Arterial blood gas analysis

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1 CONTINUING PROFESSIONAL DEVELOPMENT By reading this article and writing a practice profile, you can gain a certificate of learning. You have up to a year to send in your practice profile. Guidelines on how to write and submit a profile are featured at the end of this article. Arterial blood gas analysis Arterial blood gas analysis pages Multiple choice questions and submission instructions page 54 Practice profile assessment guide page 55 A reader s practice profile page 25 NS227 Woodrow P (2004) Arterial blood gas analysis. Nursing Standard. 18, 21, Date of acceptance: December Aim and intended learning outcomes This article aims to give nurses an understanding of the main gas and acid-base measurements derived from an arterial sample, so that they can interpret results of samples from patients in their care. After reading this article you should be able to: Describe what acid-base balance is, and its significance for homeostasis of the blood. Discuss with junior colleagues the significance of carbon dioxide measurement. Explain to a junior colleague how compensation occurs, and how it can be identified from blood gas samples. Introduction With increasing numbers of acutely ill patients in most wards, nurses often see arterial blood gases (ABGs) being taken by medical colleagues and, in some areas, by other nurses. ABGs can aid medical diagnosis, but nurses may be the first clinical staff to receive the results. Understanding the significance of these results, and knowing when medical help needs to be summoned urgently, can improve patient care. Nurses taking samples need to be able to interpret results. Understanding diagnostic results can make nursing care more holistic for the patient and rewarding for nurses. This article describes how nurses can analyse ABG samples. Blood gases may be analysed from capillary samples. Differences between arterial and capillary results are so slight that for practical purposes they can be considered identical. Information in this article therefore also applies to analysing capillary samples. Although commonly referred to as blood gases or ABGs, most machines supply other results, such as electrolytes and metabolites, that are useful for patient care, but which are not gases or necessarily related to respiratory function. This article describes how to interpret the main ABG results. It does not discuss how to take samples, errors that can occur when taking samples, or care of arterial lines. The sample In a few specialist areas, such as intensive care units, patients may have an arterial line inserted, which enables samples to be obtained easily and painlessly. However, arterial lines are dangerous and should not be used where the patient is not monitored and observed continuously by staff familiar with the potential dangers. In most wards and departments, obtaining an ABG sample necessitates an arterial stab taking blood with a syringe and needle from an artery (usually the radial artery) in a similar way to taking blood from a vein. As arteries are deeper than veins, arterial stabs are painful. Local anaesthetics should be used (Hope et al 1998), but in the author s experience rarely are. Arterial bleeds take longer to stop than venous ones. Sheehy and Lombardi (1995) recommend pressing on arterial sites for five minutes, although if patients have prolonged clotting or bleeding disorders, pressure may be needed for longer. Removing pressure too soon may cause haematoma or bruising. Once the sample has been obtained, nurses may be asked to transport, or arrange transport for, the sample. Because cells in blood are living, gas exchange and metabolism continue, so delays in analysing samples cause increasingly inaccurate results. Beaumont (1997) recommends analysing samples kept at room temperature within 15 minutes. Unless blood gas analysers are available in or very near the ward, samples should therefore be cooled to reduce metabolism, so prolonging the time available for reliable analysis. Common practice has been to insert the syringe into some ice. Clutton- Brock (1997) suggests that this prolongs the reliable sampling time to 60 minutes. However, some In brief Author Philip Woodrow MA, RGN, DipN, Grad Cert Ed, is Practice Development Nurse, Critical Care, East Kent Hospitals NHS Trust, Canterbury, Kent. philip.woodrow@ ekht.nhs.uk Summary With increasing use of arterial blood gas analysis in various ward and other hospital settings to aid medical diagnosis and management, nurses who can interpret results are often able to initiate earlier interventions and understand the reasons for medical interventions. This article enables nurses to interpret such results. Key words Oxygen therapy Respiratory disorders These key words are based on subject headings from the British Nursing Index. This article has been subject to double-blind review. Online archive For related articles visit our online archive at: and search using the key words above. february 4/vol18/no21/2004 nursing standard 45

