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Acid base electrolytes > ABG > Flashcards

ABG Flashcards

1
Q

Normal pH

A

7.35 - 7.45

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2
Q

How to convert kPa to mmHg

A

x 7.5

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3
Q

ABG interpretation

A

Oxygenation
What is the primary acid base disturbance
Is there compensation
Is the compensation adequate
Is a metabolis acidosis or alkalosis present - how severe
What is the anion gap
What is the delta gap
What is the cause
Hb
Electrolyte changes

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4
Q

What effect does an alteration of CO2 have on pH

A
  • For every 10mmHg increase in PaCO2 the pH will decrease by 0.08 not accounting for bicarbonate compensation
  • If chronic then for every 10mmHg increase in pH expect a pH decrease of 0.003 due to renal compensation
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5
Q

Normal bicarbonate

A
  • Normal 22-26 (24) (venous 2 lower than arterial)
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6
Q

ABG bicarbonate accuracty

A

Calculated based on Henderson Hasselbach equation

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7
Q

Why is utilising bicarbonate level for acid base calculations used? Why is this flawed

A
  • Using the bicarbonate level to determine changes in H+ and acidosis utilises the change in bicarbonate reflexing an equivalent amount of acid hidden by its buffering mechanism however it can also be altered by
    ◦ Compensatory pCO2 that occurs due to hyperventilation
    ◦ Pre-existing alkalosis - meaning metabolic acidosis occurs even in presence of a high HCO3
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8
Q

Define base excess

A
  • Dose of acid/alkali required to return blood to pH 7.4 at 37 degrees and pCO2 of 40mmHg and Hb 150g/L
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9
Q

Which type of base excess is used for Copenhagen tests? Why?

A

◦ Standard base excess uses ECF rather than whole blood - as it is heterogenous and cannot easily be sampled with ABG machine calculates the SBE of anaemic blood with Hb 50g/L using the actual base excess –> (cBase(Ecf))
‣ Standard base excess used for Copenhagen tests

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10
Q

What is the difference between standard base excess and actual base excess?

A

◦ Standard base excess uses ECF rather than whole blood - as it is heterogenous and cannot easily be sampled with ABG machine calculates the SBE of anaemic blood with Hb 50g/L using the actual base excess –> (cBase(Ecf))
‣ Standard base excess used for Copenhagen tests

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11
Q

Negative base numbers reflect?

A

Base deficit, or acid excess
The amount of acid required to be taken away to reduce the system back to baseline

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12
Q

Actual base excess is what? Why is this valuable and why is this different to measuring bicarbonate only?

A

◦ Actual base excess - (cBase(B)c.) Represents the metabolic contribution to the change in base excess - eliminiating pH, CO2 and temperature values as unadjusted values would suffer from the same failings as using bicarbonate concentration as you don’t know whether it is a respiratory acid base disturbance or purely metabolic.

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13
Q

What equation calculates base excess

A

Van Slkye

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14
Q

Flaws in actual base excess (3)

A

‣ Does factor in plasma-erythrocyte buffering (not however its role in the ECF)
‣ Encounters problems with the way CO2 equlibrates across ECF therefore with derangements in PCO2 it becomes more inaccurate;
- additionally the contribution of phosphate and albumin are not accounted for in the Van Slyke equation –> standard base excess factors this in better

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15
Q

WHy is base excess used instead of bicarbonate

A

◦ Standard base excess accounts for non bicarbonate buffering
◦ Elevated anion gap should be accompanied by an equal decrease in SBE
‣ If raised anion gap BUT normal SBE then metabolic alkalosis present pre-existing with new HAGMA
‣ If SBE has changed more than anion gap then non anion gap acidosis present

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16
Q

Severity of metabolic changes is classified by

A
  • The candidate is asked to stratify the severity of the acid-base disturbance according to the magnitude of the SBE derangement. The specific numbers are 4, 10 and 14 (or -4, -10 and -14) corresponding to mild, moderate and severe categories
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17
Q

Anion gap calculation and normal limits

A
  • Na - Cl - HCO3
  • Normal: 12 +/- 2 (10-14)
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18
Q

