CHAPTER ABG Analysis in Clinical Setting

117 Rajesh Mahajan, Suman Sethi

INTRODUCTION defined by the ratio of PCO2 to HCO3 and not by absolute Acid-Base balance is an intricate concept which requires an value of either one alone.5,6 intimate and detailed knowledge of the body’s metabolic Overview of Fundamentals of Acid-Base Disorder pathways used to eliminate the H+ ion. Accurately Normal metabolism of proteins and nucleotides generates interpreting acid-base balance requires simultaneous about 100 mmol H+ per day in the form of sulphuric and measurements of arterial pH and plasma electrolytes, phosphoric acids. By comparison, hydration of CO2 to as well as knowledge of compensatory physiologic form H CO generates 12,500 mmol H+ per day. mechanisms. In this article, we’ll review normal acid-base 2 3 physiology, acid-base disturbances, and lab techniques Carbon dioxide transport and mathematical calculations used to identify the cause 1. Transport of carbon dioxide in the blood is of acid-base derangements. considerably more complex. A small portion of carbon dioxide, about 5 percent, remains BASIC PHYSIOLOGY unchanged and is transported dissolved in blood. Acid-base Chemistry 2. The remainder is found in reversible chemical pH combinations in red blood cells or plasma. Some The concept of pH was put forward by the Danish chemist, carbon dioxide binds to blood proteins, principally Soren Peter Sorensen in 1909 to refer to the negative hemoglobin, to form a compound known as logarithm of hydrogen ion (H+) concentration. An increase carbamate. in the pH indicates a proportionate decrease in the 3., About 88 percent of carbon dioxide in the blood is [H+] and a decrease in the pH indicates a proportionate in the form of ion. increase in the [H+].1 Carbon dioxide enters blood in the tissues because its pH = – log [H+] local partial pressure is greater than its partial pressure The new generation of blood gas machines will report in blood flowing through the tissues. As carbon dioxide the H+ as well as the pH. Acid is an H+ donor andbase is enters the blood, it combines with water to form carbonic H+ acceptor.2 The intra and extracellular buffer systems acid (H2CO3), a relatively weak acid, which dissociates into minimize the changes in H+ that occur as a result of + - hydrogen ions (H ) and bicarbonate ions (HCO3 ). Blood addition of an acid or alkali load to the acidity is minimally affected by the released hydrogen (ECF), 60% of the acid load is buffered in the intracellular ions because blood proteins, especially hemoglobin, are fluid (ICF). The most important buffer is the imidazole effective buffering agents.7 ring of the histidine in the hemoglobin molecule. The The natural conversion of carbon dioxide to carbonic bicarbonate/carbonic acid is a weak buffer.3 acid is a relatively slow process; however, carbonic However the presence of carbonic anhydrase, the high anhydrase, a protein enzyme present inside the red blood solubility of CO2 and the ability of kidney to synthesize cell, catalyzes this reaction with sufficient rapidity that it new bicarbonate and above all the efficient removal of is accomplished in only a fraction of a second. Because

CO2 by lungs make it a powerful buffer. All buffers in a the enzyme is present only inside the red blood cell, common solution are in equilibrium with the same H+ ion bicarbonate accumulates to a much greater extent within concentration. Therefore, whenever there is a change in the red cell than in the plasma. The capacity of blood to the H+ ion concentration in the CSF, the balance of all the carry carbon dioxide as bicarbonate is enhanced by an buffer system changes at the same time – the isohydric ion transport system inside the red blood cell membrane principle. It is therefore enough to study one buffer that simultaneously moves a bicarbonate ion out of the system in order to evaluate the acid base status of ECF.4 cell and into the plasma in exchange for a chloride ion. The Henderson-Hasselbalch equation, with its reliance on The simultaneous exchange of these two ions, known logarithms and antilogarithms is long andcumbersome as the chloride shift, permits the plasma to be used as a and when attempting to deal with clinical situations. storage site for bicarbonate without changing the electrical 8 Kassirer and Bliech have rearranged the Henderson charge of