2 Box 1. ph (overall acid-base balance) normal <7.35 = acidosis >7.45 = alkalosis anecdotal claims have been made that ice immediately against the syringe wall causes haemolysis (breakdown of erythrocytes), causing inaccurate results: lower ph and oxygen (PaO 2 ), higher carbon dioxide (PaCO 2 ) and potassium (K + ) (Gosling 1995). So anecdotal recommendations are to place the syringe in iced water. However, if transporting a container of iced water causes a further delay, it is debatable whether this method achieves any greater accuracy. Delay before measurement may also cause inaccuracies from separation of blood cells and plasma. Which way measurements are affected depends on whether mainly plasma or mainly cells are inserted into the machine. Samples should therefore be mixed well during transportation, by rolling the syringe (like a cement mixer). Vigorous shaking should be avoided, as this may cause haemolysis. TIME OUT 1 Re-read the above paragraph; identify what you would need to safely transport a sample to the nearest usable blood gas analyser. If you identify any items that are not available in your clinical area, inform your ward manager. Analysis Measured results, suggested normal values and the sequence of printing results vary between machines, largely depending on how they have been programmed locally. This article identifies the most important results for most adult patients, but if additional measurements are used in your place of work, you should find out the normal range and what abnormalities may suggest about patients conditions. There are four main groups of results that will be analysed on most samples: ph. Respiratory function (oxygen, carbon dioxide, saturation). Metabolic measures (bicarbonate, base excess). Electrolytes and metabolites. This article focuses on the first three aspects. Electrolyte and metabolite measurements are useful but are additional to, rather than part of, gas analysis, so are not discussed here. When results are analysed, information about the patient, such as his or her identification number and body temperature, may be fed into the machine. Depending on how the machine is programmed, some information may be optional, but will be printed above the analysed results. As with any machine, there can be slight differences between different measurements ( drift ), so changes of less than 10 per cent are generally not considered significant. Temperature Machines provide the option to measure results at the patient s own temperature or at a default temperature of 37 C. Dissociation of gases, and therefore all results derived from gases, are affected by temperature. This can be illustrated by re-analysing samples at different temperatures. Therefore, some people consider that gases should be measured at the patient s temperature. However, body temperature varies between different sites, and if the recorded temperature changes because a different site is used, for example, axilla is replaced by tympanic measurement, or if recording of temperature was inaccurate then results may differ without any change in the patient. Thus, it is generally considered safer to measure all samples at the default temperature of 37 C, where any trends will be from a consistent baseline. The author s own preference is to sample all results at 37 C; however, to avoid variation in readings between different practitioners, it is important that all people measuring ABGs in a clinical area follow the same practice. Wards and units should therefore make team decisions about whether or not to enter patients temperatures. TIME OUT 2 Obtain a printout, or copy down results, from an ABG analysis (if none is available in the notes of any patients on your ward, specialised areas such as critical care may be able to provide you with a copy). Note down why the patient was admitted, any other relevant history and treatment, and why the gas sample was taken. If you obtain more than one printout, select one to use while reading this article. Was the sample analysed at 37 C or at the patient s temperature? If you have the