Why does albumin matter to anion gap

A
  • Low albumin falsely elevates the anion gap by 2.5 for every 10 albumin below 40
    ◦ i.e. for every 4g/L of albumin below 40 drop the normal limits of anion gap by 1
    ◦ So for albumin of 20 the anion gap is 7
    Therefore in absence of albumin anion gap is 2
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19
Q

Do you correct Na for glucose in calculations of anion gap

A

No

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20
Q

NAGMA causes

A

◦ Exogenous
‣ Normal saline infusion
‣ Exogenous acid - TPN, calcium chloride
◦ GIT
‣ Bicarbonate loss from diarrhoea or high output fistulas
‣ pancreatic/biliary drainage
‣ Ureteroileostomy or ureterosigmoidoscopy
◦ Renal
‣ Renal insufficiency
‣ RTA1 (distal)
‣ Carbonic anhydrase inhibition
‣ Aldosterone antagonists or Addisons
◦ Resp - chronic hypoventilation

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21
Q

NAGMA assessment to differentiate renal causes from non renal?

A

◦ Urinary anion gap = Na + K - Cl
◦ Positive gap = renal causes of NAGMA e.g. RTA
‣ Renal acidification defect
◦ Normal or negative urinary anion gap = GIT cause of NAGMA
‣ The approprioate acidification of the urine is occuring

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22
Q

HAGMA causes

A

◦ G - glycols - ethylene or propylene
◦ O - Oxoproline –> acetamenophin metabolite
◦ L - L lactate
◦ D - D lactate - PCM, short gut, lorazepam and phenobarbitol solutions
◦ I - iron overdose
◦ M - Methanol and other toxic alcohols
◦ A - aspirin and ASAs
◦ R - renal failure and uraemia
◦ K - ketoacidosis - starvation, ETOH, DKA

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23
Q

Differentiating HAGMA causes

A

Osmolar gap - measured minus calculted. -4 to +10 normal. Elevations suggest unmeasured toxic alcohols but also all the other contributors to HAGMA can raise it; or hyperproteinaemia/hyperlipidaemia

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24
Q

What is the delta gap and how to calculate it?

A
  • Compares the change in anion gap to the change in HCO3 to assess for simultaneous disorders; it should be a 1:1 relationship
  • CHange in AG / change in HCO3 = AG -12 / 24 - HCO3
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25
Q

What values for delta gap mean what

A

◦ <0.4 = NAGMA ONLY - none of bicarbonate change explained by anion gap change
◦ 0.4 - 0.8 = NAGMA and HAGMA
◦ 0.8-1.0 = purely due to a high anion gap metabolic acidosis*
◦ 1.0-2.0 = still purely a high anion gap metabolic acidosis
◦ >2 = HAGMA w/ metabolic alkalosis OR co-existing chronic respiratory acidosis causing raised HCO3

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26
Q

What assumptions does the delta gap make?

A

◦ Bicarbonate contributes all the buffering of metabolic acid base disturbances (its actually 75%)
◦ All buffering occurs in extracellular fluid - incorrect as the intracellular compartment is important in buffering e.g. lactate being processed intracellularly in the liver. 60% of total buffering in acidosis occurs by intracellular protein and phosphate, and 30% in metabolic alkalosis
◦ Acid anions have the same distribution space and clearance mechansismsas H+ –> incorrect e.g. lactate cleared in the liver (slower) –> delta ratio of 1.6 for lactate HAGMA not uncommon

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27
Q

How long does metabolic compensation take?

A
  • In general maximum metabolic compensation will take 2-3 days
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28
Q

What is the maximum and minimum possible bicarbon

A

+12 to 15
-20

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29
Q

What is the maximum and minimum possible CO2 for compensation

A

10mmHg to 60-80mmHg

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30
Q

Boston rules

A

Boston rules the “1-4-2-5” and “1.5+8 or 0.7 + 20” rules, using the actual bicarbonate value.

