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Boards: AcidBase/Fluids/Electrolytes > Dibart Acid Base > Flashcards

Dibart Acid Base Flashcards

1
Q

What is the range of [H+] compatible with life?

A

16 - 160 nEq/L

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2
Q

How do you calculate the pH from the [H+]?

A

pH = - log 10 [H+]

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3
Q

Describe the Law of Mass Action

A

the velocity of a reaction is proportional to the concentration of the reactants

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4
Q

What does the dissociation constant represent?

A

indicates how much an acid will dissociate into H+ and its base.

the higher the Ka the stronger the acid and the more dissociation

(pKa is the -log of this constant)

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5
Q

How do you calculate the pH from the acid base cc and pKa?

A

pH = pKa + log ([base]/[acid])

note
H = Ka [acid]/[base]

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6
Q

What pKa is the most efficient buffer?

A

if it’s within one unit of the pH (6.4-8.4 most efficient)

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7
Q

What is the solubility coefficient for CO2?

A

0.03

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8
Q

How much does PCO2 decrease for every 1.0 mEq/L decrement in HCO3- mEq/L?

A

by 0.7 mm Hg

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9
Q

What are the most efficient dissociable side groups of proteins for buffering?

A

histidine residues (pKa 6.4-7.0)
amino-terminal amino groups (pKa 7.4-7.9)

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10
Q

What protein accounts for 80% of the nonbicarbonate buffering capacity of blood?

A

hemoglobin

plasma proteins only 20%

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11
Q

What are the most important intracellular buffers?

A

proteins and phosphates

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12
Q

List 3 intracellular organic phosphate buffers

A

adenosine triphosphate
adenosine diphosphate
2,3-diphosphoglycerate

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13
Q

How fast is the renal buffering response?

A

begins within hours
takes 2-5 days to reach maximal effect

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14
Q

What is the expected HCO3- change for an acute versus chronic respiratory acidosis?

A

pCO2 increase by 1 mm Hg

> > acute&raquo_space; HCO3- increase 0.15 mEq/L
chronic&raquo_space; HCO3- increase by 0.35 mEq/L

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15
Q

What is the expected HCO3- decrease for an acute or chronic respiratory alkalosis?

A

pCO2 decrease by 1 mm Hg
» acute&raquo_space; HCO3- decrease by 0.25 mEq/L
» chronic&raquo_space; HCO3- decrease by 0.55 mEq/L

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16
Q

How is total CO2 content measured versus calculated?

A

measured: strong acid added to blood sample&raquo_space; will dissociate and donate H+&raquo_space; all HCO3- will bind with H+&raquo_space; all carbon will become CO2

equation:
CO2 content = 0.03 x PCO2 + HCO3-

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17
Q

What is base excess?

A

amount of strong acid or base required to titral 1 L of blood to pH of 7.4at 37 C and PCO2 held constant at 40 mm Hg

reflexts metabolic acid base disturbances (negative acidosis, positive alkalosis)

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18
Q

How does the pH differ between venous and arterial blood?

A

lower in venous blood

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19
Q

What are the major anions and cations of the extracellular fluid?

A

cations
* Na
* K
* Ca
* Mg

anions
* Cl
* bicarbonate
* plasma proteins
* organic acid anions (e.g., lactate)
* P
* sulfate

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20
Q

How do you calculate the anion gap?

A

AG = (Na+ + K+) - (Cl- + HCO3-)

reality - AG does not exist - this gap is filled by unmeasured cations and anions (UA UC)

AG = UA - UC

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21
Q

What is a normal AG in dgos versus cats?

A

dogs 12-24 mEq/L

cats 13-27 mEq/L

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22
Q

how can alkalemia increase lactic acid production?

A

stimulates phosphofructokinase

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23
Q

In hypoalbuminemia, how much does the AG decrease for every 1.0 g/dL decease in albumin?

A

2.4-3.0 mEq/L

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24
Q

What constitutes Atot?

