L3 Haemorrhagic Shock Flashcards
Father of Triage?
Baron Larrey
Main morbidity from extended tourniquet application (>10 Hours)
Nerve Injury
Complications of Analgesia in hemorrhagic shock?
- Opiates are given to a severely injured person:
Depressive effect on Medulla=> respiratory/cardiovascular depression - Ketamine i.v. Or intranasal is promising (dissociative)
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
- 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
Primary cause of death in Trauma?
Haemorrhage accounts for 80% of deaths
Best Therapy for Hemorrhage?
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
Test to index the amount of coagulopathy in the patient
Significance of Latency, Amplitude, Shape of Tail?
Thromboelastography
Latency= Clotting Factors
Amplitude=Platelets
Tail= Fibrinolysis
What does this Thromoelastography reveal?
Normal
What does this Thromoelastography reveal?
How to treat?
Factor Deficiency ( Late, coagulation cascade is not functioning properly)
Treat with Fresh Frozen Plasma (FFP)
What does this Thromoelastography reveal?
How to treat?
Platelets deficient or malfunctioning (small delay, decreased amplitude)
Treat with Platelet infusion
What does this Thromoelastography reveal?
How to treat?
FIbronolysis is overactive: Fibrin dissolving clots
too rapidly
Treated with Tranexamic Acid
What does this Thromoelastography reveal?
Hypercoagulation (No sign of fibrinolysis)
What does this Thromoelastography reveal?
Disseminated Intravascular Coagulation (DIC stage 1)
What does this Thromoelastography reveal?
Disseminated Intravascular Coagulation (DIC stage 2)
Clotting Factors Exhausted due to overuse in initial stage
_____________________________:
- A synthetic version of lysine
- Helps clotting (Fibrinogen has a lot of lysine)
- Anti-fibrinolysis (Inhibits Plasminogen becoming plasmin)
Tranexamic Acid
How is haemorrhage detected by the body?
Oxygen and glucose delivery to brain is key
Monitored variables
- Blood pressure
- Blood volume
- Blood oxygen content
Locations of Baro/Chemoreceptors?
Baroreceptors: Located at origin of the vertebral artery
Chemoreceptors: Located at vertebral and carotid arteries
MOA of Atrial Volume Receptors?
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
Classes of Hemorrhage?
New vs. Old Models of Absorption/Filtration into interstitial space?
NO absorption on venous side of circulation:
- ∏ of interstitial space is higher than thought
- P of interstitial space can be subatmospheric
Regulation of Cerebral Blood Flow?
Mechanism?
When it fails?
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
Symtoms/Signs of Hemorrage?
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
Summary of dealing with Hemmorage?
- Diagnose bleeding
- Arrest the bleed
- Transfuse
- Monitor clotting status
Hallmarks of Irreversible Shock?
- Falling Cardiac output
- Lactate acidosis
- Endotoxaemia
- Endothelial disturbance
- Lethal triad (Coagulopathy, Acidosis, Hypothermia)
Physiologic response to shock?
