aoe A SELF - INSTRUCTIONAL MONOGRAPH ON ARTERIAL BLOOD GAS COLLECTION AND INTERPRETATION OF ACID-BASE DISORDERS. CORALIE C. DIOQUINO-DIMACALLI, M.D. Section of Nephrology, Department of Medicine University of the Philippines ManilaTABLE OF CONTENTS Page Introduction . 1 Objectives al Recommended Preparation aaell L. Indices of an Arterial Blood Gas 2 1, The Technique of ABG Specimen Collection 2 UI. Common Errors in ABG Collection ot Review Questions 1, 11 & HT 6 TV, The Henderson and Henderson-Hasselbalch Equations... 7 V.. The pH and {HJ Relationship 8 VL. ABG Interpretation A. Definition of Terms 10 B. The Serum Anion Gap 10 C. Stepwise Approach to ABG Interpretation i Review Questions IV, V & VI 20 Answers to Review Questions 21 References 2B Recommended Follow-up B INTENDED USERS This module is for medical students who ate entering their clinical rotation, It is also for medical residents and fellows in training or for anvone interested in learning the proper technique of ABG collection and interpretation ESTIMATED STUDY TIME 2 hours eden ene ee eeeINTRODUCTION ABG and correct interpretation of the ABG report, therefore, are essential to its utility as a diagnostic tool. This module will help you lear the proper technique of collecting an ABG ‘specimen and will provide you with a step by step guide to the interpretation of an ABG report. OBJECTIVES At the end of this module, the leamer should be able to: J} Fumerate the typical indices, with their normal values, in an arterial blood gas report. [istin proper order the steps emploved in the collection of an ABG specimen Recognize the common errors in ABG specimen collection Apply the Henderson and Henderson-Hasselbalch equations Convert a given pH to its hydrogen ion concentration, ‘Compute for the anion gap. Interpret an ABG result NObaun RECOMMENDED PREPARATION Before going over this material, the leamer must have some prior knowledge of acid-base Physiology, including acid base homeostasis, He must also have boon introdiced ta clinical ‘medicine, specifically conditions that may present with acid-base problems2. Select the appropriate puncture site. BS a. Explain the procedure and its importance to the patient. b. Choose the artery from which you are to draw the blood gas. Usually the radial artery at the area of the wrist is picked as the site, but other accessible arteries in the extremities can be used These include the brachial artery in the upper extremities and the femoral artery in the lower extremities. ¢. Feel for the pulse with vour index and middle fingers. (See Figure 2.) 4. Perform the modified Allen testo check for the patency of the ulnar artery. (1) Ask the patient to clench his fist tighthy (2) Using your index and middle fingers, apply pressure on both the radial and ulnar pulse of the clenched fist to obstruct blood flow. (3) Ask the patient to open his fist. You should observe a blanched palm (4) Release pressure on the ulnar artery. If the ulnar artery is patent, the palm should become flushed or pink within 5 to 15 seconds as blood rushes to the distal arteries of the hand. This normal response is considered to be a positive response to the modified Allen test. Failure of the palm to become flushed within the specified time, which is a negative response, suggests that the ulnar artery is not patent. If the response is negative, radial artery puncture on that hand should be avoided. ©. Make sure that the pulse that you select is palpable. Choose another site if you are not satisfied with the pulse. 3. Collect the sample. 