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year 2 renal > Acid Base Balance 1 & 2 > Flashcards

Acid Base Balance 1 & 2 Flashcards

1
Q

why are acid/base balance important and what happens if it is disturbed?

A

Metabolic reactions are exquisitely sensitive to the pH of the fluid in which they occur. Relates to the high reactivity of H+ ions with Pr- = changes in configuration and function, especially enzymes

Acid/Base disturbances = all sorts of metabolic disturbances

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2
Q

pH of ECF is very closely regulated

Normal pH of arterialized blood is 7.4 = free [H+] of 40 x 10-9 moles/l or 40 x 10-6 mmoles/l

what is the important of free H+?

A

Only free H+ ions contribute to pH

Other plasma constituents are present in mmoles eg Na+, K+, Cl-, glucose etc. So [H+] is one millioneth that of other plasma constituents

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3
Q

does hte body produce H+?

A

yes

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4
Q

what ar ethe 2 main sources of H+?

A

respiratory acid

metabolic acid (non-respiratory acid)

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5
Q

how is respiratory acid a source of H+?

A

CO2 + H2O <=> H2CO3 <=> H+ + HCO3-

Formation of carbonic acid is not normally a net contributor to increased­ acid because any ­increase in production = decrease in ventilation

Problems occur if lung function is impaired

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6
Q

hwo is metabolic acid a source of H+?

A

via metabolism

a) inorganic acids: eg S-containing amino acids = H2SO4 and phosphoric acid is produced from phospholipids
b) organic acids: fatty acids, lactic acid. On a normal diet, there is a net gain to the body of 50-100 mmoles H+ per day

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7
Q

Major source of alkali is oxidation of what?

A

organic anions such as citrate

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8
Q

what do buffers do?

A

Minimize changes in pH when H+ ions are added or removed

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9
Q

what equation is this:

pH = pK + log⁡[A-]/[HA]

A

Henderson-Hasselbalch equation

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10
Q

what is the Henderson-Hasselbalch equation?

A

defines the pH in terms of the ratio of [A-]/[HA] NOT the absolute amounts

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11
Q

what is the most important extracellular buffer? and what is the equation?

A

The most important is the bicarbonate buffer system

H2CO3 <=> H+ + HCO3-

pH = pK + log⁡ [HC03-]/[H2CO3]

pK = 6.1 so in plasma at pH 7.4, 7.4 = 6.1 + log⁡ [HC03-]/[H2CO3]

1.3 = log 20, so the ratio of [HCO3-]/[H2CO3] in blood at 7.4 is 20:1, Need 20 times more bicarbonate

The quantity of H2CO3 depends on the amount of CO2 dissolved in plasma, depends on solubility of CO2 and Pco2

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12
Q

how do you calculate the standard biocarbonate?

A

The quantity of H2CO3 depends on the amount of CO2 dissolved in plasma, depends on solubility of CO2 and Pco2

Solubility of CO2 in blood at 37°C = 0.03 mmoles/l/mmHg, PCO2 = 0.225 mmoles/l/kPa PCO2

So, at a normal Pco2 of 40mmHg, 5.3kPa, [H2CO3]= 40 x 0.03 mmoles/l or 5.3 x 0.225mmoles/l =1.2mmoles/l

Since the ratio of [HCO3-]/[H2CO3] in blood at 7.4 is 20:1, [HCO3-] = 24mmoles/l = “Standard bicarbonate”

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13
Q

what is the normal value and ranges for pH?

A

pH =7.4 Range 7.37-7.43

Range of pH compatible with life: 6.8-7.8 (US), 7.0-7.6(UK)

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14
Q

what is the normal value and rages for pCO2?

A

pCO2 = 5.3kPa Range 4.8- 5.9

= 40mmHg 36-44

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15
Q

what si the normal value and range of [HCO3-]?

A

[HCO3-] = 24mmoles/l Range 22-26

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16
Q

The Henderson-Hasselbalch equation can be more simply written as what?

A

pH = [HCO3-]/PCO2

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17
Q

The unique importance of the bicarbonate buffer system is crucial:

increased ­H+ + HCO3- <=> H2CO3 <=> H2O + CO2

describe what is happening?

A

Basic mechanism by which it acts as a buffer is evident, an ­increased ECF H+ drives the reaction to the right, so that some of the additional increased ­H+ ions are removed from solution and therefore a change in pH is reduced

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18
Q

increased ­H+ + HCO3- <=> H2CO3 <=> H2O + CO2

If this was an ordinary buffer system then increased­H+ drives the reaction to the right and what would happen?