either the plasma or the red blood cell. + equation that relates H (instead of pH) to PCO2 and Hemoglobin acts in another way to facilitate the transport HCO3– and have derived an expression, which has great of carbon dioxide. Amino groups of the hemoglobin clinical utility. molecule react reversibly with carbon dioxide in solution H+ = 24 x PCO2/HCO3- to yield carbamates. A few amino sites on hemoglobin are It is important to emphasize that H+ ionconcentration is CRITICAL CARE 554 sometimes between three and five days, to retain or to retain days, five remove HCO and three between sometimes response to arespiratorydisorder takes much longer, to carbonicacid(H the exquisitesensitivityofchemoreceptors in themedulla H equation: the via related are They respectively. buffers respiratory adequate (thatis, PaCO of ventilation andperfusion. Ifalveolar ventilation is This canresultfromhypoventilation oramismatch PaO If anarterialbloodgasresultshowshypoxemia (low The oxygen alveolar–arterial tension difference and alveolar the between arterial oxygentensions. difference the by assessed disturbance. The nature ofthehypoxemia canbefurther is almostcertainlycausedbyaventilation-perfusion A PaO Oxygenation HCO derangement ofboth arterial bloodgasresultshowstwoimbalances– As ageneralrule,whencompensationispresentthe a metabolic disorder, where HCO compensatory systemexiststomaintainhomeostasis. In blood, a For anydisturbanceofgastensionsinarterial changes Compensatory as partofacid–basehomeostasis.TheHCO Bicarbonate isaweak basethatisregulatedbythekidneys Bicarbonate bicarbonate orcarbamate. these twoevents, mostcarbondioxideistransportedas in thetissues and leaves capillaries in thelung. Between metabolism mustexistinthefreeformasitentersblood Virtually every moleculeofcarbondioxideproducedby free carbondioxideeasilycrosses biologic membranes. change orbinding,yet thispoolisimportant,becauseonly transported freeinphysicalsolutionwithoutchemical 5 percentofcarbondioxideinthebloodis Only hemoglobin molecule. of the state ofoxygenation on the to bindcarbondioxidedepends labile thatis,theirability The alveolar–arterial difference, or gradient, can be gradient, or fraction ofinspiredair estimated only iftheoxygen difference, alveolar–arterial The ventilation toretainor remove CO occur almost immediately toaltertherateanddepthof excreted bythekidneys,respiratorycompensationcan calculating the difference between the alveolar (PAO alveolar and arterial(PaO the between difference the calculating in ventilation-perfusion, orboth.Thisisassessed by to hypoventilation, or is secondary to a disturbance it mustbedeterminedwhether thehypoxemiaisrelated and theotherisduetocompensation. or decreased corresponding topH)istheprimaryproblem parameter thatmatches the pHtrend(thatis,is increased pH.If pHisleaningtoward acidosis or alkalosis,thenthe imbalance istheprimarydisturbanceobtainedfrom blood. Together, CO arterial bloodreflectsthemetaboliccomponentof 2 O +CO 2 ) andinadequatealveolar ventilation (highPaCO 2 that is less than expected indicates hypoxemia. 2 

3 H - asrequired. 2 CO 2 ) oxygentensions. 3 2  CO 2

and HCO HCO 2 3 ) orH is normal), then thehypoxemia 10 3 9 ˉ andPaCO 3 - +H + . Renalcompensationin 3 - actasmetabolicand + 3 ˉ may be retainedor 2 . This occurs due to 10 2 . A cluetowhich 3 ˉ measuredin 2 2 ), ) 9 FiO increasing and smoking cigarette age, with increases O2, range is 5–15 mmHg. The difference, expressed as P (A–a) watervapor pressureareknown. A normalreference vasculature. However, the result is non-specific in thepatient’s non-specific andagain clinical featuresareessentialfordiagnosis. is pathology actual result the defining the However, vasculature. disease of theairways, lungparenchymaor pulmonary a patient suggests aventilation-perfusion mismatch related to In difference. breathing room air, aP(A–a)O2 greaterthan15mmHg alveolar-arterial the increase All causes of hypoxemia, apartfrom hypoventilation, formula P(A–a)O2 =3+(0.21xpatient’sage). in PaCO HCO alkalosis brought about by H+ secretionand HCO by about alkalosis brought (COPD) is secondarily compensated for by as itoccurs in chronicobstructive airway disease hyperventilation).the otherhandprimaryrespiratory On compensated for bysecondary respiratory alkalosis (by other components,e.g.aprimarymetabolicacidosis is change in an appropriate with acid