A

plasma proteins and phosphate

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25
Q

Compare the net gain and net loss of HCO3- and H+ in the liver and kidneys

A

liver
* metabolizes aminoacids&raquo_space; releases NH4+ in the process
* NH4+ synthesized to urea (urea cycle)&raquo_space; uses CO2 and produces H+ and titrates HCO3-

kidneys
* excrete NH4+ - diverts some of the ureagenesus
* net gain of HCO3-
* net loss of H+

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26
Q

What are the 2 transport mechanisms for H+ excretion in the kidneys?

A

Na+ - H+ - antiporter (NHE3) - 2/3

H+ATPase - 1/3

also H+K+-ATPase in the intercalated cells of the collecting ducts - quantitatively less important

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27
Q

Where are what percentages of HCO3- absorbed in the tubules?

A
  • 80% proximal tubules
  • 10% thick ascending limb of the loop of Henle
  • 6% distal convoluted tubule
  • 4% collecting duct
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28
Q

Describe how HCO3- is absorbed in the proximal tubules

How does this differ in the collecting ducts?

A
  • basolateral NaK-ATPase&raquo_space; decreased IC Na+ cc
  • NaHE3&raquo_space; H+ moves luminally
  • H+ binds with filtered HCO3-&raquo_space; H2CO3
  • CA IV facilitates H2CO3 to H2O and CO2
  • CO2 enters cells (diffuses easily)
  • CO2 binds with IC H2O
  • CA II facilitates H2O + CO2 becoming H2CO3
  • H2CO3 dissociates to H+ and HCO3-
  • H+ moves again EC with NaHE3
  • HCO3- absorbed basolaterally via electrogenic basolater 3HCO3-/Na+ cotransporter

collecting ducts:
* H+ secreted via H+ATPase instead of NaHE3
* HCO3- exits basolaterally via Cl-HCO3- exchanger

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29
Q

What is the main determinant for the tubular maximum of HCO3-?

A

How much Na is reabsorbed

volume depletion - more Na reabsorbed - increased HCO3- absorption

volume expansion - opposite

other determinant: Cl content in ultrafiltrate - if more Cl available for Na reabsorption&raquo_space; less HCO3- absorbed with Na
inverse relationship between serum Cl cc and renal HCO3- absorption

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30
Q

How does serum K cc affect HCO3- reabsorption?

A

hypokalemia&raquo_space; more K exchanges for H+ on the basolateral membrane to reach ECF

H+ available for excretion and thus HCO3- absorption

hyperkalemia vice versa

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31
Q

Explain how ammonia production and excretion in the kidneys contributes to acid base balance

A

ammonia produced from glutamine
glutamine&raquo_space; glutaminase&raquo_space; glutamate + NH4+

glutamate&raquo_space; glutamate dehydrogenase&raquo_space; alpha-ketoglutarate + NH4+

2 possible ways for alpha-ketoglutarate

  • oxidizes&raquo_space; alpha-ketoglutarate + 2H+ –> CO2 + H2O + 2 HCO3-
  • gluconeogenesis&raquo_space; glucose + 2 HCO3-

HCO3- absorbed via electrogenic 3HCO3-Na cotransporter

NH4+ secreted by taking place og H+ in NaHE3 exchanger

NH4+ reabsorbed via taking K place in NaK2Cl contransporter in the ascending thick loop of henle
» NH4+ dissociates and NH3 forms

NH3 will move interstitially (cannot move luminal here because thick ascending loop of henle impermeable to NH3 and move to tubular fluid of collecting ducts (can do that because lipophilic and easily crosses membranes)

collecting ducts have high H+&raquo_space; binds with H+ and forms NH4+&raquo_space; remains in tubular fluid and is excreted

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32
Q

If you infused a strong acid (e.g., HCl) into a patient what are the different steps of buffering?

A
  • immediately some buffered by plasma HCO3- (40% buffer) MINUTES&raquo_space; CO2 produced exhaled
  • some immediately buffered by plasma proteins and phosphate but less important
  • some enters RBC to be buffered (10%, hemoglobin!)
  • 30 min later&raquo_space; acid distributes to interstitial fluid&raquo_space; again HCO3- most important buffer
  • hours later&raquo_space; H+ enters intracellular water (50% of the buffering)
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33
Q

By what mechanisms (2) does HCO3- decrease in chronic metabolic acidosis?

