(V)ABG interpretation Kristian Hecht PGY-3 EM With thanks to Marc, Mark and Dr. Rigby

Outline Why is everyone using VBG’s anyway? Basic Review Lists that you have to remember (D’oh!) Calculations you can do at the bedside A BS-free approach to the ABG Cases Special circumstances

Basic Review

Why do we care about ABGs? Aids in diagnosis Provides clues about clinically unrecognized disorders May indicate what treatments are needed Helps assess progress of illness or therapy

What’s bad about ABG’s ABG’s are invasive Painful, even with lido! Have potential complications Local hematoma Arterial dissection thrombosis (rarely) Technically difficult, esp. in kids and elderly, thus, several attempts may be required.

ABG Vs. VBG Can you use a venous gas to replace an ABG in the ED? What are the mean differences between arterial and venous samples? Are they clinically significant?

Canadian prospective observational study in the ED (CJEM January 2002 Vol 4, No 1) N=218 pts Pts requiring ABG simultaneous venous sampling Correlation coefficients and mean differences were calculated Also 45 academic ED physicians were surveyed to determine the minimal clinically important difference in each variable

The mean differences (95% CI) in arterial and venous samples were: pH = 0.036 (0.030 - 0.042) pCO2 = 6.0 (5.0 - 7.0) mmHg HCO3 = 1.5 (1.3 - 1.7) mEq/L

Can be used to follow trends These differences were considered greater than the minimum clinically significant differences identified in the survey Concluded that although highly correlated, the differences between them preclude using them interchangeably Can be used to follow trends 58% response rate to their survey 0.05 ph units, 6.6mmHg PCO2, 3.5mEq/L HCO3

Since 2002 Arterial Blood Gas Analysis: Are Its Values Needed for the Management of Diabetic Ketoacidosis? Ann Emerg Med. 2005;45:550-551 Good correlation between arterial and venous pH and HCO3 The case for venous rather than arterial blood gases in diabetic ketoacidosis Emerg Med Australas. 2006 Feb;18(1):64-7 Review article analyzing the validity of venous BG sampling in DKA In patients with DKA the weighted average difference between arterial and venous pH was 0.02 pH units Venous HCO3- was 1.88 higher than arterial

Principles of Acid-Base Normal serum pH is maintained within a very narrow range of 7.36-7.44 Equal to [H+] 447 - 355μM pH>7.8 or <6.8 is incompatible w/life

Principles of Acid-Base pH is maintained by 3 systems Physiologic buffers Lungs Kidneys Disorders in any of these systems leads to alterations in blood pH

Physiologic Buffers 1) Bicarbonate-carbonic acid buffer system H+ + HCO3- ↔ H2CO3 ↔ H2O + CO2 2) Intracellular blood protein buffers Hemoglobin w/o this venous blood would be pH 4.5 3) Bone Reservoir of bicarb and phosphate BCABS: open ended, continuous removal of organic acid is possible with exhalation of CO2. Primary contributor Hemoglobin can buffer large amounts of acid. Venous blood would be at a ph of 4.5 if not for Hgb

Lungs Changes in pH sensed by chemoreceptors Drop in pH Increase in pH Peripherally (carotid bodies) Centrally (medulla oblongata) Drop in pH Increased minute ventilation Lowers PaCO2 Increase in pH Decreased ventilatory effort Increases PaCO2

Kidneys Play no role in acute compensation 6-12hrs Acidosis Active excretion of H+ Retention of HCO3- >6hrs of Alkalemia Active excretion of HCO3- Retention of H+ Predominantly in the form of NH4 (ammonium)

Normal ABG parameters pH 7.40 PCO2 40 mmHg [HCO3] 24 mM Anion Gap = 12 - 15

Terminology Acidemia: blood pH < 7.35 Acidosis: a physiologic process that, occurring alone, tends to cause acidemia e.g.: metabolic acidosis from increased ketoacid production in DKA If the patient also has an alkalosis at the same time, the resulting blood pH may be low, normal or high

Terminology Alkalemia: blood pH > 7.45 Alkalosis: a primary physiologic process that, occurring alone, tends to cause alkalemia i.e.: respiratory alkalosis from hyperventilation If the patient also has an acidosis at the same time, the resulting blood pH may be high, normal or low.

Terminology Primary acid-base disorder: One of the four acid-base disturbances that is manifested by an initial change in HCO3- or PaCO2. Compensation: The change in HCO3- or PaCO2 that results from the primary event. Compensatory changes are not classified by the terms used for the four primary acid-base disturbances. You cannot overcompensate for an Acid-Base disturbance i.e. a patient who hyperventilates (lowers PaCO2) solely as compensation for MAc does not have a RAlk, the latter being a primary disorder that, alone, would lead to alkalemia. In simple, uncomplicated MAc the patient will never develop alkalemia.