opportunity, ask why. ph The normal range is (Box 1). Potential hydrogen (ph) concentration of ions measures acidity or alkalinity. Acids are chemicals that can release (donate) hydrogen ions (H + ), while alkalis are chemicals that can absorb (receive) hydrogen ions. The ph scale measures moles per litre, and ranges between 1 (absolute acid) and 14 (absolute alkali): car batteries contain strong acids, with a ph of about 2.0; resting gastric ph is less than 3; many citrus fruits have a ph of 4; sodium hydroxide, a strong alkali, has a ph of 13. Such extremes of acidity or alkalinity in blood would be fatal. The main acid in blood, carbonic acid, is fortunately weak. Chemically, neutral ph is 7.0. But human blood 46 nursing standard february 4/vol18/no21/2004

3 is slightly alkaline, normally ranging between 7.35 and Therefore, blood ph below 7.35 is termed acidotic and that above ph 7.45 is alkalotic. The ph scale is a negative logarithm. A logarithm presents large numbers in a few, more easily managed, figures. A negative logarithm similarly represents small numbers, with many decimal points, in a more manageable and safer form. There are only millimole (40 nanamoles, nmol) of hydrogen ions in each litre of blood. However, slight changes in concentration can be life-threatening doubling or halving acid concentration alters ph by 0.3 (Box 2), while moving one whole figure on the ph scale causes a tenfold change in hydrogen ion concentration (Fletcher and Dhrampal 2003). The normal blood ph of means that the hydrogen ion concentration is normally 3.5 x 10-8 to 4.5 x 10-8 per litre of blood. Slight changes in ph affect enzyme activity (Hornbein 1994), while acidity increases oxygen dissociation from haemoglobin (the Bohr effect) and impairs cardiac contraction (= negative inotrope). Blood ph below 7.0 or above 8.0 makes survival very unlikely. Acidosis occurs more often than alkalosis, but both are life-threatening. Complications are cumulative as blood ph moves progressively further from the normal range. ph measures the overall acid-base balance of the blood sample. Acid-base balance is affected by both respiratory and metabolic function. An abnormal ph does not identify whether problems are respiratory or metabolic (or both) in origin. In health, the body attempts to maintain homeostasis. As homeostasis of blood ph is to maintain , an abnormality of one component (for example, metabolic acidosis) may stimulate an opposing abnormality of the other component (for example, respiratory alkalosis) to maintain a normal ph. This is called compensation, and it can only be identified by looking at ph together with both respiratory and metabolic results. Anaerobic metabolism from poor perfusion, such as during shock, produces lactic acid (Babb and Farmery 2003). Although this is a weak acid, increased levels can cause life-threatening metabolic acidosis. Lactate is a metabolite measured by some analysers. Normal blood lactate level is 1mmol/l or less. TIME OUT 3 Look at the sample results you have selected. Is the acid-base balance normal? If not, is it acidic or alkalotic? Respiratory function Blood gas analysis measures PaCO 2 (partial pressure of arterial carbon dioxide). PaO 2 (partial pressure of arterial oxygen). SaO 2 (saturation of haemoglobin by oxygen). Box 2. Hydrogen ion concentration ph 7.7 = 20nmol/l H + ph 7.4 = 40nmol/l H + ph 7.1 = 80nmol/l H + ph 6.8 =160nmol/l H + (= mmol/l) Box 3. PaCO 2 Normal: kPa <4.5 = hypocapnia, respiratory alkalosis >6.0 = hypercapnia, respiratory acidosis (Cornock 1996) Some printers omit the lower case a. With capillary or venous samples, if the machine is informed of the source of the sample, a small c or v may be printed. Venous samples are very rarely taken, but might be used to measure electrolytes and metabolites. In the UK, gases are almost always measured in kilopascals (kpa), however, some countries, including the United States, use millimetres of mercury (mmhg). As US texts, and old texts from the UK, give gases in mmhg, you may need to be able to convert these figures. One millimetre of mercury (1mmHg) equals 0.133kPa, so dividing mmhg by 7.5 approximates to kpa. Carbon dioxide (PaCO 2 ) The normal range is kPa (Box 3). The amount of carbon dioxide in the atmosphere is normally insignificant (about 0.04%). Carbon dioxide is produced by body cells as a waste product of metabolism. The respiratory centres in the brainstem respond primarily to the level of arterial carbon dioxide. So, with healthy respiratory centres and lung function, hypercapnia (>6.0kPa) stimulates