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Interpretation of Arterial Blood Gases 2009 Surgery Oxford

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  Interpretation of arterialblood gases Claire BaylisChris Till  Abstract  Arterial blood gas analysis is a frequently used and extremely useful clin-ical tool. Doctors of all levels understand the results to varying degrees.This article aims to explain some of the more important points and thushelp with interpretation of results. Not all of the results produced bya blood gas analyser are measured; the machine calculates some itself.The three things the machine actually measures are the pH of theblood and the partial pressures of both oxygen and carbon dioxide.Doctors within the specialty often run high-dependency units and there-fore it is important for surgeons to be able to understand and act onabnormal results. One of the most commonly held misconceptions isthe need to withdraw supplemental oxygen in order to establish if a patient is hypoxic. This is not necessary and the reasons are detailedin this short article. Abnormalities in acid e base disturbance and theconcepts of buffering, compensation and the effects of altitude are alsodiscussed. The final part of this article is a stepwise guide to interpreta-tion of blood gases. Keywords  acidosis; alkalosis; buffers; carbon (dioxide); oxygen  Acid e base physiology  The concept of pH (literally the  power   of   hydrogen ) was intro-duced in 1909 by Danish chemist Søren Peder Lauritz Sørensen.pH is the measure of the activity of dissolved hydrogen (H þ ) ionsin a solution. pH is the negative logarithm to base 10 of theconcentration of hydrogen ions in solution where ‘p’ denotespower and ‘H’ hydrogen. Because it is a logarithmic scale, a smallchange in pH is indicative of a large change in H þ ion concen-tration ([H þ ]) in the  opposite  direction. A change in pH of 0.3approximately doubles or halves the [H þ ]. A change in pH of 1reflects a 10-fold change in [H þ ].  pH   ¼  log  10 ½  H  þ  Pure water is said to be neutral, having a pH at 25  C of 7.0.Solutions with a pH less than 7.0 are said to be acidic and thosegreater are alkaline. A solution of strong acid has a pH of 0 anda strong alkali has a pH of 14, thus the pH scale runs from 0 to 14.Maintaining a normal pH is an important part of homeostasis.Abnormal acid e base balance can lead to protein denaturationand enzyme inactivation. The pH of blood is normally around7.35 e 7.45, which is known as physiological pH. The rangecompatible with life is greater than this, around 6.80 e 7.70.Every 24 h approximately 60 mmol/l of H þ ions are producedas an end product of normal metabolism. These H þ ions take theform of organic acids (amino acids or lactic acid), which areoxidized to carbon dioxide (CO 2 ) and water, or inorganic acids(HCl, H 2 SO 4 , H 3 PO 4 ), which are excreted by the kidneys.The transport of CO 2  has a profound effect on the acid e basestatus of the blood and the body as a whole. Normally, the lungsare responsible for most of the CO 2  removal, excreting over10,000 mEq of carbonic acid every 24 h. The kidneys also havean important role, but excrete much less CO 2  (less than 100 mEq/24 h). As a result, alveolar ventilation  e  which determines CO 2 elimination  e  has the greatest control over acid e base balance. Buffers A buffer is a solution that resists change pH when small amountsof acid or alkali are added. An acidic buffer consists of a weakacid and a salt of the acid. The equation for any buffer system isas follows:  HA 4  H  þ þ  A  Where A  is any anion (e.g. chloride, Cl  ) and HA is undisso-ciated acid (for example hydrochloric acid, HCl). The addition of a strong acid to this solution shifts the equation to the left. TheH þ ions are ‘used up’ in the formation of undissociated acid.When a base is added, the H þ ions react with the OH  ions andform water (H 2 0).An acid is a substance that dissociates, giving H þ ions.A base is a substance that accepts H þ ions.An alkali is a substance that dissociates, giving OH  ions.The pKa (defined as the logarithm to