Fluids, acid-base and electrolytes Flashcards

1
Q

5 mechanism of oedema formation:

A
  1. Venous hypertension
  2. Hypoproteinemia
  3. ↑microvascular permeability
  4. Impaired lymph flow
  5. ↑negativity of interstitial fluid pressure
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2
Q

4 mechanism of antiedema formation:

A
  1. ↑ interstitial hydrostatic pressure
  2. ↑ lymph flow
  3. ↓ interstitial colloid osmotic pressure
    1. ↑ trans-serosal flow in organs with potential spaces
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3
Q

characteristics that lead to longer half-life for artifical colloids:

A

larger MW
High molar substitutions
higher C2:C6 ratio

e,g, VetStarch 6% 130/0.4/9:1
Means:
6% - 6% tetrastarch solution
130 – Average MW in kDa
0.4 – 4 hydroxyethyl group substitutions per 10 glucose molecule
9:1 – C2:C6 ratio

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4
Q

Definition of fluid responders:

A

10-15% increase in stroke volume

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5
Q

Implicated mechanism for coagulopathy secondary to HES:

A

decreased platelet function

decreased concentrations of von Willebrand factor, factor VIII coagulant activity (FVIII:C), factor VIII-related antigen, factor VIII ristocetin cofactor

impaired fibrinogen polymerization

a dilutional coagulopathy.

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6
Q

what does CVP measure?

A

hydrostatic pressure of the intrathoracic vena cava just outside of the RA. Approximate RA pressure that’s similar to right ventricular pressure at end diastole, approximate preload

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7
Q

Predominant gas type for room air embolism:

A

Nitrogen

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8
Q

At or above which COP can the risk of oedema be decreased?

A

15mmHg

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9
Q

Osmolal gap that indicates unmeasured solutes

A

Osmolal gap > 10mOsm/kg above calculated indicates an unmeasured solute is present in large amounts.

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10
Q

Other than unmeasured solutes what else can confound an increased osmolal gap

A
  • secondary to pseudohyponatremia secondary to hyperlipidaemia, marked hyperglycaemia or hyperproteinemia
  • activiated charcoal containing propylene glycol or glycerol
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11
Q

Possible mechanisms for AKI from HES usage:

A

Renal tubular damage due to
i) hyperoncotic induced renal dysfunction => decreased GFR
ii) HES reabsorbed into PT cells via pinocytosis => osmotic nephrosis, cellular oedema, apoptosis

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12
Q

what is urine osmolality used for?

A

To assess concentrating ability of the kidneys especially if many high MW molecules could be present

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13
Q

Net effect of PTH:

A

increase Ca and decrease phosphate

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14
Q

Net effect of calcitriol

A

increases both calcium and phosphate

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15
Q

What is the active vitamin D?

A

Calcitriol

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16
Q

What is the Ca-P product?

A

total Ca (mg/dL) x phosphate (mg/dL)

17
Q

What happens when Ca-P product > 60

A

increases risk of mineralisation

18
Q

Effect of acidosis on phosphate:

A

↓ HPO42- due to renal elimination with H+

19
Q

Main sites of Mg reabsorption in the kidneys

A

Loop of Henle

20
Q

List 7 functions of Mg:

A
  1. Production and use of ATP
  2. Co-enzyme for membrane Na-K ATPase pump
  3. Calcium ATPase and proton pumps
  4. Protein and nucleic acid synthesis
  5. Regulation of vascular smooth muscle tone
  6. Cellular second messenger systems
  7. prevent apoptosis
21
Q

List 5 adverse effects for bicarb therapy:

A
  • electrolytes: increase Na, decrease K and Ca
  • decrease tissue oxygenation due to increased Hgb affinity to oxygen
  • intracellular acidosis
  • paradoxic CSF acidosis
  • hypercapnia
22
Q

Listed 4 differences between distal RTA and proximal RTA

A
  • distal RTA is a problem with H+ excretion in collecting duct, where proximal RTA is a problem with bicarb reabsorption in PT
  • urine pH > 6 in distal RTA and ph < 5.5 in proximal RTA despite acidemia
  • when NH4Cl is administered, urine pH remains > 6 in distal RTA
  • when alkali is administered to normalise plasma bicarb urinary excretion of bicarb in proximal RTA increase > 15%, where distal RTA remains normal < 5%. Therefore larger doses of bicarb is required for proximal RTA tx.
23
Q

Electrolytes correlate well between venous and arterial samples, except for which one?

A

Chloride is lower in systemic venous blood due to the Hamburger effect (chloride shift)

24
Q

Which parameters (2) differ between IO samples and venous/arterial samples:

A

potassium and PCV

25
Q

Name 3 ways sodium/lithium heparin can affect blood gas analysis

A
  • false hypoCa or Mg due to chelation
  • artificial increase NaCl and decrease K (dilutional)
  • artifically elevate PaO2
26
Q

Recommendation to keep heparin < ___% of blood volume

A

4%

27
Q

If a blood gas sample is left out at room temp, at what rate can lactate form?

A

0.01mmol/L per minute with concomitant decrease BE and pH

28
Q

What can cause artificial hyperkalaemia in a blood gas sample (3):

A

hemolysis, thrombocytosis, leukocytosis

29
Q

Main finding of 2017 Critical care medicine article: Cl content of fluids used in large volume resus is associated with reduced survival

A

-Chloride load was significantly associated with mortality even when controlling for total fluids, age and baseline severity.
- each 100mEq increase in Cl load associated with 5.5% increase in hazard of death over one year
- relationship between chloride load and hyperchloremic acidosis and AKI is less clear

30
Q

most common side effects (3) of bicarb therapy found in 2018 BICARB-ICU trial?

A

metabolic alkalosis
hypernatraemia
hypocalcaemia
(no life-threatening complications)

30
Q

What did the BICARB-ICU study find? 3 main findings:

A

Overall population: Sodium bicarbonate infusion was not associated with improvement in organ failure at day 7 and cause of death at day 28 in patients with severe metabolic acidemia

Patients with AKI at enrolment: Na bicarb decreased primary composite outcome and day 28 mortality

Bicarb decreased need for RRT during ICU stay