RAO, NAGENDRANATH ARTERIAL BLOOD GAS MONITORING Indian J. Anaesth.

2002;: 46 (4) : 289-297

289

ARTERIAL BLOOD GAS MONITORING

Prof. S. Manimala Rao1 Dr. V. Nagendranath2
Introduction In order to understand and interpret ABGs one has to have a clear knowledge regarding the nomenclature, physiology and types of acid base disorders. These are first discussed, followed by the section Rapid interpretation of arterial blood gases. Disorders of acid base balance can complicate many disease states and occasionally the abnormality may be so severe as to be life threatening. Monitoring of ABGs is an essential part in the anaesthetic management of the high-risk patients as well as in the care of critically ill patients in the ICU. Since both areas manifest sudden and life threatening changes in all systems concerned, a thorough understanding of acid base balance is mandatory for any physician, and the anaesthesiologist is no exception. Common terms and definitions pH : It is the negative logarithm of the hydrogen ion concentration. A complete definition requires that the logarithm is defined as being to the base ten and the concentration measured as activity in moles per liter. A linear change in logarithmic scale does not indicate a linear change in the variable. It indicates a proportionate change. Neutral pH : It is the pH at which there are equal numbers of H+ ions and OH ions. Water is more ionized at body temperature than at room temperature; neutral pH is 6.8 rather than 7.0. This is also the average pH inside the cell. The body preserves neutrality (pH 6.8) inside our cells, where most of the bodys chemistry occurs, and maintains the blood at pH 7.4, which is 0.6 pH units on the alkaline side of neutral. Logarithm : It is helpful to think of power. Thus 103 = 1000 and log (1000) = 3. When the pH changes by 0.3 units, e.g., from 7.4 to 7.1 the hydrogen ion concentration doubles (from 40 - 80 nmol.L1).
1. Professor & Head. 2. Associate Professor Dept. of Anaesthesiology & Intensive Care, NIMS, Hyderabad Correspond to : Prof. S. Manimala Rao Nizams Institute of Medical Sciences Panjagutta, Hyderabad 500 082. (A.P.)

Respiratory acid and respiratory acidosis : Carbon dioxide is the respiratory acid it is the only acid, which can be exhaled. Strictly speaking carbon dioxide is a gas, not an acid. Carbonic acid is only formed when combined with water. Nevertheless, clinicians customarily regard carbon dioxide and respiratory acid as synonymous. Respiratory acidosis is a high PCO2 with a low pH. Metabolic acids and metabolic acidosis : The term metabolic acids includes all of the bodys acids except carbon dioxide. Metabolic acids are not respirable; they have to be neutralized, metabolized, or excreted via the kidney. Metabolic acidosis is a pH, which is more acid than appropriate for the PCO2. This definition emphasizes the importance of the respiratory component to the overall pH. The pH is always a product of the two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the PCO2, i.e., any change in the pH unexplained by the PCO2 indicates a metabolic abnormality. Acidosis and alkalosis : Acidosis is an abnormality, which tends to produce an acidic pH unless there is a dominating, opposing alkalosis. Alkalosis is the opposite and tends to produce an alkaline pH unless there is a dominating, opposing acidosis. Bicarbonate : In acid-base determinations, the concentration (in millequivalents per liter) of the bicarbonate ion (HCO3) is calculated from the PCO2 and pH. Because it is also altered by both the respiratory and the metabolic components (see below under physiology), it cannot be an ideal measure of either. Base excess (BE) : It is a measure of metabolic acid level, and is normally zero. The blood base (total base) is about 48 mmol L1 depending on the haemoglobin concentration. Changes are termed excess or deficit. It is helpful to remember that the phrase this patient has a base excess of minus ten means, this patient has a metabolic acid excess (acidosis) of 10 mEqL1. The base excess may be used to estimate the amount of treatment (neutralization) required to overcome the metabolic acidosis (or alkalosis). H+ ion and pH pH is the negative logarithm to the base 10 of the hydrogen ion concentration in nmol.L1. An increase in

