ABG - Monograph J Holmes

8/6/2019 ABG - Monograph J Holmes

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ArterialArterialArterialArterial

BloodBloodBloodBloodGasesGasesGasesGases

Dr John L HolmesDirector Emergency Medicine , Mater Adult Hospital, Brisbane, Australia


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C O N T E N T S

SUBJECT PAGE

What's it all about? 3

Ventilatory and Pulmonary Function 3

Alvelar Gas Equation 3

Using the Alveolar Gas Equation 4

The A-a Gradient 5

Predicting the normal A-a Gradient 6

The Alveolar Gas Equation in Pulmonary Disease 9

Approximation to the Alveolar Gas Equation 11

Acid Base Disturbances 12

Physiology of Acid Base Homeostasis 13

Henderson Hasselbach Equation 13

ABGs in Acid Base Disturbances 14

Scheme for Interpretation of ABG results 15

Acid Base Nomogram 16

Metabolic Acidosis 17

The Anion Gap 17

Increased Anion Gap Acidosis 18

Normal Anion Gap Acidosis 19

Metabolic Alkalosis 20

Respiratory Acidosis 21

Rspiratory Alkalosis 23

Mixed Acid Base Disorders 24

Clinical Examples of Acid Base Disorders 25

Summary 28

Formulae and Rules of Thumb 29


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ARTERIAL BLOOD GASES

In medicine many laboratory tests may be ordered as a matter of "routine" or on the offchance that something just might turn up to help explain a patient's condition. One ofthe frequently performed laboratory tests in the Emergency Department is the analysis

of arterial blood gases (ABG's). It is often not realised that the ABG's have thepotential to reveal far more information than may initially be suspected from a casualperusal of the numberers on the computer screen or print out.

The following is the hitchhiker's guide to arterial blood gases. Hopefully after readingthese notes you may be persuaded to take a little extra time to sit down and analyseABG results and to think about what they imply. You might learn more about yourpatient than you suspected!

WHAT'S IT ALL ABOUT?

There are two main reasons for performing ABGs:

1. To assess ventilatory and pulmonary function2. To assess acid base disturbance

1. VENTILATORY AND PULMONARY FUNCTION

The PaCO2 gives an indication of VENTILATION ie: a measure of the adequacy of themovement of gas in and out of the alveoli.

The PaO2, (when related to the FiO2 and PaCO2) gives an indication of PULMONARYFUNCTION ie: the efficacy of gas exchange between the alveoli and the blood.

The key to all this is the ALVEOLAR GAS EQUATION but before discussing this wefirst have to understand some basic terminology.

A lower case "a" stands for "arterial" thus PaO2 = the partial pressure of oxygen inarterial blood.

An upper case "A" stands for "alveolar" thus PAO2= the partial pressure of oxygen inalveolar gas.

"F" stands for "fractional concentration" and "i" for "inspired". Thus FiO2 = "Fractionalconcentration of inspired oxygen" and is usually expressed as a decimal fraction. Webreathe atmospheric air at an Fi O2 of 0.21.

OK, here's the ALVEOLAR GAS EQUATION:

PAO2 = PiO2 - PaCO2 + F

R

where R is the Respiratory Quotient and usually = 0.8

and F is a negligible correction factor.

This equation states that:


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The partial pressure of oxygen in the alveolar gas

is equal to

the partial pressure of oxygen in the inspired gas

minus

the partial pressure of carbon dioxide present in the alveolar gas.

In other words, there is a reciprocal balance between the amount of oxygen andcarbon dioxide in the alveoli.

Because carbon dioxide diffuses readily across biological membranes, the alveolarpartial pressure of CO2 is equal to its partial pressure in arterial blood. Hence thePACO2 term can be replaced with the more useful PaCO2. (which we can measure).

And because dividing by O.8 is the same as multiplying by 5/4, the equation becomes:

PAO2 = PiO2 - 5 . PaCO2

4

IMPRINT THIS EQUATION ON YOUR BRAIN - it will prove to be of inestimable valuewhenever you need to interpret ABG's. You'll also be surprised to find out that ABGswhich initially may seem to imply that all is well with a patient, may actually reveal amore sinister degree of pulmonary dysfunction (and sometimes vice versa).

USING THE ALVEOLAR GAS EQUATION

It is necessary to first determine the partial pressure of inspired oxygen (ie: PiO2).

The partial pressure of an individual gas is proportional to its fractional concentration inthe gas mixture, thus:

PiO2 = Patmos - PH2O X FiO2

where PH

2O

= the Saturated Vapour Pressure of Water ( = 47 mmHg at 37

o

C). Inthe respiratory tract, the inspired air becomes fully saturated with water vapour and thismust be corrected for.

Atmospheric pressure at sea level = 760 mmHg, thus for a person breathing room airat sea level (where FiO2 = 0.21)

PiO2 = (760 - 47) x 0.21 = 150 mmHg

If the patient was breathing 35% oxygen

PiO2= (760 - 47) x 0.35 = 250 mmHg

What does the alveolar gas equation predict in the "normal" situation for a personbreathing room air?