A

the ­increased products would begin to push the reaction back to reach a new equilibrium position, where only some of the additional H+ ions are buffered

In any normal buffer system the products would stop the reaction happening and make it go slower and make it reverse back the other way

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19
Q

is the bicarbonate an ordinary buffer system?

A

no

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20
Q

how is the bicarbnate buffering system not an ordinary buffering system?

A

the reaction is pulled to the right, greatly increasing the buffering capacity of the bicarbonate

Ventilation removes the product of CO2 and cant participate in the backwards reaction any more and increases capacity of this buffer system dramatically

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21
Q

does the bicarbonate buffering system eliminate the H+?

A

Important to note that H+ has NOT been eliminated from the body. Instead the HCO3- has buffered the H+ and the respiratory compensation has greatly ­ increased the buffering capacity so that free H+ions are prevented from contributing to the pH

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22
Q

Elimination of H+ from the body is by the _______ and this excretion is coupled to the regulation of plasma _______

A

kidneys

[HCO3-]

pH = [HCO3-] = renal regulation

Pco2 = respiratory regulation

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23
Q

what are other buffers in the ECF?

A

Plasma proteins Pr- + H+ <=> HPr

Dibasic phosphate HPO42- + H+ <=> H2PO4- monobasic phosphate

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24
Q

what are intracellular buffers?

A

Primary intracellular buffers are proteins, organic and inorganic phosphates and, in the erythrocytes, haemoglobin

Buffering of H+ ions by ICF buffers cause changes in plasma electrolytes, since to maintain electrochemical neutrality, movement of H+ must be accompanied by Cl- as in red cells or exchanged for a cation, K+

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25
Q

In acidosis, the movement of K+ out of cells into plasma cause?

A

can cause hyperkalaemia = depolarization of excitable tissues = ventricular fibrillation and death

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26
Q

Bone carbonate provides what?

A

an additional store of buffer, very important in chronic acid loads as in chronic renal failure = wasting of bones

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27
Q

Are buffers important?

A

Buffers are incredibly important:

50-100 mmoles H+ per day from diet. If present as free H+ in total body water = pH of 1.2-2.4!! In fact arterial pH remains remarkably constant at 7.4, as long as the lungs and kidneys are working normally.

So H+ is successfully buffered until the kidney excretes it

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28
Q

where is metabolic acid buffered?

A

43% buffered in plasma, primarily with HCO3- 57% in cells

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29
Q

where is repsiratory acid buffered?

A

97% of buffering occurs within cells, Hb particularly important, rest with plasma proteins

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30
Q

[HCO3-] = ____ regulation

Pco2 = ___________ regulation

A

renal

respiratory

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31
Q

The kidney regulates [HCO3-] by mechanism?

A
  1. Reabsorbing filtered HCO3-
  2. By generating new HCO3-

Both of these processes depend on active H+ ion secretion from the tubule cells into the lumen

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32
Q

What is the mechanism for the reabsorption of HCO3-?

A

a) Active H+secretion from the tubule cells
b) coupled to passive Na+ reabsorption
c) filtered HCO3- reacts with the secreted H+ to form H2CO3. In the presence of carbonic anhydrase on the luminal membrane = CO2 and H2O
d) CO2 is freely permeable and enters the cell
e) Within the cell, CO2 = H2CO3 in the presence of carbonic anhydrase (present in all tubule cells) which then dissociates to form H+ and HCO3-
f) The H+ ions are the source of the secreted H+
g) The HCO3- ions pass into the peritubular capillaries with Na+
h) Bulk of HCO3- reabsorption occurs in the proximal tubule >90%

Although the HCO3- reabsorbed is not the same ion as was filtered, the net effect is the same. HCO3- is a large charged molecule, by converting it to CO2 it is much easier to save this valuable buffer

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33
Q

what is the importance of HCO3- reabsorption?

A

GFR =180l/day [HCO3-] = 24mmoles/l = 4320 mmoles HCO3- filtered per day. Must be reabsorbed, since failure to do so = to adding H+ to the ECF

There is no excretion of H+ ions during HCO3- reabsorption

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34
Q

in humans what is the iminmum and maximum urine pH?

