Acid Base Disorders

Plan to spend at least 30-60 minutes preparing for this talk by using the Interactive Board for Learning/Preparing and clicking through the graphics animations as well as the Presenter Board. Notably, the Interactive Board for this talk contains more detailed information than the Presenter Board. You may choose to include as much or as little detail from the Learning or Preparing Board, but we recommend spending ~ 15 min going through the general structure/ framework and spending the remaining 10-15 min on practice cases. 

Print out copies of the Learner’s Handout so learners can take notes as you walk through different components of an ABG, the steps in identifying an acid base disorder, and how to calculate compensation. All clickable elements are indicated by a cursor element as well as with shading. 

• Objective 1 (Components of an ABG) – Ask your learners to identify the basic structure of an ABG and normal values for each of the respective components. Click each component to reveal the normal values and the nomenclature for derangements outside normal values. There is frequent confusion about the difference between “-emia” and “-osis”. Ask your learners to differentiate between the two. 
• Objective 2 (Steps for ABG interpretation) – Walk through the four basic steps of interpreting an ABG and identifying an acid-base disorder.
  • Step 1: Identify the primary acid-base status. What is the pH? Is the patient acidemic/alkaleimic/normal pH? Click on step 1 to reveal each of these components. Do not click on the “acidemia,” “normal pH,” or “alkalemia” buttons until you are ready to navigate to those pages.
    • Identify the primary process driving the acid-base process. Look at the pCO2 and HCO3 to identify the primary process (or processes). For example, in a patient with acidemia, we would expect the HCO3 to be low if a metabolic acidosis was the primary process. If a respiratory acidosis was the primary process driving the acidemia, we would expect a high PCO2. The first set of simplified practice cases help solidify recognizing these patterns. 
  • Step 2: For all patients, regardless of what the primary process is, there should be an evaluation for an anion gap metabolic acidosis (AGMA). An AGMA can be present even in the setting of another primary respiratory or primary metabolic process. For patients with an AGMA, we need to further assess if there's another concurrent metabolic process going on with the delta-delta. These calculations are discussed more in depth on the “acidemia” and “normal pH” page. 
  • Step 3: Lastly, after identifying the primary process, we should calculate whether there is a compensatory process. 
• Objective 3 (Differential diagnoses) – We recommend starting with “acidemia”. Clicking on this button will direct you to the acidemia page and both 1) walk through the different steps discussed in the framework above, but also provide a differential diagnosis for each acid base disorder. 
  • Acidemia: Click on metabolic or respiratory to reveal the differential diagnosis. Challenge your learners to determine to come up with a differential. 
    • Metabolic acidosis: An anion gap (AG) should be calculated in all patients, but especially in those with an metabolic acidosis. A pop-up further describes what the AG is and how to calculate this. 
      • Patients with an AGMA further need a “delta-delta” calculated. We prefer calculating the “residual HCO3” which may be more intuitive. Take the measured – expected AG (which should be calculated based off of the albumin), and add this difference back to the measured HCO3. This essentially accounts for the AGMA and asks “what acid/base process is left over after accounting for the AGMA?” If this HCO3 is normal, the AGMA accounted for the entire acid-base derangement. If this HCO3 is high, there is a concurrent metabolic alkalosis. If this HCO3 is low, then there is a concurrent metabolic acidosis (nongap). You may click on the AGMA to reveal a differential diagnosis. 
      • Patients with a nongap metabolic acidosis (NAGMA) can be further worked up with a urinary anion gap, though this is less commonly used. Generally, nongap acidoses are comprised of processes that result in HCO3 loss either through the gut or kidneys. 
    • Respiratory acidosis: This differential can be separated into processes that result in decreased CO2 elimination or increased CO2 production. 
  • Normal pH: Often this is a result of a mixed acid base disorder. 
  • Alkalemia: 
    • Metabolic alkalosis is often associated with GI or renal loss of H+. They are generally divided into Cl- responsive and non-responsive causes. Click on “response to IVF” to identify Cl- responsive causes. 
    • Respiratory alkalosis causes most commonly include fever/sepsis, CNS processes, PE
• Objective 4 (Compensation) – Teach the general principles of compensation. Respiratory system compensates for metabolic processes and this occurs on the order of minutes. Metabolic compensation occurs with the kidneys for pulmonary processes, which can take several days. There is a lot of detail on this slide, but most of these are not necessary to remember. The most common acid-base derangement is metabolic acidosis, so focus on Winter's formula and the “thumb rule” as a quick short cut. 
  • If there is inadequate compensation or “overcompensation”, this indicates a mixed process. Compensatory processes will never overcompensate or fully correct pH to normal.
• Cases – There are several cases for this talk. Depending on your learning level, you may choose to include or omit any of the cases.
  • The first set of cases (~5 min) are an oversimplified algorithm to recognize/identify the primary processes and what is likely the compensatory process. Please note to learners that they will actually have to look at the degree of change and calculate based on equations (or by looking at base excess/deficit) to determine if the expected change to truly determine whether there is compensation. For example, when PCO2 declines/ rises acutely, the HCO3 will decrease/ increase simply as a result of buffering processes in the blood. 
  • Cases 1-3 are simpler cases, 4-5 are more complex cases.