Bleeding Physiology Flashcards
What volumes of blood loss define each class of Haemorrhagic shock
Class I - <750ml
Class II - 750-1500ml
Class III - 1500-2000ml
Class IV - >2000ml
Pulse rate and BP in each class of Haemorrhagic shock
Class I - <100, normal
Class II - 100-120, normal
Class III - 120-140, decr
Class IV - >140, decr
How does pulse pressure change in different classes of Haemorrhagic shock
Class I - normal/incr
Class II - decr
Class III - decr
Class IV - decr
Resp rate and urine output in different classes of Haemorrhagic shock
Class I - 14-20, >30ml/hr
Class II - 20-30, 20-30ml/hr
Class III - 30-40, 5-15ml/hr
Class IV - >35, negligible
What type of processes govern the response to bleeding
Inflammatory
What is the vascular response to trauma
Incr capillary permeability -> WBCs move to interstitium -> fluid moves from EVS to IVS -> incr central venous volume to maintain normal CO
What potential harmful effect can occur when crystalloid fluids are given in trauma
Oedema
How can crystalloid fluids lead to oedema when given in trauma
Fluid forced from IVS to EVS -> oedema -> multi organ failure
Impacts of vagal tone in trauma
Can be activated by neural pathways (eg eyes)
Involved in inflammatory oathways and inflammatory mediators release
Innervates spleen
Release of TNF in trauma
Affects CVS function
Clotting factors in the intrinsic, extrinsic, and common pathways
I - XII, XI, IX, VIII
E - VII, III
C - X, V, II, I, XIII
Which process in the clotting cascade involves tissue factor
Extrinsic (actives factor X with factor VIIa)
What factors inhibit the clotting cascade
TFPI
Antithrombin
Protein C
Thronbomodulin
Protein S (activates protein C + thrombomodulin to active Protein C)
How does trauma impact the fibrinolysis system
Overactivates system
Factors leading to trauma induced coagulopathy (TIC)
Fibrinolysis
Inflammation
ATC - acute traumatic coagulopathy
Hypothermia
Acidaemia
Haemorrhage -> loss, dilution
Why may hypercoagulability and hyperfibrinolytic blood be beneficial in trauma
Prevents clotting due to Hypovolaemic, low flow state
CVS response to bleeding
Initial tachycardia then bradycardia
Hypotension
Confounders in the CV response to bleeding
Age
Medications
3 main reflexes to haemorrhage
Arterial baroreceptor reflex
Cardiac vagal C fibre reflex
Arterial chemoreceptor reflex
Arterial baroreceptor reflex
Haemorrhage -> stretch receptors in wall of aortic arch and carotid sinus detect less stretch -> decr vagal tone and incr sympathetic activity -> sympathetic peripheral vasoconstriction
Where are the arterial baroreceptors
Aortic arch
Carotid sins
Effect of activating arterial baroreceptor reflex during haemorrhage
Sympathies peripheral vasoconstriction
Cardiac vagal C fibres reflex in haemorrhage
Cardiac vagal C fibres in left ventricle myocardium activated by circulating components and reduced preload -> decr SVR -> vagal bradycardia and hypotension
Where are cardiac vagal C fibres
Left ventricle myocardium
Effect of cardiac vagal C fibre activation in haemorrhage
Vagal bradycardia
Hypotension
Arterial chemoreceptor reflex
Incr CO2 or decr O2 -> chemoreceptors in carotids and aortic bodies activated -> incr resp rate
Arterial chemoreceptor reflex in haemorrhage
Decr bloodflow mimics incr CO2/decr O2 -> chemoreceptors activated -> incr resp rate
How can the arterial chemoreceptor reflex effect cardiac C fibres
Arterial chemoreceptors activated -> incr resp rate -> cardiac C fibres inhibited
How does sBP, HR, RR, and GCS change during bleeding
sBP - maintained then rapid drop
HR - tachy then Brady
RR - tachy
GCS - reduced
How does sBP, HR, RR, and GCS change with increasing injury level
sBP - hypertensive
HR - tachy
RR - tachy
GCS - reduced
3 components of lethal triad
Coagulopathy
Acidosis
Hypothermia
Conditions that mimic Haemorrhage
Head injury
Eviscerated abdomen
Periosteum
Obstructive shock
What causes BP RR HR and GCS changes in head injury that mimic haemorrhage
Massive catecholamine release
What nerve causes a decr in HR and BP in eviscerated abdomen and periosteum
Vagal nerve
Damage control resuscitation
Maintain haemostatic competence in a pt that is actively bleeding
Aims of DCR
Early haemorrhage control
Permissive hypotension
Limit fluid infusions
Finessed targeting if Coagulopathy
Why should fluid infusions be limited in haemorrhage
Avoid diluting coagulation factors
Code red criteria
sBP <90
Poor response to initial fluid resuscitation
Suspected active haemorrhage
TXA dose in massive haemorrhage
1g IV TXA bolus over 10 mins then 1g IV infusion over 8hrs
What is done after bleeding is controlled in a code red
Repeat FBC and clotting screen
Give platelets if count <100
Give cryoprecipitate if fibrinogen <1.5g/L
Give FFP to keep PT/APTT >1.2x normal
Keep temp >36
Keep CA2+ >1.0
Aims of damage control surgery
Haemorrhage control
Manage sepsis
Protect from further injury
Maintain haemostasis
Protect cells and organs
Preserve endothelium
AIM of ICU after haemorrhage
Restore physiology