2. Swab the chosen site with 70% isopropyl alcohol or povidone iodine antiseptic solution. , Get the prepared syringe and remove the needle cover. Hold the syringe as if you are holding a pencil with the bevel facing upward. ©. Ifthe radial artery has been chosen as the site, extend the wrist to about 30 degrees with the palm upward by placing a rolled towel or cloth beneath the wrist. Position the chosen pulse between the index finger and middle finger of your opposite hand, 4. Insert the needle into the artery at a 45 degree angle, opposite the blood flow, with the bevel of the needle facing upward. (See Figure 3.) € Advance the needle slowly until blood is seen at the hub of the needle, If the needle hhas been advanced too deep. withdraw the needle slowly until blood is seen at the hub of the needle. It is allowable to redirect the needle, but only after it has been ‘withdrawn to just beneath the skin. Arterial blood is identified by flashing of blood as it enters the hub of the needle. pulsations during filling and auto-filling of the syringe without withdrawal of the plunger. ‘That is, the plunger automatically rises due to the arterial pressure Collect 2.5 ml of blood. &. Withdraw the syringe and needle and apply pressure over the puncture site. Digital pressure should be applied over the puncture site for a minimum of five (8) minutes, A femoral artery puncture will require a longer pressure time. You may ask someone to assist vou in applying pressure while you prepare the sample for transport, but make sure you inspect the site two (2) minutes after pressure for any bleeding. If oozing occurs, you may have to apply pressure for a longer period of time.4. Prepare the specimen for transport a. After withdrawing the needle from the skin, make sure that no bubbles have centered the syringe. Expel any air bubble by advancing the plunger into the syringe ‘with the needle in an upright position. b. Insert the needle into the rubber stopper and make sure that the seal is airtight. Be careful not to puncture yourself doing this, Ifan airtight wrap is available, use it to keep the svringe airtight after removing the ncedle. . Swirl the syringe between the fingers of your two hands to ensure that heparin is distributed evenly. This will help prevent clotting 4. Place the airtight syringe into your previously prepared ice container. (See Figure 4) The ideal temperature is between | and 4 degrees Centigrade. 5. Transport the specimen to the laboratory immediately.lll. COMMON ERRORS IN ABG COLLECTION ‘Most of the errors in blood gas measurements arise from improper sampling technique and blood specimen handling. These include the following’ 1. Dilution with heparin The volume of heparin should be less than 5% of the blood volume of the sample. Too much heparin results in a dilution of the sample. The effect on the ABG isa drop in paCO- and a potential increase in pH. The paO; is not affected by heparin dilution. This error can be avoided by following the proper technique as discussed in the previous section on preparing the svringe and the needle (Ib-d), 2. Air contamination Any air bubble trapped in the syringe may falsely increase the paQz. Since air contains nearly’ no carbon dioxide, paCO; of the blood sample will potentially decrease causing the pH to rise. Thus an airtight seal is necessary. 3. Venous sampling or adimixture ‘Venous sampling often results from drawing blood from a hypotensive patient. This can be avoided by observing the characteristics of arterial blood as discussed in the previous section on drawing the sample (3e). Venous admixture can occur ‘specially’ when the vein lies in close proximity to the artery. It may result from Pushing the needle too deep beneath the artery and from repeated re-directioning and re-positioning of the needle, Since the pO, of venous blood (pvO2) is only 40 mm Hig and the pyCO: is 48 mm He. admixture with arterial blood will drastically lower the pa, and increase the paCO:, Venous contamination should be suspected when there is a large disparity between the patient's clinical status and the blood gas data. Ifa pulse oximeter is available, it may serve as a crosscheck of the oxygen saturation (Sa0,) measured by an ABG. For example, a saturation of 92% via pulse oximeter and an Sa0; of 75% via an ABG would strongly suggest that the blood gas obtained may not be arterial, If this occurs, another ABG specimen should be drawn, 4. Failure to cool the blood Iced samples remain stable for about two hours. Failure to cool the blood can result in continued red blood cell metabolism. This causes an increase in paCO;. a resultant decrease in pH and a lowering of the