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Blood gases and acid–base balance 

Blood gases and acid–base balance
Author(s):

Stephen Chapman

, Grace Robinson

, John Stradling

, Sophie West

, and John Wrightson

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date: 29 November 2021

Interpretation of ABGs 1

Normal ranges

Breathing air: PaO2 >12kPa (>10 in normal elderly), PaCO2 4.6–5.9.

How to take

  • ABGs Best taken from radial, rather than brachial, artery due to dual radial/ulnar supply to hand. Use a heparinized syringe; analyse immediately or within 30min if kept on ice.

Always record date, time, and the % inspired O2.

  • Arterialized capillary sample An underused technique. Uses small glass pre-heparinized tube to draw up blood from a lancet puncture on the bottom end of the ear lobe. Blood gas machine must take microsamples (most do). PaCO2 levels are accurate enough for clinical practice, but good arterialization, with rubefacients (Algipan/Deep Heat) or heat and vigorous rubbing, are required for an accurate PaO2; the latter is less important, as oxygenation can be assessed by oximetry. Can easily be performed by nursing staff to monitor response to NIV and O2 therapy.

The three main things blood gases tell you about gas exchange

  • How much is the patient ventilating their alveoli? This is derived from the PaCO2. PaCO2 ≥6kPa ≈ underventilating, PaCO2 ≤4.5kPa ≈ overventilating

  • Is the PaO2 high enough to adequately oxygenate tissues and prevent anaerobic metabolism? PaO2 >6kPa (SaO2≈ 80%) is probably adequate; PaO2 >7kPa (SaO2 >87%) is definitely adequate

  • Is there evidence of V/Q mismatch? Evidence of low V/Q units is derived from the calculated A–a O2 gradient.

The two main things blood gases tell you about acid–base balance

(see later section on acid–base balance)

  • What is the respiratory component to an abnormal pH? This is derived from the PaCO2

  • What is the metabolic component to an abnormal pH? This is derived from the standard base excess/deficit.

The A–a gradient calculator graph sets out the graphical representation of gas exchange

(see Fig. A1.1)

  • Point ➀ = pO2 and pCO2 (virtually zero) of inspired air (atmospheric pressure ≈ 100kPa; air is 21% O2, and air is slightly ‘diluted’ by water vapour pressure (7kPa) following humidification by upper airways). 21% of 100–7 = 20kPa. (Point ➁ = pO2 and pCO2 when breathing 24% O2 via a Ventimask, and point ➂ = pO2 and pCO2 when breathing 28% O2 via a Ventimask.)

  • Point ➃ = theoretical pO2/pCO2 of alveolar gas when breathing air, if all the O2 removed and replaced by CO2 (equivalent to extreme hypoventilation and impossible!), when the respiratory quotient (RQ = CO2 produced/O2 consumed) is 0.8 (usual value)

  • The line between ➀ and ➃ ✌ with a gradient of 0.8, describes all possible combinations of alveolar gas, towards ➀ if ventilating more and towards ➃ if ventilating less, called the alveolar air line

  • Point ➄ = area in which PaO2 and PaCO2 of arterial blood sit normally. If lungs are perfect gas exchangers, then blood leaving the lungs and entering systemic arterial circulation (➃) should be perfectly equilibrated with the alveolar gas (A).

  • However, the mixed venous point = ➅ ✈ or the pulmonary arterial blood) is well to the left of the alveolar air line. This is because capillary PO2 falls more kPa than the PCO2 rises during gas exchange in the tissues (CO2 solubility curve is steeper than PaO2–SaO2 solubility, or dissociation curve)

  • Thus, if the lungs fail to oxygenate returning mixed venous/pulmonary arterial blood properly (e.g. area of consolidation, or low V/Q due to asthma/COPD), then it is as if mixed venous blood has bypassed the lung and ‘leaked’ into the arterial blood, which therefore drags the eventual arterial PaO2/PaCO2 point to the left of the alveolar air line, e.g. point ➆ ✎

Fig. A1.1 pCO2 vs pO2: alveolar air lines and A–a gradient calculator.

Fig. A1.1 pCO2 vs pO2: alveolar air lines and A–a gradient calculator.