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the pH indicates a proportionate decrease in the [H+] and a decrease in the pH indicates a proportionate increase in the [H+]. pH = - log10[H+] H = 10pH Various rules of thumb have been proposed for interconversion. Taking into account ease of calculation and range of clinical accuracy the best is the one proposed by Burden et al.1 The useful conversion range is pH 7.10 to 7.60 (H+ concentration 79-25 mmolL1). The method works by treating the two decimal digits of pH in this range as if they were a whole number between 10 and 60. If this number is subtracted from 83, the result is very close to H+ concentration. In reverse, subtracting H+ concentration from 83 yields two decimal digits of the corresponding pH, e.g. if H = 71; 83 - 71=12, therefore the pH = 7.12 (actual value is 7.15). If pH is 7.50; 83-50=33, therefore [H+] = 33, pH 7.33 and the actual value is 7.32.
Table I - Represents the pH values and corresponding H ion concentrations
pH 6.70 6.75 6.80 6.85 6.90 6.95 7.00 7.05 7.10 7.15 7.20 7.25 7.30 7.35 [H+] nmol/L 200 178 158 141 126 112 100 89 79 71 63 56 50 45 pH 7.40 7.45 7.50 7.55 7.60 7.65 7.70 7.75 7.80 7.85 7.90 7.95 8.00 [H +] nmol/L 40 35 32 28 25 22 20 18 16 14 13 11 10

imidazole ring of the histidine in the haemoglobin molecule. The bicarbonate/carbonic acid is a weak buffer. However the presence of carbonic anhydrase, the high solubility of CO2 and the ability of kidney to synthesize new bicarbonate and above all the efficient removal of CO2 by lungs make it a powerful buffer. All buffers in a common solution are in equilibrium with the same H+ ion concentration. Therefore, whenever there is a change in the H+ ion concentration in the CSF, the balance of all the buffer system changes at the same time the isohydric principle.2 It is therefore enough to study one buffer system in order to evaluate the acid base status of ECF. The Henderson-Hasselbalch equation, with its reliance on logarithms and antilogarithms is long and cumbersome and when attempting to deal with clinical situations, this equation has been found wanting. Kassirer and Bliech have rearranged the Henderson equation that relates H+ (instead of pH) to PCO2 and HCO3 and have derived an expression, which has great clinical utility.3 H+ = 24 x PCO2/HCO3 It is important to emphasize that H + ion concentration is defined by the ratio of PCO2 to HCO3 and not by absolute value of either one alone. ACID-BASE Normal metabolism of proteins and nucleotides generates about 100 mmol H+ per day in the form of sulphuric and phosphoric acids. By comparison, hydration of CO2 to form H2CO3 generates 12,500 mmol H+ per day. Carbon dioxide transport 1) In Dissolved form : Carbon dioxide is twenty times more soluble in water than oxygen. One millilitre of plasma will dissolve 0.0006 ml of carbon dioxide per mmHg partial pressure. 100 ml of plasma with a PCO2 of 40 mmHg therefore carries about 2.4 ml CO2 in solution. This is about 5% of total CO2 carriage. 2) As carbamino compounds : Carbon dioxide combines directly with terminal amine groups in blood proteins and haemoglobin. 5 -10% of CO2 carriage occurs in this way. The exact figure depends on the haemoglobin concentration. As bicarbonate: The remaining 85 -90% of carbon dioxide is carried by blood in the form of bicarbonate ions. Carbonic anhydrase in red cells accelerates the formation of H2CO3 from dissolved

The new generation of blood gas machines will report the H+ as well as the pH. Acid is an H+ donor and base is H+ acceptor. The intra and extracellular buffer systems minimize the changes in H+ that occur as a result of addition of an acid or alkali load to the extracellular fluid (ECF), 60% of the acid load is buffered in the intra cellular fluid (ICF). The most important buffer is the

3)

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carbon dioxide. The H2CO3 then dissociates into H+ and bicarbonate ion. Histidine buffers in the haemoglobin molecule accept the H +, and bicarbonate ions diffuse out of the red cell (an inward chloride shift occurs to maintain electroneutrality). This removal of H+ and HCO3 from the red cell cytoplasm promotes further H2CO3 formation and dissociation. Control of hydrogen ion concentration The hydrogen ion environment is tightly controlled over a variety of time periods: 1) 2) 3) Seconds: buffer systems Minutes: CO2 excretion by the lungs Hours to days: renal excretion of H+, reabsorption of HCO3

The main buffer system, which is also the one examined by blood gas analysis, is the carbonic acid/ bicarbonate buffer, with normal values shown here:
CO 2+H 2 O (1.2mmol.l1)

H2CO3 ( mol.l1)

H+ (40mmol.l1)

HCO3 (24mmol.l1)