respiratory centres to increase the rate and depth of breathing, which removes more carbon dioxide. Similarly, hypocapnia (<4.5kPa) reduces the stimulus to breathe, so decreasing the respiratory rate and depth. Arterial carbon dioxide levels therefore indicate ventilation, the amount of air moving in and out of the alveoli. In health, respiratory responses can restore a life-threatening ph of 7.0 to 7.2/7.3 in three to 12 minutes (Guyton and Hall 2000). Hypoventilation, which may occur in conjunction with respiratory failure, may lead to hypercapnia and hypoxia, because of the inability to remove sufficient carbon dioxide to maintain normal levels. Inadequate ventilation may necessitate ventilatory support, such as non-invasive ventilation (BTS 2002) or the respiratory stimulant doxapram (BTS 1997). Hypocapnia occurs with hyperventilation. This is only likely to be seen with: february 4/vol18/no21/2004 nursing standard 47

4 Panic attacks. Artificial (over-)ventilation. Compensation for metabolic acidosis. With panic attacks, causes should be identified and if possible resolved, and the patient reassured. If hypocapnia causes problems, it can be reversed by the patient rebreathing his or her own carbon dioxide (using a paper bag), but this is usually only necessary in first-aid situations. Artificial overventilation can be adjusted by reducing ventilator settings (rate and/or volume). Compensatory metabolic acidosis should usually not be treated, as the compensation maintains haemostasis; however, the cause of acidosis often requires treatment. Carbon dioxide is often referred to as a potential acid. Chemically, an acid has to contain hydrogen ions, which carbon dioxide does not. However, when carbon dioxide produced by cells diffuses into capillary blood it mixes with water (the main component of blood) to form carbonic acid: CO 2 + H 2 O H 2 CO 3. Arterial carbon dioxide therefore indicates the amount of carbonic acid, so hypercapnia creates a respiratory acidosis, while hypocapnia creates a respiratory alkalosis. Carbonic acid has two useful properties for human blood physiology: it is weak and unstable. Being a weak acid, large amounts of carbonic acid would be needed to create a life-threatening acidosis, so respiratory acidosis occurs only if excessive amounts of carbon dioxide are retained. Its instability means that it dissociates (breaks down) easily, which is why the arrow in the above formula points both ways. Carbonic acid usually dissociates back into water and carbon dioxide, carbon dioxide being removed through the lungs and excess water being removed in urine. Oxygen (PaO 2 ) The normal range is kPa (Cornock 1996). Oxygen is literally vital for cells, and so for organs and the body, to survive. However, prolonged use of high concentrations can cause toxic damage. Precise levels for oxygen toxicity are debated but are often considered to be >60% oxygen for >24 hours (Hinds and Watson 1996). So if a patient is hyperoxic (PaO 2 >13.5kPa), supplementary oxygen for prolonged use should be reduced. Significant hyperoxia almost never occurs unless patients are given high concentration supplementary oxygen. More often, patients have hypoxia (PaO 2 <11.5kPa), as a result of respiratory Box 4. Respiratory failure Type 1 PaO 2 <8kPa PaCO 2 <6kPa Type 2 PaO 2 <8kPa PaCO 2 >6kPa (BTS 2002) failure, and need supplementary oxygen to maintain adequate tissue oxygenation. For short-term use during acute crises, such as during or immediately after cardiac arrest, oxygen toxicity is not an issue, so maximal (100%) oxygen should be given. Hypoxia may be caused by hypoventilation, in which case carbon dioxide will be raised. But oxygen is far less soluble than carbon dioxide, so any disease increasing the fluid barrier between alveolar air and pulmonary blood (for example, pulmonary oedema, chest infection) may cause hypoxia while carbon dioxide remains normal (normocapnia). Hypoxic patients need oxygen; without oxygen, tissue cells die. Contrary to widespread belief, only per cent of patients with COPD may become apnoeic if given more than 28% oxygen (Bateman and Leach 1998). However, medical gases are drugs, which legally require a prescription. Nurse-initiated oxygen therapy may be covered in some areas by patient group directions, but in other areas nurses initiating oxygen should remember their individual accountability (NMC 2002). Where urgent treatment is necessary to preserve life, there is a legal (Dimond 2002) and professional (NMC 2002) expectation that nurses will act in patients best interests. Saturation (SaO 