A
  • through buffering the acid
  • hypocapnia decreases renal HCO3- reabsorption
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34
Q

At what pH does myocardial contractility begin to decrease?

A

below 7.20

suspected to be caused by IC acidosis leading to displacement of Ca ins from critical binding sites on contractile proteins

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35
Q

List the different cardiovascular effects of acidosis

A
  • decreased cardiac contractility
  • arrhythmias
  • arterial vasodilation
  • impaired catecholamine responses
  • venous vasoconstriction&raquo_space; venous congestion
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36
Q

how does acidosis affect the oxygen-hemoglobin dissociation curve?

A

right shift

offset within 6-8 hours due to RBC decrease of 2,3-diphosphoglycerate&raquo_space; back to the left/normal

37
Q

What type of acidosis will cause hyperkalemia?

A

acute mineral acidosis

not seen with organic acidosis

38
Q

How does chronic acidosis affect calcium homeostasis?

A
  • displaces Ca from binding site&raquo_space; increased free ionized Ca cc
  • release of buffres from bones (calcium carbonate)&raquo_space; osteodystrophy + hypercalciuria
39
Q

What causes distal renal tubular acidosis?

A

impaired H+ excretion in the collecting ducts

40
Q

What are the clin path hallmarks of distal renal tubular acidosis?

A
  • increased urine pH > 6.0 (without UTI with urease producing bacteria!)
  • acidosis

confirmed diagnosis: ammonium chloride tolerance test

41
Q

What causes proximal renal tubular acidosis?

A
  • impaired renal HCO3- reabsorption
42
Q

In a patient with proximal RTA with metabolic acidosis, what is the expected renal pH?

A

appropriately low renal pH because distal acidifying ability preserved

eventually HCO3- will settle at a different stabilized plasma HCO3- concentration

43
Q

What are the components of the fanconi syndrome?

A
  • proximal RTA
  • glucosuria
  • defects in absorbing P, Na, K, uric acid, amino acids
44
Q

How can you diagnose proximal RTA?

A
  • low urine pH (< 5.5 to 6)
  • hyperchloremic metabolic acidosis
  • normal GFR

after alkali therapy to normalize plasma HCO3- cc
* increased urine pH (> 6.0)
* increased urinary fractional excretion of HCO3-

45
Q

What is the most common complication from alkali therapy in patients with proximal RTA?

A

hypokalemia

through increased distal delivery of Na and HCO3-

46
Q

What are the main differences between proximal and distal RTA

A

Both:
* hypercalciuria
* hyperphosphaturia
* bone resorption > more severe in distal RTA
* hypokalemia

Distal RTA
* nephrocalcinosis and nephrolithiasis
* hypokalemia is more severe
* potassium wasting is improved with NaHCO3- administration
* lower alkali therapy required
* plasma HCO3- can be more severe
* low fractional excretion of HCO3-
* urine pH high

Proximal RTA
* potassium wasting is worsened with NaHCO3- administraiton
* higher alkali therapy required
* has other tubular defects
* urine pH low
* high fractional excretion of HCO3- if plasma HCO3- cc normal

47
Q

How does parenteral nutrition cause hyperchloremic metabolic acidosis?

A
  • amino acids&raquo_space; broken down to urea in the liver&raquo_space; H+ and NH4+ production

also: hypophosphatemia during refeeding&raquo_space; reduces renal excretion of titratable acids

48
Q

How does metabolic acidosis develop in hypoadrenocorticism?

A
  • aldosterone enhances Na reabsorption in collecting ducts&raquo_space; tubular lumen more negative&raquo_space; enhances H+ secretion
  • directly stimulates H+ via H+-ATPase pump in collecting ducts

decreased H+ secretion if these effects are diminished

49
Q

Fill in the blanks

A
50
Q

Which EG compound is primarily responsible for the metabolic acidosis?