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The normal value of PaCO2 = 40 mmHg and PiO2 O2 = 150 mmHg

Substituting these values into the alveolar gas equation, we get:


4

= 150 - 5 . 40

4

= 150 - 50

= 100 mmHg

In a healthy young adult, the alveolar oxygen tension approximates the arterial oxygentension ( ie: PAO2 = PaO2 ) and hence our "normal" subject should have a PaO2 ofapproximately 100 mmHg.

THE A - a GRADIENT

Nothing in life, however, is perfect, and gas exchange between the alveoli and theblood is not 100% efficient. Usually the arterial partial pressure of oxygen is somewhatless than the alveolar oxygen tension.

The difference between the calculated PAO2 and the measured PaO2 is the A - agradient. It is written in a variety of ways including P(A-a)O2 or (A -a)DO2.

Factors Influencing the A - a gradient

1. Age2. Inspired oxygen partial pressure of oxygen & PAO23. Pulmonary disease

1. Age

For young people it's OK to have an A - a gradient of up to 15 mmHg on air and ittends to get bigger with advancing age.

A useful rule of thumb is that the maximum A - a gradient (breathing air) should equalapproximately one third the age.


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2. Inspired partial pressure of Oxygen

On supplemental oxygen, the A - a gradient is widened, but the extent of this isinfluenced by a number of factors including the shape of the oxygen dissociation curveand the degree of intrapulmonary shunting (V/Q mismatch).

In normal lungs there is relatively little widening of the A -a gradient with increasingFiO2. However, when there is a significant degree of V/Q mismatching, the A - agradient does widen markedly with increasing FiO2 (see fig:4).

Predicting the Normal A-a Gradient

This formula relates normal A-a gradients to the effects of both AGE and PAO2 :

A - a gradient = Age + PAO2 - 23

3 5

Consider a 60 year old man breathing 50% oxygen and with a PaCO2 of 40 mm Hg.

From the alveolar gas equation, the PAO2 = (713 X 0.5) 5 X 40/4 = 307 mmHg.

He may thus be expectedto have an A - a gradient of 60/3 + 307/5 - 23 = 58 mmHgand his PaO2 should be around 307 - 58 = 249 mmHg.

If his measured PaO2 was significantly less than this, then there would be a strong

possibility of pulmonary disease.

PAO2 mmHg

150

140

130

120

110

100

90

80

70

60

50

40

30

20

10

00 100 200 300 400 500 600 700 800

A - a gradientmmHg

80604020

Age (years)

Fig. 1. A - a gradient as a function of Age and PAO2


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Fig. 2. PaO2 as a function of Age and FiO2 (assuming a PaCO2 of 40 mmHg)

age (years)

PaCO2mmHg

120

110

100

90

80

70

60

50

40

30

20

10

0

20

PaO2 mmHg

0 20 40 60 80 100

30

40

100

90

80

50

70

60

A -agr adie nt

Fig. 3 PaO2 as a function of Age and PaCO2 (breathing room air)

age (years)

FiO2600

550

500

450

400

350

300

250

200

150

100

50

0

1.0

0.60

0.50

0.35

0.21

PaO2 mmHg

0 20 40 60 80 100


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3. The A - a Gradientin Pulmonary Disease

In pulmonary disease, the A - a gradient is increased.

NOTE: The A -a gradient is NOT affected by just alveolar hypoventilation alone.

There are three pathological causes of increased A - a gradient in pulmonary disease:

1. Ventilation / perfusion inequality (most important)

2. Barriers to gas diffusion from the alveolus into the blood.

3. Arterio - venous "shunts"

PAO2 mmHg

500

400

300

200

100

0

A - a gradientmmHg

0 100 200 300 400 500 600 700 800

50%

20%

15%

5%

1%

Fig. 4 Effect on A-a gradient of increasing PAO2 at differing degrees of V/Q mismatch


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THE ALVEOLAR GAS EQUATION IN PULMONARY DISEASE

To give an idea of how to apply the alveolar gas equation in practice, we'll considersome clinical scenarios.

Case 1

A 54 year old man presents with dyspnoea and fever. He has pleuritic chest pain andcough and on examination he has an area of bronchial breathing at the left base. CXRis suggestive of left lower lobe pneumonia.

You have taken ABG's with the patient breathing oxygen at 35% (FiO2 = 0.35).

The results are: pH = 7.35PaO2 = 92PaCO2 = 46

HCO3 = 26BE = -2SpO2 = 97%

We shall ignore the acid/base parameters in this case and concentrate on therespiratory function. The question to be answered is: Is there a significant degree ofpulmonary impairment?

At first glance, these gas results seem reasonable - the PaO2 = 92 which is OK andthe PaCO2 is only minimally elevated (46 mmHg normal range 35 45).

