Question 2

College Answer

To adequately answer this question, candidates must be able to demonstrate that they recognised this to be a major haemorrhage. When a weight and a volume are supplied it is expected the percentage blood loss would be calculated and the shock graded or the haemorrhage at least described as severe. Often the consequences were omitted. Consequences were best described in organ systems e.g. CV, renal, metabolic. Many candidates failed to mention the patient would be hypotensive and tachycardic. A good answer should include mention, and provide explanations, of the mechanisms for the following compensatory responses:
· Activation of both baroreceptors and chemoreceptors and their consequences
· The sympathetic nervous system response
· Fluid shifts
· Renal effects - most candidates mentioned the urine output would be decreased but
did not provide a mechanism for this
Endocrine effects, eg secretion and actions of ADH, ACTH/Cortisol

Reference: Textbook of Medical Physiology, Guyton and Hall, Foundations of Anaesthesia:
Basic Clinical Science, Hemmings and Hopkins

Discussion

• Staging of blood loss is in terms of % of circulating volume lost:
  • Four classes (ATLS): <15% of volume, 15–30%, 30–40% and > 40%
  • Loss of 1000ml of blood (20% of the total circulating volume) in a 70kg subject  represents most of the stressed volume.
  • Loss of 2000ml of blood = 40% of the circulating volume = severe haemorrhagic shock
• Hypovolemia and cardiovascular compensation
  • Baroreflex activation and chemoreceptor activation.
  • Decreased vagal stimulus; thus increased heart rate
  • Sympathetic activation, which has multiple effects:
    • Increased peripheral vascular resistanc
    • Redistribution of blood flow away from the cutaneous and splanchnic circulation
    • Stimulation of systemic catecholamine release from adrenal glands, which produces an increased systemic effect in addition to the peripheral sympathetic nervous system effecs
    • Stimulation of vasopressin release via the projections from the nucleus of the solitary tract to the hypothalamus
    • Stimulation of renin release by sympathetic stimulation of the juxtaglomerular cells, and due to lower renal perfusion
• Transcapillary fluid redistribution and isovolaemic anaemia
  • ​​​​​​​Vasoconstriction of arterioles results in reduced capillary hydrostatic pressure
  • This results in a change in the Starling relationship in the microcirculation
  • The result is a movement of free water out of the interstitial space and into the intravascular space
  • This dilutes the blood volume and decreases the haematocrit, decreasing the haemoglobin concentration of the blood, but restoring some of the circulating volume
• Renal fluid/electrolyte conservation and haemopoiesis
  • ​​​​​​​​​​​​​​Renin secretion causes:
    • Vasoconstriction (by angiotensin)
    • Increased sodium retention (by aldosterone)
  • Vasopressin release causes:
    • Vasoconstriction (by V1 receptors)
    • Increased water retention (by V2 receptors)
  • Venous hypotension decreases atrial natriuretic peptide secretion,
    which causes:
    • Decreased renal blood flow
    • Decreased urinary water and sodium excretion
  • The net effect is decreased urine output and increased retention of sodium and water
  • Erythropoiesis  is stimulated by EPO release from the kidney, stimulated by decreased oxygen delivery 

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