A

Glycolic acid

51
Q

which calcium oxalate crystal is normal in health and which is more indicative for EG?

A

Ca-oxalate dihydrate - occasionally found in normal patients

Ca-oxalate monohydrates rarely seen except from EG tox

52
Q

What are the most common causes of metabolic alkalosis in small animals?

A
  • vomiting of stomach contents
  • administration of diuretics
53
Q

What is the response of kidneys to gastric HCl loss?

A

H+ lost –> HCO3- cc in plasma and kidneys increase
» natriuresis, kaliuriesis, suppression of acid excretion + bicarbonaturia

insufficient and limited because concurrent volume depletion
» kidneys try to retain Na&raquo_space; more HCO3- absorption
» aldosterone secretion&raquo_space; increases H+ excretion

> > K loss from kaliuresis
K will exchange with H+ to move EC&raquo_space; H+ moves IC in tubular cells&raquo_space; more excretion

54
Q

What will inhibit the kidneys ability to excrete alkaline load?

A

volume depletion (decreased GFR and Na avidity)
Cl deficiency and Na avidity

55
Q

How does acid base status affect lactate production?

A

increaed intracellular pH increaes phosphofructokinase activity&raquo_space; more lactic acid production

56
Q

What are the main buffering mechanisms from alkali loads?

A
  • 68% remains in the ECF - of which only 1% is converted by H+ ions donated by proteins
  • 32% titrated by intracellular buffers
57
Q

List organic anions that can lead to a source of alkali when metabolized

A
  • lactate
  • ketoacids
  • citrate (blood transfusions)
58
Q

Why does hypochloremia perpetuate metabolic alkalosis from gastric volume loss?

A

Na avidity caused by ECV depletion&raquo_space; if Cl deficit&raquo_space; Na reabsorbed in exchange for H+ and K+ instead of together with Cl-

> > paradoxical aciduria (high H+ excretion despite alkalosis)

59
Q

How can Cl- supplementation correct some of the alkalosis from gastric fluid loss?

A

more Cl available for Na absorption

Na+ absorption will now use less H+ and K+ ions in exchange (also helps with hypokalemia)

> > allows urinary HCO3- excretion

must restore Cl as a resobable anion so HCO3- isn’t used instead

60
Q

Explain how diuretic administration causes alkalosis

A

leads to increased distal nephron Na+ delivery –> more Na absorbed here in exchange for K+ and H+

more Cl lost in ratio to Na&raquo_space; less Cl available as anion for Na+ absorption&raquo_space; more HCO3- absorbed

causes hypokalemia&raquo_space; transcelular H+ shift IC&raquo_space; more H+ lost via Na-H+ exchange

RAAS stimulation increases Na-H+ and Na-K+ exchange

61
Q

How should hypokalemia from vomiting-induced alkalosis be best treated?

A

Chloride supplementation to assure K retention in the kidneys

e.g., KCl over KPhos

62
Q

What is more sensitive in triggering changes in respiration, PaCO2 or PaO2 changes?

A

PaCO2

63
Q

Which peripheral chemoreceptor plays the most important role in PaO2 sensing and affecting respiration?

A

carotid body

aortic arch also but minimal role compared

64
Q

Name the alveolar ventilation equation

A

VA = constant x (VCO2 / PaCO2)

constant around 0.863

65
Q

What percentage of CO2 remains dissolved in plasma versus as HCO3-, or bound to proteins??

A

8 % (PaCO2)

81% (HCO3-)

11% (mostly carbaminohemoglobin)

66
Q

Explain how respiratory acidosis causes hypochloremia

A

increased CO2 –> + H2O –> H2CO3 –> HCO3- + H+

H+ increases intracellularly including tubular cells –> more NaHE3 exchange
collecting ducts:
H+ binds with NH3 –> NH4+ –> excredet with Cl-

reabsorbed HCO3- crosses basolaterally via HCO3-Cl- exchanger –> more chloride lost

–> chloruresis

67
Q

How does chloruresis from respiratory acidosis affect the strong ion difference (SID)?

A

increases SID

68
Q

How does hypercapnia affect the cardiovascular system?