Interpretation of ABGs 2

  • The horizontal distance between the actual arterial point and the ‘ideal’ alveolar air line (e.g. ➄ minus ➆, 3.5kPa) is called the alveolar to arterial (A–a) gradient and is a measure of how efficiently mixed venous blood is equilibrated with alveolar gas, i.e. it is a measure of V/Q mismatch, right-to-left shunts, and very severe lung fibrosis (through reduced diffusion across the alveolar capillary membrane). As well as being read off the graph, it can be mathematically calculated, as shown in Fig. A1.2.

Fig. A1.2 Calculation of inspired PO2 breathing air, 24 or 28% O2. Air, 21% of (100 – 7) ≈ 20kPa (where 100kPa is atmospheric pressure, and 7kPa is water vapour pressure due to the inspired air being humidified); 24%, 24% of (100 – 7) ≈ 23kPa; 28%, 28% of (100 – 7) ≈ 26kPa.

Fig. A1.2 Calculation of inspired PO2 breathing air, 24 or 28% O2. Air, 21% of (100 – 7) ≈ 20kPa (where 100kPa is atmospheric pressure, and 7kPa is water vapour pressure due to the inspired air being humidified); 24%, 24% of (100 – 7) ≈ 23kPa; 28%, 28% of (100 – 7) ≈ 26kPa.

In Fig. A1.1, the alveolar air line depends on the % inspired O2, and the two extra lines for 24% and 28% O2 are shown. In the calculation, the PIO2 has to be adjusted accordingly (see Fig. A1.2).

In normal lungs, matching of V/Q is not totally perfect due to relative underperfusion of the apices and overperfusion of the bases (gravity effects on pulmonary arterial blood flow, not fully compensated for by hypoxic vasoconstriction of pulmonary arterioles). These imperfections in V/Q and direct drainage of some of the cardiac muscle venous blood into the LV cavity, and hence systemic arterial circulation, lead to a small A–a gradient, 1–2kPa in the young and middle-aged and 2–3kPa in the elderly. Figures in excess of these values are abnormal and indicate areas of low V/Q or increased shunt.

Use of A–a gradient diagram: examples

Case 1

Consider point W in the pO2–pCO2 graph (see Fig. A1.3), the blood gases on air of a young non-smoker complaining of chest pain 7 days post-operatively. The PaO2 of 13 is normal. Does this reassure you or does it provide supporting evidence for a PE? Ask the following questions:

  • How much is the patient ventilating? PaCO2≈ 2; therefore ≤4.5kPa and indicates hyperventilation

  • Is the patient adequately oxygenated? PaO2 >7kPa; therefore OK

  • Is there an abnormal A–a gradient? Read off graph, horizontal line between W and alveolar line, or calculate:

Fig. A1.3 Examples of using A–a gradient.

Fig. A1.3 Examples of using A–a gradient.

20 – [13 + (2/0.8)] ≈ 4.5kPa

>2kPa, hence yes; therefore, the V/Q matching is not normal.

This provides supporting evidence for a PE but could just as well be due to consolidation from pneumonia, for example.

  • Remember, PaO2 cannot be used to assess V/Q matching in the lung without an associated PaCO2 to tell you ‘what the PaO2 ought to be’.

Case 2

Consider point X on the pO2–pCO2 graph (see Fig. A1.3). These are the gases on air from a young man following an overdose of methadone tablets.

  • How much is the patient ventilating? PaCO2≈ 11; therefore ≥6kPa and indicates hypoventilation

  • Is the patient adequately oxygenated? PaO2 only 6kPa; therefore not enough and needs extra O2

  • Has the patient got an A–a gradient?

20 – [6 + (11/0.8)] ≈ 0.8kPa

<2kPa, hence no; therefore, there is nothing wrong with the lungs, despite the abnormal gases; this represents pure hypoventilation.

After a messy stomach washout, he is sent to the ward and 24h later is febrile. Gases on 24% O2 are point Y on the graph; thus, both PaCO2 and PaO2 are better.

  • How much is the patient ventilating? PaCO2 just ≥6kPa; therefore is still hypoventilating a bit

  • Is the patient adequately oxygenated? PaO2 >7kPa; therefore adequately oxygenated

  • Has the patient got an A–a gradient?