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31
Q

Expected HCO3 for changes in CO2 (i.e. metabolic compensation rules)

A

Respiratory acidosis (primary)
* Acute change in HCO3 -> For every 10 mmHg increase in PaCO2, the HCO3- will rise by 1 mmol/L
◦ 1:10
* Chronic change in HCO3 –> For every 10 mmHg increase in PaCO2, the HCO3- will rise by 4 mmol/L
◦ 3-4 : 10

Respiratory alkalosis:
* Acute change in HCO3 - reduced 2 for every 10 change
◦ For every 10 mmHg decrease in PaCO2, the HCO3- will fall by 2 mmol/L
* Chronic change is 5 for every 10
◦ For every 10 mmHg decrease in PaCO2, the HCO3- will fall by 5 mmol/L

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32
Q

Cheat rule instead of winters formula for metabolic acidosis calculations

A
  • QUICK GENERAL RULE - PaCO2 should be the last 2 digits of the pH if pH 7.1 - 7.6
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33
Q

Metabolic acidosis predicted CO2

A

◦ Expected CO2 = (1.5 x HCO3) + 8 (+/- 2) - Winters formula
◦ 1 meq/L HCO3 increase —> PaCO2 increase by 0.6mmHg

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34
Q

Expected PaCO2 for metabolic alkalosis

A
  • Expected PaCO2 = (0.9 x HCO3) + 9
  • Boston rule = PaCO2 = (0.7 x HCO3 ) + 20
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35
Q

Copenhagen rules

A
  • Acute change in PCO2 will not change the SBE
    ◦ The standard bicarbonate and base excess values use a normalised CO2 value
  • Expected change chronically in SBE to a rise in CO2 is 0.4x the change in PaCO2
  • Metabolic acidosis
    ◦ expected CO2 = 40 + (1x SBE)
  • Metabolic alkalosis
    ◦ Compensatory change in CO2 will be proportional to 0.6x the SBE
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36
Q

Normal PaO2

A

75 - 100

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37
Q

aA ratio is what

A

PaO2 / PAO2 –> i.e. arterial vs expected alveolar
Normal >75%

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38
Q

What is the response to hypoxia

A
  • The body begins to compensate for low O2 at <60mmHg; fails at <20mmHg
  • Response physiologically
    ◦ Increased minute volume
    ◦ Pulmonary artery vasoconstriction - reduced perfusion to hypoxic alveoli which can precipitate heart failure
    ◦ Increased cardiac output - HR
    ◦ Increased RBC
39
Q

Alveolar gas equation

A
  • Alveolar gas equation
    ◦ PaO2 = (FiO2 x (Patm - pH20)) - (PaCO2/ respiratory quotient)
    ◦ The pAO2 = (FiO2 x (760 - 47)) - (PaCO2 x 1.25)
    ‣ Normal PaO2 75 - 100 (99 at room air)
    ‣ If normal PaCO2 but supplemental O2 then PaO2 = 713 x FiO2 - 50
    ‣ Respiratory quotient based on protein/carb/fat intake assumed to be 0.8
40
Q

Aa gradient is normally
How do you calculate expected normal

A
  • A-a gradient - age/4 + 4
    <20 or 5-10 depending on source
41
Q

Problems with Aa gradient

A

‣ Under-estimated in fever
‣ Values increase in supine patient
‣ Decreased accuracy with increasing FiO2

42
Q

‣ Hypoxia with normal PO2 (a/A ratio) suggests

A

hypoventilation or low atospheric oxygen (low pressure)

43
Q

Hypoxia with low Aa ratio

A
  • Intrapulmonary V/Q mismatch e.g. intrapulmonary or intracardiac shunt
    * Diffusion defect
    ◦ If A-a >20 but normal CXR suggestive of PE
    * Increased oxygen extraction ratio - could use mixed venous sample to determine same.
44
Q

What percentage of shunt can CO2 remain normal up to?

A

PCO2 remains normal until shunt >50% and can even be decreased with hyperventilation

45
Q

What reasons might someone be shunting

A

Atelectasis, consolidation
Intrapulmonary shunt - AVM
Intracardiac shunt

46
Q

What is P50? What two methods of calculating it are there? Why are they different?

