Trauma/ hemorrhage Flashcards

1
Q

Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class II

A

(15–30% loss), tachycardia and subtle changes in mentation are observed.
Blood pressure normal

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1
Q

Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class I

A

(up to 15% loss), clinical symptoms of volume loss are not readily observed.

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2
Q

Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class III

A

circulatory shock and requires immediate intervention
(30–40% loss), marked tachycardia, impaired mentation, and measurable hypotension occur.

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3
Q

Advanced Trauma Life Support (ATLS) classes of hemorrhage:
Class IV

A

circulatory shock and requires immediate intervention
(> 40% loss), these vital signs are further deranged and may lead to a complete loss of consciousness

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4
Q

Compensatory mechanisms for declining intravascular volume: immediate

A

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

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5
Q

Compensatory mechanisms for declining intravascular volume: intermediate

A
  1. Transcapillary shifts (fluid from interstitium + IC –> IV)
  2. RAAS activation
    a. Ang II - vasomotor tone
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6
Q

Compensatory mechanisms for declining intravascular volume: late

A

net positive fluid balance occur in patients 1–48 hours after survival of the initial insult

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7
Q

Compensatory mechanisms for declining intravascular volume: immediate - depressor reflex

A

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

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8
Q

Location of baroreceptors
What do they detect?

A

Aortic arch, carotid sinus, left atrium
BP

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9
Q

Location of chemoreceptors
What do they detect?

A

Aorta, carotid artery
Hypoxemia

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10
Q

How do local tissue factors regulate vasomotor tone?

A

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

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11
Q

Describe intrinsic myogenic autoregulation in normal states and during hemorrhage

A

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

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12
Q

Angiotensin II

A
  • 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
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13
Q

Vasopressin release stimulated by

A

increased osm, decreased ECV

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14
Q

Vasopressin - actions

A

V1 - arterioles - vasoconstriction
V2 - CD - inserts aquaporins - promotes water reabsorption
Increases thirst

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15
Q

Aldosterone

A

Increases Na reabsorption in the DCT

16
Q

Compensated hemorrhagic shock/ acute compensatory shock - PE findings

A

Tachycardia
Narrow pulse pressure
Vasoconstriction - prolonged CRT
Increased RR - decreased CaO2 and perceived O2 debt

17
Q

Phases of decompensated shock

A

early/acute and late
or
compensatory reversible, decompensated reversible, decompensated irreversible

18
Q

Irreversible shock

A

systemic vasodilation, decreased cardiac filling pressures, myocardial systolic depressionm widespread cellular dysfunction

19
Q

Acute traumatic coagulopathy (ATC) - factors

A

20-30 min post-injury
considered unrelated to the actual loss, consumption, inhibition, or dilution of hemostatic factors or platelets

20
Q

Proposed precipitating factors of ATC (6)

A
  1. tissue injury
  2. hypoperfusion (shock)
  3. systemic inflammation
  4. metabolic acidosis
  5. hypothermia
  6. hemodilution
21
Q

ATC - two main drivers

A
  1. Shock due to ongoing tissue hypoperfusion
  2. Severity of tissue injury
22
Q
A