Carbonic acid itself quickly dissociates either into hydrogen ion and bicarbonate or carbon dioxide and water. It represents a transitional state and is present in only micromolar quantities. Oxygenation Interpretation of PO2 requires knowledge of the sigmoid oxyhaemoglobin dissociation curve. The sigmoid shape derives from the fact that haemoglobin consists of four subunits, and binding of oxygen to one subunit facilitates the binding of oxygen to the other units. The characteristic points on the curve are: 1) The arterial point 2) The mixed venous point 3) The P50 PO2=100mmHg (13.3kPa) PO2=40mmHg (5.3kPa) PO2=27mmHg (3.6kPa)
Oxygen Dissociation Curve

Buffer systems consist of equilibrium mixtures of weak acids and their salts, they provide a sink for H+ or OH- ions, minimizing the pH change in response to acid/ alkali loads. Buffers are most effective when both components are present in equal concentration. This occurs when the pH is equal to the negative logarithm of the equilibrium constant (PKa) for the reaction concerned. Useful buffering occurs over a range of one pH unit either side of the optimum pH. The primary buffers in extracellular fluid are (in order of importance): 1) Carbonic acid/bicarbonate: H2CO3/HCO3 2) Haemoglobin/histidine residues (38 per molecule): HHb/Hb 3) Plasma protein/histidine residues: HPr/Pr 4) Phosphate: H2PO4/HPO4 (pKa = 6.1)

SO2=97.5% SO2=75% SO2=50%

(pKa = 6.8) (pKa = 6.8)

Despite having a pKa distant from normal plasma pH, the carbonic acid/bicarbonate system has a very high buffering capacity, since large quantities of carbonic acid can be accumulated or disposed of by modification of breathing. At pH 7.4, histidine is the only amino acid residue that readily accepts a hydrogen ion. The large numbers of histidine in haemoglobin make it a very effective buffer. Plasma proteins contain fewer histidines and are therefore less active as buffers. Phosphate is present in low concentrations in extracellular fluid, and is therefore of minimal importance. It is a primary intracellular buffer however, and has an important buffering function in urine, facilitating H+ excretion.

Hb saturation

(pKa = 6.8)

PO2 (kPa)

Binding of oxygen to haemoglobin results in conformational changes to the molecular subunits, making the histidine residues less ready to accept H+. So deoxyhaemoglobin is a better H+ acceptor than is oxyhaemoglobin, allowing deoxygenated blood to transport more CO2 (in the form of H+ + HCO3), for a given PCO2, than oxygenated blood does this is called the Haldane effect. Deoxygenated haemoglobin is also more ready to bind CO2 in the form of carbamino compounds at terminal amine groups. Conversely, the

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presence of H+ reduces haemoglobins affinity for oxygen, so a low pH shifts the dissociation curve to the right, making haemoglobin more ready to give up O2 at a given PO2 the Bohr effect. The Bohr and Haldane effects make useful physiological sense - the high O2 environment of the lungs oxygenates haemoglobin and so causes H+ release and reformation of CO2 to be expired, while the high CO2 environment of the tissues acidifies red cells and so facilitates oxygen release. A summary of factors affecting the oxyhaemoglobin dissociation curve is as follows: Left shift (increase O2 affinity) Alkalosis Hypocarbia Temperature 2,3 DPG Right shift (decreased O2 affinity) Acidosis Hypercarbia Temperature 2,3 DPG -

rises and PCO2 falls, whereas the HCO3 concentration remains unchanged. The alpha stat concept refers to the use of 37oC temperature-uncorrected pH and PCO2 values, whereas the pH stat concept refers to the use of pH and PCO2 values corrected to the patients core temperature.4 Hiramatsu et al have used the pH stat strategy in Deep Hypothermic Circulatory Arrest (DHCA) and found that Cerebral Blood Flow (CBF) was greater during cooling with a better preservation of cytochrome aa3 values.5 With few exceptions, the appropriate clinical interpretation of blood gas values is better accomplished using the alpha stat strategy and this is an universal practice. Combination of pH stat and alpha stat is adopted in complex congenital cardiac lesions along with DHCA. Acid base disorders Several definitions that are used to describe disturbances in acid base status are useful in understanding acid base disorders Acidemia A H + ion above the normal range of 36-44 nmolL1, pH less than 7.36 Acidosis A process that would cause acidemia, if not compensated Alkalemia A H+ below the range of 36-44 nmolL1, pH greater than 7.44 Alkalosis A process that would cause alkalemia if not compensated There are mainly two types of disorders, respiratory and metabolic. They may be compensatory or non compensatory. Changes in pH that are primarily a result of changes in PCO2 are termed respiratory disorders. On the other hand changes in pH brought about by changes in bicarbonate and other buffer bases are termed primary metabolic disorders. Basically there are four primary acid-base disorders viz. respiratory acidosis, metabolic acidosis, respiratory alkalosis and metabolic alkalosis. Compensation usually occurs in a primary acid base disturbance with an appropriate change in other components, e.g. a primary metabolic acidosis is compensated for by secondary respiratory alkalosis (by hyperventilation). On the other hand primary respiratory acidosis as it occurs in chronic obstructive airway disease (COPD) is secondarily compensated for by metabolic alkalosis brought about by H+ secretion and HCO3 absorption by the kidneys. While the former takes a few minutes to achieve the result, the latter may take days to weeks to be fully established.