But let's now plug these numbers into the alveolar gas equation:


4

= (760-47) X 0.35 - 5 X 46

4

= 249.6 - 57.5

= 192 mmHg

The MEASURED PaO2 = 92 mmHg

Thus the A - a gradient = 192 - 92 = 100 mmHg

The predicted normal A -a gradient for this man is:

Normal A - a = AGE / 3 + PAO2 / 5 - 23

= 54 / 3 + 192 / 5 - 23

= 33 mmHgThe patient thus has a significantly increased A - a gradient which implies that there isa large degree of pulmonary dysfunction, even though he is maintaining an adequatePaO2 on supplemental oxygen therapy.Looking at it from another angle, if we apply the normal A-a gradient for his age wewould expect his measured PaO2 to be at least 192 33 = 159 mmHg on this FiO2


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Case 2

A 21 year old female is found comatose in the street, possibly as the result of a drugoverdose. She is somewhat cyanosed and you are concerned that she may haveaspirated vomitus. Her arterial blood gases on room air are:

pH = 7.29PaO2 = 71PaCO2 = 58HCO3 = 25BE = -1SpO2 = 82%

Using the alveolar gas equation:


4

= (760-47) X 0.21 - 5 X 58

4

= 149.7 - 72.5

= 77 mmHg


Thus the A - a gradient = 77 71 = 6

This is a low A -a gradient and tells us that the patient's hypoxaemia is due solely tohypoventilationand notdue to pulmonary disease (including aspiration).

The correct initial management of this patient is to assist her ventilation using bag &mask. However, note that she still needs supplemental oxygen until she is breathingup moreadequatelyas she will undoubtedly, after she is given naloxone.

Case 3

A 45 year old woman is brought into the Emergency Department following a motorvehicle accident in which she sustained multiple injuries including blunt trauma to thechest. She is conscious but distressed.

She is administered high flow oxygen at an estimated concentration of 60% and hasthe following arterial blood gases:

pH = 7.29PaO2 = 151

PaCO2 = 52HCO3 = 22BE = -3SpO2 = 97%


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Initial assessment of thses results suggests that oxygenation appears to be adequate,though there is an elevated PaCO2 of 52 suggesting underventilation.

Using the alveolar gas equation:


4

= (760-47) X 0.60 - 5 X 52

4

= 427.8 - 65.0

= 363 mmHg


Thus the A - a gradient = 363 - 151 = 212

The estimated normal A -a gradient for this lady breathing 60% oxygen is beapproximately:

= AGE / 3 + PAO2 / 5 - 23= 45/3 + 363/5 - 23= 65

The significantly widened A -a gradient in this case tells us that, despite maintaining anadequate PaO2 of 151 mmHg on supplemental oxygen, this patient nevertheless hasa significant degree of pulmonary dysfunction IN ADDITION to her hypoventilation.She should have a PaO2 = 363 65 = 298 mmHg. Her ABGs are consistent withpulmonary contusion or haemothorax etc.

The above cases illustrate that the careful assessment of ABG's using the alveolar gasequation can give us a lot more information about a patient's pulmonary status thaninitial reading of the results might suggest.

In some cases, as in patients 1 and 3 above, an adequate PaO2 on supplementaloxygen may be obscuring underlying pulmonary pathology. Conversely, patient 2 is anexample of where hypoventilation gives the impression of pulmonary pathology butwhere in fact lung function per seis adequate.

Approximation to the Alveolar Gas Equation

For most circumstances the alveolar gas equation can be approximated to :

PAO2 = 7 X %O2 - PaCO2 - 10

Applying this formula to the first example above (54 y.o. man on 35 % oxygen):

PaO2 = 92


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PaCO2 = 46

PAO2 7 X 35 - 46

245 - 46

199 mmHg

When calculated using the original formula:

PAO2 = (760-47) X 0.35 - 46 X 5/4= 250 - 58= 192 mmHg

2. ACID - BASE DISTURBANCES

Acid/base physiology can be fairly daunting but unfortunately we do have to know asmattering of this subject, so the following is a primer. Luckily, when it comes toworking out what is going on from the ABG's, there are a few rules of thumb which canaid in interpretation. We shall come to these later.

BASIC PHYSIOLOGY OF ACID/BASE HOMEOSTASIS

The pH of body fluids is maintained within a narrow range by homeostatic mechanismsof which there are three major players:

1. Kidneys2. Lungs / Respiratory centre3. Buffer systems

Of the various buffering systems in the body, by far the most important is theBICARBONATE - CARBONIC ACID system.

Importantly, the variables in this system (bicarbonate and PaCO2) are independentlyregulated by the kidneys and central respiratory centre respectively.

We thus talk about the metabolic and respiratory components of acid/base

homeostasis and by measuring the plasma bicarbonate and PaCO2 in arterial blood,we get an indication of the aetiology of any underlying acid/base disturbance.

Either the bicarbonate or PaCO2 may be primarilydisturbed depending on whether thefundamental problem is metabolic or respiratory in origin. In addition, both may besecondarily altered in compensation for other acid/base abnormalities.

The important chemical relationship representing the bicarbonate buffer system is:

CO2 H2O+ H2CO3 + H2CO3-

H+


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Derivation of the Henderson - Hasselbalch Equation

[H+] . [HCO3

-]

Ka = b definition[H2CO3]

[HCO3-]

and log Ka = log [H+] + log

[H2CO3]

[HCO3-]

- lo Ka = - lo H+

- lo[H2CO3]

[HCO3-]

Thus pKa = pH - log[H2CO3]

[HCO3-]

And pH = pKa + log[H2CO3]

Now the plasma concentration of carbonic acid is directly proportional to the partialpressure of CO2 in the plasma, the solubility coefficient being 0.03 mmol/litre/mmHg.