A

In humans, minimum urine pH = 4.5.-5.0, maximum » 8.0

Usually, net production of 50 -100 mmoles H+ per day

If present as free H+ ions in urine volume of 1litre = pH = 1. Stinging!! Fortunately, buffered in urine

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35
Q

What acts as buffers?

A

Several weak acids and bases act as buffers. Most is done by dibasic phosphate, HPO42-, also uric acid and creatinine

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36
Q

Importance of the formation of titratable acidity is what?

A

it generates new HCO3- AND excretes H+

Only used for acid loads

The process is called “titratable acidity” because its extent is measured by the amount of NaOH needed to titrate urine pH back to 7.4 for a 24hour urine sample

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37
Q

how are H+ removed?

A
  1. Na2HPO4 in the lumen. One Na+ is reabsorbed in exchange for secreted H+. This monobasic phosphate removes H+ from the body
  2. The source of the new HCO3- is indirectly CO2 from the blood. It enters the tubule cells, combining with H2O to form carbonic acid, in the presence of carbonic anhydrase, which then dissociates to yield H+, used for secretion, and new HCO3- , which passes with Na+ into the peritubular capillaries
  3. Occurs principally in the distal tubule. This is where, phosphate ions, not reabsorbed by the proximal tubule Tm mechanism, become greatly concentrated because of removal of up to 95% of the initial filtrate
  4. Process is dependent on Pco2 of the blood
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38
Q

Distal tubule is site of formation of titratable acidity because……

A

Distal tubule is site of formation of titratable acidity because un-reabsorbed dibasic phosphate becomes highly concentrated by the removal of volume of filtrate

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39
Q

ammonium excretion does what?

A

Major adaptive response to an acid load, generates new HCO3- AND excretes H

40
Q

ammonium excretion is only done for acid loads, describe how this removes H+

(in the distal tubule)

A

NH3 is lipid soluble, NH4+ is not. This differential solubility is basis for mechanism

NH3 is produced by deamination of amino acids, primarily glutamine, by the action of renal glutaminase within the renal tubule cells

NH3 moves out into the tubule lumen, where it combines with secreted H+ ions to form NH4+ which combines with Cl- ions (from NaCl) to form NH4Cl which is excreted. (Distal tubule mechanism)

The new HCO3- passes with Na+ ions into the peritubular capillaries

41
Q

where is the source of secreted H+ form in ammonium secretion?

A

The source of the secreted H+ is again CO2 from the blood

42
Q

describe the process of ammonium excretion in the proximal tubule

A

In the proximal tubule, there is an NH4+/Na+ exchanger so NH4+ ions formed within the cells pass out into the lumen

Net effect is the same

Ammonium formation happens in the cells in the proximal tubule and uses a sodium transfer to get into the lumen to be excreted

43
Q

can NH4 cross the cell membrane?

A

NH4 cant cross membrane as large charged molecule, but NH3 can as it is lipid soluble

44
Q

what si the activity of renal glutaminase depedent on?

A

exquisitely pH dependent

When intracellular pH falls =­increased renal glutaminase activity and therefore more NH4+ produced and excreted

45
Q

what is the main adaptive response of the kidney to acid loads? and how long does it take?

A

This ability to augment NH4+ production is the main adaptive response of the kidney to acid loads

It takes 4-5 days to reach maximal effect because of the requirements of ­increased protein synthesis

Normally only 30-50 mmoles H+ per day are lost as NH4+, but this can ­increase to 250 mmoles/l in the presence of severe acidosis

It also takes time to switch off the ability to make NH4+ when there is excess of alkali

46
Q

If renal or respiratory function is abnormal, or any acid or base load overwhelms the body, a change in pH occurs

decreased pH =

increased pH =

A

acidosis

alkalosis

47
Q

respiratory disorders affect what?

A

Pco2

48
Q

what does renal disorders affect?

A

[HCO3-]

49
Q

what is Respiratory Acidosis?

A

pH has fallen and it is due to a respiratory change, so Pco2 must have increased. Respiratory acidosis results from reduced ventilation and therefore retention of CO2

retention of carbon dioxide

50
Q

what are acute causes of respiratory acidosis?

A

drugs which depress the medullary respiratory centres, such as barbiturates and opiates

Or Obstructions of major airways

51
Q

what are chronic causes of repsiratory acidosis?

A

lung disease eg bronchitis, emphysema, asthma

52
Q

what is the response to respiratory acidosis?