A
  • p50 - shift in the oxyhaemoglobin curve direction expected
    ◦ p50 (st) vs p50
    ‣ Difference between values reflects magnitude of Bohr’s effect and temperature on oxyhaemoglobin dissocation curve
    ‣ Thus, in the presence of a normal p50(st) and an abnormal p50 one would conclude that the curve has shifted purely because of pH, pCO2 and T°.
    ◦ p50 (st) is abnormal in presence of abnormal 2,3 DPG levels and rarer dyshaemoglobinaemias (sulfhaemoglobin)
    ‣ If p50 is abnormal by an equal amount the curve is shifted left due to this
47
Q

How to calculate osmolality

A

Osmolality gap
* Helpful when methanol and ethylene glycol levels not available, beware assuming ETOH is the cause of increased osmolality gap in drunk people
* Measured osmolality - calculated osmolality
◦ Normal gap -4 to +10
* Calculated serum osmolality = 2Na + Ur + ETOH + glucose

48
Q

Causes of raised osmolality gap

A
  • Raised osmolality gap causes

Unmeasured
◦ Body additives
‣ ETOH
‣ Methanol
‣ Ethylene glycol
‣ Propylene glycol
‣ Isopropyl glycol
‣ Acetone
‣ Mannitol

Measureable
◦ DKA
◦ AKA - alcoholic ketoacidosis
◦ Severe lactic acidosis
◦ Shock
◦ Trauma
◦ CRF
◦ Hyper lipid anemia
◦ Hyper protein anemia
◦ ^^Mg

49
Q

How does pH affect K

A
  • 0.1 decrease in pH increased K by 0.5 (vice versa)
50
Q

Corrected Na

A

Corrected Na for glucose = Na + (glucose - 5/3)

51
Q

What factors precipitate a metabolic alkalosis

A

Chloride depletion
Bicarbonate excess
Potassium depletion

52
Q

What factors maintain a metabolic alkalosis

A

Chloride depletion
Potassium depletion
Volume contraction
Reduced GFR

53
Q

What reasons might chloride be low

A

◦ Failed input - dietary chloride deprivation
◦ Losses
‣ GI losses
* Gastric losses by vomiting or drainage
* Diarrhoea
* Gastrocystoplasty
‣ Diuretics: loop or thiazides
‣ Cystic fibrosis (loss due to high sweat chloride content)
◦ Posthypercapneic state

54
Q

What reasons might bicarbonate be high

A

◦ Iatrogenic alkalinisation
◦ Recovery from starvation
◦ Hypoalbuminemia

55
Q

Why might potassium be depleted

A

◦ Mineralocorticoid overactivity
‣ Primary hyperaldosteronism
‣ Mineralocorticoid oversupplementation
◦ Hypertension associated
‣ Severe hypertension
‣ Liddle’s syndrome - ENaC channel.
◦ Bartter and Gitelman syndromes
◦ Exogenous
‣ Licorice (glycyrrhizic acid)
‣ β-lactam antibiotics
‣ Laxative abuse
‣ Clay ingestion

56
Q

How to differeniate response to metabolic alkalosis

A
  • Urinary chloride
    ◦ <10 indicates volume depletion and give NaCl
    ◦ >20 - volume expanded, hypokalaemia, Bartter/Gitelman syndrome, hyperaldosteronaemia and will be resistant to NaCl
57
Q

For each 10mmHg rise in PCO2 wehat impact does this have on HCO3 and pH

A

HCO3 rise by 0.08mmol/L
pH drop by 0.07
Rise in H+ by 8nmol/L

58
Q

Metabolic acidosis causes what change in PCO2 per mmol/L change in HCO3

A

0.1mmHg of PCO2 decrease per 1mmol/L decrease in HCO3

59
Q

What effect does temperature have on pH and PCO2

A

pH increased by 0.017 units for every 1 degree decrease in temperature

PaCO2 decreases by 4.5% for every 1 degree decrease

60
Q

What is alpha STAT and pH STAT

A

ALpha STAT is when the blood sample is warmed and measured at normal temperature - as the histidine residues pKa changes in parallel with the pH change intracellular function l;ikely maintained

pH STAT uncorrected temperature - arterial pH and PCO2 are maintained at constant values during cooling so CO2 content becomes greater

61
Q

How is the traditional Henderson Hasselbach approach to acid base different to Stewart?