basedisturbance (FiO of changesinPCO are primarilyaresult compensatory. ChangesinpHthat and metabolic.Theymaybecompensatory or non- There aremainlytwotypesofdisorders, respiratory compensated Alkalosis – A process that wouldcausealkalemiaifnot greater than7.44 Alkalemia– A H+belowtherangeof36-44nmolL–1,pH compensated Acidosis – would causeacidemia,ifnot A processthat nmolL–1, pHlessthan7.36 Acidemia – A H+ionabove thenormalrangeof36-44 disorders in acid base statusare useful in understandingacid base disturbances describe to used are that definitions Several Acid basedisorders and hisPaCO In respiratoryacidosis, the patient’s pHislessthan7.35 acidosis Respiratory alkalosis. metabolic acidosis,respiratoryalkalosisand primary acid-basedisorders viz. , primary metabolicdisorders. Basically there arefour termed are bases buffer other and bicarbonate in changes On theotherhandchangesinpHbroughtaboutby produced. The relationship between PaCO weeks tobefullyestablished. to days take may latter the result, the achieve to minutes absorption bythekidneys.Whileformer takes a few to maintain normal PaCOto maintain of normal.Theamount alveolar ventilation necessary that causes hypercarbia, oraPaCO normal). Alveolar hypoventilation istheonlymechanism ARTERIAL BLOOD GAS MEASUREMENTS NOMENCLATURE FOR INTERPRETATION CLINICAL OF 2 . An expectedP (A–a)O2 2, 3 usually 0.21 on room air), barometricpressureand usually 0.21onroomair), -determines arterial pH.Generally,acute increases 2 13 areaccompanied byonlyminimalchanges in Compensation usually occurs in aprimary 2 isabovelimit of upper (the 45mmHg 2 aretermedrespiratorydisorders. 2 varies dependinguponCO 14

can be calculated usingthe can be 2 above theupperlimit 2 and plasma 3 – 2

CHAPTER 117 555 3   HCO 19 Normal Normal 2   PaCO Normal Normal . It is defined as the 2 11     pH of 40 mmHg. The –] 3 12 2 ] + [HCO – 18 ABG Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis amount of acid required to restore a liter of blood to amount of acid required to restore its normal pH at a PaCO Normal AG is 12 ± 4mEq/l. Conditions resulting in resulting AG is 12 ± 4mEq/l. Conditions Normal metabolic acidosis other than hydrochloric acidosis usually lead to a decrease in the serum bicarbonate in serum rise concentration without a concomitant AG. chloride thereby increasing the Delta ratio is related to defined as: the AG and buffering, and is AG/decrease in bicarbonate] Delta ratio = [increase in the bicarbonate levels when occur can ratio delta high A at the onset of the metabolic acidosis are already elevated either due to a pre-existing metabolic alkalosis, or as a A low compensation for pre-existing respiratory acidosis. normalanion gap with hyperchloremic delta ratio occurs acidosis. of all the gap (AG) represents the concentration Anion by the and is measured anions in the plasma unmeasured following formula: AG = [Na+] - [Cl Delta Ratio Estimate of Base Excess/Deficit Estimate The metabolic component of the acid–base balance is reflected in the base excess. pH and PaCO from blood derived This is a calculated value increases in metabolic alkalosis and decreases (or becomes (or decreases and alkalosis in metabolic increases but its utility in in metabolic acidosis, negative) more interpreting blood gas results is controversial. idea of the metabolic some While the base excess may give the interpretation. nature of a disorder, it may also confuse secondary be primary or may acidaemia alkalaemia or The does or alkalosis. The base excess to respiratory acidosis not take of the metabolic into account the appropriateness disorder, thus limiting utility its response for any given when interpreting results. causes of metabolic alkalosis respond to treatment treatment to respond alkalosis of metabolic causes with patient’s the If solution. chloride sodium 0.9% metabolic his 15 mmol/L, than less is concentration chloride above urine chloride levels is saline-responsive; alkalosis metabolic indicate non-saline-responsive 25 mmol/L saline-responsive resulting in The mechanisms alkalosis. or renal GI loss, diuresis, alkalosis include metabolic responsive Non-saline from hypercapnia. compensation excess from mineralocorticoid alkalosis results metabolic the Fluid administration is or potassium depletion. metabolic foundation for treatment for saline-responsive of extreme alkalosis, the patient alkalosis. In cases be may alkalosis dilute hydrochloric acid. Saline-resistant given the underlying etiology. is treated by addressing