base 10 of the acid disso-ciation constant, Ka) is equivalent to the pH at which 50% of thesubstance is ionized. The relationship between pH, pKa andionized and unionized concentrations is shown in Figure 1. Themaximal buffering effect occurs when the pKa is equal to the pHof the solution the substance is in, thus the amount of free anion(A  ) is equal to the amount of undissociated acid (HA).The effectiveness of a buffer depends on the quantity avail-able and its pKa. The closer the pKa of the buffer is to the pH of   pH =  pKa + log 10  [  A ][ HA ] The relationship between pH, pKa and the concentrationsof ionized [A   –  ] and unionized [HA] acid. When [A   –  ] = [HA], log  10  [A   –  ]/[HA] = 0; thus pH = pKa Figure 1 Claire Baylis  MB ChB  is a Year 3 Specialty Trainee in Anaesthesia, in theNorth Western Deanery. Conflict of interest: none declared. C/O Anaesthetic Department, Royal Lancaster Infirmary, Ashton Road,Lancaster LA1 4RP, UK. Chris Till  BM FRCA  is a Consultant in Anaesthesia and Intensive CareMedicine, Royal Lancaster Infirmary, UK. CRITICAL ILLNESS AND INTENSIVE CARE II SURGERY 27:11  470    2009 Elsevier Ltd. All rights reserved.  the solution, the more effective it is. Three main buffers exist inhumans e proteins, haemoglobin (Hb) and bicarbonate (HCO 3  ).Different buffers exist in blood and intracellular fluid (ICF).Haemoglobin has six times the buffering capacity of plasmaproteins. Reduced Hb is a weaker acid and therefore a betterbuffer than oxyhaemoglobin. In blood, HCO 3  is the mostsignificant buffer. H þ ions combine with HCO 3  and are thenremoved from the body in the form of CO 2  and H 2 O. CO 2  þ  H  2 O 4  H  2 CO 3 4  H  þ þ  HCO  3 The pKa of bicarbonate is 6.1, low compared to blood pH.Bicarbonate is, however an effective buffer due to the largequantity available and the fact that it is an ‘open-ended’ buffersystem. The body has the ability to alter CO 2  and HCO 3  levelsindependently via either the lungs or kidneys.The addition of H þ ions to blood results in an increase inH 2 CO 3 , which in turn leads to an increase in CO 2  (as they are inequilibrium), which is excreted via the lungs. This is explainedby the Henderson e Hasselbalch equation for bicarbonate.  pH   ¼  6 : 1 þ log 10   HCO  3  ½  H  2 CO 3  ¼  6 : 1 þ log 10   HCO  3  0 : 03   PCO 2 In ICF, proteins and phosphate are the main buffers. Oxygen Oxygen is carried in two forms in blood, dissolved in plasma orin combination with haemoglobin. The amount of oxygen dis-solved in blood is proportional to the partial pressure of oxygen,usually expressed in kilopascals (kPa). For each kPa, 0.027 mloxygen is dissolved per 100 ml blood. Every 100 ml of normalarterial blood contains 0.3 ml dissolved oxygen.Oxygenisalsotransportedcombinedwithhaemoglobin.Haemis an iron e porphyrin compound, joined to the protein globin. The‘globin’ consists of   four polypeptide chains , each of which has theability to combine and form a reversible compound with oxygen. O 2  þ  Hb 4  HbO 2 Each Hb molecule can therefore bind four oxygen molecules.Every 100 ml of normal arterial blood with a [Hb] of 15 g/dlcontains approximately 20 ml of oxygen e of which only 1.5% isdissolved in plasma.As each oxygen molecule binds, there is a conformationalchange in haemoglobin, increasing its affinity for oxygen. Thischange facilitates oxygen loading and unloading and is thereason for the sigmoid shape of the oxygen dissociation curve.Haemoglobin e oxygen saturation refers to the percentage of available binding sites that have combined with oxygen. Arterialblood has an oxygen saturation of approximately 97% (corre-sponding to a PaO 2  of 13.5 kPa). Mixed venous saturation Mixed venous blood is blood from the superior vena cava andinferior vena cava after it has mixed in the right heart. Blood issampled from the pulmonary artery by means of a pulmonaryartery catheter. Normal mixed venous saturation ( SvO 2 ) is 75%(corresponding to a PaO 2  of 5.3 kPa). This can be a useful tool incritically ill patients and can help to distinguish between sepsisand cardiogenic shock as a cause of hypotension. An  SvO 2 > 75%suggests that oxygen supply exceeds demand. This may be thecase in sepsis. In this instance, there may be adequate oxygensupply but the tissues are unable to take up and use the oxygen.This results in a higher percentage of oxygen in venous blood.Conversely, an  SvO 2  < 75% suggests demand exceeds supply. Incardiogenic shock there may be an increase in demand foroxygen, which is not met by an increase in supply. This results ina reduced venous oxygen saturation.  