Shock / Bleeding / Haemorrhage

Shock

Acute circulatory failure resulting in inadequate tissue perfusion

  1. Distributive shock
  2. Obstructive shock

 

[Response to reduced circulating volume]

 

Haemorrhage

  1. Primary - at time of injury
  2. Reactionary - within 24hs (due to build up of blood pressure)
  3. Secondary - Thrombus degradation by infective organisms

 

Hormonal regulation of fluid volume (important in SHOCK)

  • Reduced circulating volume results in reduction of blood pressure
  1. Detected by carotid sinus/aortic arch baroreceptors: Sympathetic response
    • Catecholamine response - vasoconstriction to maintain BP, increase FOC, increase cardiac output
    • Stimulation of B2 adrenoceptors in kidneys kicks off RAS response
  2. Decrease in renal blood flow / renal perfusion pressure: Renin-Angiotensin-Aldosterone response
    • B2 stimulation releases renin; converts angiogensinogen to angiotensin I
    • angiotensin I converted to angiotensin II by ACE (in the lungs, also degrades bradykinin)
    • Angiotensin II potent vasoconstrictor
    • Angiotensin II stimulates the release of aldosterone (from zona glomerulosa) which promotes Na/water resorption from DCT
  3. Stress hormone release - corticosteroids from adrenal cortex
    • Salt/water retention
  4. Increase in plasma osmolarity: ADH (produced in paraventricular and supraoptic nuclei) response
    • Osmoreceptors detect a rise in osmolarity (from loss of volume)
    • Stimulates the release of vasopressin (aka anti-diuretic hormone) - potent vasoconstrictor
    • ADH (via increase cAMP, aquaporin) stimulates resorption of water from DCT/CCD
  5. Reduced renal perfusion stimulates EPO production (long term)
  • Increase in fluid volume
  1. Distention of cardiac atria - leads to release of ANP: promotes diuresis
  2. Increase in brain naturetic peptide (BNP increased in "cardiac failure")

 

Type Pathology Features Managment
Anaphylactic      

Cardiogenic

...resulting from myocardial dysfunction

  • Cardiac index < 2.2l/min/m2 + PAOP > 16mmHg
  • Tissue hypoxia persists despite adequate volume replacement

 

Causes

  • AMI
  • Arrythmias
  • Stunning post bypass
  • Myocardial contusion
  1. Reduced cardiac index
    • Cool peripheries
    • Reduced CRT
    • Oliguria
    • Reduced consciousness
  2. Raised venous pressure
    • Pulmonary oedema
    • Raised JVP
    • Hepatomegaly from venous engorgement

Pathophysiology

  1. Right shift of Frank-Starling curve
  2. Progressive increase in oxygen demand
  3. Increased lactic acidosis

Investigations:

  • ECG: arrythmia, MI
  • CXR - Pulmonary oedema features: (1) Cardiomegaly (2) Kerley B lines above costophrenic angle (3) Interstitial shadowing of pulmonary oedema (4) Hilar "Bats wings" (5) upper lobe blood diversion
  • Echo - valvular lesions; estimation of ejection fraction, ventricular contractility
  • Pulmonary artery catherisation - elevated venous pressure, reduced cardiac index <2.2l/min/m2; PAOP >16mmHg, decreased venous sats
Hypovolaemic shock

Causes

  • Haemorraghic (may be occult)
  • Burns
  • Dehydration (inadequate intake, excess loss: DKA)

Severity of blood loss

  % Loss
Volume loss
Class I 0-15% <750mls
Class II 15-30% 750-1500mls
Class III 30-40% 1500-2000mls
Class IV >40% >2000mls
  1. Suspect occult loss
    • Fractures - pelvis (1-3l); femoral (1-2l); Tibial (0.5-1l)
    • Blunt chest/abdominal trauma
    • Obstetric haemorrhage: abruptio, placenta accreta, placenta previa
  2. Resuscitate
  3. Stop bleeding
Neurogenic (cf spinal shock) Loss of sympathetic outflow following spinal cord injury    
Septic Shock in the presence of sepsis

Hypoperfusion

Hypotension

Organ dysfunction