2 16 15 is increased, - 3 levels to maintain a levels 18

- 3 or potassium. In the presence + 19 - results in an increase in pH. increase in an - results 3 - is key to determining if the patient key to determining is - ions move from the extracellular fluid 3 + 17 is reduced, causing an increase in pH. The is reduced, causing . However, over a period of 1 to 3 days, renal renal 1 to 3 days, period of a over . However, 2 3 load, H load, + near normal or normal pH. This causes a mixed acid-base near normal or normal pH. This causes at directed is alkalosis respiratory of Treatment disorder. and correcting the underlying etiology. For discovering from anxiety, have example, if a patient is hyperventilating ventilated him breathe into a paper bag. In mechanically reducing the patients with mechanical overventilation, or tidal volume will increase PaCO minute ventilation and reduce pH. of an H of Metabolic alkalosis Metabolic alkalosis occurs when HCO In general, the kidneys attempt to preserveexchanging it for excreted H sodium by Metabolic acidosis in the amount of an increase is Metabolic acidosis production of acids excess either from absolute body acid, and potassium. loss of bicarbonate, sodium, or excessive include , Causes of metabolic acidosis of bicarbonate through and loss diabetic ketoacidosis, through the diarrhea or bicarbonate wasting severe kidneys or gastrointestinal (GI) tract. Respiratory alkalosis occurs critical care, respiratory alkalosis in Common when PaCO Chronic respiratory acidosis occurs secondary to a chronic to a chronic secondary occurs acidosis respiratory Chronic chronic example, in ventilation—for in alveolar reduction pulmonary obstructive as chronic such lung diseases coma, causes are: sedation, other main disease COPD, or kyphoscoliosis severe disorders, neuromuscular pneumothorax sarcoidosis, Fibrosis, obesity, pulmonary or effusion, chronic obstructiveairway disease, parenchymal disease etc. pulmonary obstruction, severe airway serum HCO serum most common cause of respiratory alkalosis is increased is respiratory alkalosis of cause common most hyperventilation, which can happen in ventilation, alveolar pregnancy, hepaticdisease, mechanical overventilation, Determining appropriate compensatory septicemia. and in HCO changes into the intracellular fluid. the cell into the extracellular outside moves potassium For this process to occur, fluid to maintain electro neutrality.significant In overall severe acidosis, depletion stores can occur despite serum hyperkalemia. This is of total body potassium diabetic to patients with given is potassium why I.V. ketoacidosis early in treatment, despite the often-elevated External and internal potassium serum potassium level. balances are regulated to maintain an extracellular fluid concentration of 3.5 to 5.5 mEq/L and a total body content of about 50 mEq/kg (40mEq/kg in females).Main causesare:hypovolemia, cardiogenic or septic shock, renal failure, hypoxia, diabetic ketoacidosis, severe diarrhea, pancreatic fistula. conservation of HCO conservation also has a concomitant metabolic disorder. In chronic In disorder. metabolic a concomitant has also respiratory alkalosis, the compensatory mechanisms result in mild reduction in plasma HCO usually as the result of excessive loss of metabolic acids. loss usually as the result of excessive Causes of metabolic alkalosis include diuretics, secretory adenoma of the colon, emesis, hyperaldosteronism, Cushing’s syndrome, and exogenous steroids. Some CRITICAL CARE 556 excluded. IfPaCO or metabolic alkalosis; but amixed disorder cannot be Elevated PaCO in the PaCO Simple acid-base disorders result inapredictablechange PaCO disorders arepresent. either noacid-basedisorderispresentorcompensating acidosis or analkalosis is present. IfpHis normal, Net deviationinthearterialpHwillindicatewhetheran pH Arterial Firstly, whetherpH,PaCO Validity oftheABGReport the procedure. of difficulty the increase not does anesthetic Local infiltrated. makes arterialpuncturelesspainfulforthepatientand be should lignocaine) 2% with alcohol or iodine,andalocalanesthetic(such as the wristforsupport.Thepuncturesiteshouldbecleaned the wrist dorsiflexed at 45°. A towel may be placed under The patient’s