[HCO3-]

Thus pH = pKa + log0.03 PaCO2

This is the famous Henderson - Hasselbalch equation.

The important thing to realise is that the RATIO of plasma bicarbonate concentration tothe PaCO2 needs to be kept constant in order to maintain a constant plasma pH. Thusif bicarbonate concentrations fall, then in order to maintain pH, PaCO2 must also fall.Conversely, if bicarbonate concentrations rise, then PaCO2 must also rise.

Irrespective of whether PaCO2 or bicarbonate is primarily disturbed, the other follows in

compensation to maintain the ratio and thus maintain pH.

The pKa of carbonic acid is 6.1. Normal serum bicarbonate = 24 mmol/L and normalPCO2 is ~ 40 mmHg. Thus the Henderson - Hasselbalch equation can be used topredict normal plasma pH:

[HCO3-]

pH = pKa + log0.03 PaCO2

24

= 6.1 + log 0.03 X 40

= 6.1 + log 20= 6.1 + 1.3

= 7.4


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Other buffer systems also have effect on acid/base homeostasis though they are notas quantifiably important as the bicarbonate system. In addition there are other renalresponses to pH disturbance.

ARTERIAL BLOOD GASES IN ACID/BASE DISTURBANCES

When confronted with a possible acid/base disturbance, it is important to determine ifthe disturbance is predominantly metabolic or respiratory in origin, and to recognise theappropriate type and degree of homeostatic compensation.

A metabolic disturbance invokes a respiratory compensation which is fairly rapid inonset. A respiratory acid/base disturbance invokes a metabolic compensatoryresponse which takes a few days to become maximal.

Scheme fo the Interpretation of Arterial Blood Gases

1. Look at the pH

Decide if acidosis or alkalosis is present. Normal range 7.35 - 7.45. Note thatcompensations for acid/base disturbances are rarely complete.

2. Look at the BICARBONATE

If then either a primary metabolic alkalosis or compensated respiratory

acidosis is present. If then either a primary metabolic acidosis or

compensated respiratory alkalosis is present.

3. Look at the PaCO2

If then either a primary respiratory acidosis or compensated metabolic

alkalosis is present. If then either a primary respiratory alkalosisorcompensated metabolic acidosis is present.

Note that underlying respiratory pathology may make interpretation difficult.

Aide memoire

Note that both the PaCO2 and the bicarbonate tend to move in the same direction.

If the PaCO2 and the bicarbonate move in the SAME direction as the pH change, thenthe problem is METABOLIC in origin.

If the PaCO2 and the bicarbonate move in the REVERSE direction to the pH change,then the problem is RESPIRATORY in origin.


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pH-

PCO2-

HCO3-

ACIDOSIS

Metabolic

Respiratory

ALKALOSIS

Metabolic

Respiratory

Figure 4: Summary Acid Base Disturbances

You will note that we have completely ignored the so-called BASE EXCESS. Thisparameter is a derived value and can sometimes be misleading. It should not benecessary for you to look at the BE (especially now that you have a goodunderstanding of what's going on with the PaCO2 and bicarbonate).

Figure 5 is an acid - base nomogram and plots the relationship between plasmabicarbonate and arterial PCO2 at different pH levels. The shaded areas show the

approximate ranges of HCO3-and PaCO2 which occur with pure acid-base

disturbances.


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Figure 5. ACID - BASE NOMOGRAM

7.7 7.6 7.5 7.4

7.3

7.2

7.1

7.0

6.9

6.8

pH50

40

30

20

10

0

PCO2 mmHg

metabolicacidosis

chronicresp

alkalosis

acuteresp

alkalosis

metabolic

alkalosis

chronicresp

acidosis

acuteresp

acidosis

20 40 60 80 1000

HCO3-

mmol/L

24


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Rules of thumb formulae which can be used to predict bicarbonate and PaCO2 levelsin various acid-base disturbances are based on this and similar nonograms.

METABOLIC ACIDOSIS

Metabolic acidosis is characterised by a primary fall in the plasma bicarbonateto lessthan 24 mmol/L.

There are three main causes:

1. Increased production or gain of non-volatile acids2. Decreased acid excretion by the kidney3. Loss of alkali from the body

H+

ions react with HCO3-to form carbonic acid (H2CO3) which dissociates to form CO2

and H2O. Increased H+

ion concentration (ie: lowered pH) stimulates ventilation andPaCO2 is reduced (despite the increased production of CO2).

Metabolic acidosis may be divided into two major groups depending on whether theANION GAP is widened or not.

METABOLIC ACIDOSIS

INCREASED ANION GAP NORMAL ANION GAP( non-volatile acids) (hyperchloraemic acidosis)

1. acid production 1. Loss of Alkali

Ketoacidosis Diarrhoeadiabeticalcoholicstarvation

OstomiesCarbonic anhydrase inhibitionRenal tubular acidosis (proximal)

Lactic acidosis

2. Exogenous acid ingestion 2. excretion of H+

ions

Salicylates HypoaldosteronismMethanol Renal tubular acidosis (distal)Ethylene glycol

3. acid excretion 1. Cationic acids

Renal failure TPNMethanol NH4ClEthylene glycol

figure 6: Causes of metabolic acidosis


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The Anion Gap is the difference between the measured anions and cations in plasma.