Acid-Base Disorders Respiratory disorders Metabolic disorders Alter the serum PaCO2 Metabolic disorders Alter the serum HCO3-

Lists you have to remember…. D’oh…

Respiratory Disorders ACIDOSIS Hypoventilation Pulmonary pathology Airway obstruction Decreased respiratory drive ALKALOSIS ↑ minute ventilation CNS disease Hypoxemia Anxiety Toxic states Hepatic insufficiency Assisted ventilation

Metabolic Disorders ACIDOSIS Anion gap metabolic acidosis Non-AG metabolic acidosis ALKALOSIS Saline responsive Saline resistant Otherwise known as chloride responsive and unresponsive

Anion Gap Metabolic Acidosis Addition of exogenous acids or Creation of endogenous acids “ Cat Mudpiles” Carbon monoxide/cyanide Alcohol/AKA Toluene Methanol Uremia DKA Paraldehyde INH/Iron Lactic Acidosis Ethylene glycol Salicylates

Normal AG Metabolic Acidosis Excessive loss of HCO3- or Inability to excrete H+ “Hard ups” Hyperalimentation/ Hyperventilation Acids/Addison’s/ Acetazolamide RTA Diarrhea/Dehydration/ Diuretics Uterosigmoidostomy Pancreatic fistula or drainage Saline (large amounts)

Saline-responsive metabolic alkalosis Volume contracted Contraction of the ECF around the constant plasma HCO3- Relative Excess Urinary chloride level <10 mEq/L Vomiting/Gastric Suction Diuretics Ion-deficient baby formula Colonic adenomas

Saline-resistant metabolic alkalosis Associated with mineralcorticoid excess Leads to ↑ Na+ reabsorption Secretion of K+ and H+ to maintain neutrality Urinary chloride >10mEq/L Primary aldosteronism Exogenous steroids Adenocarcinoma Bartter’s Syndrome Cushing’s disease Ectopic adrenocorticotropic hormone Exogenous mineralocorticoids are Licorice and chewing tobacco

Calculations that can help you

Henderson-Hasselbalch equation Check validity of laboratory measurements obtained H+ = 24 x PaCO2 ÷ HCO3 = 40 nEq/L HCO3 calculated on ABG with HH eqn HCO3 measued on Chem 6

Respiratory Compensation Compensation PaCO2 : HCO3- Acute Resp Acidosis 10 : 1 Acute Resp Alkalosis 10 : 2 Chronic Resp Acidosis 10 : 3 Chronic Resp Alkalosis 10 : 4

Metabolic Compensation Compensation PaCO2 : HCO3- Metabolic Acidosis 10 : 10 Metabolic Alkalosis 10 : 7.5

“The Corey Slovis approach to acid-base abnormalities” A no bull@#$% approach for non-nephrologist

Slovis 6-step approach to ABG Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Check the numbers Need both Chem 6 and blood gas Know your normal values Does the blood gas make sense? Are there any immediate hints to the diagnosis

The ABG rules 1) Is it an Acidosis or Alkalosis Look at the pH (>7.45, <7.35) 2) Is it Respiratory or Metabolic Metabolic = pCO2 + pH ∆ in same direction Resp = pCO2 + pH ∆ in opposite direction 3) Is it a pure respiratory acidosis? ↑pCO2 : ↓pH = 1:1

Calculate the AG Na+ – [HCO3- + Cl] Normal = 5-12 Upper limit of normal is 15

Unmeasured ions Mg2+ Ca2+ K+ Albumin PO43- Acetate HCO3- Na+ Cl-

Anion Gap HCO3- Na+ Cl-

Anion Gap For example: give me an ‘M’ Methanol intoxication Methanol oxidized to formic acid Formate- + H+ + HCO3-  Formate- +  CO2 + H2O

Add Formic acid Anion Gap HCO3- Na+ Cl-

Formate- Anion Gap HCO3- Na+ Cl-

Narrow AG? Sure, add more unmeasured cations, as carbonate or chloride e.g. FeCl2 MgCl2

Add MgCl2 Anion Gap HCO3- Na+ Cl-

Mg2+ Anion Gap HCO3- Na+ Cl-

Rule of 15 HCO3- + 15 = pCO2 = pH (last 2 digits)

Rule of 15 Used in acidosis Derived from the Henderson Hasselbalch equation It predicts what resp compensation will do to the pCO2 and the pH If the Rule is broken then another process other than just resp compensation exists