arm is placed palm-up on a flat surface, with 1) as it is easy to palpate and has a good collateral supply. Blood is usuallywithdrawnfromtheradialartery(Figure andanalysis Sampling be followed tointerpretthe ABG report. of interpretation ABG report.Thefollowingsequencemay and athoroughphysicalexaminationareessentialforthe base disturbance. Therefore, a carefully obtainedhistory as withsymptomsthathave nothingtodowiththeacid- that develop as a consequence of the disturbanceas well disturbance. Theymayalsopresentwithmanifestations symptoms duetotheetiologicalcausethatresultedin Patients withacid-basedisturbancesmaypresent Assessment Clinical directions, itis indicative ofa mixeddisorder. disorder cannotbeexcluded. respiratory alkalosis or metabolicacidosis; but amixed equation oracid-basenomograms. Bach Hassel Henderson- the using confirmed be should 30 minutes with little effect on the accuracy of the results. sample, thebloodcanbestoredoniceforapproximately analysis promptly.Ifthereisanydelayinprocessingthe ensure accuracy,itisimportanttodeliver thesamplefor be insertedatananglejustdistaltothepalpatedpulse heparinized syringewitha23or25gaugeneedleshould radial artery should be palpatedfor a pulse, and a pre- INTERPRETATION OF THE ABG REPORT 2 andHCO 2 and HCO 3 – 2 andHCO 2 andHCO Fig. 1:Allen's Test 18 3 -. Low PaCO 3 – indicate respiratory acidosis – indicaterespiratory 2 andHCO 3 19 - showachange inopposite 16 2 and HCO 3 11 - arecompatible 3 - indicate 1 The measured in allpatientswithmetabolicacidosis. present aloneorconcurrently(Table 2).The AG shouldbe high anionandnormalgapvarieties, whichcanbe paraproteinemia. Metabolic acidosis can be divided into laboratory reflect can error, metabolicalkalosis,hyperphosphatemia,or but acidosis metabolic indicate bromide, or iodide. Elevated values most commonly presence of aparaproteinemiaorintoxicationwithlithium, laboratory errororhypoalbuminemiabutcandenotethe Calculating theAnionGaps Calculating differ, amixeddisorderispresent. is unlikely.Iftheexpectedvalues andtheactualvalues values and the actualvalues match, a mixed disorder base disorders is showninTable 1below.Iftheexpected The expectedcompensatory response for simple acid- ResponseCompensatory intoxication. multiple myeloma, bromideintoxication,andlithium chemical laboratory, and detection of such disorders as base disorders, assessment of qualitycontrolinthe entity is used in thedetectionand analysis of acid- subtracted from the serum sodium concentration. This the as sum ofserumchlorideandbicarbonateconcentrations defined is laboratory, chemical the in measured The serum anion gap,calculatedfrom the electrolytes acidosis. When {(Na anhydrase inhibitors, proximal and distal renal tubular carbonic fistulas), diversion,pancreatic ureteral or biliary include gastrointestinallosses ofbicarbonate(diarrhea, hypocapnia. Conditions causing normal AG acidosis failure, administrationof hydrochloric acid and post- acidosis, moderate degreeofrenal IV renal tubular type potassium include hyperaldosteronism, normal tohigh the serumpotassiumlevels. Normal AG acidosis with a Normal AG metabolic acidosis can be groupedas per poisoning]. lactic acidosis; E =ethylene glycolpoisoning;S=salicylate P =paraldehydeingestion;Iisoniazid overdosage;L= ketoacidosis (also alcoholic ketoacidosis and starvation); MUDPILES [M =methanol;Uuremia;Ddiabetic with themnemonic of elevated AG metabolicacidosis can be remembered gap indicates anon renal causeof acidosis. renal fromnon-renal causes. A negative urinaryanion compensation with partialrespiratory Metabolic alkalosis Pure metabolicacidosis Pure metabolicalkalosis Pure respiratoryacidosis Pure respiratoryacidosis Pure respiratoryalkalosis Condition Table 1:Comparing Acid-base imbalances compensation with partialrespiratory Metabolic acidosis 20 Low values mostcommonly indicate + +K + ) -Cl - ] canhelpindistinguishing High High High Low Low Low Low pH 18 Normal Normal Paco High High High Low Low 16 2 Normal Normal Normal 17 HCO High High Causes Low Low 3 CHAPTER 117 557 J 1980; J Assoc Semi Nephrol Semi Clinical application Clinical application Thorac Cardiovasc Surg Cardiovasc Thorac Rapid estimation of plasma CO2 plasma estimation of Rapid BJA 1997; 78:479. Clinical physiology of acid-base 1988; 32:365-8. Ann Emerg Med 1990; 19:1310-3. 11. 