Alveolar gas equation The alveolar gas equation describes the relationship between theactual arterial partial pressure of oxygen (PaO 2 ) and what wouldbe the expected alveolar (PAO 2 ) for a given  fraction of inspiredoxygen (FiO 2 ) .Oxygen is almost completely taken up by blood as it passesthe alveolus, hence the partial pressures in the alveolus andarterial blood should be approximately equal. Arterial bloodcan be sampled and the PaO 2  measured. The differencebetween the two values (actual PaO 2  and expected PAO 2 ) isknown as the ‘A e a gradient’. Physiological shunting of blood(i.e. blood leaving the left ventricle that has bypassedthe pulmonary circulation) produces a normal gradient of 0.5 e 2 kPa. An increase in A e a gradient is present if there ismore deoxygenated blood leaving the left ventricle due toa pathological process. The equation can be used to establish theextent of hypoxia, without needing to remove supplementaryoxygen. PiO 2  is the partial pressure of inspired oxygen . In dry gas, PiO 2 ¼  barometric pressure    FiO 2 . Inhaled air is humidified as itpasses through the respiratory tract, so that by the time it reachesthe alveoli, it is completely saturated with water vapour. Thesaturated vapour pressure (SVP) of water at 37  C is 6.3 kPa. Thepercentage of oxygen in the air is unaffected by altitude (21%)however, the partial pressure of oxygen is. For this reason,barometric pressure must also be taken into account. At sealevel, barometric pressure (P B ) is 101.3 kPa.Other gases notably CO 2 , are present in the alveolus and thepartial pressure of these must also be taken into account. Therespiratory quotient is the ratio ofthe amount of CO 2  produced foreach molecule of O 2  used in metabolism. This number varies, but0.8 is taken to be normal for someone with a balanced diet. ThepartialpressureofCO 2  isdivided bytherespiratoryquotient (RQ).  PAO 2  ¼  PiO 2    PaCO 2  RQ  where  PiO 2  ¼  FiO 2  ð  P   B   SVPH  2 O Þ For example: For an FiO 2  of 0.4 (that is 40% oxygen) anda PaCO 2  of 5.3 kPa at sea level, the partial pressure of alveolaroxygen (PAO 2 ) would be 0.4    (101.3  6.3)  5.3/0.8  ¼  30.85kPa. Thus, for a normal human receiving 40% oxygen (FiO 2  0.4)a PAO 2  of 30.85 kPa would be expected, which assuminga normal A e a gradient, this would produce a PaO 2  of approxi-mately 30 kPa. As a shortcut, subtract ten from FiO 2  to give theexpected PAO 2  in kPa. For an FiO 2  of 40%, a PAO 2  of approxi-mately 30 kPa would be expected. CRITICAL ILLNESS AND INTENSIVE CARE II SURGERY 27:11  471    2009 Elsevier Ltd. All rights reserved.   Altitude Altitude causeshypoxiadue toa reduction inPiO 2 , notthe oxygenpercentage.Pressuredecreasesexponentiallyasaltitudeincreases,roughly halving for every 5500 m above sea level. The barometricpressure at the summit of Mount Everest (an altitude of8400 m) is30 kPa. Hypoxia leads to hyperventilation, due to stimulation of peripheral chemoreceptors. The increase in minute ventilationreduces PaCO 2 , producing a respiratory alkalosis. This can causecerebral oedema and symptoms such as fatigue and dizziness,known as altitude sickness. After 24 e 48 h, cerebrospinal fluid pHis normalized by movement of HCO 3  out of CSF. After a few days,blood pH is near normalized by renal excretion of bicarbonate. AspH begins to normalize, ventilation can again increase.  PiO 2  ¼  FiO 2  ð  P   B   SVPH  2 O Þ Sealevel :  PiO 2  ¼  0 : 21 ð 101 : 3  6 : 3 Þ ¼  19 : 95 kPa Everest :  PiO 2  ¼  0 : 21 ð 30  6 : 3 Þ ¼  4 : 98 kPa It can be seen from these equations that although the inspiredpercentage of oxygen remains the same, the inspired  partial pressure  is considerably lower.Conversely, pressure increases below sea level increasing thePiO 2.  