Rule of 15 Creates a new set point for the pCO2 pCO2 appropriate = normal compensation pCO2 too low = superimposed primary resp alkalosis pCO2 too high = superimposed primary resp acidosis Note: as HCO3 falls below 10 you need to use the formula HCO3 x 1.5 + 8 = expected pCO2

Examples of rule of 15 1) HCO3=20, pCO2=35 pH= 7.35 Pure wide gap metabolic acidosis with an appropriate 2ndary resp alkalosis 2) HCO3=10, pCO2=20 pH= 7.32 pCO2 is too low. Superimposed primary resp alkalosis 3) HCO3=10, pCO2=32 pH= 7.14 pCO2 is too high. Superimposed primary resp acidosis

Delta Gap Checks for “hidden” metabolic process Based on the 1:1 concept that ↑AG = ↓HCO3 Upper limit of AG = 15 Normal HCO3 = 24 Bicarb too high = metabolic alkalosis Bicarb too low = Non-gap metabolic acidosis

Examples of delta gap AG=20 HCO3=19 AG=22 HCO3=8 AG=26 HCO3=20 ∆AG = 5 and ∆HCO3 = 5 No hidden process AG=22 HCO3=8 ∆AG = 7 and ∆HCO3 = 16 Bicarb too low = additional normal AG metabolic acidosis AG=26 HCO3=20 ∆AG = 11 and ∆HCO3 = 4 Bicarb too high = superimposed metabolic alkalosis

Osmolar Gap Use if an unexplained anion gap acidosis 2Na + BUN + Glucose = calculated gap OG = Measured – calculated Upper limit of normal is ~10 If higher consider toxic alcohols

Intermission http://www.youtube.com/watch?v=RcL6DwSufMI

Confused???? Lets hit the cases

Case #1 19yo male presents with 2 week hx of abdominal pains and blurred vision Na =135 BUN =30 pH = 7.30 Cl =100 Glucose =38 pCO2 = 30 K =6.0 pO2 = 100 HCO3 =15

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #1 Anion Gap Metabolic acidosis with appropriate resp compensation DDx = MUDPILES Diagnosis: DKA

Case # 2 36yo M presents with altered LOC. He is markedly agitated, febrile and hyperventilating Na =140 pH = 7.32 Cl =100 pCO2 = 20 K =3.8 pO2 = 80 HCO3 =10

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #2 con’t Anion gap metabolic acidosis And Resp alkalosis Two immediate things you have to think about? ASA overdose Sepsis

Case #3 84yo F found down in her apartment with altered mental status Na =140 pH = 7.16 Cl =104 pCO2 = 64 K =3.2 pO2 = 80 HCO3 =28

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #3 Pure respiratory acidosis DDx Pulmonary pathology Airway obstruction Decreased respiratory drive

Case #4 48yo known diabetic presents with 4d hx of abdominal pains, vomiting and severe diarrhea Not eating so stopped insulin Na =130 BUN =40 pH = 7.30 Cl =105 Glucose =29 pCO2 = 30 K =4.8 pO2 = 100 HCO3 =15 Is this DKA???

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #4 cont Is this DKA? Non-AG Metabolic Acidosis DDx = HARDUPS Most likely secondary to severe diarrhea

Case #5 22yo F presents with retrosternal chest pain and describes SOB during her biology exam Na =135 BUN = 9 pH = 7.46 Cl =101 Glucose = 7.8 pCO2 = 35 K =4.0 pO2 = 100 HCO3 =23

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #5 cont Respiratory alkalosis DDx: CNS disease Hypoxemia Anxiety Toxic states Hepatic insufficiency Assisted ventilation

Case #5 cont Respiratory alkalosis DDx: CNS disease Hypoxemia Anxiety Toxic states Hepatic insufficiency Assisted ventilation

Case #6 You are about to place the ETT in a crashing patient when the RT shoves the following ABG into your face with no patient history at all… Na =138 pH = 7.25 Cl =108 pCO2 = 25 K =5.0 pO2 = 100 HCO3 =10

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #6 cont You explain to her that this is obviously…. Wide gap metabolic acidosis with appropriate respiratory compensation DDx: MUDPILES Delta gap indicating an additional non-AG metabolic acidosis DDx: HARDUPS

Case #7 35-year-old man with renal insufficiency admitted to hospital with pneumonia and the following lab values Na =145 pH = 7.52 Cl =98 pCO2 = 30 K =2.9 pO2 = 62 HCO3 =21

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #7 Three separate acid-base disorders !!! 1) Acute respiratory alkalosis Acute hyperventilation due to pneumonia 2) Concomitant metabolic acidosis From renal disease 3) Hypokalemic metabolic alkalosis From excessive diuretic therapy The result of all this acid-base abnormality? Blood gas values that are indistinguishable from those of simple acute respiratory alkalosis.

