leads to forward heart failure. May be due to LHS heart disease [pulmonary oedema, tachypnoea, cyanosis, pleural effusion (cats)] or RHS heart disease [ascites, jugular distension/pulses, pleural effusion (dogs)].
      - Distributive shock
        
        Intravascular fluid is distributed across the body in an abnormal way. This may be due to generalised vasodilation, increased vessel permeability, decreased cardiac contractility due to cytokines (sepsis)/platelet activating factor (anaphylaxis), or DIC (occlusion of microvessels causing decreased venous return). Occurs in animals with SIRS (sepsis, severe pancreatitis, major tissue trauma, neoplasia, burns) or anaphylaxis.
  - - - Increased CO & SVR
        
        Catecholamines (baroreceptor reflex/chemoreceptors cause sympaticotonus & Ad/NAd release - chronotropy, inotropy, peripheral vasoconstriction and central vasodilation).
    - - Aldosterone causes sodium retention and increased intravascular volume. ADH also binds to principal cells, allowing water reabsorption from the collecting duct.
    - - RAAS (baroreceptors of JGA decrease impulse firing and renin is released. Angiotensin 1 converted to angiotensin 2, which is a potent vasoconstrictor and also stimulates aldosterone release.
- - - - Further reduced rectal temp, worsening tachycardia (dogs 150-170) or bradycardia (cats <100bpm), MM pallor with normal CRT, weak femoral pulses + dorsal pedal pulses only just palpable, further decreased mentation (becoming obtunded).
    - - Worsening tachycardia (dogs 170-220bpm) or bradycardia (cats), MM extremely pale/white with prolonged CRT, femoral pulse very weak or 'thready' with a dorsal pedal that is no longer palpable. extremely obtunded with cold extremities.
  - - - Dogs in Addisonian crisis (vomiting, diarrhoea, lethargy, weakness, anorexia, PU/PD) will have weak pulses, bradycardia (hyperkalaemia) and poor CRT. The HR may actually be in the normal range despite other findings of hypovolaemia - it is an inappropriate bradycardia due to hyperkalaemia!
      - MMs will remain pale despite appropriate fluid therapy of the severely anaemic patient.
      - Mentation will remain depressed with TBI despite appropriate fluid therapy.
- - - - Perfusion parameters
      - Urine output
      - Blood gases
      - Lactate
      - Base deficit
- - - - Anaemic and hypoproteinaemic (and coagulopathic) patients. Use within 8hrs if collected fresh.
    - - Anaemic.
    - - Coagulopathies or acute hypoproteinaemia (long-term stored plasma used for hypoproteinaemia as platelets inactivated).
  - - - DEA 1.1 -ve dogs should only receive DEA 1.1 _ve blood
      - DEA 1.1 +ve dogs can receive DEA 1.1 +ve or -ve blood
    - - Blood types A, B and AB
      - B highly immunogenic (high anti-A Ab titre), so never give B cat A blood.
      - AB cats (<5%) should receive only A or AB blood