This increases the partial pressure of O 2  in the alveolus andmore is taken up into arterial blood. Hyperbaric chambers can beused to deliver a higher PiO 2  than would otherwise be possibleby increasing the percentage. Oxygen dissociation curve The normal haemoglobin e oxygen dissociation curve is shown inFigure 2. The curve is shifted to the right by increased CO 2 ,temperature, diphosphoglycerate and [H þ ]. Thus in the tissuesthere is better unloading of oxygen for a given PCO 2 . Conversely,decreased CO 2 , temperature, [diphosphoglycerate] and [H þ ]shifts the curve to the left. This improves oxygen binding inpulmonary capillaries. The leftward shift is accentuated ataltitude.Pulmonary vasoconstriction occurs as a result of alveolarhypoxia. This leads to an increase in pulmonary artery pressuretherefore work of the right heart. This can cause right ventricularhypertrophy. Carbon dioxide carriage CO 2  is carried in the blood in three forms, the concentrations of which differ in venous and arterial blood. CO 2  is 20 times moresoluble than oxygen and 10% of venous CO 2  is dissolved inblood. Most CO 2  in blood is in the form of bicarbonate (HCO 3  ).Bicarbonate formation results initially from the combinationof CO 2  with H 2 O to form carbonic acid (H 2 CO 3 ). This reaction isslow in plasma, but fast in red blood cells due to the presence of an enzyme (carbonic anhydrase). This subsequently dissociatesinto H þ ions and HCO 3  (see above). Some liberated H þ ions bindto reduced haemoglobin which is present in peripheral blood.Reduced haemoglobin is less acidic, and is therefore a betterproton acceptor. Conversely, HbO 2  in pulmonary capillarieshelps unload CO 2  a phenomenon known as the Haldane effect.The affinity of haemoglobin for O 2  reduces in the presence of a low pH, such as in tissues. This helps with unloading of O 2  e a phenomenon known as the Bohr effect. Both the Haldane andBohr effect result in CO 2  loading at the tissues and O 2  unloading.Some CO 2  takes the form of carbamino compoundsor carbamates. These compounds are formed by combination of CO 2  with the terminal amine groups of circulating proteins.Of these, globin is the most important.  Hb :  NH  2  þ CO 2 4  Hb :  NH  : COOH  ð carbaminohaemoglobin Þ This reaction occurs rapidly without enzymes. Reduced haemo-globin can bind more CO 2  than oxygenated Hb, thus O 2 unloading facilitates CO 2  binding (Figure 3).  Anion gap The sums of positive and negative charges in the body are equal,resulting in electrical neutrality. The main positively chargedions (cations) are sodium (Na þ ) and potassium (K þ ), theconcentrations of which can be measured. Similarly, it is possibleto measure the concentrations of the principal negatively chargedions (anions), chloride (Cl  ) and HCO 3  . The difference betweenthe cations and anions is known as the  anion gap .  Anion gap  ¼ ð½  Na þ þ½  K  þ Þð½ Cl  þ½  HCO  3  Þ The normal range is 10 e 18 mmol/l and is due to the presence of unmeasured ions such as magnesium and phosphate. An 801006040202610141822Total O 2 Dissolved O 2 O 2  combinedwith Hb     %     H    b   s   a   t   u   r   a   t    i   o   n    O    2    c   o   n   c   e   n   t   r   a   t    i   o   n    (   m    l    /   1   0   0   m    l    ) 0 Partial pressure of oxygen (kPa) 3.5 5.3 13.5 The normal haemoglobin-oxygen dissociation curve.Partial pressures of oxygen corresponding to saturations of 50%, 75% (mixed venous blood) and 97% (arterial blood)are shown Figure 2   Venous 30% Carbamino compounds60% HCO 3  10% DissolvedArterial 5% Carbamino compounds90% HCO 3  5% Dissolved CRITICAL ILLNESS AND INTENSIVE CARE II SURGERY 27:11  472    2009 Elsevier Ltd. All rights reserved.  