Acidosis, hypercarbia and increased temperature are all features of the local circulation in metabolically active tissues, and they all increase oxygen unloading from haemoglobin. 2,3 DPG levels are low in stored blood, making it relatively ineffective at unloading oxygen in the tissues. The high affinity of HbF for oxygen is due to its relative insensitivity to 2,3 DPG. Oxygen content of blood depends on both haemoglobin saturation and haemoglobin concentration, with an additional largely trivial contribution from dissolved O2. Each gram of haemoglobin can combine, under ideal conditions, with 1.39 ml of oxygen. But carboxyhaemoglobin and methaemoglobin are both present in normal blood, so the conventional figure for oxygen carrying capacity of haemoglobin is 1.34 ml.gl. Oxygen dissolves in plasma to the extent of only 0.00003 ml.l-1.mmHg-1, so that 100 ml of blood at normal arterial PO2 transports only 0.3 ml O2. In contrast, if the haemoglobin concentration is 15 g.dl1, the same 100 ml of arterial blood will carry 15 x 1.34x97.5%=19.6 ml of oxygen associated with haemoglobin. Effect of temperature When blood is cooled, CO2 becomes more soluble reducing its PCO 2 by about 4.5% per oC fall in temperature and the pH rises by about 0.015 per oC fall in temperature. Available evidence suggests that homeostatic mechanisms center around protein buffers and enzymes, specifically the alpha imidazole group on histidine residues, the so called alpha stat regulation. This mechanism requires that, with hypothermia the pH

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The changes in PCO2, pH and HCO3 depending upon the type of disorder are given in table 2.
Table 2: Primary and expected compensatory changes in acid base disorders.
Primary disorder Characteristic primary changes [H + ] Expected (normal) in vivo response For each mmolL1 fall in [HCO3], PaCO2 falls by 1 mmHg

Respiratory alkalosis Main causes: anxiety, encephalitis/meningitis, salicylates, acute asthma, pulmonary embolus, hypoxia at altitude. Reduction in CO 2 drives the bicarb buffer equilibrium towards the production of carbonic acid. Protein and haemoglobin buffers release H+, limiting the rise in pH. Bicarbonate levels fall by about 2 mmol.l-1 for every 10 mmHg fall in PCO2. After 6-12 hours, renal H+ excretion and bicarbonate reabsorption are reduced, pH falls towards normal, and bicarbonate is further reduced. Chronic respiratory alkalosis with renal compensation is therefore associated with a bicarbonate fall of up to 5 mmol.l-1 for each 10 mmHg fall in PCO2, but this compensation will take one or two days to become complete. Metabolic acidosis Main causes: hypovolaemia, cardiogenic or septic shock, severe hypoxia, diabetic ketoacidosis, renal failure, diarrhoea, pancreatic fistula. The presence of excess H+ is compensated to some extent by protein and haemoglobin buffers. The bicarb buffer equilibrium is driven towards CO2 production, which drives an initial increase in breathing to maintain normal carbonic acid levels. Bicarbonate is consumed, and therefore falls. Over the next 12-24 hours H+ diffuses into the brain, and drives a further increase in ventilation, which lowers carbonic acid levels and induces a compensatory respiratory alkalosis. (Lactic acid is produced by all cells, including brain cells, and therefore produces a faster respiratory response than do ketoacids, which are produced by the liver and must diffuse into the brain across the blood-brain barrier.) Once compensation is established, PCO2 is reduced by 1-1.3 mmHg (0.130.17 kPa) for each mmol.ll fall in bicarbonate. Because of the slow equilibration of CSF H+ with blood pH, hyperventilation may persist for 12-24 hours after blood pH returns to normal. Metabolic alkalosis Main causes: vomiting, nasogastric suction, gastric fistula, steroids, diuretic therapy, inappropriate sodium bicarbonate administration, massive blood transfusion (citrate metabolised to bicarbonate). Reduction in H+ is compensated to some extent by release of hydrogen ions from protein and haemoglobin buffers. The bicarb buffer equilibrium is pushed towards increasing bicarbonate levels and decreasing carbonic acid. Ventilation falls immediately