paOs. Ifice is not available, the ABG sample should be analyzed within 20 minutes of its extraction, ‘The table below summarizes the effects of the common ABG collection errors on the pH, paCO: and paQ, values. Table 2_ Effects of ABG collection errors on pH, paCO: and paOs ‘ABG COLLECTION ERROR pH | paco, | paO; 1_ Dilution with heparin tC | Dec |" NC 2. Air contamination INC_|_DEC_|_ INC 3. Venous admixture [pec | INC | DEC “4. Failure to cool blood, ia [SDE GHE| REINGH [DEG Legend: INC = increase. DEC = decrease. NC = no changeREVIEW QUESTIONS 1, I & Ii {Enumerate the five typical indices of an ABG report and indicate their corresponding IT Below are 14 key steps in the collection of an ABG specimen. Number them according to the correct order in which they are performed. ——— Draw 0.1 cc of heparin into the syringe. Apply digital pressure over the puncture site Insert the needle into a rubber stopper Check that the plunger of the syringe slides easily into the barrel ‘Choose the arterial site for ABG collection. Swab the chosen arterial site ‘Transport the specimen to the laboratory Explain the ABG procedure to the patient Collect 2.5 mi of blood Expel any air bubble in the syringe Place the airtight svringe in a container with ice, Expel any excess heparin —— Insert the needle into the chosen site, Perform the modified Allen test TIL. True or False. Encirele T ifthe statement is true and F ifthe statement is false T T T F F 2 6 Arterial blood may be identified by pulsations during auto-filing of the syringe In ABG specimen collection, the volume of heparin should be more than 5% of the blood volume of the sample Failure to cool an ABG specimen to 4 degrees Centigrade may result in an increase in paCOs and a decrease in pH ‘Air contamination of an ABG sample results in a decrease in paCQ, and an increase in both pH and pa0. Venous contamination should be suspected when there isa large disparity between the patient's clinical status and the blood gas data Too much feparin results in an increase in paCO; and a decrease in pH. ‘Check your answers on page 21IV. THE HENDERSON AND HENDERSON-HASSELBALCH EQUATIONS ‘Acid-base homeostasis is maintained in the body by: (1) buffering, both intracellular and extracellular, (2) acid excretion by the kidneys in the form of ammonium, biphosphate or free hydrogen ion, and (3) carbon dioxide excretion by the lungs during respiration. The most important extracellular buffer is the bicarbonate system. The dissociation constant for carbonic acid (Ke) can be calculated using the equation HHO.) Ke = [H:COs] below: ‘whére (H"] is the hydrogen ion concentration, [HCOs] is the bicarbonate concentration and [H:COs] is the carbonic acid concentration. Henderson utilized the equation above to solve for the [H']. He came up with the following equation by extrapolation: Kellf,COs) ~ [H'] = [HCOs) Since itis difficult to measure [HCO], the dissolved carbon dioxide concentration is used in its place. The dissolved carbon dioxide concentration in meq/L can further be calculated by ‘multiplying paCO, (mm Ha) by a conversion factor of 0.03 (meq/L/mm Hg). ‘The Ke is a known value of approximately 800, Substituting these values therefore into the equation above, the ‘modified equation will appear as follows: - 800 x 0.03 paCO, I] = (HCO, 24 x paCO, IH] = {HCO} From the above equations, it is quite clear that in order to maintain the same hydrogen ion ‘concentration. a process which is accomplished by buffering, a decrease or increase in [HCO] will necessitate a corresponding decrease or increase in paCOs, respectively. This is the so-called compensatory response The Henderson-Hasselbalch equation, which appears below, is the chemical equation ‘which provides the basis for determining manv common blood gas measurements. It utilizes the bicarbonate system and describes the fixed inter-relationships between paCO,, pH and HCOs. All Hasselbalch did was to take the negative log on both sides of the Henderson equation. He came up ‘with the following HCO) pH = pKe+ log [H:COs| where pK is the negative log of the dissociation constant of carbonic acidKnowing thatthe pKe is equal to 6.1. and thatthe (H:COs] can be ‘computed as 0.03 x paCO2, as explained above, this equation can now be modified as follows: IHCOs) PH =6.1 +log OO3EpaCOy is equation i utilized by the ABG machine to compute forthe (HCO) after the pHi and paCO, have been determined by ther corresponding ciectrodes V. THE pH AND [H*] RELATIONSHIP Table 3. Relationship between arterial pH and (Hin the physiologic range PH | [1° nanoeg/t, 7.80 16 7.70 20 7.60 6 7:50 32 740 0 7330 so 720 68 7310 80 7.00 100 9 6.80 160, Since the relationship between pH and (HJ is roughly linear between 7.20 and 7. 