Fluid resuscitation Flashcards

1
Q

Define the ROSE principle of fluid therapy

A

R = resuscitation (within minutes)
O = optimization (hours)
S = stabilization (days)
E = evacuation (weeks)

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2
Q

Draw the Frank-Starling and Marik-Phillips curve and show potential consequences of a fluid bolus based on preload

What happens to these curves in the face of sepsis?

A

See picture

With sepsis, the EVLW curve is shifted to the left

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3
Q

Give examples of what can be used as fluid challenges

A
  • Mini fluid bolus (5 mL/kg over 5 min)
  • Passive leg raise
  • Valsalva effects (heart-lung interactions)
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4
Q

What does the “Gray zone” refer to in assessment of fluid responsiveness

A

Values of assessment that have a Sp and a Se < 90% for assessment of fluid responsiveness - where fluids might be beneficial or not

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5
Q

What is the percentage of volume of crystalloids that stay in the intravascular space 30 min after administration of a bolus

A

25%

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6
Q

What are beneficial effects of hypertonic saline

A
  • Plasma volume expansion (by 3-5 times the volume administered) but transient
  • Arteriolar vasodilation
  • Reduced endothelial swelling
  • Weak positive inotrope and coronary vasodilation
  • Immune modulatory effects (decreased neutrophil activation, decreased cytokines)
  • Improves cerebral perfusion pressure
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7
Q

What is the maximum rate of administration of hypertonic saline? Why?

A

1 mL/kg/min
Faster rates can inhibit central and peripheral vasomotor centers and cause bradycardia and vasodilation from acute hyperosmolarity

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8
Q

What is Oxyglobin made off

A

Ultrapurified bovine hemoglobin

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9
Q

What are the pharmacological characteristics describing the different colloid solutions

A
  • Weight-average molecular weight (WAMW) = mean of molecular weights of molecules
  • Number average molecular weight (NAMW) = median of molecular weights of molecules
  • Molar substitutions (MS) = number of hydroxyethyl residues per glucose subunit
  • Ratio of hydroxyethyl substitutions at C2 versus C6 position (C2:C6) = determines where alpha-amylase will attach for hydrolysis

-> larger MW, with higher degree of substitution, and higher C2:C6 ratio associated with longer half life

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10
Q

What are suggested mechanisms of HES-associated AKI

A
  • Reabsorption of HES molecules in the proximal tubule leading to osmotic swelling / vascuolization of the cells
  • Decreased glomerular filtration due to increased colloid oncotic pressure
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11
Q

What are suggested mechanisms of HES-associated coagulopathy

A
  • Decreased platelet function (reduced GPIIb/IIIa receptor which normally binds vWF and fibrinogen)
  • Decreased vWF concentrations
  • Decreased factor VIII activity and ristocetin cofactor activity
  • Impaired fibrinogen polymerization
  • Dilutional coagulopathy
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12
Q

How much plasma is required to increase albumin by 0.5 g/dL

A

22.5 mL/kg

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13
Q

How to calculate the dose of albumin to deliver

A

Albumin deficit (g) = 10 * 0.3 * BW (kg) * (desired albumin - patient albumin)]

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14
Q

What hypersensitivity can be seen after administration of human albumin to dogs

A

Type I (anaphylaxis) and type III (immune complex disease).

  • Human albumin should never be administered more than once.
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15
Q

List adverse effects of resuscitative fluid therapy

A
  • Organ edema (-> lung injury, GI dysmotility and increased translocation, etc.)
  • Increased risk of arrhythmias and decreased contractility
  • Dilutional coagulopathy
  • Activation of inflammatory cascade (increased TNF-alpha, IL-6, IL-8, IL-10, phospholipase A2 activation) - worse with racemic LRS (effect of D-lactate)
  • Endothelial glycocalyx degradation
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16
Q

What is Turbostarch

A

A mix of 23.4% NaCl and 6% hydroxyethyl starch in a 1:2 ratio (given at total volume of 3-5 mL/kg)

17
Q

Definition of massive transfusion

A

Transfusion of:
- Entire blood volume in 24h
- 50% blood volume in 3-4h
- Blood products at 1.5 mL/kg/min (=90 mL/kg/h) for 20 min

18
Q

What is hypotensive resuscitation vs delayed resuscitation

A

Hypotensive resuscitation = resuscitation to a SBP of 90 of MAP of 60 for a few hours until definitive control of hemorrhage

Delayed resuscitation = withholding all fluid resuscitation until definitive control of hemorrhage (for a few minutes)

19
Q

Possible sites of IO catheterization.
Which ones have the highest success rates and allow higher flow rates?

A
  • Medial surface of proximal tibia
  • Trochanteric fossa of the femur
  • Wing of the ilium
  • Greater tubercle of the humerus

Highest success and flow with humerus and femur

20
Q

List complications of IO catheterization

A
  • Fracture
  • Fat embolism
  • Fluid / drug extravasation
  • Osteomyelitis
  • Nerve injury
  • Hemorrhage
  • Compartment syndrome (higher risk with hypertonic infusion)
21
Q

Describe the push-pull technique vs the reinfusion technique to sample blood from a central venous catheter

A

Push-pull:
- Stop your infusions, clean your injection ports, flush the catheter
- With an empty syringe, aspirate and re-inject blood in the catheter 3 times (a volume of at least 3 times the dead space of the catheter)
- Pull your sample
- Flush catheter

Reinfusion:
- Stop your infusions, clean your injection ports, flush the catheter
- In a syringe with 0.5-1.5mL of heparinized saline 4U/mL, draw blood (3-6 times the dead space volume of the catheter)
- Pull your sample
- Reinject first syringe to patient
- Flush catheter
* Make sure not to do it too often to hemodilute and heparinize patient

22
Q

Colloids tend to remain in the intravascular space rather than redistribute to the interstitial space. How are starch molecules cleared from the intravascular space?

A

Clearance depends on the rate of absorption by tissues (liver, spleen, kidney, heart), uptake by the reticuloendothelial system,xlearence through urine and bile and enzymatic degradation to small particle by serum amylase.

23
Q

What is the CVC collapsibility equation and what value represents hyper/hypovolemia?

A

CVCcl = (CVCd max - CVCd min) / CVCd max

> 50% –> hypovolemia
< 50% –> Hypervolemia

24
Q

What are 2 hypothesized mechanisms to explain the pathophysiology of HES-associated AKI?

A
  1. Swelling of the proximal tubular cells due to osmotic nephrosis from reabsorption of the HES molecules
  2. Hyperoncotic induced renal dysfunction: HES –> increase in COP –> decreased GFR when coupled with low renal perfusion pressure (alteration in intraglomerular colloid forces)