Multi-organ failure and critical illness Flashcards
Pathophysiological responses to haemorhage and reduced MAP (3)
Baroreceptor (immediate)- Increases SNS and reduces PNS, increasing HR and ionotropy and causing arteriolar and venous constriction
Endocrine- catecholamine and steroid release
Reduced renal perfusion (mins to hours)- RAA axis activation causing Na and water retention increasing circulatory volume
ABC treatment in trauma
A-intubate
B-ventilate (increases oxygenation and decreases O2 requirement of patient)
C-IV access and fluid resuscitation
Side effects of anaesthetic induction agents in trauma
Vasodilation and hypotension (vasoconstriction stops) - can lead to hypovolaemic cardiac arrest (responds to treatment)
Treatment of hypovolaemic cardiac arrest
CPR, adrenaline, blood, resuscitation (reacts well to increased volume and adrenaline)
5 sites of major blood loss in trauma
‘Blood on the floor and 4 more’
1) External
2) Chest
3) Abdomen
4) Pelvis and retro peritoneum
5) Around long bone fractures esp. femur
Typical ABG result in trauma
Metabolic (lactic) acidosis with respiratory compensation if possible (Can’t if on ventilator)
Effect of crush injuries on serum potassium
Rises as released by burst cells
Does Hb level show blood loss?
Not immediately, concentration isn’t changed by bleeding, need to wait until after fluid resus.
Fluid replacement in major haemorrhage
Don’t give too much clear fluid as dilutes Hb clotting factors and platelets so makes you bleed.
Give blood, FFP and platelets eraly
Major haemorrhage protocol
Triad of death in major haemorrhage
Hypothermia from cold fluids and environment - decreases coagulation
Acidosis from anaerobic resp due to hypoperfusion - decreases heart performance
Coagulopathy from cold, bleed more, more acidotic etc. LOOK AT DIAGRAM
Medications in major haemorrhage
Tranexamic acid and vasopressor
Imaging to find source of bleeding
CT if stable enough, CXR and pelvic XR in resus if not
Preferred type of imaging in spinal trauma
MRI
Type of CT used
Dual bolus CT with contrast
What are high density lesions in brain on CT caused by?
Blood - contrast doesn’t get to brain
What kind of damage is found at post mortem in traumatic brain injuries?
Hypoxic-ischaemic damage
Mechanism of hypoxic-ischaemic damage in traumatic brain injuries
Inflammation increases ICP causing inadequate cerebral blood flow and distortion of vital structures.
Why does ABC need treating before can treat D (brain injury)?
Brain needs steady oxygen from cardiac output - need good cerebral oxygen supply before can treat brain injuries
Perfusion rate of brain
750mls/min
How is cerebral blood flow maintained as MAP changes?
Constricts as MAP increases and vice versa - fails at extremes though (<70 and >160)
How does the brain initially cope with decrease in cerebral blood flow and what happens drops too low?
Initial it increases oxygen extraction from the blood. When flow is below 20ml/100g/min get failure of electrical function (symptoms) and below 10 you get failure of ionic pumps so K out and Na in (cell death)
CPP(Cerebral Perfusion Pressure)=
MAP-ICP
Ideal CPP
60-70mmHg
How does brain compensate for increase in ICP (e.g a bleed)?
Loses CSF and Venous blood - can only lose a certain amount so becomes uncompensated after that