A

Need to protect pH so need to increase­ [HCO3-]

The increased­ Pco2 will = increased­ secretion of H+ and ­increased HCO3-. Acid conditions stimulate renal glutaminase so get more NH3 produced, BUT, it takes time

So there is ­increased generation of new HCO3- as well as ­increased reabsorption, because having generated more HCO3- , the increased­ Pco2 will also ­increase the ability to reabsorb it

53
Q

However, although the renal compensation to ­ increase HCO3- protects the pH in respiratory acidsosis, it does not correct the original disturbance, what does?

A

Only restoration of normal ventilation can remove the primary disturbance

54
Q

what are the valvues like in chronic respiratory acidosis?

A

in chronic respiratory acidosis eg in bronchitis, blood gas values are never normalised

They may be eg pH 7.32, Pco2 65mmHg (8.67 kPa), [HCO3-] 38 mmoles/l

The underlying disease process prevents the correction of ventilation, but because the kidney maintains high [HCO3-], the pH is protected

55
Q

Patients with lung disease will always have aberrant Pco2 and [HCO3-], but as long as ____ function is not impaired, __ can be maintained at a level compatible with life

Problems arise when patients with lung disease develop ____ dysfunction

A

kidney

pH

renal

56
Q

what is respiratory alkalosis?

A

Alkalosis of respiratory origin so must be due to a fall in Pco2 and this can only occur through increased ventilation and CO2 blow-off

57
Q

what are the acute causes of respiratory alkalosis?

A

voluntary hyperventilation, aspirin, first ascent to altitude

58
Q

what are the chronic cause of respiratory alkalosis?

A

long term residence at altitude, decreased Po2 to <60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation

59
Q

what is done to protect pH in repsiratory alkalosis?

A

To protect pH, [HCO3-] should decrease

Alkaline conditions are dealt with by the HCO3- reabsorptive mechanism

If decreased Pco2, less H+ is available for secretion, therefore less of the filtered load of HCO3- is reabsorbed so HCO3- is lost in the urine

Again, ventilation must be normalized to correct the disturbance

60
Q

what is metabolic acidosis?

A

An acidosis of metabolic origin must be due to a decreased [HCO3-]

So, decreased [HCO3-], either due to ­increased buffering of H+ or direct loss of HCO3-

61
Q

How do you protect pH in metabolic acidosis?

A

To protect the pH, Pco2 must be decreased

62
Q

what are the causes of metabolic acidosis?

A
  1. increased­ H+ production, as in ketoacidosis of a diabetic (acetoacetic acid, b- hydroxybutyric acid) or in lactic acidosis
  2. Failure to excrete the normal dietary load of H+ as in renal failure
  3. Loss of HCO3- as in diarrhoea
    ie failure to reabsorb intestinal HCO3-

can be an excess of protons or a lack of bases

63
Q

what happens to breathing in metabolic acidosis?

A

The resulting acidosis stimulates ventilation so that Pco2 falls

The ­increase in ventilation is in depth rather than rate, may be very striking, reaching a maximum of 30 l/min cf normal 5-6 l/min when the arterial pH falls to 7.0

This degree of hyperventilation = Kussmaul breathing = an established clinical sign of renal failure or diabetic ketoacidosis. Very serious

64
Q

metabolic acidosis:

Normally the kidneys correct the disturbance by restoring _______ and getting rid of __ ions

A

[HCO3-]

H+

65
Q

Normally the kidneys correct the disturbance by restoring [HCO3-] and getting rid of H+ ions

Problem: Source of H+ ions is the carbonic acid from CO2, but the respiratory compensation lowers the Pco2 to protect the pH!!!!!!!!

what is the explanation?

A
  1. Compensations for A/B disturbances are always in the same direction as the initial disturbance. Remember pH is defined as the ratio of [HCO3-]/ PCO2. However they are never quite to the same extent ie not complete, so pH not restored to 7.4
  2. Complete compensation would remove the drive to correct the original disturbance. Survival value of this is that if there were no pressure to correct initial disturbance, a further perturbation may push the system so far that compensation can no longer be effective
  3. Because of the decreased Pco2, the total amount of H+ secreted by the renal tubule will be less than normal BUT because the plasma [HCO3-] and therefore filtered load of HCO3- is reduced to an even greater extent , a smaller fraction of total H+ is needed for HCO3- reabsorption and therefore a greater proportion is available for excretion in the form of titratable acid and NH4+
66
Q

increased metabolic H+ within the body causes what?