A
  • vasodilation
  • decreased myocardial contractility
  • increased HR and CO
  • tachyarrhythmias

overall typically no change in BP

69
Q

After recovery from metabolic acidosis, how long does the compensatory respiratory alkalosis last?

A

24-48 hours –> this lag can cause a respiratory alkalosis

70
Q

Does chronic respiratory alkalosis cause hypokalemia?

A

No - only with acute respiratory alkalosis - due to translocation of K+ into cells and renal losses - short lived effect and even acutely only mild

71
Q

How long does it take for maximum respiratory compensation for an acute metabolic acidosis to occur?

A

17-24 hours

72
Q

How is inappropriate compensation defined?

A

If PCO2 or HCO3- differs by more than 2 mm Hg/ mEq/L from the expected value

73
Q

Which acid base disturbances actually compensate efficiently enough to cause a normal pH?

A

chronic respiratory alkalosis (>14 days)
long-standing respiratory acidosis (>30 days)

74
Q

What are the differentials for metabolic alkalosis or acidosis associated with a decreased or increased Atot, respectively?

A

alkalosis - hypokalemia

acidosis - hyperphosphatemia

75
Q

List 3 calculations to assess whether an acid base disturbance is due to a change in SID or not

A

SID = strong ion difference

[Cl-] gap
chloride normal - chloride corrected
chloride corrected –> chloride x (Na normal/ Na patient)

normal Cl dog 110, cat 120
normal Na dog 146, cat 156
> 4 hypochloremic alkalosis
< -4 hyperchloremic acidosis

[Cl-]/[Na+] ratio
< 0.72- 0.74 hypochloremic alkalosis
> 0.78-0.8 hyperchloremic acidosis

[Na+] - [Cl-]
< 32 hyperchloremic acidosis
> 40 hypochloremic alkalosis

76
Q

By how much does a decrease in Alb by 1 g/dL change the AG?

A

will decrease AG by 4.1 mEq/L

77
Q

How can [P] change the AG?

A

contribution is usually negligible
hyperphosphatemia though can increase AG

0.58 times mEq/L P change

78
Q

How do you calculate the simplified strong ion gap?

A

Dog
SIG simplified = Alb x 4.9 - AG

cat
= Alb x 4.58 - AG + 9

if - 5 mEq/L&raquo_space; suspicious for increase un unmeasured strong anion

79
Q

What are the 3 components of the strong ion approach?

A

PCO2
Atot
SID

80
Q

What are the main determinants of Atot?

A

Albumin
globulin
inorganic phosphate

81
Q

What are the determinants of changes in SID?

A

strong ion difference

[HCO3-]
BE
[Na+]
[Cl-]

increase SID&raquo_space; strong ion metabolic alkalosis
decrease SID&raquo_space; strong ion metabolic acidosis

82
Q

What are the potential causes for strong ion difference alkalosis?

A
  • contraction/concentration alkalosis (decreased plasma free water and increased [Na+])
  • decreased [Cl-]
83
Q

What is the usual cause of chloride-resistant metabolich hypochloremic alkalosis?

A

hyperaldosteronism
hyperadrenocorticism

84
Q

What are the potential causes for SID acidosis?

A
  • decrease in [Na+] / dilutional acidosis
  • increase in [Cl-]
  • increase in concentration of other strong ions (e.g., lactate, ketones, sulfates)
85
Q

What is the quation for the effect of albumin on base excess

A

= 3.7 x (Alb normal - Alb patient)

86
Q

What is the equation for the effect of phosphate on base excess?

A

mmol/L
= 1.8 x [P]

mg/dL
= 0.58 x [P]

87
Q

What is the equation for the contribution of free water changes on base excess?

A

= 0.25 x (Na patient - Na normal)

88
Q

What is the equation for the effects of Chloride on base excess?

A

= Cl normal - Cl corrected

89
Q

What is the equation for the SIG?

A

strong ion gap = Na + K - Cl

SIG = A- - AG

Boards: AcidBase/Fluids/Electrolytes (13 decks)

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