( Na+

+ K+

) - (Cl-

+ HCO3-)

Although there is electrical neutrality, there is normally an anion gap of up to 15 mmol/L

due to the presence of negatively charged moieties (especially proteins) which are notusually measured in standard laboratory testing.

An increase in the anion gap is found when there is an accumulation of anionic forms

of non-volatile acids (eg: acetoacetate, lactate, SO42-

, PO43-

etc).

Thus acidosis due to the accumulation of non-volatile acids is known as increasedanion gap metabolic acidosis.

In non-anion gap acidosis there is no change in the levels of non-volatile acids.However, there is usually loss of bicarbonate (which is compensated for by a rise inchloride ion) or decreased excretion of hydrogen ions by the renal tubules.

Non-anion gap acidosis can also be caused when there is the administration of cationicacids (as in TPN). These forms of acidosis are also known as hyperchloraemicacidosis.

INCREASED ANION GAP ACIDOSIS

There is an accumulation of non-volatile acids either through increased production,ingestion or decreased excretion.

1. Increased Acid Production

1.1 Ketoacidosis:

Diabetes: There is accumulation of acetoacetate and beta-hydroxybutyrate.

Alcoholism: Often middle aged females following a period of starvation. Beta-hydroxybutyrate is the predominant ketone and this may lead to ketosis beingmissed as routine testing usually only detects acetoacetate.

Starvation: Mild ketosis is due to increased fat metabolism.

1.2 Lactic Acidosis:

Tissue hypoxia and subsequent anaerobic glycolysis usually secondary to shock(including sepsis) or respiratory failure.

May be associated with liver necrosis, leukaemia, solid tumours or diabeticketoacidosis.

Drugs and Toxins: biguanides, alcohol, cyanide, salicylates etc.

TPN. - Fructose metabolism

Congenital enzyme defects


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2 Exogenous acid ingestion or administration

2.1 Poisoning:

Ethylene glycol: Metabolised to aldehydes and oxalic acid.

Salicylates: Produce build up of endogenous organic acids (acetoacetate,lactate, pyruvate) due to impairment of carbohydrate metabolism.

Methanol: Oxidised by alcohol dehydrogenase to formaldehyde and formicacid. Formic acid is buffered to formate but also blocks carbohydratemetabolism leading to accumulation of organic acids.

3. Decreased Excretion of Non-volatile Acid

3.1 Chronic Renal Failure:

Principal defect is decreased excretion of NH4+

and other non-volatile acids such assulphate and phosphate.

There may also be some renal wasting of bicarbonate.

NORMAL ANION GAP ACIDOSIS

The loss of bicarbonate is balanced by an increase in chloride ion thereby maintainingelectrical neutrality.

1. Loss of Alkali

1.1 Gastrointestinal Losses:

From diarrhoea, pancreatic fistulae, "ostomies".

1.2 Carbonic Anhydrase Inhibition:

Carbonic anhydrase is required for tubular conservation of bicarbonate which is thus

lost in the urine when the enzyme is inhibited. At the same time HCl is reabsorbed.

1.3 Proximal Renal Tubular Acidosis

A defect in the proximal renal tubule leads to decreased reabsorption of bicarbonateand large losses of bicarbonate in the urine.

2. Dilution of Bicarbonate Concentration

Extracellular fluid volume expansion by normal saline dilutes bicarbonateconcentration.


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3. Decreased Excretion of H+

Ion

3.1 Hypoaldosteronism

Aldosterone promotes Na+ conservation and H+ and K+ excretion. Inhibition ofaldosterone thus causes H+ ion retention (and hyperkalaemia) which also decreasesNH3 production.

3.2 Potassium sparing diuretics

These inhibit the distal tubular secretion of acid and potassium.

RULES OF THUMB IN METABOLIC ACIDOSIS

If pH = 7.XY, then PaCO2 XY

(eg: pH = 7.29, PaCO2 29)

C = 1 B + 10 (C = PaCO2 and B = Bicarbonate)

eg: If Bicarbonate = 16 mmol/L, PCO2 should be approx. 16 X 5/4 +10 = 30 mmHg

METABOLIC ALKALOSIS

Characterised by a primary increase in the plasma bicarbonate (> 28 mmol/L)

Pathophysiology

There is either a net gain of bicarbonate ora net loss of hydrogen ion.

Normally there is very efficient renal excretion of excess bicarbonate, so for alkalosis tobe maintained, an additional mechanism is required whereby bicarbonate issignificantly reabsorbed or regenerated.

Clinically the maintenance of metabolic alkalosis is most often associated withextracellular fluid volume deficit. During ECF contraction, the renal conservation ofsodium under the influence of aldosterone takes precedence over acid/basehomeostasis. In these circumstances there is NaCl depletion and most Na

+ions are

paired with HCO3-. The reabsorption of Na

+from the renal tubules therefore also

results in the reabsorption of HCO3-

into the plasma, thereby maintaining alkalosis.This can be treated by the administration of Normal Saline which provides Cl

-ions in

place of HCO3- ions.