Metabolic acidosis

- [HCO 3 ] -

Metabolic alkalosis

[H + ]

[HCO 3 ]

For each mmolL1 rise in [HCO3], PaCO2 rises by 0.75 mmHg; however, PaCO2 does not exceed 55mmHg For each mmHg rise in PaCO2, plasma [H+] rises by 0.75 nmolL1 For each mmHg fall in PaCO2, plasma [H+] falls by 0.30 nmolL-1 For each mmHg fall in PaCO2, plasma [H+] falls by 0.75 nmolL1 For each mmHg fall in PaCO2, plasma [H+] falls by 0.15 nmolL1

Acute respiratory acidosis

[H + ]

PaCO 2

Chronic respiratory acidosis

[H + ]

PaCO 2

Acute respiratory alkalosis

[H + ]

PaCO 2

Chronic respiratory alkalosis

[H + ]

PaCO 2

Respiratory acidosis Main causes: sedation, coma, neuromuscular disorders, severe kyphoscoliosis or obesity, pulmonary fibrosis, sarcoidosis, pneumothorax or effusion, chronic obstructive airway disease, airway obstruction, severe pulmonary parenchymal disease. Retention of CO2 drives the bicarbonate buffer equilibrium towards production of H+ and HCO3. H+ is buffered by protein and haemoglobin, limiting the fall in pH. Bicarbonate levels rise by about 1 mmol.l1 for every 10mmHg (1.3 kPa) rise in PCO2. Therefore even quite extreme hypercarbia will not push bicarbonate over 32 mmol.l-1 acutely. After 6-12 hours, however, renal H+ excretion increases causing the generation and reabsorption of bicarbonate. Bicarbonate levels then rise further, while pH returns towards normal. Chronic respiratory acidosis with metabolic compensation will therefore raise bicarbonate by as much as 4 mmol.l-1 for each 10 mmHg rise in CO2, but this compensation will take one or two days to become complete.

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to maintain normal carbonic acid levels. After 12-24 hours, rising CSF pH may induce a further fall in ventilation to produce a compensatory respiratory acidosis - this rarely involves a rise in PCO2 to more then 55 mmHg (7.3kPa), since oxygenation must be maintained. Metabolically alkalotic patients may be sufficiently sick from their underlying disease so that the respiratory compensation is absent and hyperventilation may occur instead. Base excess From the above it is clear that CO2 and bicarbonate levels are inextricably linked, and interpretation of mixed respiratory/metabolic disorders is very complicated if only pH, PCO2 and bicarbonate levels are available. What is required is a measure of metabolic acid/base status which is separated from the effects of CO2. Several parameters have been used in the past, including standard bicarbonate and buffer base, but the most frequently used today is base excess. Base excess is defined as the amount of fully-ionised acid which would be required to return the patients blood to pH 7.4 when the CO2 has been adjusted to 40 mmHg (5.3 kPa). It is derived from nomograms or calculations, based on experimental results produced by Siggaard-Andersen. Units are mmol.l-l. Positive values indicate metabolic alkalosis, negative values metabolic acidosis. To correct a metabolic acidosis, the following quantity of sodium bicarbonate is suggested in the Advanced Life Support manual: NaHCO3 dose (mmol) = base excess (mmol.ll) x body weight (kg)/3 (8.4% sodium bicarbonate solution contains 1 mmol NaHCO3 per ml). Body weight divided by three is a rather generous estimate of extra-cellular fluid volume, so this equation is estimating the bicarbonate dose to fully correct ECF acidosis. Bear in mind, however, that most of the ECF lacks the protein and haemoglobin buffers present in blood, and much of it equilibrates only slowly with blood. Therefore small doses of bicarbonate (50-100 ml) should be titrated against repeated estimates of pH and base excess. Anion gap This is a useful concept in the assessment of the cause of metabolic acidosis, though an understanding of the concept is probably of more use than the parameter itself. Electrical neutrality in body fluids is attained by the following balance:

Cations Na+ K+ Ca++ Mg++ SulphateTotal

[+] mmol.l-1 140 4.5 5 1.5 1 151

Anions ClHCO3ProteinPhosphateOrg. acid Total

[-] mmol.l-1 104 24 15 2 5 151

Anion gap is calculated as [Na+]-([Cl]+[HCO3]) and is usually 12 mmol.l-l. It is increased if K+, Ca++ or Mg++ concentrations fall or if protein levels rise; it falls if potassium, calcium or magnesium levels rise or plasma proteins decrease. But if these values are normal, the anion gap is due to the presence of metabolic acids. If there is a rise in metabolic acids, bicarbonate will be consumed by association with H+ and there will therefore be a shift in the anionic distribution from bicarbonate to metabolic acids, and the anion gap will increase. This occurs classically in lactic acidosis, ketoacidosis and most kinds of renal failure. However, if chloride rises simultaneously with the bicarbonate fall, the two effects offset each other, and no change in anion gap is seen. This is hyperchloraemic acidosis, which occurs in renal tubular acidosis, early renal failure, diarrhoea, ureteric diversions and carbonic anhydrase-inhibitor treatment. Mixed acid base disorders Suppose a patient has low pH and is therefore acidemic. In this setting, a low plasma HCO3 concentration indicates metabolic acidosis and a high PCO2 indicates respiratory acidosis. Similar reasoning can lead to the diagnosis of a combined metabolic and respiratory alkalosis in a patient with an elevated pH, a high plasma HCO3 and a low PCO2. A knowledge of the extent of renal and respiratory compensations allows mixed disorders to be diagnosed, e.g. a patient with a salicylate overdose is found to have the following result: pH 7.45, PCO2 20, HCO3 13 The slightly high pH indicated that the patient is alkalemic. This can be due to a high HCO3 concentration or a low PCO2. Since only the latter is present the primary diagnosis is respiratory alkalosis, most likely acute, given the history. In this disorder, the body buffers will reduce

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the plasma HCO3 concentration by 2 mEqL1 for every 24 to 20 mEqL1 as the PCO2 drops acutely from 40 to 20 Torr. The actual HCO3 of 13 mEqL1 is lower than expected, suggesting that the patient has a combined, respiratory alkalosis and metabolic acidosis. Also, renal and respiratory compensations return the pH toward but rarely to normal. Thus, a normal pH in the presence of changes in the PCO 2 and HCO 3 concentrations immediately suggests a mixed disorder.6 Blood gas monitors The pH, PCO2 and PO2 measurements are normally accomplished by blood gas analysers using an arterial blood sample fed into the analyser as and when the acid base status is required. Improvements in technology have paved the way for blood gas monitors which display the same results online. A blood gas monitor is a patient dedicated device that measures arterial pH, PCO2 and PO2 without permanently removing blood. A sensor that operates via optical detection of altered light is an optode. Either transmission based or fluorescence based chemistries can be used as indicators for optode microsensing. They are operable with a 20G arterial catheter and do not negatively affect continuous pressure measurement, obtaining of blood samples or routine function of the arterial catheter system. They are stable and consistent for at least 72 hours. To avoid patient interface problems with intraarterial devices, an extra-arterial fluorescent optode system has been developed. This device locates the pH, PCO2 and PO2 fluorescent optodes within a sensor cassette that is inserted in series with the arterial catheter tubing system near the patients wrist. To measure pH, PCO2 and PO2, a stopcock closes the system to the IV fluid source, which then allows arterial blood to flow into the sensor cassette when a sub-atmospheric pressure is created in an upstream reservoir. The placement of the reservoir is such that only IV fluid enters the reservoir. The stopcock is then returned to its original position so that the reservoir is isolated and fluid flow from the pressurized bag is restored, by allowing BP monitoring to continue. The minimal blood flow occurring in the sensor cassette does not interfere with optode function. Results are displayed within 90 seconds. Advantages 1. They furnish immediate and continuing blood gas trends.

2. 3. 4,

They reduce blood loss incident to obtaining data. They reduce the risks of nosocomial infection. They reduce the exposure of personnel to patients blood.