50, one Sap compute for the [Hj mathematically using the following formulas: For pH > 7.40, [H"] = 40 x (0.8)'. where x represents the number of tenths above 7:40 For pH <7.40, |H"] = 40 x (1.287, where y represents the number of teaths below 740 For example, 2 pH of 70, which is 0.1 or one tenth above 7.40, would give an IH} of 40 x (0.8)! or 32.mea/L. A pH of 7.60, which is 0.2 or evo tenths above 7.40, would give an [HI] of 40 Pal) oF 25.6. shich is rounded ofF to 26 meg/L. A pH of 7.30, which is 0.1 or one tenth below 740. would yield an (H"] of 40 x (1.28) or $0 meq/L Using this formula then, what is the (H"] for a pH of 7.20? "Fou artived at an answer of 62.5 or 63 nanoea/L then yu have gotten the concept rightNow, how does one determine the 1H’ of pH values between tenths? All one has to do is ‘imerpolate. For example, to get the [H'] of a pH of 7.35, Just follow the following steps: |. Determine the {HJ of the lower pH value in tenths From Table 1, the [H"} fora PH of 7.30 = 50 nanoeq/L. Alternatively, you can use the formula [H"] = 40 x (1.25)! = 50, 2. Determine the [H" of the higher pH value in tenths From Table 1. the [H'] fora pH of 7.40 = 40 nanoea/L 3. Determine the difference between the values obtained from Step Nos. 1 and 2 above, 50 - 40 = 10 nanoeq/L 7.40. 10/10 = I nanoea/L. This gives you the [HI for every 0.01 or one hundredth pH level between 7.30 and 7.40. 5. Multiply your answer in Step No.4 by the desired number of hundredth places. Inthis ase, pH of 735 coresponds to 5 hundredth places, ‘Thug Tnanoeg/L x 5 = 5 nanceq/L & Subtract the value obtained in Step No. 5 from the value obtained in Step No. 1 50 - 5 = 45 nanoeg/L. This gives You the [HJ for a pH of 7.35 "Now, use the same steps to determine the [H' fora pH of 7.27Vi. ABG INTERPRETATION OF ACID-BASE DISORDERS ‘Let us assume that the ABG specimen has been properly collected and that there are no sampling errors. How does one now interpret the ABG report? For the next section ofthis module, we shall go through a stepwise approach to ABG interpretation, We shall be Concentrating on the acid-base interpretation solely for this section. The interpretation of the oxygenation status will not be touched on, but can be reviewed from the recommended references that appear atthe end of this module. Before going through the stepwise approach to ABG interpretation. 1 shall fist define terms that will be used and introduce the concept of the serum anion gap A. Definition of Terms For purposes of uniformity, let me define the following terms: Acidemia - refers to a blood pH less than 7.35 1 2. Allealemia - refers to a blood pH more than 7.45 3. Acidosis - refers to a process which causes a decrease in pH 4. Alkalosis - refers to a process which causes an increase in pH 5. Metabolic - refers to a problem in bicarbonate concentration, It may be a metabolic acidosis which results from a decrease in bicarbonate concentration, or a metabolic 7.40 ACIDOSIS ALKALOSIS a PaCOz> 40 [HCOs}<24 — paCO, < 40 {HCO,] > 24 RESPIRATORY METABOLIC RESPIRATORY METABOLIC Based on the above figure. since [HCO] is < 24 and paCO, is > 40, both metabolic and respiratory acidosis are present ¢. Determine the deviation from normal ABG indices, (1) For the respiratory component, % deviation is computed as follows ni Ct normal paCO; x 100, % deviation = where normal paCO;= 40 Plugging in the value of 45 for actual paCO2, 5-40 a Yedeviation = 40 x 100 = 40. x 100= 12.5% (2) For the metabolic component. % deviation