increase in unmeasured ions will either increase or decrease thegap. Blood gas analysis All blood gas analysers directly measure pH, PaO 2  and PaCO 2 .The inverse relationship between pH and [H þ ] is approxi-mately linear over the middle of the clinical range. pH reduces by0.1 for every 10 nmol/litre increase in [H þ ] (Table 1). [H þ ] is measured using an ion-selective electrode with ion-sensitive glass. The [H þ ] within the electrode is maintained ata constant level by the action of buffers in the solution. As bloodis exposed to the other side of the glass, a potential differencedevelops across it in proportion to the [H þ ] in the blood sample.Other types of ion-selective electrode can be used to measureNa þ , K þ and Ca 2 þ . Compensation Compensation for abnormalities in acid e base balance can beeither metabolic or respiratory. For a primary metabolic distur-bance, the compensatory mechanism will be respiratory. Forexample, in diabetic ketoacidosis the minute ventilationincreases, increasing elimination of CO 2  in an attempt to returnthe pH to normal.Respiratory acidosis from hypoventilation will eventually leadto HCO 3  retention by the kidneys and correction of pH  e a process that takes several days. Long-term CO 2  retention willresult in an increase in HCO 3  and may be associated witha normal pH. Restoration of normal CO 2  will result in a metabolicalkalosis as the HCO 3  will remain elevated for a considerabletime after the CO 2  is corrected.Normally an elevated CO 2  is the main stimulus for breathing.Long-term retention of CO 2  such as in obstructive airwaysdisease will eventually lead to a reduced sensitivity of the brain(respiratory centres) to CO 2  and the ‘‘hypoxic drive’’ will takeover as the main stimulus to breathe. This can lead to furtherrespiratory depression and a further increase in CO 2  if oxygen isadministered. Only a handful of patients fall into this category . If in doubt oxygen should be administered to hypoxic patients and senior help called.Three main terms are used in reference to compensation. Uncompensated:  Acid e base disturbance. No attempt at correc-tion of the pH. Partially compensated:  Acid e base disturbance. Some attemptto correct pH but pH not within the normal range. Fully compensated:  Acid e base disturbance. Complete correc-tion of the pH back to normal.It is important to note that over-compensation does not occur. If this appears to have occurred, it is most likely to be iatrogenic. Base excess The base excess (or deficit if it is negative) refers to the amount of base (in mmol) that would be required to restore 1 litre of blood tonormalpH( assumingCO 2 isnormal ),at37  C.Ifthereisadeficitof base,thereisametabolicacidosisandbasewouldhavetobeaddedto correct the pH. If there is a base excess, there is a metabolicalkalosisandbasewouldhavetoberemovedtonormalizepH.IftheCO 2  was elevated, this base excess could be compensatory. Temperature correction The solubility of CO 2  and O 2  in blood increases as temperaturedecreases. This can result in a falsely low partial pressure readingon the blood gas analyser.  Actual bicarbonate This is an estimate of whole blood [HCO 3  ], calculated bysubstituting PCO 2  for H 2 CO 3  in the Henderson e Hasselbalchequation. Standard bicarbonate This is the [HCO 3  ] that would result from equilibrating whole,arterial blood  in vitro  with a gas with PCO 2  ¼  5.3 kPa. It iscalculated and cannot be directly measured. Lactate Lactate is the end product of anaerobic glycolysis. The normalrange for blood lactate is 0.6 e 2.0 mmol/litre. If there is an O 2 CO 2 O 2 H 2 O H 2 OO 2  O 2 CO 2 Dissolved Tissue     C   a   p    i    l    l   a   r   y   w   a    l    l PlasmaRed blood cell Dissolved C        a      r       b        a      m      i         n      o      H        b         HbO 2 HHbHCO  –3 Hb  – CI  – K + CI  – Na + HCO  –3  H + CO 2 CO 2  + H 2 O H 2 CO 3 CACO 2 Gas exchange in a tissue capillary Figure 3pH H D concentrationnmol/l mol/l 9.0 1 10  9 8.0 10 10  8 7.4 40 10  7.4 7.3 50 10  7.3 7.0 100 10  7 Table 1Primary Compensation ACIDOSIS Respiratory PCO 2  [  HCO 3  [ Metabolic HCO 3  Y  PCO 2  Y ALKALOSIS Respiratory PCO 2  Y  HCO 3  Y Metabolic HCO 3  [  Often none Table 2 CRITICAL ILLNESS AND INTENSIVE CARE II SURGERY 27:11  473    2009 Elsevier Ltd. All rights reserved.
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