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Sem3: ANAT20050 Trauma > L3 Haemorrhagic Shock > Flashcards

L3 Haemorrhagic Shock Flashcards

1
Q

Father of Triage?

A

Baron Larrey

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2
Q

Main morbidity from extended tourniquet application (>10 Hours)

A

Nerve Injury

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3
Q

Complications of Analgesia in hemorrhagic shock?

A
  • Opiates are given to a severely injured person:
    Depressive effect on Medulla=> respiratory/cardiovascular depression
  • Ketamine i.v. Or intranasal is promising (dissociative)
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4
Q

Lethal triad of Trauma?

Mechanism:

  • ___________=> vasodilation=> additional loss of heat
  • ___________=> constriction of blood vessels=> further deprives tissues of blood => worsening anaerobic metabolism
  • ___________=> depresses liver=> reduces the formation of fibrinogen=> worsening coagulopathy
  • _____________=> loss of heat=> hypothermia
A
  • Coagulopathy: Severe tissue damage=> cascades=> can get out of control. Can lose a lot of platelets and other clotting factors. Addition of saline further dilutes factors
  • Acidosis: Loss of blood=> system reacts shutting down non-vital organs. Switch to anaerobic metabloims=> acidosis. Acidosis increases the degradation of fibrinogen
  • Hypothermia: other factors contribute to hypothermia which in turn worsens them

Mechanism:

  • Acidosis=> vasodilation=> additional loss of heat
  • Hypothermia=> constriction of blood vessels=> further deprives tissues of blood => worsening anaerobic metabolism
  • Hypothermia=> depresses liver=> reduces the formation of fibrinogen=> worsening coagulopathy
  • Loss of more blood (coagulopathy)=> loss of heat=> hypothermia
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5
Q

Primary cause of death in Trauma?

A

Haemorrhage accounts for 80% of deaths

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6
Q

Best Therapy for Hemorrhage?

A

Best Overall: 1:1 Fresh frozen Plasma: Packed red cells

Lactated Ringer’s solution=Hartmann’s solution (Buffering)

  • Lactate metabolized by the Liver (Cori Cycle) => Glucose
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7
Q

Test to index the amount of coagulopathy in the patient

Significance of Latency, Amplitude, Shape of Tail?

A

Thromboelastography

Latency= Clotting Factors

Amplitude=Platelets

Tail= Fibrinolysis

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8
Q

What does this Thromoelastography reveal?

A

Normal

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9
Q

What does this Thromoelastography reveal?

How to treat?

A

Factor Deficiency ( Late, coagulation cascade is not functioning properly)

Treat with Fresh Frozen Plasma (FFP)

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10
Q

What does this Thromoelastography reveal?

How to treat?

A

Platelets deficient or malfunctioning (small delay, decreased amplitude)

Treat with Platelet infusion

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11
Q

What does this Thromoelastography reveal?

How to treat?

A

FIbronolysis is overactive: Fibrin dissolving clots
too rapidly

Treated with Tranexamic Acid

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12
Q

What does this Thromoelastography reveal?

A

Hypercoagulation (No sign of fibrinolysis)

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13
Q

What does this Thromoelastography reveal?

A

Disseminated Intravascular Coagulation (DIC stage 1)

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14
Q

What does this Thromoelastography reveal?

A

Disseminated Intravascular Coagulation (DIC stage 2)

Clotting Factors Exhausted due to overuse in initial stage

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15
Q

_____________________________:

  • A synthetic version of lysine
  • Helps clotting (Fibrinogen has a lot of lysine)
  • Anti-fibrinolysis (Inhibits Plasminogen becoming plasmin)
A

Tranexamic Acid

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16
Q

How is haemorrhage detected by the body?

A

Oxygen and glucose delivery to brain is key

Monitored variables

  • Blood pressure
  • Blood volume
  • Blood oxygen content
17
Q

Locations of Baro/Chemoreceptors?

A

Baroreceptors: Located at origin of the vertebral artery

Chemoreceptors: Located at vertebral and carotid arteries

18
Q

MOA of Atrial Volume Receptors?

A

Volume receptors when stimulated by stretch: Signal via vegas nerge=>mediulla=> hypothalamus (Tonic Inhibition of ADH)

  • In blood loss: Inhibition of ADH reduced=> more ADH=> reduction in urine output
  • Getting into pool, blood is pushed up from the periphery=> stretch volume receptors => increased ADH inhibition => triggering urge to urinate
19
Q

Classes of Hemorrhage?

A
20
Q

New vs. Old Models of Absorption/Filtration into interstitial space?

A

NO absorption on venous side of circulation:

  • ∏ of interstitial space is higher than thought
  • P of interstitial space can be subatmospheric
21
Q

Regulation of Cerebral Blood Flow?

Mechanism?

When it fails?

A

Autoregulation: within 50-150mmHg there is no change in blood below to the brain.

Mechanism: Works because the smooth muscle surrounding vessels leading to the brain senses BP

  • Drop pressure=> Dilate
  • Increase in pressure => Constrict

When it Fails: Oxygen and sugar supply to the brain fails when mmHg <50 => CNS disturbances (confusion, hostility) => lethargy/coma

22
Q

Symtoms/Signs of Hemorrage?

A

Symptoms (Patient Complaint)

  • Intense thirst (ANGII Crosses BBB)
  • Dry mouth (Give ice cubes, not water)
  • Weakness (Vasoconstriction of peripheral vessels => weak supply to muscles)
  • Faint (Constricted vessels limits flow to brain)
  • Tinnitus, flashing lights (Retina most sensitive organ, first to fail under hemorrhagic conditions)

Signs (Physician Observed)

  • Pallor, cold, clammy
  • Fast and “thready ” pulse
  • Air hunger
  • Contricted veins
  • Oliguria/anuria
  • Confusion
23
Q

Summary of dealing with Hemmorage?

A
  • Diagnose bleeding
  • Arrest the bleed
  • Transfuse
  • Monitor clotting status
24
Q

Hallmarks of Irreversible Shock?

A
  • Falling Cardiac output
  • Lactate acidosis
  • Endotoxaemia
  • Endothelial disturbance
  • Lethal triad (Coagulopathy, Acidosis, Hypothermia)
25
Q

Physiologic response to shock?

A
26
Q
A

Sem3: ANAT20050 Trauma (16 decks)

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