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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

A

diarrhea

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
Q

Hyperkalemia inhibits what in the kidney?

A

ammonia synthesis -> metabolic acidosis and further exacerbates Hyperkalemia

26
Q

ECG changes w/ hyperkalemia around what value?

A

> 6
Peaked when =10

Wide QRS, merging with T when greater -> V Fib

Hyperkalemia is the most dangerous

27
Q

Tx of hyperkalemia

A
  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
Q

Normal Mg-

location ?

A

1.8-2.5
located in the bones (2/3)

intracellular (1/3)

29
Q

hypomagnesium affects

A

hypokalemia and hypocacemia - more difficult to Tx

30
Q

normal phos

A

3-4.5

stays in bones 85% ‘remainder intracellular

31
Q

most common cause of sever hypophosphatemia

A

Alcohol abuse (less absorption)and DKA

32
Q

Anion gap

A

Na - (Cl + bicarb)

normally ~12
- reflects ions in serum but unmeasured (proteins, phosphates, organic acids, sulfates)

33
Q

Effects of acidosis

A 
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
Q

Effects of alkalosis

A

Decreases cerebral blood flow
L shift in oxygen-Hgb curve to fascilitate loading of Oxygen
Arrythmias
Tetany and seizures

35
Q

Salicylate poisoning causes

A

Respiratory Alkalosis w/ metabolic acidosis

36
Q

Arterial blood gas

CO2 elv think?
low?

HCo3 level elv think?
low think?

A

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
Q

Normal AG acidosis - hyperchloremic metabolic acidosus

Causes?

A

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
Q

features of metabolic acidosis

A

Hyperventilation - kussmauls breaths - compensatory

Decreased CO and tissue perfusion

39
Q

Winter’s formula

expected PaCO2 =

A

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
Q

With metabolic acidosis PaCO2 should?

Metabolic alkalosis PaCO2 should?

A

PaCO2 should decrease as compensation(hyperventilate)

PaCO2 should increase as compensation (hyperventilate)

failure -> additional primary respiratory acid base ongoing

41
Q

Causes of metabolic alkaosis

A

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
Q

Resp acidosis due to?

A

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
Q

Compensation in resp Acidosis

A

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
Q

Increase in PaCO2 ->

A

increased cerebral blood flow

-> increased CSF pressure -> CNS depression

45
Q

Respiratory alkalosis causes

A

alveolar hyperventilation

anxiety, sepsis, PE, pneumonia, Mechanical ventilation, pregnancy, liver disease, medication (salycilate)

46
Q

Acute and chronic compensation for respiratory alkalosis

A

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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