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IBSc PHEM Applied Science > Bleeding Physiology > Flashcards

Bleeding Physiology Flashcards

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1
Q

What volumes of blood loss define each class of Haemorrhagic shock

A

Class I - <750ml
Class II - 750-1500ml
Class III - 1500-2000ml
Class IV - >2000ml

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2
Q

Pulse rate and BP in each class of Haemorrhagic shock

A

Class I - <100, normal
Class II - 100-120, normal
Class III - 120-140, decr
Class IV - >140, decr

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3
Q

How does pulse pressure change in different classes of Haemorrhagic shock

A

Class I - normal/incr
Class II - decr
Class III - decr
Class IV - decr

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4
Q

Resp rate and urine output in different classes of Haemorrhagic shock

A

Class I - 14-20, >30ml/hr
Class II - 20-30, 20-30ml/hr
Class III - 30-40, 5-15ml/hr
Class IV - >35, negligible

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5
Q

What type of processes govern the response to bleeding

A

Inflammatory

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6
Q

What is the vascular response to trauma

A

Incr capillary permeability -> WBCs move to interstitium -> fluid moves from EVS to IVS -> incr central venous volume to maintain normal CO

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7
Q

What potential harmful effect can occur when crystalloid fluids are given in trauma

A

Oedema

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8
Q

How can crystalloid fluids lead to oedema when given in trauma

A

Fluid forced from IVS to EVS -> oedema -> multi organ failure

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9
Q

Impacts of vagal tone in trauma

A

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

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10
Q

Clotting factors in the intrinsic, extrinsic, and common pathways

A

I - XII, XI, IX, X
E - VII
C - X P, II, I, XIII

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11
Q

Which process in the clotting cascade involves tissue factor

A

Extrinsic (actives factor X with factor VIIa)

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12
Q

What factors inhibit the clotting cascade

A

TFPI
Antithrombin
Protein C
Thronbomodulin
Protein S (activates protein C + thrombomodulin to active Protein C)

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13
Q

How does trauma impact the fibrinolysis system

A

Overactivates system

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14
Q

Factors leading to trauma induced coagulopathy (TIC)

A

Fibrinolysis
Inflammation
ATC - acute traumatic coagulopathy
Hypothermia
Acidaemia
Haemorrhage -> loss, dilution

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15
Q

Why may hypercoagulability and hyperfibrinolytic blood be beneficial in trauma

A

Prevents clotting due to Hypovolaemic, low flow state

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16
Q

CVS response to bleeding

A

Initial tachycardia then bradycardia
Hypotension

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17
Q

Confounders in the CV response to bleeding

A

Age
Medications

18
Q

3 main reflexes to haemorrhage

A

Arterial baroreceptor reflex
Cardiac vagal C fibre reflex
Arterial chemoreceptor reflex

19
Q

Arterial baroreceptor reflex

A

Haemorrhage -> stretch receptors in wall of aortic arch and carotid sinus detect less stretch -> decr vagal tone and incr sympathetic activity -> sympathetic peripheral vasoconstriction

20
Q

Where are the arterial baroreceptors

A

Aortic arch
Carotid sins

21
Q

Effect of activating arterial baroreceptor reflex during haemorrhage

A

Sympathies peripheral vasoconstriction

22
Q

Cardiac vagal C fibres reflex in haemorrhage

A

Cardiac vagal C fibres in left ventricle myocardium activated by circulating components and reduced preload -> decr SVR -> vagal bradycardia and hypotension

23
Q

Where are cardiac vagal C fibres

A

Left ventricle myocardium

24
Q

Effect of cardiac vagal C fibre activation in haemorrhage

A

Vagal bradycardia
Hypotension

25
Q

Arterial chemoreceptor reflex

A

Incr CO2 or decr O2 -> chemoreceptors in carotids and aortic bodies activated -> incr resp rate

26
Q

Arterial chemoreceptor reflex in haemorrhage

A

Decr bloodflow mimics incr CO2/decr O2 -> chemoreceptors activated -> incr resp rate

27
Q

How can the arterial chemoreceptor reflex effect cardiac C fibres

A

Arterial chemoreceptors activated -> incr resp rate -> cardiac C fibres inhibited

28
Q

How does sBP, HR, RR, and GCS change during bleeding

A

sBP - maintained then rapid drop
HR - tachy then Brady
RR - tachy
GCS - reduced

29
Q

How does sBP, HR, RR, and GCS change with increasing injury level

A

sBP - hypertensive
HR - tachy
RR - tachy
GCS - reduced

30
Q

3 components of lethal triad

A

Coagulopathy
Acidosis
Hypothermia

31
Q

Conditions that mimic Haemorrhage

A

Head injury
Eviscerated abdomen
Periosteum
Obstructive shock

32
Q

What causes BP RR HR and GCS changes in head injury that mimic haemorrhage

A

Massive catecholamine release

33
Q

What nerve causes a decr in HR and BP in eviscerated abdomen and periosteum

A

Vagal nerve

34
Q

Damage control resuscitation

A

Maintain haemostatic competence in a pt that is actively bleeding

35
Q

Aims of DCR

A

Early haemorrhage control
Permissive hypotension
Limit fluid infusions
Finessed targeting if Coagulopathy

36
Q

Why should fluid infusions be limited in haemorrhage

A

Avoid diluting coagulation factors

37
Q

Code red criteria

A

sBP <90
Poor response to initial fluid resuscitation
Suspected active haemorrhage

38
Q

TXA dose in massive haemorrhage

A

1g IV TXA bolus over 10 mins then 1g IV infusion over 8hrs

39
Q

What is done after bleeding is controlled in a code red

A

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

40
Q

Aims of damage control surgery

A

Haemorrhage control
Manage sepsis
Protect from further injury
Maintain haemostasis
Protect cells and organs
Preserve endothelium

41
Q

AIM of ICU after haemorrhage

A

Restore physiology

IBSc PHEM Applied Science (18 decks)

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