Rapid interpretation of ABG The fundamental for any interpretation is to recognize the cause of the problem, which once evaluated can lead to a systematic management. In approaching the evaluation of blood gas and acid-base disturbances in the body the following scheme is suggested: 1) The patients history and clinical condition should be carefully reviewed. 2) The adequacy of alveolar ventilation should be assessed. 3) The alveolar-to-arterial oxygen tension gradient should be calculated. 4) Plasma electrolytes should be measured and the anion gap calculated. 5) The acid-base status of the body should be determined. What are the components of an ABG report? 1) Patient data I.P. No., sex, age. 2) Clinical status FiO2, R.R. or ventilatory settings. 3) Arterial O2 tension (PaO2). 4) Arterial CO2 tension (PaCO2). 5) pH 6) Bicarbonate in mEqL1 7) Base excess 8) Haemoglobin 9) O2 content 10) O2 saturation 11) Temperature 12) Serum K+ values The usual questions one asks after the availability of data for evaluation of acid-base status are: 1) Is there an acid-base disorder? 2) If so, is it primary or compensatory? 3) Whether it is simple or mixed 4) And finally what is the aetiology? A thorough history and careful evaluation of the patient at the bedside yields clues to the understanding of the disorder. An acute disorder is not compensated and it may clearly be evident from the history. The evaluating person must thoroughly understand that compensation only attempts to restore the abnormal state to near normal but never to a total correction. The respiratory compensation for primary metabolic process and the renal compensation for chronic respiratory acidosis are very effective whereas the respiratory compensation for metabolic alkalosis has a ceiling at a PaCO2 of 55mmHg. Before understanding to interpret the arterial blood gases one should be fairly thorough with the normal values, which are given in the following table.

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S.No.
1. 2. 3. 4. 5. 6.

Value
pH PaO2 O2 saturation PaCO2 HCO BE
3

Arterial blood
7.40 (7.35 7.45) 80-100 mmHg 95%

Mixed venous
7.36 (7.31 7.41) 35-40 mmHg 70-75% 41-51 mmHg 22-26 mEqL -2 to +2
1

and BE will become negative. On the other hand loss of acid by vomiting or ingestion or accumulation of HCO3- will lead to an increase in bicarbonate and BE values. BE values refer not only to bicarbonate, but also to proteins and haemoglobin which are the other buffer bases. 6. Metabolic abnormalities -HCO3or BEmetabolic alkalosisacid or HCO3- HCO3or BEmetabolic acidosis acid-or HCO3 pH is maintained for, by two major mechanisms. One is compensation i.e. it alters the component not primarily responsible for the abnormality. Secondly by correction, pH is normalized by altering the component that is primarily responsible for the abnormality. The body always strives to maintain a balance between HCO3 and PaCO2 of 20:1. At this ratio the pH is normal. For every 10 mmHg rise or fall in PaCO2 from 40 mmHg, there is an increase or decrease in pH by 0.08 units. For e.g. PCO2 - 20 (40 + 20 = 60 mmHg) pH 0.08 x 2 = 0.16 pH = 7.4 0.16 = 7.24

35-45 mmHg 22-26 mEqL -2 to +2

1

Arterial or venous blood sample It is traditional to draw arterial blood for PaO2, PaCO2 and pH measurements. It is the best indicator of how well the lungs are oxygenating. However in the haemodynamically unstable patient, mixed venous blood is a close approximation of acid-base status of the times. It has been recommended that central venous blood can be analysed in such situations. In analyzing the data follow a sequence of order 1. Check pH. It indicates acidemia or alkalemia pH <7.35 acidemia the process causing academia is acidosis pH >7.45 alkalemia the process causing alkalemia is alkalosis Both processes may be occurring simultaneously, the pH indicates the stronger one 2. Check PO2, which indicates oxygenation. 3. Check PCO 2 , which indicates ventilation. Hypoventilation leads to more dissolved CO2 in blood leading to higher PaCO2. Conversely hyperventilation is a state caused whenever there is not enough dissolved CO2 in blood i.e. the lungs are excreting far more CO2 by excessive ventilation. CO2 is always considered an acid as it combines with H2O to form weak acid viz. H2CO3, which in turn breaks down to H+ and bicarbonate HCO3. H+ is buffered by plasma proteins, whereas CO2 is eliminated by the kidney as acid in urine and by lungs as CO2 gas. Respiratory abnormalities - PCO2 respiratory acidosis - ventilation PCO2 respiratory alkalosis - - ventilation Check bicarbonate and BE. These two indicate whether the primary disorder is metabolic or respiratory. These two are influenced only by metabolic processes other than respiratory disturbances that affect a patients pH. If metabolic process causes accumulation of acid or loss of bicarbonate, the HCO3- values drop below normal