Case #8 Elderly man from nursing home with hx of RA Profound weakness and areflexia + poor oral intake for days Current meds: Sleeping pills PRN Prednisone 45mg daily Na =145 pH = 7.58 Urine Cl = 74 mmol/L Cl =86 pCO2 = 49 K =1.9 pO2 = 84 HCO3 =45

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #8 Con’t Metabolic Alkalosis w/ Resp alkalosis (10:7.5) ? Saline responsive or resistant Resistant DDx? Primary aldosteronism Exogenous steroids Adenocarcinoma Bartter’s Syndrome Cushing’s disease Ectopic adrenocorticotropic hormone Why is the K+ so low? Mineralcorticoid excess results in sodium reabsorption. To maintain neutrality the kidney must pump out H+ and K+

Case #9 EMS called for 38yo male increasingly agitated and incoherent paramedics noted he appeared "drunk" but normal vital signs and 02 Sats BP 110/70, HR 72, T 36°C, RR 24, Sat 97% RA Thirty minutes later: GCS fell to 9 (E2/M4/V3) RR ↑ 30 breaths/min No focal neurologic signs Physical examination was otherwise unremarkable PEA arrest requiring resuscitation with Epi

Case #9 Labs: Na =153 BUN = 5.9 pH = 6.49 Cl =108 Glucose = 6.0 pCO2 = 62 K =5.4 Cr = 174 pO2 = 100 HCO3 =5

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case # 9 Cont What would be appropriate resp compensation for this metabolic acidosis? HCO3 x 1.5 + 8 = expected pCO2 pCO2 should = ~16 Acid-Base abnormality? Severe AG metabolic acidosis Secondary severe Resp Acidosis

Case #9 Cont Anything else you would like? What is the Osmolar Gap? Serum Osmolarity = 487 mOsm Serum EtOH < 2.2mmol/L What is the Osmolar Gap? 169 mEq/L Diagnosis? Severe methanol intoxication Serum methanol = 37mmol/L Patient died

Case #10 60yo male seriously ill on arrival to ED Vomiting dark brown fluid ‘every hour or two’ for about a day plus several episodes of melena Past history of alcoholism, cirrhosis, portal hypertension Examination: Jaundiced, sweaty, clammy and tachypnoeic BP 98/50, pulse 120/min Peripheries were cool Abdomen soft and nontender Signs of chronic liver disease present

Case #10 Cont Labs: ABG: Na = 131 Cl = 85 K = 4.2 Glucose = 2.88 mmol/L BUN = 8 mmol/L Creatinine = 78 umol/L Lactate = 20.3 mmol/l Hgb = 62 g/L Albumin = 20g/L ABG: pH = 7.10 pCO2 = 14 mmHg pO2 = 103 mmHg HCO3 = 4 mmol/l

Approach Check the numbers Apply the ABG rules Calculate the AG If Acidosis apply the rule of 15 (+/- 2) If Acidosis apply the delta gap (+/- 4) Check the osmolar gap

Case #10 Cont WG metabolic acidosis with appropriate respiratory compensation Likely lactic acidosis Is there a secondary metabolic process? ∆AG = 27 and ∆HCO3 = 20 But…… Does anyone know what the Figge Correction is

Case #10 Cont Does a low serum albumin affect the measurement of the anion gap? Yes! If albumin <40 g/l = for every decline of 10 g/l subtract 4 from the normal value of the AG Therefore the ∆AG = ∆HCO3 and it is a pure WG metabolic acidosis

Case #11 28yo F known asthmatic and 8 months pregnant presents with increasing SOB over 24hrs She has been taking her inhalers with no effect Exam In resp distress, diaphoretic, and looking very tired Auscultation reveals no wheezing

Case #11 Cont ABG Are you concerned about her? pH = 7.36 PO2 = 90 PCO2 = 45 HCO3 = 22 Are you concerned about her?

Case #11 Physiologic changes of pregnancy Physiological hyperventilation results in respiratory alkalosis with compensatory renal excretion of bicarbonate These changes alter normal ABG values: pH 7.4-7.45 PO2 = 95-105 mm Hg PCO2 = 28-32 mm Hg, HCO3 = 18-21 mEq/L.

Case #11 Cont Even though the ABG does not at first glance appear worrisome A pCO2 of 45 at this stage in pregnancy likely represents a significant degree of CO2 retention Potentially impending resp failure!!!

Name that Acidosis Distinctive Breath Renal Failure DKA Renal Failure Uremia Refractory Seizures INH Xray diagnosis Iron ingestion Blindness Methanol 1° Resp Alkalosis ASA GI Bleed Lactic acidosis U/A diagnosis Ethylene glycol

Thanks!