A
  1. Immediate buffering in ECF and then ICF
  2. Respiratory compensation within minutes
  3. Renal correction of the disturbance takes longer to develop the full response to increase­ H+ excretion and generate new HCO3- because renal glutaminase takes 4-5 days to reach maximum. As HCO3- starts to increase­, repiratory compensation begins to wear off until eventually get rid of all excess H+
67
Q

in metabolic acidosis, respiratory compensation ______ the ____ correction, but ______ the pH, much more important

A

dleays

renal

protects

68
Q

what is metabolic alkalosis? and what is done to protect the pH?

A

[HCO3-] must have increase­ and Pco2 will ­increase to protect the pH

69
Q

what are the causes of metabolic alkalosis?

A
  1. increased H+ ion loss - vomiting loss of gastric secretions
  2. ­ increased renal H+ loss - aldosterone excess, excess liquorice ingestion
  3. Excess administration of HCO3- is unlikely to produce a metabolic alkalosis in subjects with normal renal function, but may do so if renal function impaired
  4. Massive blood transfusions can lead to metabolic alkalosis because bank blood contains citrate to prevent coagulation, which is converted to HCO3-, but need at least 8 units to have this effect

The greatly increased­ filtered load of HCO3- exceeds the level of H+ secretion to reabsorb it, even in the presence of ­ Pco2, so the excess is lost in the urine. Again, respiratory compensation delays renal correction, but protects the pH

70
Q

name a, b, c and d

A

increase

decrease

increase

increase

71
Q

name e, f, g and h?

A

dcerease

increase

decrease

decrease

72
Q

name i, j, k and l

A

increase

decrease

decrease

decrease

73
Q

name M, N, O and P

A

decrease

increase

increase

increase

74
Q

A decrease in pH (acidosis) is CAUSED by either what?

A
75
Q

An increase in pH (alkalosis) is CAUSED by either what?

A
76
Q

how do you tell between chronic and acute respiratory acidosis?

A

Note that for a given increase in Pco2, there is a smaller decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis

77
Q

Note that for a given increase in Pco2, there is a smaller decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis

why is this?

A

Answer lies in mechanisms used to raise [HCO3-]. NH3 production takes 4-5 days to be fully turned on. So initially can only raise [HCO3-] by titratable acid, so limited. With time, can use NH3 production which has a considerable capacity to raise [HCO3-]

A similar difference is seen between acute and chronic respiratory alkalosis because of the delay in turning off NH3 production. In contrast to renal compensations, which need time to reach completion, respiratory compensations occur in minutes so no differences

78
Q

Important to realize that acid/base disorders don’t just occur in isolation and in otherwise healthy individuals

Consider a badly controlled diabetic in ketoacidosis = (1)

This patient, despite the best advice, has always smoked, = chronic bronchitis = (2)

Patient has a haemorrhage = (3)

ie combined metabolic and respiratory acidosis

A

1 - metabolic acidosis

2 - respiratory acidosis

3 - lactic acidosis

79
Q

carrying on from previous flashcard:

blood/gas values: pH = 6.99, Pco2 = 60mmHg (8kPa), [HCO3-] = 13mmoles/l

What would you suggest to help him?

And let us not forget Potassium. The high acidity will cause Hyperkalaemia as H+ ions are buffered intracellularly in exchange for K+ ions. Danger of Ventricular Fibrillation.

A
  1. Insulin (+ glucose if non-diabetic), stimulates cellular uptake of K+

BUT?????

  1. Also for hyperkalaemia, calcium resonium, either oral or pr (per rectum), exchanges Ca2+ ions for K+ ions (12-24 hours)
  2. Ca gluconate (iv) = decreased excitability of heart, stabilizes cardiac muscle cell membranes
80
Q

The kidneys that are so important in Acid/Base balance are the same ones that are so important in regulating ECF volume and composition.

Consider a bad case of vomiting:

loss of NaCl and H2O = ……….

loss of HCl = …………

A

hypovolaemia

metabolic alkalosis

81
Q

what happens in a case of bad vomiting?

