Fluid Resuscitation Flashcards

1
Q

define hypotension

A

it is difficult to classify but generally

  • a BP <90/60 mmHg
  • >40 mmHg below normal
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2
Q

how does hypotension occur in sepsis

A
  • bacteria produce toxins which stimulate the immune system to produce cytokines eg TNF alpha
  • these increase NO production in vascular smooth muscle which causes vasodilation
  • fall in TPR, leads to a fall in BP = TPR x CO(=HR x SV)
  • endothelial dysfuntion and capillary leak leads to decreased intravascular volume
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3
Q

NO production

A
  • continuously produced by vascular endothelium from amino acid L-arginine through NOS enzyme
  • potent vasodilator, short action
  • shear stress on vascular endothelium stimulates calcium release from vascular endothelial cells and activation of NOS
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4
Q

consequences of hypotension

A
  • Leads to hypoperfusion in tissues which causes hypoxia and organ dysfunction
  • Hypoxia leads to anaerobic metabolism, which produces lactic acid as a byproduct
  • This causes a progressive metabolic acidosis with a raised anion gap, which leads to detrimental effects:
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5
Q

detrimental effects of metabolic acidosis

A
  • exacerbates vasodilatation , reducing TPR further
  • decreased myocardial contractility, reducing CO
  • generalised impaired function of cells
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6
Q

what does hypoperfusion cause in kidneys

A

acute kidney injury

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7
Q

immediate fluid management - sepsis 6

A
  • 500ml 0.9% saline STAT
  • repeat boluses of fluid as required
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8
Q

signs of hypovolaemia

A
  • Cool peripheries (though may be warm)
  • Clammy
  • Dry mucous membranes
  • Decreased JVP
  • Tachycardia
  • Hypotension, postural drop is evident first
  • Skin turgor
  • Mottling of skin
  • Poor urine output
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9
Q

monitoring of fluid

A
  • HR, BP, RR
  • Sepsis 6: serum lactate and urine output
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10
Q

what is the normal serum lactate level

A

<1.8 mmol/L

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11
Q

what does elevated lactate suggest

A
  • tissue hypoperfusion/hypoxia - anaerobic metabolism
  • in the context of sepsis, suggests severe illness or organ dysfunction as a result of tissue hypoperfusion
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12
Q

how is urine output best monitored

A
  • urinary catheter - more accurate and can give hourly volumes
  • also option of recording urine volume
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13
Q

normal urine output

A

should be at least 0.5ml/kg/hr

(heavier patients produce more)

anything less than this is oliguria

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14
Q

what does oliguria indicate in sepsis

A

renal hypoperfusion

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15
Q

crystalloid fluids

A
  • eg 0.9% NaCl and Hartmanns solution
  • cheap and widely available
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16
Q

Hartmanns solution

A

a crystalloid that contains additional electrolyes

generally only used for surgical procedures

17
Q

colloids fluids

A
  • eg Gelofusin
  • theoretically, should maintain oncontic pressure, however this does not translate in practice
  • expensive
18
Q

which fluids carry a small risk of anaphylaxis

A

colloids and albumin (colloids>)

19
Q

albumin

A
  • a natural colloid that maintains oncotic pressure
  • derived from donated blood samples
  • there is a small risk of infection - HepC
20
Q

where is albumin made

A

liver

21
Q

blood as a fluid

A
  • the most physiological colloid
  • increases oxygen carrying capacity
  • scarce resource
22
Q

what is there a risk of with blood fluid replacement

A
  • there is a risk of transfusion reaction - type II hypersensitivity
  • Anti-blood group Ab bind to the surface of circulating donor RBCs
  • There is an overwhelming systemic inflammatory response, which can occur after only 1ml of blood has been transfused
23
Q

what should never be used in fluid resuscitation

A

dextrose 5% - exits the intravascular space took quickly to do any good

24
Q

how much fluid do most patients require to restore euvolaemia

A
  • 2l
  • if in doubt, always give too much rather than too little
25
Q

how can overload oedema be managed

A
  • loop diuretic eg IV furosemide
  • inhibit NaCl transporter in the Loop of Henle, decreasing blood volume
26
Q

further management of a patient who is still hypotensive despite optimized fluid resuscitation/euvolaemia restored

A
  • inotropic support/vasoconstrictors eg nor/adrenaline
  • cause vasoconstriction ± increased myocardial contractility
  • adminstered through a central venous catheter in HDU/ICU