2 ) The normal level is about 97%. Most readers will be familiar with oxygen saturation from pulse oximetry. Pulse oximeter probes measure saturation of haemoglobin in peripheral (capillary) blood (SpO 2 ). The saturation measured in an ABG sample is the SaO 2. However, differences between SpO 2 and SaO 2 are in practice negligible, both often being referred to as SO 2. Oximetry readings may be falsely high as a result of: Carbon monoxide (for example, from smoking a cigarette) (Dobson 1993). Bright light, especially fluorescent light and heat lamps (Fox 2002, Ralston et al 1991). Whereas most oximeter finger probes have effective light shields, ear probes do not, and finger probes are contoured for a finger, not the ear. Shading probes with the hand may result in a more accurate, lower, reading. Falsely low oximetry readings may be caused by: Poor perfusion (Jensen et al 1998), such as from vascular disease, vasoconstriction (Keenan 1995), severe shock (Keenan 1995) or very irregular heart rhythms. Shivering (Stoneham et al 1994). High blood bilirubin levels (bilirubinaemia) (Dobson 1993). Dark nail varnish, especially blue or black (Wahr and Tremper 1996). Intravenous dyes, such as methylene blue (Fox 2002). The relationship between partial pressure of oxygen in arterial blood (PaO 2 ) and saturation of haemoglobin in arterial blood by oxygen (SaO 2 ) is complex, shown graphically by the oxygen saturation curve (Figure 1). This S-shaped curve represents significant changes in PaO 2 with minimal changes in SaO 2 48 nursing standard february 4/vol18/no21/2004

5 at higher levels (the plateau of the curve); changes in SaO 2 accelerate while changes in PaO 2 reduce at lower levels (the steep part of the curve). Saturation measures the percentage of haemoglobin (Hb) that is saturated by oxygen. It does not measure Hb. So, if two patients both have oxygen saturations of 97%, but one has an Hb of 14g/dl and the other has an Hb of 7g/dl, the first has 97% of 14g/dl saturation and the second has 97% of 7g/dl, giving the first patient nearly twice the amount of oxygen in the arterial blood. Blood gas samples usually measure Hb, so the Hb should be checked when considering the significance of oxygen saturation. Respiratory failure Respiratory failure results in inadequate oxygen in the blood. The British Thoracic Society (2002) defines respiratory failure as an arterial oxygen level below 8kPa (Box 4). With respiratory failure, arterial carbon dioxide levels may be low, normal or high. Carbon dioxide is 20 times more soluble than oxygen (Waterhouse and Campbell 2002), so diseases that increase the fluid barrier between alveolar air and pulmonary blood, such as pulmonary oedema, may cause hypoxia while carbon dioxide levels remain normal (normocapnia). This is called type 1 respiratory failure, and is defined as PaO 2 below 8kPa and PaCO 2 below 6kPa (BTS 2002). When breathing is shallow (for example, in COPD) or slow, insufficient carbon dioxide will be removed from the blood, causing high blood carbon dioxide (hypercapnia) in addition to hypoxia. This is called type 2 respiratory failure, and is defined as PaO 2 below 8kPa and PaCO 2 above 6kPa (BTS 2002). Bicarbonate is produced in various parts of the body, including the liver and kidneys. Low levels of bicarbonate are caused either by extensive buffering or by impaired/delayed response to produce sufficient buffer, such as with liver failure. Carbonic acid, the main acid in blood, can dissociate into bicarbonate and a free hydrogen radical, resulting in production of bicarbonate from respiratory acidosis. Conversely, bicarbonate and a hydrogen radical (a single H + atom) can form carbonic acid: CO 2 + H 2 O H 2 CO 3 HCO H + So bicarbonate, used to measure metabolic acidbase balance, can be increased as a result of hypercapnia. Therefore, from the measured bicarbonate and carbon dioxide, analysers calculate how much bicarbonate results from respiratory dysfunction and subtract this from the actual bicarbonate, to provide a computer estimation. This is the standardised bicarbonate (SBC; standardised figures are sometimes identified by std ) and represents a more accurate estimation of metabolic function. When gases are relatively normal, actual and SBC are similar or identical, but abnormal carbon dioxide levels can cause significant differences. Using standardised rather than actual levels is therefore logical; however, all staff should use the same measurement, as alternating between standardised and actual levels could result in patients being treated for differences in