2006; 54:720-4. Hasten A, Berg B, Inerot S, Meth L. Importance of correct of Importance L. Meth S, Inerot B, Berg A, Hasten gas analysis. the results of blood for of samples handling Acta Anaesthesiol Scand from pH and total CO2 content. N Eng J Med 1965; 272:1067. from pH and total CO2 RK. Templin WT, Peruzzi Shapiro BA, ed. 1994:230-31. ofblood gases. 5th et al. pH strategies and cerebral energetics Hiramatsu T, circulatory arrest. after before and 1995; 109:948. Burton David Rose. andelectrolyte disorders. 4th ed. 1994:508. An approach to interpret arterial A, Sharma SK. Mohan AK, editor. Clinical medicine Agarwal bloodgases. In Association A publication of Indian update - 2006.Vol. IX. Medical Jaypee Brothers New Delhi: Clinical Medicine. of Publishers2006; 73-81. guide simple A T. Wardle C, Gwinnutt T, Brown P, Driscoll Brothers Medical toblood gas analysis. New Delhi: Jaypee Publishers; 2002. and SPL. Enzyme studies II. The measurement Sörenson in enzymatic meaning of hydrogen ion concentration 1909; 21:131-200. BiochemischeZeitschrift processes. paper pages 131-134 and 159-160 of the Excerpts from available at http://dbhs.wvusd.k12.ca.us/webdocs/Chem- September 21 on Accessed History/Sorensonn article.html. 2006. R. Shapiro BA, Harrison RA, Cane RD, Kozlowski-Templin ed. Chicago; Year Clinical application of blood gases. 4th Book Medical Publishers, Inc.; 1989. disorders. stepwise approach to acid-base A Fall PJ. and for metabolic acidosis Practical patient evaluation 2000; 107:249-50, 253-4, 257- Med other conditions. Postgrad 8 passim. Narins RG, Emmetta practical approach. Medicine (Baltimore) disorders: M. Simple and mixed acid-base arterial blood gases and acid-bas balance. BMJ 1998; arterial blood gases 317:1213-6. Burden and McMullan. Physiology 9th ed. of Medical JE. Textbook AC, Hall Guyton 1996: 390. HL. JP, Bleich Kassirer 59:161-87. and interpreting of oxygen: assessing ABC AJ. Williams 1998; balance. BMJ acid-base and gases arterial blood 317:1213-6. A, Robinson G. New look at the Beasley R, McNaughton Lancet 2006; 367:1124-6. oxyhemoglobin dissociation curve. gap acidosis. Anion K, Szerlip HM. Ishihara 1998; 18:83-97. An approach to mixed Wrenn K. The delta (delta) gap: acid-base disorders. disorders. acid-base Diagnosing AK. Ghosh Physicians India Kruse JA, CadnapaphornchaiP. The serum osmole gap. Crit Care 1994; 9:185-97.

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+ 15 reflects 2 reflects the oxygenation 2 ) 3 17 ketones Renal tubular acidosis Renal failure acetazolamide Carbonic anhydrase inhibitors (e.g. for glaucoma) (e.g. saline) Dilution with hyperchloremic solutions or biliary diversion Pancreatic acid equivalents Administration of inorganic acid or hydrated or excretion of Na well Ketoacidosis, Renal failure (severe) Renal failure Lactic acidosis hypoxia, tumors L: tissue not status changes; syndrome, mental D: short bowel lab measured by routine alcoholic Ketoacidosis: diabetic, with respiratory (usually associated Salicylate alkalosis) glycol Ethylene 5 - oxoprolinuria - induced Acetaminophen (pyroglutamic aciduria) Diarrhea (loss HCO • • • Ureterosigmoidostomy • • • • • Table 2: Causes of Acidosis Table anion gap High • • - - • • Poisonings - - - Methanol - Normal anion gap • CONCLUSIONS OSMOLAR GAP OSMOLAR Measuring arterial blood gases can be a useful adjunct useful be a can gases arterial blood Measuring to the assessment of patients with either acute or chronic acidaemic if the patient is The results show diseases. a or alkalaemic and whether the cause is likely to have respiratory or metabolic component. The PaCO Osmolar gap = Measured osmolality - Calculated osmolality Osmolar gap = Measured osmolality abnormal when gap >10 mOsm/l is considered Osmolar high causing Conditions formula. using this calculated ethanol, ethyleneglycol, include AG metabolic acidosis ethanol and propylene methanol, acetone, isopropyl glycol poisoning. Calculated osmolality =Glucose (mg/dl) +2[Na+ (mEq/l)]/18 + osmolalityCalculated =Glucose (mg/dl) +2[Na+ (mEq/l)]/18 (mg/dl) /2.8 nitrogen Blood urea Osmolar gap is also useful in differentiating the causes of causes the differentiating in useful also is gap Osmolar calculated gap is Osmolar acidosis. metabolic AG elevated osmolality from by subtracting the calculated serum shown below. measured osmolality using the formula alveolar ventilation and the PaO and ventilation alveolar