23 – [11 + (6.5/0.8)] ≈ 4.2kPa

(remember, the PIO2 is 23kPa, because he is on 24% O2.)

>2kPa, hence yes; therefore may have developed an aspiration pneumonia.

Three things blood gases tell you about gas exchange

  • How much is the patient ventilating their alveoli?—PaCO2

  • Is the PaO2 high enough to adequately oxygenate tissues and thus prevent anaerobic metabolism?

  • Is there any evidence of a V/Q mismatch, assessed from the A–a gradient for O2?

Acid–base balance

Normal ranges

pH 7.37–7.43 (H+ 37–43nmol/L), PaCO2 4.7–5.9, base excess ± 3mmol/L.

Interpretation

Acid–base relationships are best plotted as a PaCO2 vs pH graph, because these are the two 1° measurements made by a blood gas machine (everything else to do with acid–base balance is calculated). This is shown in Fig. A1.4.

Fig. A1.4 Acid–base balance: PaCO2–pH. Lines running top left to bottom right are the iso-bicarbonate lines labelled as absolute [HCO3–] (in brackets) or as a base excess/deficit (relative to a [HCO3–] of 25meq/L), hence can be – (metabolic acidosis) or + (metabolic alkalosis).

Fig. A1.4 Acid–base balance: PaCO2–pH. Lines running top left to bottom right are the iso-bicarbonate lines labelled as absolute [HCO3] (in brackets) or as a base excess/deficit (relative to a [HCO3] of 25meq/L), hence can be – (metabolic acidosis) or + (metabolic alkalosis).

Normal acid–base is the area labelled N, the pH between 7.37 and 7.43, the PaCO2 around 5kPa. As ventilation is decreased or increased (PaCO2 going up or down, respectively), the pH will change, the amount depending on the buffering capacity of the blood (CO2 is an acid gas, combining with water to give [H+] and [HCO3] ions). Without buffering, the pH would fall disastrously following small rises in PaCO2. This buffering capacity depends mainly on Hb and other proteins, producing the normal buffer line running through N on the graph.

Therefore, acute hypoventilation and hyperventilation will move the patient up and down this line, in the direction b or c, respectively. If the hypoventilation at point b becomes chronic (e.g. as it may in COPD), then the kidney retains bicarbonate (by excreting [H+]) to try and correct the pH towards normal, and the patient moves onto a new iso [HCO3] buffer line displaced to the right, e.g. the one labelled +10meq/L (35meq/L). The degree of displacement represents the metabolic component to the acid–base status and, in this case, because the [HCO3] has risen, will be higher than the normal figure of about 25meq/L. When the raised figure is quoted relative to the normal 25meq/L (by subtracting 25), this is called the base excess. Thus, buffer lines to the right of the normal buffer line represent a metabolic alkalosis or base excess.

These figures are calculated, assuming a normal or ‘standard’ PaCO2, called the ‘standard bicarbonate’ (SBC on the blood gas machine printout) or ‘standard base excess’ (usually BE). The other similar figures on some printouts (usually HCO3 and TCO2) are calculated at the patient’s actual PaCO2 and are not much use.

Chronic hyperventilation

(e.g. at altitude due to the hypoxia) produces the opposite, a resorption of [H+] by the kidney, and the buffer line shifts to the left, giving a negative value for the ‘base excess’, a base deficit. Thus, a metabolic acidosis compensates for a respiratory alkalosis. Note that these corrections rarely bring the pH back to normal, as there needs to be an error signal to keep the correction process going.

A metabolic acidosis

(such as in ketoacidosis) will also move the line to the left (a), producing a base deficit (or negative base excess), followed by hyperventilation to try and correct it (i.e. a respiratory alkalosis to correct a metabolic acidosis). This pure ventilatory stimulation in the absence of abnormal lungs often produces deep breathing, with little increase in rate, and is called Kussmaul’s breathing. Thus, lines to the left of the normal buffer line represent a metabolic acidosis or base deficit.

Important point—

a metabolic acidosis, e.g. due to anaerobic metabolism (and hence lactic acid production), can reverse the compensatory metabolic alkalosis 2° to chronic hypercapnia, e.g. during a COPD exacerbation with severe hypoxia, thus removing the ‘evidence’ for previous chronic CO2 retention.

