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Med 1 > Fluids, Lytes and Acid Base disorders > Flashcards

Fluids, Lytes and Acid Base disorders Flashcards

1
Q

Total body water

A

60% men

50% women

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2
Q

Intracellular fluid -

Extracellular fluid -

  • plasma =
  • interstitial fluid =
A

TBW = total body water= 50-60% of weight*

ICF= 2/3 TBW or (40% weight)*

ECF=1/3 TBW or (20% weight)*

  • plasma (1/3 ECF) (5%* of weight)
  • interstitial (2/3 ECF)(15%* of weight)
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3
Q

Totals

Normal output

Normal intake

A

out: 800-1500 mL urine per day, minimum 500-600 to excrete wait

intake 1500mL

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4
Q

3 reasons for oliguria

A

low blood flow to kidney
kidney problem
post renal obst

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5
Q

Normal urine output is

A

0,5-1.0 mL/kg/hr

low output sign of volume depletion

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6
Q

Maintenance fluids

4/2/1 rule

A

Use D5 1/2 saline (dextrose inhibits musclet breakdown)

4mL/kg 1st 10kg
2mL/kg next 10kg
1mL/kg for every kilo over 20

ex 70kg -> 40mL/kg +20mL + 50mL = 100mL/hr

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7
Q

hyponatremia and hypernatremai are due to

A

too much or too little water

symptoms when <120Na

head trauma ECF osm decreases, water shifts into brain cells increasing ICP so keep serum Na normal or slightly high

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8
Q

hypervolumia and hypovolumemia are due to

A

too much or too little Na

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9
Q

hypotonic hyponatremia

A

true hyponatremia

serum osm = <280mOsm/kg

Hypovolemic (total body Na is LOW)

  • low urine Na, compensation for extrarenal losses, diaphoreis, 3rd spacing
  • High urine Na, renal Salt loss is likely w/ diuretics and decreased aldosterone or ATN

Euvolemic - no ECF expansion/contracion
- SIADH, polydypsia, post op ,hypothyroidism, oxytocin,

Hypervolemic - low urine Na, water retaining
- CHF , nephrotic syndrome, liver disease

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10
Q

Isotonic hyponatremia - pseudohyponatremia

A

increase in plasma olds lowers plasma Na concentration but amount of Na is normal

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11
Q

Hypertonic hyponatremia

A

osmotic shift of water out of cells due to gradient
- hyperglycemia, mannitol, radiocontrast

every 100 hyperglycemic, Na decreases by 3

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12
Q

When faced w/ hyponytremia 1st look at?

A

serum osm

  • high -Hypertonic hyponytremia
  • normal - pseudohyponytremia

Low - TRUE hyponytremia

  1. assess ECF status
    - Hypovolemic vs euvolemic vs Hypervolemic
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13
Q

Tx for hyponytremia

A

120-130 - withhold free water

110-120 - loop diuretics w/ saline

<110 or symptomatic give 2% saline, no more than 8mmol/L in the 1st 24 hrs to prevent central pontine demyelination

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14
Q

Diabetes insipitius is

A

isovolemic hypernytrmia

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15
Q

Free water deficit calc

A

water deficit = TBW (1-actual Na + desired Na)

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16
Q

Corrected calcium in hypoalbuminemia

A

Ca + 0.8 (4 - serum alb)

Ca usually bound to albumin.
physiological ionized free Ca is controlled by PTH independent of albumin levels

hypoalbum the total Ca is low but ionizesd may be normal when corrected

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17
Q

acute alkalotic state and Ca

A

ionized Ca may be low despite normal serum Ca

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18
Q

low magnesium is associated w/

A

low Ca

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19
Q

Tx of hypercalcemia

A
  1. IV fludis

diuretics - further inhibit Ca reabsorption

bisphosphonates, Calcitonin

20
Q

hypokalemia

A

alkalosis and insulin shift K into cells (give bicarb when high and insulinw/glucose)