is computed as follows: [normal HCO - actual HCO, % deviation = normal HCO; x 100, where normal HCO, = 24 Plugging in the value of 20 for the actual HCOs, 24:20 a “edeviation= 24 x 100 = 24. x 100 = 16.67% 4. Compare the % deviation from normal for both disorders as computed ine, The higher deviation indicates the primary or dominant disorder. Since the metabolic deviation (16.67%) is higher than the respiratory deviation (12.5%). this ABG represents a primary or dominant metabolic acidosisStep No. 4. Check the compensatory response, Table 5 on the next page lists some equations of compensation for simple acid-base disorders. Different references give many other methods of computing for the compensatory response, but we shall adopt this for the rest of the exercise Table 5. Simple Acid-Base Disorders: Compensatory Response and Equations of Compensation PRIMARY INITIATING ‘COMPENSATORY | EQUATION OF COMPENSATION. DISTURBANCE CHANGE RESPONSE | METABOLIC DEC HCO, | DEC pCO: EXP pCO: = 1.5.x (HCO,) 8-2 ACIDOSIS METABOLIC INC HCO; INC pco- EXP pCO; = 0.9.x [HCO] +9 4/-2 ALKALOSIS RESPIRATORY ACIDOSIS ACUTE INC pCo; INC HCO; AIHCOs] = 0.1 x ApCO, +/-3 CHRONIC INC pco; INC HCO; AIHCOs}= 0.4 x ApCO, 1/4 RESPIRATORY ALKALOSIS ACUTE | DEC pco, DEC HCO; ATHCOs}= 0.1.0.3 x ApCO; NCR |IOepcos DEC HCO, AIHCOs] = 0.2-0.5 x ApCO, DEC = decrease. INC= increase, EXP = expected. A= change a. Determine the compensatory response for the primary or dominant disorder. The compensatory response for a metabolic acidosis is a decrease in paCO;, Looking back at Table § above. the expected paCO;can be computed as follows expected paCO; = 1.5x[HCOs] +8 4/- 2 Plugging in the value of 20 for {HCOs} expected paCO; = (1.5 x 20) +8 = 3048 4/-2=38 47-2 5. Compare the expected compensatory response with the actual value If the actual value falls within the expected range of compensation, the patient has a simple primary or dominant acid-base disorder. Ifthe actual valve falls bevond the expected ranec of compensation. the patient has a mixed acid-base disorder For this patient, the actual paCO: of 45 mm Hg, is definitely beyond the expected range of 36-40. Thus. this patient has a mixed acid-base disorder. IF there 1s a mixed acid-base disorder, determine the secondary disorder. Remember that fora primary metabolite disorder, the compensatory respiratory ‘sponse may be an inerease or decrease in paCO:. Ifthe actual paCOs is higher than the expected range, the patient has a secondary respiratory acidosis, Ifthe actual aC O. is lower than the expected range, the patient has a secondary respiratory alkalosis. For a primary respiratory disorder, the compensatory metabolic response may be an increase or decrease im [HCO.|, IF the actual [HCO] is higher than the expectedTange, the patient has a secondary metabolic alkalosis, Ifthe actual [HCO,] is lower than the expected range. the patient has a secondary metabolic acidosis ‘The primary acid-base disorder of this patient is a metabolic acidosis. Since his, actual paCO> of 45 is higher than the expected paCO,, this patient has a secondary respiratory acidosis. Thus. so far we have determined that the patient has a mixed metabolic and respiratory acidosis. Step No.5. Always calculate for the anion gap. Use the formula for anion gap: AG = [Naj - (ICl] + |HCOs). Given Na = 148, Cl= 100 and HCO: = 20. then AG = 148 - (100 + 20)= 148 - 120 8 ‘The normal AG is 12 +/- 4 meq/L. Any value more than normal suggests the existence of a high anion gap metabolic acidosis, A normal gap does not rule in or rule out a NAG metabolic. acidosis. In this case, since the calculated anion gap of 28 is higher than 12 +/-4, this patient has a high anion gap metabolic acidosis. Thus far. we ean qualify further that this patient has a mixed high anion gap metabolic acidosis and respiratory acidosis. Step No. 6. Use the Delts/Deltas when spplicable. ‘The delta/déltas are utilized to determine the presence of combined metabolic disorders. Any of the following combinations is possible: a high anion gap with a normal anion gap metabolic acidosis, a high anion gap metabolic