A

Henderson Hasselbach assumed HCO3 behaves as an independent variable and the concentratoin of this determines the metabolic component of pH balance

HCO3 however varies with CO2 and can confuse metabolic interpretation

62
Q

What are the 3 laws determining H+ according to Stewarts theory

A

1/ Law of electroneutrality in aqueous solutions
2/ Law of mass action - dissociation equilirbia of all incompletely dissocited substances must be satisfied
3/ Law of conservation fo mass - total concentration is the suma of concentration of dissociated and undissociated substanes

63
Q

How does a decreased strong ion difference cause acidosis?

A

Decreased strong ion difference means that there are more measured anions usual, water dissociated more H+ and OH- to restore electropneutrality

64
Q

Atot normal range in Stewarts strong ion theory

A

12 - 24

65
Q

Increased Atot in Stewarts strong ion theory means what?

A

Acidosis
Increased phosphate in renal failure causes acidosis
Decreased Atot in hypoalbuminaemai causes alkalosis

66
Q

What is the classical method of describing causes of lactate rise?

A

Type A - impaired tissue perfusion
- Local
- Global
Type B
- B1 - disease state
- B2 - Drug related
- B3 - inborn errors of metabolism

67
Q

What are reasons for impaired tissue perfusion leading to lactic acidosis

A

Type A (lactic acidosis due to impaired tissue perfusion)
• anaerobic muscular activity (sprinting, generalised convulsions)
• tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia)
• reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning)

68
Q

What are the disease states that lead to lactic acidosis not related to hypoperfusion (B1)

A
  1. LUKE - leukaemia, lymphoma
  2. TIPS - thiamine, infection, pancreatitis, short bowel
  3. FAILURES - hepatic, renal, diabetic
69
Q

Why does sepsis lead to lactic acidosis

A

• Endogenous catecholamine release and use of adrenaline as an inotrope
• Circulatory failure due to hypoxia and hypotension
• Cytopathic hypoxia – widespread microvascular shunting and mitochondrial failure
• Inhibition of pyruvate dehydrogenase (PDH) by endotoxin
• Coexistent liver disease

70
Q

What is the most likely benefit of giving bicarbonate in lactic acidosis

A

Severe pulmonary hypertension and right heart failure to optimise RV function
Severe IHD where lactic acidosis is thought to contribute to arrhythmia risk

71
Q

Describe how lactate is related to hydrogen ions?

A

Lactate production from pyruvate CONSUMES a hydrogen ion intracellular alkalinising the intracellular fluid. Anaerobic metabolism in of itself does NOT produce H+

Metabolic acidosis does occur concurrently with raised lactate likely by concurrent process related to ATP turnover which lowers pH
1. ATP —> ADP produces H+
2. Inorganic phosphate fromATP buffers free proton before being reincorporated into aerobic metabolism to produce ATP
3. If net ATP production lags behind production then protons leave cell via Na/H exchanger

Therefore increased lactate can occur without increased acidosis if increased ATP hydrolysis doesn’t occur

72
Q

What medications are in particular involved with lactic acidosis?

A

Acute drugs
◦ adrenaline
◦ nitroprusside infusion

Chronic drugs
◦ beta-agonists e.g. salbutamol
◦ salicylates
◦ anti-retroviral drugs
◦ paracetamol
◦ biguanides

Other
◦ ethanol intoxication in chronic alcoholics
◦ methanol
◦ cyanide
◦ fructose
◦ sorbitol

73
Q

B3 causes of lactate rise

A

◦ congenital forms of lactic acidosis with various enzyme defects — e.g. pyruvate carboxylase deficiency, glucose-6-phosphatase and fructose-1,6-bisphosphatase deficiencies, oxidative phosphorylation enzyme defects)
* Type B3 was said to be the consequence of inborn errors of carbohydrate metabolism.