Finally, a metabolic alkalosis, e.g. during hypokalaemia (when the kidney is forced to use [H+], instead of [K+], to swap for the sodium that needs resorbing from the tubular fluid), moves the buffer line to the right (d) but with only limited hypoventilation available to compensate, due to the inevitable ventilatory stimulation the attendant hypoxaemia produces.

Thus, the mixture of respiratory and metabolic contributions to a patient’s acid–base disturbance can be established by plotting the PaCO2 and pH on the graph.

Anion gap

The anion gap [(Na+ + K+) – (Cl + HCO3)] shows the amount of other anions, apart from [Cl] and [HCO3], that exists and helps differentiate the cause of any metabolic acidosis. Depending on methods of measurement, the normal value is between 8 and 16mmol/L (or meq/L) and mainly due to albumin. High anion gap indicates loss of [HCO3] without a subsequent increase in [Cl]. Electroneutrality is maintained by increase in anions such as ketones, lactate, [PO4], and [SO4]. Because these anions are not part of the anion gap calculation, a high anion gap results.

An acidosis with a normal anion gap will be a simple HCO3/Cl exchange such as might occur, e.g. in:

  • Renal tubular acidosis

  • Acetazolamide therapy

  • [HCO3] loss from profuse diarrhoea.

An anion gap is likely to be present, e.g. when the metabolic acidosis is due to:

  • Diabetes, starvation, or alcohol-induced ketoacidosis (ketones are acids)

  • Renal failure (although can be in the normal range too)

  • Lactic acidosis

  • Salicylate poisoning

  • Methanol poisoning

  • Ethylene glycol (antifreeze) poisoning.

Three things arterial samples tell you about acid–base balance

  • Is there a ventilatory/respiratory component from an abnormally high or low PaCO2?

  • Is there a metabolic component evidenced by a shift of the buffer line to the left or right, numerically the base excess (or deficit)?

  • If there is a metabolic acidosis, is there an increased anion gap?

Further information

Williams AJ. ABC of O2.  Blood gases and acid–base balance http://www.bmj.com/cgi/content/full/317/7167/1213.

Conversion between arterial O2 saturation and O2 tension (Hb dissociation curve)

See Fig. A1.5 and Table A1.1.

Table A1.1 Conversion chart*

% saturation

kPa

mmHg

98

15.0

112

97

12.2

92

96

10.8

81

95

9.9

74

94

9.3

70

93

8.8

66

92

8.4

63

91

8.1

60

90

7.7

58

88

7.3

55

86

6.8

51

84

6.5

49

82

6.2

47

80

5.9

45

75

5.4

40

70

4.9

37

65

4.5

34

60

4.2

31

55

3.8

29

50

3.5

27

* Assumes a normal position of the Hb dissociation curve; kPa and mmHg conversion factor: 7.5 × kPa ≈ mmHg.

A fall in pH (more acidotic) or a rise in body temperature will move the dissociation curve to the right. This has the effect of making the PaO2 higher for any given SaO2, e.g. at pH 7.20, a measured saturation (e.g. by oximetry) of 90% is equivalent to a higher PaO2 of 9.7kPa (73mmHg) than the usual 7.7kPa (58mmHg); a rise in body temperature to 41°C will do the same, and the effects of pH and temperature are additive.

Conversely, for a given PaO2, pyrexia and acidosis will lower the SaO2 and thus O2 carriage to the tissues. A PaO2 of 7.7kPa (58mmHg) will normally give an SaO2 of 90%, but, if the temperature rises to 41°C and pH falls to 7.20, then the SaO2 falls to 70%.

Increasing 2, 3-DPG levels shift the curve to the right, but levels fluctuate unpredictably and any changes are small.

Changes in body temperature are often the reason why measured pulse oximetry saturations apparently ‘do not agree’ with the measured blood gases (pH is taken into account in the theoretical calculation of SaO2 by blood gas analysers, but the patient’s correct body temperature is rarely entered and thus is not taken into account). This is particularly important in hypothermia when the curve is left-shifted, leading to impaired O2 unloading. Furthermore, an apparently adequate oximetry reading can mask a low PaO2, which will further lessen O2 availability to the tissues (although somewhat mitigated by the reduced metabolic rate of hypothermic tissues).