acidosis with a metabolic alkalosis, and a normal anion gap metabolic acidosis with a metabolic alkalosis. Tables 6 and 7 summarize the delta/delta formulas and indicate how they should be interpreted. For a high anion gap metabolic acidosis, use the delta AG/delta [HCOs}. For a ‘normal anion gap metabolic acidosis, use the delta [ClJ/delta [HCOs} Since this patient has a high anion gap metabolic acidosis, we shall apply the formula for delta AG/delta [HCOs], The patient's computed AG is 28 and his [HCO,] is 20. Substituting these values into the formula: delta AG patient's AG - normal AG 28:12 16 delta [HCO;] = normal [HCO:| - patient's [HCOs] = 24-20 = 4 Since the delta AG of 16 is much higher than the delta |HCOs] of 4, this indicates that the patient probably already had an existing bicarbonate level that wes higher than expected. ‘Therefore the patient has a mixed high anion gap metabolic acidosis and a metabolic alkalosis. Thus, so far we have alread’ identified the following acid-base disorders in this patient: high anion gap metabolic acidosis, respiratory acidosis and metabolic alkalosis.Table 6. Delta AG/Delta HCO3 DELTA ANION GAP/DELTA HCO3 ‘Use when a high anion gap (AG) metabolic acidosis is diagnosed DELTA AG PATIENT'S AG - NORMAL AG DELTAHCO3 = NORMAL HCO3 - PATIENT'S HCO3 Assume normal AG = 12, normal HCO3 = 24 INTERPRETATION: If DELTA AG = DELTA HCO3: PURE AG METABOLIC ACIDOSIS If DELTA AG DELTA HCO3: AG METABOLIC ACIDOSIS + METABOLIC ALKALOSIS Table 7. Delta Chloride/Delta HCO3 DELTA CHLORIDE/DELTA HCO3 ‘Use when a normal anion gap (NAG) metabolic acidosis is diagnosed DELTA CI PATIENT'S Cl - NORMAL Cl DELTAHCO3} = NORMAL HCO3 - PATIENT'S HCO3 Assume normal C1= 100, normal HCO3 = 24 INTERPRETATION, if DELTA Cl= DELTA HCO3: PURE NAG METABOLIC ACIDOSIS | MDELTACl DELTA HCO}. NAG METABOLIC ACIDOSIS + METABOLIC ALKALOSIS —__+———_ METABOLIC ALKALosis | Step No. 7. Summarize the acid-base disorders and look for specific etiologies for the acid base disorders {n summary this patient's ABG showed the following acid-base disorders: |. primary high anion gap metabolic acidosis 2. secondary respiratory acidosis 3. metabolic alkalosis Can We now explain cach ofthis acid-base disorders? From Step No, 1, we were actually able to predict the presence ofall ofthese disorders ‘The high anion gararegbel acidosis could te stowed to the renal flue, Tt.can also be duc toa lactic acidasis ft ensued during theardiopulmonary arest and resuscitation. The respiratory acidosis was probably a result of hypoventilation during the arrest, You will remember that the ABG was taken ahr three ampules ‘of sodium bicarbonate had been given. This could explain the metabolic alkalosis found on ABG interpretation Although for this particular case, the acid-base disorders were quite easy to predict, in Clinical practice the acid-base disorders may not be vey evident. Take for example the ease of a ‘comatose patient brought to the Emergency Room by some by-standers who saw him unconscious in the side walks of Rizal Park. The ABG in such a patient will be very useful and can direct the scarch for the etiology of his coma as well as aid in managing a not-so-very-obvious acid-base disorder, Tables 4, 8, 9 and 10 list some disease conditions that manifest with the various acide base disorders. Oftentimes however disease conditions can present with multiple acid base abnormalities as presented in Table 11 Table 8. Causes of metabolic alkalosis URINE CHLORIDE < 10 meq/day URINE CHLORIDE > 20 meq/day VOMITING OR GASTRIC DRAINAGE DIURETICS (DISCONTINUED) POST-HYPERCAPNEA, CHLORIDE DEFICIENCY SYNDROME. CONGENITAL CHLORIDE DIARRHEA NORMAL BLOOD PRESSURE. BARTTER’S SYNDROME SEVERE POTASSIUM DEPLETION DIURETICS (CURRENT) HYPERCALCEMIA INCREASED BLOOD PRESSURE HIGH ALDOSTERONE LOW RENIN PRIMARY HYPERALDOSTERONISM ADENOMA HYPERPLASIA CARCINOMA, HIGH RENIN RENOVASCULAR HYPERTENSION MALIGNANT HYPERTENSION RENIN-SECRETING TUMOR LOW/NORMAL ALDOSTERONE. LOW RENIN EXCESS CORTICOSTERONE. DRUGS (LICORICE) NORMALHIGH RENIN | CUSHING’S SYNDROME, i ECTOPIC ACTH SECRETIONTable 9_ Causes of respiratory