74
Q

What is D lactate?

A

D lactate is isomer of lactate produced by intestinal bacterial and not by humans — it is not detected on standard lactate assays — a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia

75
Q

Alternate system to lactate rise

A

Increased production
1. Lack of O2 - circulatory collapse, regional ischaemia, hypoxia, lack of oxygen carrying capacity
2. Failure of electron transport chain - Drugs and toxic alcohols
3. Metabolic process
- Inborn
- Pyruvate dehydrogenase inactitivity (thiamine, sepsis)
4.Upregulated glycolysis
- Beta action, catecholamine excess, malignancy

Reduced clearance
- hepatic/renal
- decreased gluconeogenesis due to ethanol and methanol or ketoacidosis

76
Q

Why might lactate clearance be reduced?

A
  • Lactic acidosis due to impaired hepatic or renal function
  • Decreased gluconeogenesis due to the ethanol and methanol
  • Decreased gluconeogenesis due to ketoacidosis
77
Q

What effect does lactate production have on intracellular acid base?

A
  • Lactate production from pyruvate consumes a hydrogen ion
    ◦ This alkalinises the intracellualr fluid
    ◦ Anaeorbic metabolism does not itself produce H+
78
Q

How does lactate production equate with acidosis

A
  • However metabolic acidosis does occur concurrently with raised lactate and likely by a concurrent process and is related to increased ATP turnover which lowers pH
    ◦ Hydrolysis of ATP to ADP produces H+
    ◦ Inorganic phosphate removed from ATP usually buffers free proton and it is then incoroportated into aeorbic metabolism to produce more ATP
    ◦ If the phosphate ion is rapidly recycled to rpodce more ATP in stressed metabolically active tissues this does not occur and if net production of ATP lags behind anaerobic production of H+ then protons will leave cell via Na/H exchanger
  • By the same logic increased lactate production can occur without acidosis if increased ATP hydrolysis does not occur
79
Q

What happens to solubility of oxygen and CO2 at low temperatures? Why does this matter for blood gasses?

A

The solubility of oxygen and carbon dioxide is increased at low temperatures -

The concentration of a solute gas in a solution is directly proportional to the partial pressure of that gas above the solution” according to Henry’s Law (k = P/C, therefore C = P/k). This assumes that temperature remains unchanged.
Temperature affects the equilibrium constant for the solvation process (k): the solubility of O2 and CO2 is increased at low temperatures. Thus at low temperatures, there will be a lower partial pressure for a higher dissolved concentration of gas
Oxygen and carbon dioxide increase in solubility as water temperature decreases, so their partial pressures will be less

Blood gas analyzers warm blood to 37°C

80
Q

What is the alpha STAT approach

A

compare results with normal results at a given temperature — samples warmed to 37C may be compared to normal results at 37C (alpha-stat approach)
At any temperature, an uncorrected pH of 7.4 and a PCO2 of 40 mmHg represents normal acid-base balance

81
Q

Which is the standard acid base approach in hypothermia?

A

Alpha STAT approach

compare results with normal results at a given temperature — samples warmed to 37C may be compared to normal results at 37C (alpha-stat approach)
At any temperature, an uncorrected pH of 7.4 and a PCO2 of 40 mmHg represents normal acid-base balance

82
Q

What will an uncorrected ABG show in hypothermic patients?

A

A warmed ABG from a hypothermic patient will show a higher PaO2, higher PaCO2, and a lower pH than that actually present in the patient’s blood in vivo

83
Q

What is the temperature correction for PaO2

A

PaO2 is decreased by 5 mmHg for each degree below 37C

84
Q

What is the temperature correction for PaCO2

A

PaCO2 is decreased by 2 mmHg for each degree below 37C

85
Q

Why does pH change with temperature?