interpretation rather than for any physiological change. Base excess (BE) The normal level is ±2 (Cornock 1996). Metabolic acid-base balance is also represented by base excess. BE measures the number of Figure 1. Oxygen dissociation curve TIME OUT 4 Review the respiratory function of the patient whose results you are analysing. Is the respiratory acid-base balance normal? If not, does the patient have a respiratory acidosis or alkalosis? What does this imply about his or her respiratory function? Identify whether you consider the oxygen status to be satisfactory. Does the patient have respiratory failure? If so, is it type 1 or type 2? Remember to check the Hb. Do you think there should be any change in the patient s oxygen therapy? If so, describe what you recommend. How do these findings compare with what you know of the patient s respiratory function? SaO 2 % Venous Arterial Shift to the right, eg from pyrexia or acidosis, which decreases the affinity of haemoglobin for oxygen Normal oxygen dissociation curve Metabolic measures Bicarbonate (HCO 3 - ) The normal range is 24-27mmol/l (Coombs 2001). Bicarbonate is the main, although not the only, chemical buffer in plasma, so levels indicate metabolic acid-base status PO 2 (kpa) february 4/vol18/no21/2004 nursing standard 49

6 Box 5. Metabolic acid-base balance Metabolic acidosis HCO 3 - /SBC BE/SBE Metabolic alkalosis HCO 3 - /SBC BE/SBE Box 6. Compensation (ph in normal range) Respiratory acidosis (PaCO 2 >6kPa) Metabolic alkalosis (SBC >28, SBE >+2) Respiratory alkalosis (PaCO 2 <4.5kPa) Metabolic acidosis (SBC <22, SBE <-2) moles of acid or base needed to return 1 litre blood to ph 7.4 (assuming PaCO 2 remains constant at 5.3kPa). It is derived from measured bicarbonate. However, like bicarbonate, it can be affected by respiratory function, so standardised base excess (SBE) is calculated, removing the respiratory element to provide a purely metabolic estimation. BE means an excess of base (alkali). With metabolic alkalosis, there is an excess of base. But with metabolic acidosis, there is a negative BE (Box 5). Sometimes printouts fail to clearly show a minus sign, but if bicarbonate is low, BE will be negative. Compared with the ph scale, BE measurement is simple. Its neutral is zero. Unlike the negative logarithmic ph scale, the BE scale is linear. The normal range is usually given as +2 to -2. TIME OUT 5 Review the metabolic results from the patient whose results you are analysing. Is the metabolic acid-base balance normal? If not, does the patient have a metabolic acidosis or alkalosis? What does this imply about his or her metabolic function? How do these findings compare with what you know of the patient s renal and other metabolic functions? Are there significant differences between actual and standardised measurements? If so, note how abnormal carbon dioxide is. Compensation In health, the body maintains homeostasis. Homeostasis of blood ph is Therefore, provided the body remains healthy enough to respond, imbalance of either respiratory or metabolic function will be compensated for by an opposite imbalance of the other (Box 6). However, while altering respiratory rate and depth can (with a healthy respiratory system) normalise blood ph in a few minutes, metabolic responses take considerably longer (hours or, sometimes, days). A patient s history often indicates which way, if any, compensation is occurring (Table 1). For example, people with COPD, and therefore hypercapnia with a chronic respiratory acidosis, often develop compensatory chronic metabolic alkalosis. Reducing respiratory acidosis (for example, using non-invasive ventilation) in these patients may result in continuing metabolic (over-) compensation, causing overall alkalosis that persists for some days. Attempts to compensate may also be incomplete, failing to normalise ph. Respiratory effects on acid-base balance, through removal of carbon dioxide, is at least as powerful as all chemical buffers combined, and may be twice as powerful (Marieb 2004). Doubling or halving the amount of air reaching the alveoli (ventilation) can alter ph by 0.2 (Marieb 2004), enough to return a severe acidosis of 7.2 to normal in three to 12 minutes (Guyton and Hall 2000). With healthy lungs, ventilation can increase 15-fold (Marieb 2004), as experienced by some athletes during vigorous exercise. Metabolic control is more complex, relying on: Hydrogen loss in urine. Production and re-absorption of chemical buffers (bicarbonate, phosphate, proteins), mainly by the liver, kidneys and gut. Production of metabolic