Similarly primary hyperaldosteronism may initiate and maintain metabolic alkalosisdue to excess excretion of H

+ions (in preference to sodium which is conserved).


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Severe hypokalaemia may also be a cause of metabolic alkalosis and also contributesto its maintenance. When serum potassium levels fall, there is exchange ofintracellular K

+for extracellular H

+ions. This movement of H

+ions into cells raises the

pH of the ECF. Also in the kidney, H+

ions are excreted in preference to K+

ions.

METABOLIC ALKALOSIS

CAUSES MAINTAINANCE

1. Loss of H+

ions

VomitingGastric drainage

Renal lossesPrimary hyperaldosteronismSecondary hyperaldosteronismCushings syndromeBartters syndromeDrugs: steroids, diuretics, carbenoxolone

extracellular fluid volumeHyperaldosteronism

Hypokalaemia (severe)

2. Gain of Bicarbonate

NaHCO3 administrationMetabolic conversion of lactate, citrate, acetate

Figure 7: Causes of metabolic alkalosis

ARTERIAL BLOOD GASES IN METABOLIC ALKALOSIS

pH and HCO3-are elevated. There is a highly variable respiratory compensation.

Increased pH leads to hypoventilation and subsequent increased PaCO2.Thus pH, bicarbonate and PaCO2 are all elevated in metabolic alkalosis.

RULE OF THUMB:

C = B / 2 + 30 (C = PaCO2 and B = Bicarbonate)

eg: If Bicarbonate = 37 mmol/L, PCO2 should be approx. 37 / 2 +30 = 49 mmHg


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RESPIRATORY ACIDOSIS

Ventilatory failure leads to CO2 retention and an increased PaCO2 due to ongoingmetabolic production of carbon dioxide.

The increased CO2 forms carbonic acid which dissociates to bicarbonate and water.Metabolic compensation occurs in chronic respiratory acidosis with the renalconservation of bicarbonate and increased secretion of acid.

RESPIRATORY ACIDOSIS

ACUTE CHRONIC

Thoracic traumaAcute respiratory disease Chronic respiratory disease

asthmaacute pulmonary oedamapneumonia / pneumonitis

COPD , emphysemachronic asthmafibrosing alveolitis

Neuromuscular disease Morbid obesity (Pickwickian)Drugs (opiates & other CNS depressants)

intracerebral pressuremeningitis, encephalitishead traumacerebral haemorrhageexpanding space occupying lesion

Brainstem stroke

Cardiac arrestFigure 8: Causes of respiratory acidosis

The underlying causes of acute or chronic ventilatory or circulatory failure should becorrected clinically. The administration of bicarbonate to "correct" a pure respiratoryacidosis is counterproductive as it is converted to CO2, compounding the underlyingproblem. 100 mmol of bicarbonate is the equivalent of giving 2.5 litres of CO2 !

RULES OF THUMB IN RESPIRATORY ACIDOSIS

In acute respiratory acidosis, the HCO3- by 0.1 mmol per 1 mmHg in the PaCO2

(due to the equation CO2 + H2O H2CO3 HCO3-

+ H+

being driven to the right).

In chronic respiratory acidosis, the HCO3- by 0.3 0.4 mmol per 1 mmHg in the

PaCO2 (due to compensatory renal reabsorption of bicarbonate).

These trends are represented in the following two formulae: (again B = Bicarbonate andC = PaCO2)

B = C / 10 + 20 (AcuteRespiratory Acidosis)

B = C / 2 + 2 (ChronicRespiratory Acidosis)


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Example : If the PaCO2 = 60 mmHg

If this were acute respiratory acidosis (eg: acute asthma), the HCO3-

should be

60/10 + 20 = 26 mmol/L. If this were chronic respiratory acidosis (eg: COPD blue bloater), the HCO3

-

should be 60/2 + 2 = 32 mmol/L.

RESPIRATORY ALKALOSIS

Essentially due to hyperventilation and loss of CO2.

RESPIRATORY ALKALOSIS

RESPIRATORY CENTRE STIMULATION OTHER

Acute hypoxia Anxiety hyperventilation syndromeasthmaacute pulmonary oedamapneumonia

ExerciseArtifical ventilationPregnancy

Chronic hypoxiapulmonary fibrosiscyanotic heart disease

altitudeFeverDrugs (salicylates, amphetamines etc)Cerebral disease / head injury

Figure 9: Causes of Respiratory Alkalosis

The loss of CO2 in hyperventilation leads to a reduction in plasma HCO3-

The degreeof compensation depends on whether the process is acute or chronic. In fullycompensated respiratory alkalosis the pH may actually return to normal (the only acid /base disturbance where compensation may be completely effective).

RULES OF THUMB IN RESPIRATORY ALKALOSIS

In acute respiratory alkalosis, the HCO3- by 0.25 mmol per 1 mmHg in the PaCO2

(due to the equation CO2 + H2O H2CO3 HCO3-

+ H+

being driven to the left).

In chronic respiratory acidosis, the HCO3- by 0.50 mmol per 1 mmHg in the

PaCO2 (due to compensatory renal excretion of bicarbonate).