acidosis ACUTE DISORDERS CHRONIC DISORDERS. "AIRWAY OBSTRUCTION ASPIRATION ‘CHRONIC OBSTRUCTIVE DISEASES LARYNGO/BRONCHOSPASM CENTRAL NERVOUS SYSTEM DEPRESSION SEDATIVES ‘CHRONIC SEDATIVE ABUSE GENERAL ANESTHESIA BRAIN TUMOR, POLIO CEREBROVASCULAR ACCIDENT. TRAUMA _ OBESITY-HYPOVENTILATION NEUROMUSCULAR DISEASE GUILLAIN-BARRE POLIO MYASTHENIC CRISIS MYOPATHIES HYPOKALEMIA MYXEDEMA ‘TOXINS AND DRUGS MULTIPLE SCLEROSIS RESTRICTED VENTILATION PNEUMONIA OBESITY HEMO AND PNEUMOTHORAX INTERSTITIAL FIBROSIS FLAIL CHEST KYPHOSCOLIOSIS| ARDS. HYDROTHORAX MISCELLANEOUS. CARDIOPULMONARY ARREST VENTILATOR MALFUNCTION VENTILATOR MALFUNCTION, Table 10. Causes of respiratory alkalosis ACUTE DISORDERS: ‘CHRONIC DISORDERS ‘CENTRAL NERVOUS SYSTEM ANXIETY ANXIETY CVA, TRAUMA cya INFECTION TUMOR SALICYLATES SALICYLATES PROGESTERONE DERIVATIVES PROGESTERONE DERIVATIVES HYPOXIA SHOCK HIGH ALTITUDE ANEMIA ANEMIA PNEUMONIA PULMONARY DISEASE. PNEUMONTA INTERSTITIAL LUNG DISEASE PULMONARY EMBOLUS RECURRENT PULMONARY EMBOLI MILD CONGESTIVE HEART FAILURE. MISCELLANEOUS GRAM NEGATIVE SEPSIS PREGNANCY VENTILATOR MALFUNCTION VENTILATOR MALFUNCTION POST-METABOLIC ACIDOSIS HEPATIC FAILURE Afr the ABG has been interpreted as we have done so above, the next step is to manage the acid-base disorder(s) identified. This topic is bevond the scope of this module. For those who ‘wish to pursue this, the references recommended at the end of the module can be utilized. ‘A summary of the stepwise approach to ABG interpretation ie given in Figure 5.Table 1). Clinical states feu associated with acid-base disorders ‘CLINICAL CONDITION METABOLIC. METABOLIC. RESPIRATORY RESPIRATORY ACIDOSIS | ALKALOSIS _| ACIDOSIS ALKALOSIS: ‘CNS DISEASE + + \VOMITING/GASTRIC + SUCTION DIARRHEA + HEPATIC FAILURE + COPD/RESPIRATORY + FAILURE, PULMONARY EMBOLI SEPSIS DIABETES RENAL FAILURE +]efele CARDIOPULMONARY ARREST. DRUGS: OVERDOSE/POISONS - + DIURETICS. | + /ACETAZOLAMIDE: + AMPHOTERICIN + HYPERKALEMIA 5 + HYYPOKALEMIA a + ‘Adepled fom: Cohen J Kassiver Teds ) Ac ese. Boson, Lie, Brown TBD SUMMARY OF STEPS IN ABG INTERPRETATION FROM THE CLINICAL SETTING OBTAIN A SIMULTANEOUS ABG AND ELECTROLYTE PROFILE, DETERMINE THE PRIMARY OR DOMINANT DISORDER. CHECK THE COMPENSATORY RESPONSE, ALWAYS CALCULATE THE ANION GAP. USE THE DELTA/DELTAS WHEN APPLICABLE, ETIOLOGIES FOR THE ACID-BASE DISORDERS, DISORDERS, 1; OBTAIN DIAGNOSTIC CLUES TO THE PRESENCE OF ACID-BASE DISORDERS SUMMARIZE THE ACID-BASE DISORDERS AND LOOK FOR THE SPECIFIC 8. PRESCRIBE A TREATMENT REGIMEN FOR ALL RECOGNIZED ACID-BASE Figure 5. Summary of steps in ABG interpretationREVIEW QUESTIONS IV, V & Vi DIRECTIONS: Use the case presented below to answer the questions that follow. GASE. A 36 vear old male with alcobolc chosis anda past history of upper gastrointestinal bleeding, hepatic encephalopathy and recurrent Pancreatitis, claimed to have been drinking heavily Until afew davs prior to admission. He sought medical atteation only after several days of Postion but fll 1S mm Hg systolic in the upright positon. His skin turgor was poor. Massive ascites and splenomegaly were present. The following laboratory exams were done at the Emergency Room: Serum BUN = 25 mmol/L |. Based on the history. what are the potential acid-base disorders? 2. What is the (H+ for the given pH? > Using the Henderson equation, compute forthe calculated (HCOs] 4. What is the primary acid-base disorder? S. What is thé compensatory response tothe primary acid-base disordet? 6 Is there a secondary acid-base disorder” If so, what is it? 7. Compute for the anion gap & TFapplicable. compute for the appropriate delta/deltas © Imerpret the value that you obtain for the delta/delta computation 10. Summarize this patient's acid-base dsorder(s). Identify the etiologies ofeach acide base disorder identified (Check your answers with those found on page 22ANSWERS TO REVIEW QUESTIONS |, I! & Ill 1. Enumerate the five typical indices of an ABG report and indicate their corresponding normal values. 1. pH=735-7.45 2. paCO, = 35 - 45 mm Hg pa0.