acids from cells and in the stomach. Absorption of acids and alkalis from the diet (and other routes, such as intravenous infusions). Most intravenous infusions are acidic; for example, in the author s workplace the ph of normal saline (0.9%) is 5.0, while the ph of 5% glucose is TIME OUT 6 Is compensation occurring in the result you have analysed? If so, from the patient s history, identify whether respiratory function is compensating for a metabolic problem or vice versa. Is compensation achieving normal ph? TIME OUT 7 Having completed your analysis of the results, discuss your findings and ideas with a colleague who is used to interpreting ABGs. If nursing and medical colleagues in your area are not used to interpreting ABG results, ask the critical care outreach team. You may like to use the case study in box 7 as an example. 50 nursing standard february 4/vol18/no21/2004

7 Table 1. Three examples of successful and unsuccessful compensation Metabolic acidosis (compensated) Temperature 36.1 ph PaCO kPa PaO kPa Temperature corrected: ph PaCO kPa PaO kPa HCO 3 act 21.6mmol/l HCO 3 std 21.7mmol/l BE act -3.5mmol/l BE std -3.4mmol/l Hb 13.5g/dl SaO % K + 4.1mmol/l Na + 139mmol/l Ca 2+ (calcium) 1.15mmol/l Cl - (chloride) 108mmol/l Glu (glucose) 5.1mmol/l Lac (lactate) 0.5mmol/l This patient has a normal ph, but is hyperventilating (PaCO 2 ). Oxygenation (PaO 2, SaO 2 ) is excessive, partly from hyperventilation, and partly from the three litres of nasal oxygen the patient was receiving. Oxygen can be discontinued, and monitored using pulse oximetry. The 100.6% saturation is machine error. Changes in gas measurements from temperature correction and in metabolic measurements from standardisation are small and insignificant. The patient has a slight metabolic acidosis. This would be the underlying problem, for which respiratory compensation is occurring. This patient had type 1 diabetes and was recovering from diabetic ketoacidosis. While blood glucose level is now normal, metabolic acidosis is reducing but persists. Lactate is normal. Respiratory acidosis with (excessive) metabolic compensation (Not temperature corrected) ph PaCO kPa PaO kPa HCO 3 act 33.3mmol/l BE 11.6mmol/l Hb 10.9g/dl SaO % This patient has an alkalosis. Ventilation (PaCO 2 ) is adequate, as the patient is receiving non-invasive ventilation for respiratory failure caused by pneumonia. Oxygen is poor. The ventilator is currently delivering only air, so supplementary oxygen needs to be added. He or she has a metabolic alkalosis. Before admission, the pneumonia had presumably caused increasing respiratory acidosis, initiating metabolic compensation to maintain normal ph. Now that ventilation has removed the respiratory acidosis, metabolic alkalosis remains, causing an overall alkalosis. Uncompensated metabolic acidosis ph PaCO kPa PaO kPa HCO 3 act 18.2mmol/l BE -8.3mmol/l K mmol/l Lactate 3.65mmol/l This patient has a severe acidosis. Gases are normal, so the patient is ventilating adequately. There is a severe metabolic acidosis, and lactate is high. Potassium is also life-threateningly high. The patient had had a cardiac arrest, and at the time this gas was taken was being hand-ventilated following successful resuscitation. Conclusion ABG analysis provides useful monitoring, especially for carbon dioxide. In most wards, taking arterial samples has traditionally been a medical role, but some specialist nurses are now taking samples and so need to be able to interpret measurements. Nurses who are not taking samples may be able to initiate earlier intervention if they are able to interpret results. Understanding results can help nurses to understand treatments and interventions, so making nursing more interesting. Like any other investigation, blood gas analysis may provide information that can be useful for treating patients. This article has described how to interpret the most important results. It has not covered every possible measurement machines may make (which vary according to programming). As you develop your skills further, you may benefit from finding out the significance, or otherwise, of other measurements. Interpreting ABG samples is a skill which, like any other, improves with practice. Unfortunately, february 4/vol18/no21/2004 nursing standard 51