These trends are represented in the following two formulae:

B = C / 4 + 14 (Acute Respiratory Alkalosis


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B = C / 2 + 4 (Chronic Respiratory Alkalosis)

again - B = Bicarbonate and C = PaCO2

Example : If the PaCO2 = 28 mmHg

If this were acute respiratory alkalosis (eg: hyperventilation syndrome), the HCO3-


If this were chronicrespiratory acidosis (eg: adaptation to high altitude), the HCO3-


MIXED ACID - BASE DISORDERS

It has been said that life wasn't meant to be easy. It is not unusual for patients to besuffering from multiple pathology. In such cases acid/base disturbances may also bemultifactorial in origin.

For example, in salicylate poisoning, direct stimulation of the respiratory centre initiallyleads to a respiratory alkalosis. However, after a few hours, the salicylates cause anuncoupling of oxidative phosphorylation resulting in an additional co-existent lacticmetabolic acidosis. Another example would be a patient with sepsis due to pneumoniawho may have both a metabolic and respiratory acidosis.

In cases such as these, interpretation of ABG's on first reading may not lead to an

obvious conclusion. However, with a bit of inspired perspicacity the primary disordercan usually be identified (usually on the basis of the history) and coexistent pathologycan be surmised. By application of the appropriate rule of thumb formulae, the clinicalimpressions can be verified. Let's illustrate the process using a clinical example:

Case 4

A 4 year old child is brought to the Emergency Department and the parents tell you hemay have taken some pills about 4 hours ago. The childs temperature is 38.5

oand

the respiratory rate is 40 per minute. The rest of the clinical examination is normal.

The ABG's (on air) are as follows:

pH = 7.50PaO2 = 119PaCO2 = 21HCO3

-= 14

BE = 3There is obviously an alkalosis (pH=7.50) and because the pH is whilst the PaCO2

and HCO3-are both , the primary disorder must be respiratory in origin.

However, is this the whole story? Because from the history this is likely to be an acuteprocess, let's plug the figures into our formula for acute respiratory alkalosis:


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ABGs 25

Predicted B = 1/4 C + 14

= 21/4 + 14

= 19 mmol/L

The measured bicarbonate (14) is actually significantly less than this. So whats goingon? The discrepancy can be explained by postulating that in addition to the majorproblem of respiratory alkalosis, there is an additional process causing a metabolicacidosis which is driving the bicarbonate even further down. This is exactly the pictureseen in acute salicylate intoxication where salicylates initially directly stimulate therespiratory centre causing hyperventilation (acute respiratory alkalosis) but later poisonaerobic glycolysis leading to lactic acidoisis.

CLINICAL EXAMPLES OF ACID - BASE DISTURBANCES

Case 5

A 68 year old man with a history of "bronchitis" presents in respiratory distress withwheeze. He is placed on low flow oxygen (estimated FiO2 = 0.25). His ABG's are:

pH = 7.34PaO2 = 86PaCO2 = 49HCO3

-= 26

BE = 0SpO2 = 87%

The primary acid/base disturbance appears to be respiratory acidosis as the pH is lowbut the PaCO2 and HCO3

-are both elevated. However, can we be sure that this is a

pure respiratory acidosis and if so is it likely to be acute or chronic?

Using the formula for acute respiratory acidosis:

Predicted Bicarbonate = PCO2 / 10 + 20= 49/10 + 20= 25

This accords well with the measured result and thus these results are consistent with apure acute respiratory acidosis.

It is instructive to analyse the respiratoryfunction also in this case. Uing the alveolargas equation as previously:


4

= (760-47) X 0.25 - 5 X 49

4

= 178 - 61


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ABGs 26

= 117 mmHg

The PaO2 = 86 and the A - a gradient = 117 - 86 = 31 mmHg.

The predicted normal A -a gradient for this man is:

Normal A - a = AGE / 3 + PAO2 / 5 - 23

= 68 / 3 + 117 / 5 - 23

= 23 mmHg

The widened A - a gradient implies pulmonary disease and corroborates a diagnosisof respiratory acidosis in this case.

Case 6

A 66 year old lady with septicaemia of unknown cause. The ABG's on 30% O2 are:

pH = 7.15PaO2 = 96PaCO2 = 29HCO3 = 10BE = -1SpO2 = 96%

The primary acid/base disturbance is a metabolic acidosis (low pH and lowbicarbonate). The PaCO2 is also low implying respiratory compensation for themetabolic acidosis. Let's try to confirm this using the equation for acute metabolicacidosis:

Predicted C = 1.25 B + 10= 13 + 10= 23 mmHg

The measured PaCO2 (29 mmHg) is higher than that predicted. The patient has notbeen able to mount a full repiratory response to her metabolic acidosis. This is

suggestive of an underlying respiratory problem and she in fact has a mixed metabolicand respiratory acidosis and is consistent with pneumonia complicated by sespsi.

