Acid-Base Pearls Part 1

The objective of this lecture is to provide a few clinical pearls on how to approach Acid-Base issues commonly seen on inpatient medicine. There is a slide component, which is used for didactic purposes, as well as a monograph section for background (see below). In part 1, we will introduce a methodology to approach clinical scenarios where Acid-Base Disturbances are key elements.

There are many excellent resources on this subject and the principles found in this lecture are an amalgam of several superb papers and monographs. Although I learned a great deal about Acid-Base physiology in Medical School and Residency, the EMCRIT podcasts by Scott D Weingart, MD were amongst some of the most valuable in my education. Please check them out.

Other resources include:
- Clinical review: Acid–base abnormalities in the intensive care unit by Lewis Kaplan and Spiros Frangos
- Physiological Approach to Assessment of Acid–Base Disturbances by Kenrick Berend, M.D., Ph.D., Aiko P.J. de Vries, M.D., Ph.D., and Rijk O.B. Gans, M.D., Ph.D
- Why Is Saline So Acidic (and Does It Really Matter?) by Benjamin AJ Reddi
- Integration of Acid–Base and Electrolyte Disorders by Julian Seifter MD

1. History and Physical Exam
2. Determination of the Primary Acid-Base Disorder and Secondary Response
3. Evaluation of the Metabolic Component of the Acid-Base Disorder
4. Evaluation for the presence of Mixed Metabolic Acid-Base Disturbances
5. Consideration of the Serum (or Plasma) Osmolal Gap
6. Evaluation of the Respiratory Component of an Acid-Base Disorder
7. Interpretation of Acid-Base Disorders in the Clinical Context

• Base Excess of -6 (aka a Base Deficit of 6)
  • What this means is that you’d have to add 6 mmol/l of base to get to a pH of 7.4
    • i.e. the patient is acidotic
• Base Excess of 4
  • i.e you’d have to add 4 mmol/l of acid to get to a pH of 7.4
    • i.e. the patient is alkalotic
      
• Normal Range
  • Normal -2 to +2
    
  • If it is outside of this range it means there is an imbalance between Cations and Anions

• This step-by-step method is adopted from Scott Weingart’s EMCRIT ACID-BASE SHEET, which is excellent!

• Blood Gas
  • An Artertial or Venous Blood Gas will do, but VBGs are much easier to get, as a a phlebotomist can draw a VBG, but at all the hospitals I’ve worked at, MDs are the one’s (with a few exceptions) who must acquire an ABG
• Lactate
  
• Albumin
  • this is a concentration, so getting one as proximal to the blood gas as possible is important as this can fluctuate
    
• Acetone
  
• Complete Metabolic Panel

• Urine Lytes (Na+, K+, Cl-)
• Urine pH
  

• If the blood pH is <7.35, the patient is acidotic
  • At this point we don’t know if it’s metabolic, respiratory or mixed, but their primary problem is acidosis
• If the blood pH is >7.45 the patient is alkalotic
  • Again, we don’t know if it’s metabolic, respiratory or mixed, but their primary problem is alkalosis
    

• If the blood gas C0₂ is > 45 they have a respiratory acidosis
  
• If the blood gas C0₂ is < 35 they have a respiratory alkalosis
  

• A strong ion is a salt that completes dissociates when put into solution
  • e.g. NaCL -> Na+ + Cl-
    
• Examples of strong ions include: Na+ K+ Ca2+ Mg2+ Cl-
  
• The difference between your strong ions is a major determinant of Acid/Base status
  
• Sodium and Chloride are the major strong ions that determine acid/base (see figure below)
• To maintain electroneutrality, the body must either lose a negative charge or gain a positive charge
  
• The Strong Ion Difference that has clinical utility is the [Na⁺] - [Cl^-]
  • Thus, SID = [Na] - [Cl]
    • Under normal conditions, this = 38
      
• Thus, 38 is a good determinant of Acid/Base status
  • If the SID is less than 38 -> think acidosis
    • You can think of this as a relative increase in chloride
      
    • This is often referred to as a “SID Acidosis”
  • If the SID is greater than 38 -> think alkalosis
    • you can think of this as a relative increase in sodium
    • This is often referred to as a “SID Alkalosis”

• The three most common causes of a “SID Acidosis” are:
  • IV Fluids
    
  • Rental Tubular Acidoses
    
  • Diarrhea

• Any fluid that has a SID of < 24 can cause an acidosis
  • 2 liters of NS (which has a SID of 0) in <24 hours is enough to cause acidosis
    • This is fascinating topic and worthy of a separate monograph, but in the meantime if you want more reading check out Scott Weingart’s post

• To work a suspected RTA up further, evaluate your Urine Studies
  • Calculate a Urine Anion Gap (Urine Na⁺ + K⁺ – Cl^-)
    • If the UAG is negative, consider other causes as unlikely to be an RTA
      • The UAG is a proxy for the ability of the kidney to secrete acid because it is hard to detect ammonium
        
      • Chloride is excreted proportionally to NH₄⁺ to maintain electroneutrality
        
      • Thus, if the kidney can’t excrete acid i.e. in an RTA, the urine Chloride will be low, and the UAG will be positive
        
    • If UAG is negative, then the kidney is secreting NH₄⁺ and Cl^- and you don’t have an RTA
      