Epi also redistributes K inside cells

21
Q

Hyperkalemia

A

acidosis and lysis of cells -> increase of K our of cells

K is shifted out in exchange of bringing in H

22
Q

most common cause of hypokalemia and nonanion gap metabolic acidosis

23
Q

most dangerous complication of hypokalemia

A

arrythmia

see flat T waves, inversion if severe

U waves

24
Q

K and digoxin

A

Hypokalemia predisposes toxicity

25
Hyperkalemia inhibits what in the kidney?
ammonia synthesis -> metabolic acidosis and further exacerbates Hyperkalemia
26
ECG changes w/ hyperkalemia around what value?
>6 Peaked when =10 Wide QRS, merging with T when greater -> V Fib Hyperkalemia is the most dangerous
27
Tx of hyperkalemia
1. Give IV Ca if see ECg changes, stabilizes the RMP, (caution if digoxin) Shift w/ glucose and insulin Na bicarb as well if severe Kayexelate -> GI K exchange resin absorb K in the colon and pooped out
28
Normal Mg- location ?
1.8-2.5 located in the bones (2/3) intracellular (1/3)
29
hypomagnesium affects
hypokalemia and hypocacemia - more difficult to Tx
30
normal phos
3-4.5 stays in bones 85% 'remainder intracellular
31
most common cause of sever hypophosphatemia
Alcohol abuse (less absorption)and DKA
32
Anion gap
Na - (Cl + bicarb) normally ~12 - reflects ions in serum but unmeasured (proteins, phosphates, organic acids, sulfates)
33
Effects of acidosis
``` R shift in oxygen-Hgn curve to facilitate unloading depresses CNS Decreases Pulm flow arrythmias impairs mycardical function hyperkalemia ``` kidneys reabsorb more bicarb(new) to maintain pH
34
Effects of alkalosis
Decreases cerebral blood flow L shift in oxygen-Hgb curve to fascilitate loading of Oxygen Arrythmias Tetany and seizures
35
Salicylate poisoning causes
Respiratory Alkalosis w/ metabolic acidosis
36
Arterial blood gas CO2 elv think? low? HCo3 level elv think? low think?
CO2 elv - respiratory acidosis or compensation for metabolic alkalosis CO2 low - resp alkalosis or compensation for metabolic acidosis HCO3 elv -metabolic alkalosis or compensation for resp acidoisis HCO3 low - metabolic acidosis or compensation for resp alkalosis
37
Normal AG acidosis - hyperchloremic metabolic acidosus Causes?
low HCo3 is associated w/ high Cl so AG remains normal Renal loss of bicarb - RTA type 2 - proximal INability to excrete H - RTA type 1 - distal GI loss of HCO2 - diarrhea, (MOST COMMON CAUSE) pancreatic fistulas
38
features of metabolic acidosis
Hyperventilation - kussmauls breaths - compensatory | Decreased CO and tissue perfusion
39
Winter's formula expected PaCO2 =
expected Pa CO2= 1.5(measured HCO3) + 8 +/-2 predicts expected respiratory compensation it now w/in range another metabolic process is going on if actual higher then expected -> respiratory acidosis (impending resp failure) if actual is lower than expected -> resp alkalosis
40
With metabolic acidosis PaCO2 should? Metabolic alkalosis PaCO2 should?
PaCO2 should decrease as compensation(hyperventilate) PaCO2 should increase as compensation (hyperventilate) failure -> additional primary respiratory acid base ongoing
41
Causes of metabolic alkaosis
usually transient - kidneys excrete excess Bicarb, need to consider mech that maintains metabolic alkalosis if persistent vomitting + NG suction of H; diuretics lose ECV w/normal Bicarb -> contraction alkalosis Volume expansion:increased mineralocorticoid secretion -> increased tubular reabsorption of Na and HCOs and excessive Cl loss inuring Cushings, k def,
42
Resp acidosis due to?
any disorder that decrease CO2 clearance alveolar hypoventilation - Primary pulm diseas - COPD - neuromuscular diseas - myasthenia graves - CNS malfunction - brainstem - Drug induced - morphine, narcotic overdose - Resp muscle fatigue
43
Compensation in resp Acidosis
renal compen w/increased HCO3 begins w/in 12-24hrs acute: 1mmol/L increase for every 10mmHg in PaCO2 Chronic: 4mmol/L increase for every 10mmHg increase in PaCO2 be careful - low oxygen may drive RR, may inhibit breathing rate w supplemental oxygen
44
Increase in PaCO2 ->
increased cerebral blood flow -> increased CSF pressure -> CNS depression
45
Respiratory alkalosis causes
alveolar hyperventilation anxiety, sepsis, PE, pneumonia, Mechanical ventilation, pregnancy, liver disease, medication (salycilate)
46
Acute and chronic compensation for respiratory alkalosis
Kidneys dump more bicarb with Acute - 10mmHg decrease in PaCO2, the plasma HCO3 decreases by 2 Chronic - 10 mmmHg in PaCO2 the plasma HCO3- decreases by 5-6mEq/L

Med 1 (11 decks)

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