A

loss of NaCl and H2O = hypovolaemia

loss of HCl = metabolic alkalosis

The hypovolaemia will stimulate aldosterone to ­ increased distal tubule Na+ reabsorption

Under conditions of avid Na+ reabsorption, (and due to loss of Cl- ), the main ion exchanged for Na+ is H+

The respiratory compensation for the metabolic alkalosis ie increased ­Pco2 helps drive the H+ secretion and exacerbates the metabolic alkalosis by adding yet more HCO3- to the plasma

82
Q

The hypovolaemia will stimulate __________ to ­ increase distal tubule ___ reabsorption

A

aldosterone

Na+

83
Q

Under conditions of avid Na+ reabsorption, (and due to loss of Cl- ), the main ion exchanged for Na+ is what?

A

H+

84
Q

The respiratory compensation for the metabolic _______ ie increased ­Pco2 helps drive the H+ secretion and exacerbates the metabolic alkalosis by adding yet more HCO3- to the plasma

A

alkalosis

85
Q

summary diagram

A
86
Q

Shows that restoration of _____ takes precedence over correction of metabolic alkalosis

A

volume

Give NaCl, restore volume, alkalosis will be corrected

87
Q

In vomiting and diarrhoea, although lose acid and alkali, become alkalotic, why is this?

A

decreased ECF volume, increased aldosterone = contraciton alkalosis

Liquorice contains glycyrrhizic acid, which is very similar to aldosterone, so that excess ingestion = metabolic alkalosis

88
Q

what is the anion gap?

A

Anion Gap = The difference between the sum of the principal cations ( Na+ and K+) and the principal anions in the plasma (Cl- and HCO3- )

Normally 14-18mmoles/L

ie (140 +4) – (104 +24) = 16mmoles/L, (due to plasma proteins)

89
Q

when may it be useful to measure the anion gap?

A

It can be useful to measure the anion gap in metabolic acidosis

90
Q

what are the patterns of metabolic acidosis in terms of anion gap? and how are they caused

A

There are 2 patterns of metabolic acidosis in terms of anion gap, in one there is no change from normal and in the other the anion gap increases

If the acidosis is due for example to a loss of bicarbonate from the gut, then the reduction of bicarbonate is compensated by an increase in chloride and so there is no change in anion gap

However in eg lactic or diabetic acidosis, the reduction in bicarbonate is made up by other anions such as lactate, acetoacetate, b-OH butyrate and so the anion gap is increased

91
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.32, [HCO-3] = 15 mM, PCO2 = 30mmHg (4kPa)

  1. Metabolic Acidosis
  2. Metabolic Alkalosis
  3. Respiratory Acidosis (acute)
  4. Respiratory Acidosis (chronic)
  5. Respiratory Alkalosis (acute)
  6. Respiratory Alkalosis (chronic)
A
92
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.32, [HCO-3] = 33 mM, PCO2 = 60mmHg (8kPa)

  1. Metabolic Acidosis
  2. Metabolic Alkalosis
  3. Respiratory Acidosis (acute)
  4. Respiratory Acidosis (chronic)
  5. Respiratory Alkalosis (acute)
  6. Respiratory Alkalosis (chronic)
A
93
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.45, [HCO-3] = 42 mM, PCO2 = 50mmHg (6.7kPa)

  1. Metabolic Acidosis
  2. Metabolic Alkalosis
  3. Respiratory Acidosis (acute)
  4. Respiratory Acidosis (chronic)
  5. Respiratory Alkalosis (acute)
  6. Respiratory Alkalosis (chronic)
A
94
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.45, [HCO-3] = 21 mM, PCO2 = 30mmHg (4kPa)

  1. Metabolic Acidosis
  2. Metabolic Alkalosis
  3. Respiratory Acidosis (acute)
  4. Respiratory Acidosis (chronic)
  5. Respiratory Alkalosis (acute)
  6. Respiratory Alkalosis (chronic)
A
95
Q

A 75 year old man has the following blood gas values:

pH = 7.31, PCO2 = 7.7.kPa, (58mmHg), [HCO3-] =36mmoles/l.

  1. It is likely that he has renal disease.
  2. He may have an acute respiratory infection.
  3. It is possible that he may have chronic bronchitis.
  4. There will be a decrease in his excretion of ammonium ions.
  5. His plasma potassium will be reduced.
A

3

96
Q

The following acid/base values were obtained:

pH = 7.25, [HCO3-] = 12mmoles/l, PCO2 = 3.3kPa (25mmHg)

a. They are indicative of a respiratory acidosis
b. The reduction in Pco2 is a result of under-breathing
c. The subject has probably been taking bicarbonate of soda
d. It could be related to impaired renal function
e. The subject may have been vomiting very badly

A

d

year 2 renal (26 decks)

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