    • UAG is NOT useful in patients with proximal RTA
      
  • Assess Urine pH
    • Type I (Distal RTA) ‐ Urine pH > 5.55
      • causes include: auto-immune, sicklers, cirrhosis, idiopathic
    • Type II (Proximal RTA) ‐ Urine pH < 5.55
      • causes: myeloma, Wilson’s, Vit D deficiency, heavy metals
    • Type IV (Distal RTA) ‐ Hyperkalemic, Urine pH < 5.5
      • Aldosterone deficiency, diabetes

• The loss of bicarbonate in the stool leads to a SID acidosis
  

• To work this up, look at the UCl
  • Urine chloride <15 means that the person may have a saline-responsive alkalosis (though this also will depend on their volume status)
    • UCl >15 means unlikely to have saline-responsive alkalosis
      

• Cyanide, Carbon Monoxide, Metformin, Didanosine,(Stavudine, Zidovudine, Linezolid, Strychnine, Emtriva, Rotenone (Fish Poison), NaAzide (Lab Workers), Apap (if Liver Fx), Phospine (rodenticide), NaMonofluoroacetate (Coyote Poison‐Give Etoh as antidote), Inh (if patient seizes), Hemlock, Depakote, Hydrogen Sulfide, Nitroprusside (If cyanide toxic), Ricin & Castor Beans, Propofol, Linezolid, Sympathomimetics (Cocaine, Methamphetamine), Jequirty peas (Abrus precatorius), Prunus Amygdalus Plants as well as Crab Tree Apple Seeds & Cassava (yucca)
  • Of note, most of the toxins under SIG acidoses will also cause elevated lactate
• Rare causes
  • Pyroglutamic acidemia (from taking tylenol in combination with severe sepsis, renal fx, or hepatic fx)
    
  • Shoshin beri beri (from severe thiamine deficiency)
    
    

• Of note, the SIG is the Gap of Unmeasured Anions
  
• This is essentially the Anion Gap, but with the added information that we can calculate the lactate and we correct for albumin
  
  SIG = (Base Deficit) + (SID – 38) + 2.5 (4.2 ‐ Albumin (g/dL)) – Lactate
• This can also be thought of as the corrected base deficit, or put a minus sign in front and it is the corrected base excess
  
• Could also be thought of as the Acid Excess (with Acid Excess = Base Deficit)
  
  Acid Excess = SIG + (38 – Patient’s SID) + 2.5(Pt’s Albumin – 4.2) + Lactate
• In other words, the acid excess seen on the VBG must be explained somehow
  • This is probably the most logical way of remembering the formula
• The Excess Acid (if there is any), could be explained completely by:
  • Lactate
    
  • Excess albumin (b/c albumin is a weak acid), though this never really happens
    
  • SID acidosis (aka non-anion gap acidosis)
    
  • Strong Ion Gap Acidosis (Uremia, DKA, AKA, Tox, D-lactic Acidosis)

• Uremia, DKA, AKA (Alcoholic KetoAcidosis)
  
• Tox
  
• ASA, ethylene glycol, methanol, propylene glycol (ativan, valium, dilantin infusions), iron, INH, & paraldehyde
  
• D-Lactic Acidosis
  • from short gut/blind loop
    • this will not show on lactate assay

• Hypercalcemia, Hypermagnesemia, Hyperkalemia, Immunoglobulins, Bromide, Nitrates, Lithium Overdose
  
  

• If the primary disturbance is respiratory and you feel it is chronic, you can calculate the expected metabolic compensation
  
• Expected Δ BE (or expected ↓ of SID) = 0.4 x (Chronic Change in CO₂)
  
• If the primary problem is metabolic acidosis
  
• Expected ↓ CO₂ = Base Deficit
  
• If the primary problem is metabolic alkalosis
  
• Expected ↑ CO₂ = 0.6 x Base Excess
  
• Formula to correct P_aCO₂ in a COPD Patient
  • 0.08 decrease in pH = for every 10 mmHg increase in PaCO2 acutely

• If the SIG is elevated and the above work up has not yielded a diagnosis, the next step is to look for an Osmolar Gap
  • Normal Osmolality is 270-290 mOsm/Kg H2O
    
    Osm Gap = Measured Osmal – (2 Na + Gluc/18 + BUN/2.8 + ETOH/3.7)
• An Osmomar Gap >10 is considered “Positive”
  • Causes of Elevated Osm Gap:
    • Methanol, Ethylene glycol (found in automotive anti-freeze), mannitol, isopropanol (isopropyl alcohol), propylene glycol (found in Lorazepam, Valium, Phenobarb, Phenytoin infusions), lithium
      
• Distinguishing between toxic alcohols
  • Methanol and Ethylene Glycol cause BOTH increase in AG and Osm Gap
    
  • Isopropyl Alcohol causes an increase in Osm Gap, but NOT AG
    
• If Osm Gap is >50
  • The etiology is almost certainly a toxic alcohol
    
• Assay for Toxic Alcohols (volatile alcohols)
  • Liquid/Gas Chromatography
• Tx for Ethylene Glycol Poisoning
  • Dialysis
    
  • Bicarb
    
  • Fomepizole (Alcohol Dehydrogenase Inhibitor)
    • Give until level of EG undetectable