Again, we can confirm that this is a respiratory proboem by analysing her pulmonaryfunction. This time well use the approximation to the alveolar gas equation :

PAO2 7 X 30 - 29 -10

171 mmHg

The predicted normal A -a gradient for this woman is:

Normal A - a = AGE / 3 + PAO2 / 5 - 23

= 66 / 3 + 171 / 5 - 23

= 33 mmHg


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The actual A-a gradient is 171 96 = 75 mmHg so there is confirmation ofrespiratory disase consistent with pneumonia.

Case 7

A 16 y.o. boy with a history of cystic fibrosis presents with yet another chest infection.The ABG's (on 35% oxygen) are:

pH = 7.40PaO2 = 116PaCO2 = 51HCO3 = 29BE = 2SpO2 = 99%

At fiirst glance there appears to be no acid/base disturbance as the pH is "normal"(7.40). However, the PaCO2 and the HCO3

-are both elevated. This occurs in both

respiratory acidosis and in metabolic alkalosis. So what's going on?It helps to know that cystic fibrosis is associated with metabolic alkalosis, so we'll startby applying the formula for metabolic alkalosis and seeing what we come up with:

Predicted C = B / 2 + 30= 29 / 2 + 30= 45 mmHg

Now the PaCO2 = 51 mmHg which is higher than predicted. However, this would beconsistent with an acute respiratory acidosis superimposed on an underlying metabolicalkalosis. This may well happen if this patient was having an acute pulmonaryinfection. The combination of a chronically compensated metabolic alkalosis plus anacute respiratory acidosis just happens to result in a "normal" pH in this case.

However . . . . . . . . . could there be another explanation? What about the possibility ofchronic respiratory acidosis in this patient? After all, CF is characterised by chroniclung disease.

OK, this time well analyse the ABG results using the formula for chronic respiratoryacidosis:

Predicted B = C / 2 + 2= 51 / 2 + 2= 28 mmol/L

This in fact is very close to the measured bicarbonate of 29 mmol/L.

So, where do we go from here? Do these ABG's represent a mixed metabolic alkalosisand acute respiratory acidosis OR a pure chronic respiratory acidosis? Perhaps asmall clue can be gleaned from the "normal" pH which makes a pure acid/basedisturbance unlikely. But as with all laboratory tests, ABG's need to be interpreted inlight of the complete clinical picture and it is at this point that clinical judgement needsto be exercised.


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The clinical picture would be most consistent with the first explanation. However, theremay be elements of all three processes involved in this case!

SUMMARYArterial blood gases can reveal a great deal of information, far more than is usuallyrealised. The principles and rules presented in these notes will help you to rationallyand usefully interpret the data you receive back from the blood gas lab. You should beable to tell a lot about your patients' respiratory function and acid/base status from onesimple blood test. But to make the most of this you must be prepared to sit down,often with pen and paper, and spend a couple of minutes analysing the data. Do notmerely glance at the result slip and be satisfied with a superficial interpretation of theresults even though with experience you should be able to rapidly recognise obviouspatterns of pathology.

The last clinical case example (case 7) illustrates the principle that laboratory tests arean aid to diagnosis only. To a large extent, lab tests, including ABG's, should be usedto confirm and quantify a clinical diagnosis. And remember above all. . . . . . . . . .

ALWAYS TREAT THE PATIENTAND NOT THE MACHINE!

John L Holmes Revised June 2008


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Summary FORMULAE & RULES of THUMB

Alveolar Gas Equation

PAO2 = 713 X FiO2 - 5 . PaCO2

4Approximation to Alveolar Gas Equation

PAO2 7 X %O2 - PaCO2 - 10

Estimation of normal A-a gradient

A - a = age + PAO2 - 233 5

RULES OF THUMB IN ACID BASE DISTURBANCES

B =1

/10C + 20 (acute acidosis)B =1/2C + 2 (chronic acidosis)

RESPIRATORY ACID - BASE DISORDERS

B =1/4C + 14 (acute alkalosis)

B =1/2C + 4 (chronic alkalosis)

C = 11/4 B + 10 (acidosis)

C =1/2 B + 30 (alkalosis)

METABOLIC ACID - BASE DISORDERS


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FORMULAE & RULES OF THUMB USING SI UNITS (kPa)

Many hospitals in Europe use SI units when reporting ABG results. There is nocompelling reason for this other than to conform to standards in other disciplines.

The conversion factor between mmHg and kPa is 0.133 and the conversion factorbetween kPa and mm Hg is 7.5

Thus 1 atmosphere = 760 mm Hg = 101 kPa

PaO2 normal range = 90 - 100 mmHg = 12 .0 - 13.3 kPaPaCO2 normal range = 35 45 mm Hg = 4.7 6.0 kPa

The formuale given above can be converted for use with SI units as follows:

Alveolar Gas Equation

PAO2 = 95 X FiO2 - 5 . PaCO2

4Estimation of normal A-a gradient

A - a = 0.04age + 0.2PAO2 - 3

B =3/4C + 20 (acute acidosis)

B = 4C (chronic acidosis)

RESPIRATORY ACID - BASE DISORDERS

B = 2C + 14 (acute alkalosis)

B = 4C + 3 (chronic alkalosis)

C = B/6 + 11/3 (acidosis)

C = B/15 + 4 (alkalosis)

METABOLIC ACID - BASE DISORDERS

Documents

ABG - Monograph J Holmes