8 Box 7. Case study Mr Watts is admitted with bronchopneumonia. He has no history of chronic respiratory disease. He has a non-productive cough. His oxygen saturation is below 86% and he is very dyspnoeic. On 100% oxygen, his blood gases are: ph 7.32 pco kPa po kPa SBC 26.0mmol/l SBE 2.4mmol/l SO 2 89% This result shows an overall acidosis, with respiratory acidosis but no metabolic compensation. This indicates a new respiratory problem. Raised carbon dioxide indicates poor ventilation, which also contributes to severe hypoxia. The sample confirms that the pulse oximetry measurement was accurate, and he is started on bilevel non-invasive ventilation. Following prn (pro re nata, or when required) salbutamol and ipratropium nebulisers, his cough becomes productive. A physiotherapist is called, achieving effective sputum clearance. One hour after physiotherapy, with bilevel non-invasive ventilation delivering 60% oxygen, his gases are: ph pco kPa po kPa SBC 26.0mmol/l SBE 2.0mmol/l SO 2 99% Mr Watts metabolic status remains unchanged, as would be expected. His carbon dioxide (and acid-base balance) levels have been restored to normal, so it is decided to discontinue bilevel noninvasive ventilation. His oxygenation is greatly improved, but it is decided to maintain 60% oxygen as non-invasive ventilation is being discontinued. Further changes can be guided by pulse oximetry. These ABGs have enabled prompt (and probably earlier than might otherwise have occurred) interventions and, following the second gas, early discontinuation of non-invasive ventilation. Mr Watts will need active treatment for his bronchopneumonia, including antibiotics, regular physiotherapy, and probably other medications and investigations. Nursing care should include frequent (at least four-hourly) respiratory observations, including rate and depth of breathing and oxygen saturation. samples are often taken when patients conditions are too poor to spend time practising interpretation. Making a second copy of the printout from the machine, or copying results on to notepaper, enables nurses to practise interpretation at a more convenient time TIME OUT 8 Now that you have completed the article you might like to write a practice profile. Guidelines to help you are on page 55. REFERENCES Babb M, Farmery A (2003) Haemorrhagic shock. Surgery. 21, 8, 208a-208e. Bateman N, Leach R (1998) Acute oxygen therapy. British Medical Journal. 317, 7161, Beaumont T (1997) How to guides: arterial blood gas sampling. Care of the Critically Ill. 13, 1, centre insert. British Thoracic Society (2002) Non invasive ventilation in acute respiratory failure. Thorax. 57, 3, British Thoracic Society (1997) Guidelines for the management of chronic obstructive pulmonary disease. Thorax. 52, Supplement 5. Clutton-Brock T (1997) The assessment and monitoring of respiratory function. In Goldhill D, Withington P (Eds) Textbook of Intensive Care. London, Chapman & Hall. Coombs M (2001) Making sense of arterial blood gases. Nursing Times. 97, 27, Cornock M (1996) Making sense of arterial blood gases and their interpretation. Nursing Times. 92, 6, Dimond B (2002) Legal Aspects of Nursing. Third edition. Harlow, Longman/Pearson Education. Dobson F (1993) Shedding light on pulse oximetry. Nursing Standard. 7, 46, Fletcher S, Dhrampal A (2003) Acid-base balance and arterial blood gas analysis. Surgery. 21, 3, Fox N (2002) Pulse oximetry. Nursing Times. 98, 40, 65. Gosling P (1995) How to guides: blood gas analysis. Care of the Critically Ill. 11, 1, centre insert. Guyton A, Hall J (2000) Textbook of Medical Physiology. Tenth edition. Philadelphia PA, WB Saunders. Hinds C, Watson D (1996) Intensive Care. Second edition. London, WB Saunders. Hope R et al (1998) Oxford Handbook of Clinical Medicine. Fourth edition. Oxford, Oxford University Press. Hornbein T (1994) Acid-base balance. In Miller R (Ed) Anesthesia. Fourth edition. New York NY, Churchill Livingstone. Jensen L et al (1998) Meta-analysis of arterial oxygen saturation monitoring by pulse oximetry in adults. Heart and Lung. 27, 6, Keenan J (1995) Pulse oximetry. Nursing Standard. 9, 35, 55. Marieb E (2004) Human Anatomy and Physiology. San Francisco CA, Benjamin/Cummings. Nursing and Midwifery Council (2002) Code of Professional Conduct. London, NMC. Ralston A et al (1991) Potential errors in pulse oximetry. Anaesthesia. 46, 4, Sheehy S, Lombardi J (1995) Emergency Care. Fourth edition. St Louis MO, Mosby. Stoneham M et al (1994) Knowledge about pulse oximetry among medical and nursing staff. Lancet. 344, 8933, Wahr J, Tremper K (1996) Oxygen measurement and monitoring techniques. In Prys-Roberts C, Brown B Jr (Eds) International Practice of Anaesthesia. Oxford, Butterworth Heinemann. Waterhouse J, Campbell I (2002) Respiration: gas transfer. Anaesthesia and Critical Care. 3, 9, nursing standard february 4/vol18/no21/2004