= 80 - 100 mm Ha HL. Below are 14 key steps in the collection of an ABG specimen. Number them according to the correct order in which they are performed. 2 Draw 0.1 ce of heparin into the syringe. 10 Apply digital pressure over the puncture site, 12. Insert the needle into a rubber stopper 1 Check that the plunger ofthe syringe slides easily into the barrel $ Choose the arterial site for ABG collection. 7 Swab the chosen arterial site 14 Transport the specimen to the laboratory. 4 “Explain the ABG procedure to the patient. 9 Collect 2.5 ml of blood. 11 Expel any air bubble in the syringe 13 Place the airtight syringe in a container with ice 3 Expel any excess heparin. 8 Insert the needle into the chosen site. 6 Perform the modified Allen test IIL. True or False. Encircle T if the statement is true and F if the statement is false. © F 1 Are iol ma eel y ples ring ago Be ge © In ABG specimen collection: the volume of heparin should be more than 5% of the blood volume of the sample @ Failure to cool an ABG specimen to 4 degrees Centigrade may result in an increase in paCO; and a decrease in pH. © F 4 Air contamination of an ABG sample results in a decrease in paCOz and an increase in bath pH and paQ:, ® Venous contamination should be suspected when there is a large disparity between the patient's clinical status and the blood gas data. T ©) 6. Too much heparin results in an increase in paCO; and a decrease in pH.SOLUTION TO pH PROBLEM ‘What is the [H’] for a pH of 7.27? 1 (H'] for pH of 7.20 = 40 x (1.25)'= 62.5 [H’] for pH of 7.30 = 40 x (1.25)! = 50 625-30= 125 125/10 = 1.25 1.25%7=875 62.5 - 8.75 = 53.75 oF $4 nanoegL. ANSWERS TO REVIEW QUESTIONS IV, V & VI Based on the history. what are the potential acid-base disorders? 2. Metabolic acidosis due to hepatic failure, alcoholic or starvation ketoacidosi and potential renal failure due to hypotension b. Respiratory alkalosis due to hepatic failure ©. Metabolic alkalosis due to vomiting and possible hypokalemia 4. Respiratory acidosis due to hypoventilation due to hypokalemia ‘What is the [H'] for the given pH? [1] = 29 nanoeg/L Using the Henderson equation, compute for the calculated [HCO] [HCO,] = 24 x 66/29 = 54.6 or $5 meq/L ‘What is the primary acid-base disorder? Metabolic alkalosis ‘What is the compensatory response to the primary acid-base disorder? Increase in pCO} Is there a secondary acid-base disorder? If so, what is it? Yes. Respiratory acidosis, Compute for the anion gap AG = 143465+56) = 143 - 121 = 22 (elevated AG) Ifapplicable, compute for the appropriate delta/deltas 8 AGIAHCO; = (22-12)(56-24) = 10/32 Interpret the value that sou obtain for the delta/delta computation, Mixed AG and NAG metabolic acidosis Summarize this patient's acid-base disorder(s). Identify the etiologies of each acid- base disorder identified. a. Primary metabolic alkalosis due to vomiting and hypokalemia . Secondary respiratory acidosis due to hypoventilation due to hypokalemia and possible CNS disease © AG metabolic acidosis due to ketcicidosis. lactic acidosis and renal insufficiency 4d. NAG metabolic acidosis possibly due to early renal failureREFERENCES Bia M and Thier SO. “Mixed Acid-Base Disorders” in Medical Clinics of North America 65 (2): 347-361, Glassock, RJ (ed.). Current Therapy in Nephrology and Hypertension, 3ed. McGraw: Hill Book Co., 1992, Kokko JP and Tannen RL (eds ). Fluids and Electrolytes. W.B, Saunders Co., 1986. Malley WJ. Clinical Blood Gases: Application and Non-invasive Alterations. W.B. Saunders Co., 1990 Narins RG and Gardner LB. “Simple Acid-Base disturbances” in Medical Clinics of North America, 65 (2): 321-346, 1981. Rose, BD. Clinical Physiology of Acid-Base and Electrolyte Disorders. McGraw-Hill Information Services Co., 1989 RECOMMENDED FOLLOW-UP ‘This module was designed to increase the competence of medical students in ABG collection and interpretation. ‘The recommended follow-up activities include a conscious effort to avoid the common errors of ABG collection when asked to extract an ABG specimen, and the utilization of this module in interpreting the ABGs of all patients assigned to the medical student during his clinical rotations