For studying states of academia or alkalemia one requires all the measurements viz. pH, PaCO2 and bicarbonate. Examples : 1. pH 7.45, PCO2 26 and HCO3 19 Here the pH is alkalotic, PCO2 indicates respiratory alkalosis and bicarbonate is low. Acute CO2 excretion (acute respiratory alkalosis) drives the hydration reaction more the left than normal, and HCO3 decreases slightly. Final interpretation is partially compensated respiratory alkalosis. 2. pH 7.48, PaCO2 55 and HCO3 38 pH is alkalotic, PCO2 indicates respiratory acidosis and bicarbonate is high. Metabolic alkalosis is partially compensated with PCO2 ceiling of 55 mmHg. 3. pH 7.13, PCO2 82 and HCO3 24 pH is acidotic, PCO2 indicates respiratory acidosis and a normal bicarbonate. This picture shows uncompensated respiratory acidosis. 4. pH 7.29, PCO2 25, HCO3 12 Here the pH is low indicating academia and the bicarbonate is low indicating a metabolic origin. Final interpretation is metabolic acidosis partially

4.

5.

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5.

compensated by a fall in PCO2 in an attempt to bring the pH towards normal. pH 7.45, PCO2 20, HCO3 13 Here the pH suggests alkalemia. PCO2 is low suggesting a respiratory alkalosis. The actual bicarbonate is lower than expected suggesting a combined metabolic acidosis and respiratory alkalosis.

Table III illustrates a schematic representation for interpretation of acid-base balance

FiO2 is the fractional inspired oxygen concentration. PaO2 is always related to FiO2. Blood gas analysis without FiO2 marking, does not really make any sense. Ratio of PaO2/FiO2 permits evaluating patients receiving various amounts of oxygen. It gives an indirect method of estimation of venous admixture. Increasing A-a gradients signify deterioration in lung function. A-aO2 gradient = 140 (PO2 torr) 5% should be substracted which is a normal physiological shunt. An A-a ratio of 0.75 is normal, 0.40-0.75 is acceptable, 0.20-0.39 is poor and less than 0.20 is very poor. PaO2 denotes the O2 tension, which does not directly relate to ventilation. But there is a reciprocal relationship between PaCO2 and PaO2. The normal PaO2 varies with age and high altitudes. Oxygen saturation (SaO2) can be calculated from the formula O2 sat% = content capacity Rapid interpretation of arterial blood gases may not be a cakewalk. But with some basic understanding and perseverance, the student will be able to do it accurately in many situations. Mixed acid-base disorders and complex conditions may pose a problem but right history and clinical evaluation may pave the way for easy interpretation. References
1. Burden and McQuillan. BJA 1997; 78:479. 2. Guyton AC, Hall JE. Textbook of Medical Physiology 9th ed. 1996: 390. 3. Kassirer JP, Bleich HL. Rapid estimation of plasma CO2 from pH and total CO2 content. N Engl J Med 1965; 272:1067. 4. Shapiro BA, Peruzzi WT, Templin RK. Clinical application of blood gases. 5th ed. 1994:230-31. 5. Hiramatsu T et al. pH strategies and cerebral energetics before and after circulatory arrest. J Thorac Cardiovasc Surg 1995; 109: 948. 6. Burton David Rose. Clinical physiology of acid-base and electrolyte disorders. 4th ed. 1994:508.

e.g. In interpretation the saturation is very useful and should give a clue to defective or abnormal haemoglobins, when PaO2 and Hb% are within normal limits but O2 saturation and content are low. Oxygen content is necessary when evaluating the adequacy of O2 delivery to tissues. To increase CaO2 one has to improve the patients haemoglobin.

OBITUARY
Dr. Sawant passed M.B.B.S. and D.A. from S.S.G. Hospital and Medical College, Baroda in 1955 and 1957 respectively. He joined Tata Memorial Hospital, Mumbai in May 1959 and worked as Head of the Dept. from 1966 to 1990. Under his dynamic leadership the dept. rose to international heights. He was very popular amongst the residents, his colleagues and all other staff members of the hospital, for his ever helpful and co-operative nature. His sudden and untimely demise on 8th April 2001, shocked not only TMH but the whole of ISA, Mumbai branch.

Dr. Narayana S. Sawant

(18-11-1928 to 08-04-2001)

May Almighty God give peace to the departed soul!