Why Order an ABG?• Aids in establishing a diagnosis• Helps guide treatment plan• Aids in ventilator management• Improvement in acid/base management allows for optimal function of medications• Acid/base status may alter electrolyte levels critical to patient status/care
Logistics• When to order an arterial line -- • Need for continuous BP monitoring • Need for multiple ABGs• Where to place -- the options • Radial • Femoral • Brachial • Dorsalis Pedis • Axillary
Acid Base Balance• The body produces acids daily • 15,000 mmol CO2 • 50-100 mEq Nonvolatile acids• The lungs and kidneys attempt to maintain balance
Acid Base Balance• Assessment of status via bicarbonate- carbon dioxide buffer system • CO2 + H2O <--> H2CO3 <--> HCO3- + H+ • ph = 6.10 + log ([HCO3] / [0.03 x PCO2])
The Terms• ACIDS • BASES • Acidemia • Alkalemia • Acidosis • Alkalosis • Respiratory • Respiratory CO2 CO2 • Metabolic • Metabolic HCO3 HCO3
Step One - Assessing pHLook at pH and determine if it is acidotic(<7.35), normal (7.35 - 7.45), or alkalotic(> 7.45).pH is the best overall indicator indetermining the acid-base status of thepatient.
Step Three - Determine metabolic involvementHCO3---------------------------Normal: 22 - 26 mEq/LMetabolic acidosis: <22 mEq/LMetabolic alkalosis: > 26 mEq/L[Standard Bicarbonate: Calculated value.Similar to the base excess. It is defined as thecalculated bicarbonate concentration of thesample corrected to a PCO2 of 5.3kPa(40mmHg).
Step Four - Assess for compensationIn pure respiratory acidosis (high PaCO2, normal[HCO3-], and low pH) we would expect an eventualcompensatory increase in plasma [HCO3-] that wouldwork to restore the pH to normal. Similarly, we expectrespiratory alkalosis to elicit an eventual compensatorydecrease in plasma [HCO3-]. A pure metabolic acidosis(low [HCO3-], normal PaCO2, and a low pH) shouldelicit a compensatory decrease in PaCO2, and a puremetabolic alkalosis (high [HCO3-], normal PaCO2, andhigh pH) should cause a compensatory increase inPaCO2. All compensatory responses work to restorethe pH to the normal range (7.35 - 7.45)
Further analysis in cases of METABOLIC ACIDOSISAnion gap = Na+ - [CL- + HCO3-]Difference between calculated serum anions andcations.Based on the principle of electrical neutrality, the serumconcentration of cations (positive ions) should equal theserum concentration of anions (negative ions).However, serum Na+ ion concentration is higher thanthe sum of serum Cl- and HCO3- concentration.Na+ = CL- + HCO3- + unmeasured anions (gap).Normal anion gap: 12 mmol/L (10 - 14 mmol/L)
Normal anion gap acidosisDisease processes that can lead to normal anion gap(hyperchloremic) acidosis. Useful mnemonic(DURHAM):a) Diarrhea (HCO3- and water is lost).b) Ureteral diversion.c) Renal tubular acidosisd) Hyperalimentatione) Acetazolamidef) Miscellaneous conditions: They include pancreaticfistula, cholestyramine, and calcium chloride (CaCl)ingestion, all of which can increase the gastrointestinalwastage of HCO3-.
Increased anion gap metabolic acidosisMethanol poisoningUremia: In end-stage renal failure in which glomerular filtration rate fallsbelow 10—20 ml/min, acids from protein metabolism are not excreted andaccumulate in blood.Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a buildup of beta-hydroxybutyric and acetoactic acids (ketoacids).Paraldehyde poisoning.Ischemia.Lactic acidosis: Lactic acid is the end product of glucose breakdown ifpyruvic acid, the end product of anaerobic glycolysis, is not oxidized toCO2 and H2O via the Tricarboxylic Acid Cycle. (Causes: hypoxia,ischemia, hypotension, sepsis).Ethylene glycol poisoning: Ethylene is metabolized by alcoholdehydrogenase to oxalic acid in the liver. Usually there is also a coexistinglactic acidosis.Salicylate poisoning