A

Cooling causes the pH of a blood sample to increase

proton dissociation is an endothermic reaction (HA <-> H+ + A-), thus colder temperatures promote equilibration to the left (ie. formation of HA, rather than H+)
the change in pH with temperature is almost linear (Ashwood et al, 1983)
‘anaerobic cooling’ of a blood sample (ie cooling in a closed system) causes the pH to increase
If required, modern blood gas machines will report the pH value for the actual patient temperature
this ‘corrected value’ is calculated mathematically from the pH measured at 37C in the machine

86
Q

What is the correction factor for pH due to temperature

A

The Rosenthal correction factor is recommended for clinical use

Change in pH = 0.015 pH units per degree C change in temperature
If the measured pH is 7.360 at a blood gas electrode temperature of 37C, then the pH at a patient temperature of 34°C is calculated as follows: pH = [7.360 + (37-34)(0.015)] = 7.405`

87
Q

Describe the pH STAT approach?

A

PaCO2 is maintained at 40 mmHg and the pH is maintained at 7.40 when measured at the patient’s actual temperature (hypothermia)
it is, therefore, necessary to add CO2 to the inspired gas (via the oxygenator) to counteract the increased solubility of CO2 at lower temperatures
Higher PaCO2 (respiratory acidosis) is targetted than for the alpha-stat approach

88
Q

Describe the alpha STAT approach? How does this related to intracellular buffering? Why does this matter?

A

alpha (degree of dissociation) in this approach specifically refers to the ratio of protonated to total imidazole of histidine residues in intracellular proteins
0.55 is considered optimal for the function of intracellular enzymes
0.55 occurs at intracellular pH 6.8 and T 37C, which is seen physiologically
paCO2 and the pH are maintained at 40 mmHg and 7.40 when measured at 37 C (i.e. blood sample is warmed to normothermia for measurement)
When a patient is cooled during hypothermic cardiac bypass, and measurements are made at the patient’s actual temperature, pH will increase and the measured pCO2 and the pO2 will decrease with lowering of the patient’s temperature
Lower PaCO2 is targetted than for the pH-stat approach

89
Q

Why would pH STAT make sense? 4

A

Argument for the pH-stat approach targetting higher PaCO2

causes cerebral vasodilatation
results in increased jugular SvO2 implying increased cerebral blood flow and oxygen delivery

causes systemic vasodilatation resulting in faster, more homogeneous cooling

counteracts the leftward shift of the haemoglobin-oxygen dissociation curve that occurs with hypothermia and hypothermia-induced alkalaemia
-increases offloading of haemoglobin to the tissues
-may increase oxygen delivery

may optimise myocardial function

90
Q

Why does the alpha STAT approach make sense

A

Targeting a lower PaCO2

maintains pN, the normal pH of neutrality
allows cellular transmembrane pH gradients, intracellular trapping of metabolic intermediates, and protein function to be maintained
this occurs because protein buffering (via the imidazole rings of histidine residues) is also temperature dependent

maintains cerebral autoregulation, which becomes uncoupled with the pH-stat approach
avoids potential problems of excess cerebral blood flow such as intracranial hypertension and increased microembolisation

the alkaline pH improves cerebral protection during the ischaemic insult

avoids errors introduced by inaccurate body temperature measurement

91
Q

What is the pH of neutrality?

A

defined as the state when [H+] = [OH–]
is temperature dependent
occurs at pH 6.8 at 37C
intracellular pH has been measured at pH 6.8 at 37C
mammalian studies also show that intracellular pH is maintained at approximately pN despite temperature changes
experimental work has shown that the imidazole ring of histidine is responsible for the maintenance of pN as it is the only endogenous buffer that has the correct pK and whose pK changes appropriately with temperature

92
Q
A
93
Q

What happens to SBE usually when there is an elevated anion gap? What does it mean if this is not the case?

A

Elevated anion gap should be accompanied by an equal decrease in SBE
‣ If raised anion gap BUT normal SBE then metabolic alkalosis present pre-existing with new HAGMA
‣ If SBE has changed more than anion gap then non anion gap acidosis present

Acid base electrolytes (4 decks)

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