Trauma/ hemorrhage Flashcards
Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class II
(15–30% loss), tachycardia and subtle changes in mentation are observed.
Blood pressure normal
Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class I
(up to 15% loss), clinical symptoms of volume loss are not readily observed.
Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class III
circulatory shock and requires immediate intervention
(30–40% loss), marked tachycardia, impaired mentation, and measurable hypotension occur.
Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class IV
circulatory shock and requires immediate intervention
(> 40% loss), these vital signs are further deranged and may lead to a complete loss of consciousness
Compensatory mechanisms for declining intravascular volume: immediate
within minutes
baroreceptor-mediated stimulation of the sympathetic nervous system = increased HR, contractility, selective vasoconstriction
Baroreceptors - detect decreased BP –> arterial and capacitance venoconstriction –> increased HR; CO maintained despite decreased preload
Chemoreceptors - detect hypoxemia and met acidosis –> increased ventilatory drive and RR
Local tissue factors = regulate vasomotor tone
Compensatory mechanisms for declining intravascular volume: intermediate
- Transcapillary shifts (fluid from interstitium + IC –> IV)
- RAAS activation
a. Ang II - vasomotor tone
Compensatory mechanisms for declining intravascular volume: late
net positive fluid balance occur in patients 1–48 hours after survival of the initial insult
Compensatory mechanisms for declining intravascular volume: immediate - depressor reflex
slow rates and lower magnitudes of blood loss
vagal-mediated bradycardia and vasodilation predominate over the baroreceptor reflex in order to preserve blood flow while minimizing blood loss
Location of baroreceptors
What do they detect?
Aortic arch, carotid sinus, left atrium
BP
Location of chemoreceptors
What do they detect?
Aorta, carotid artery
Hypoxemia
How do local tissue factors regulate vasomotor tone?
decreases in PaO2 and production of local metabolites (eg, CO2 , H+ ) –> vasodilation via release of prostaglandins, nitric oxide, and adenosine, allowing capillary recruitment and redistribution of blood flow
Describe intrinsic myogenic autoregulation in normal states and during hemorrhage
regulates vessel tone in response to changes in local blood pressure
normal conditions - only a fraction of capillaries in organs are open to allow the passage of RBCs
hemorrhage - the number of open capillaries increases proportionally to the degree of tissue hypoxia
recruitment of capillaries promotes oxygen diffusion by decreasing the distance to tissue beds and increasing the surface area available
Angiotensin II
- NE release from adrenal medulla and sympathetic nerve terminals
- vasopressin
- aldosterone
- thirst
- Na reabs in proximal tubule (activating Na-H antiporter)
- preferential efferent arteriolar vasoconstriction
Vasopressin release stimulated by
increased osm, decreased ECV
Vasopressin - actions
V1 - arterioles - vasoconstriction
V2 - CD - inserts aquaporins - promotes water reabsorption
Increases thirst