The Curious Case of the Acidemic Asthmatic


This is a fictional and educational case - any resemblance real patient information is entirely unintentional.



The Case


A 34-year-old female with a history of moderate persistent asthma presents to the ED with shortness of breath. Her illness started 3 days prior with a URI. Over the next few days, she became more short of breath and developed chest tightness, wheeze, cough and insomnia. Albuterol nebs are no longer helping.


Asthma since a young child. Major triggers - pollen, dust, weather changes, viral illness. She was intubated once in her 20s. Now taking fluticasone/salmeterol, montelukast and albuterol PRN.

    Other Data:


    • Moderate distress, uncomfortable
    • Accessory Muscle use, speaking in full sentences
    • Bilateral expiratory wheeze (all lung fields)


    • HR 120
    • RR 26
    • BP 155/72
    • SpO2 100% on 2L NC

    Other Data:

    • CMP: Normal
    • CBC: Normal


    • Initial ABG: 7.32/44/150/23

    • Initial Lactate 3.0 mEq/L




    She was given: 80mg IV methylprednisolone, albuterol nebs x6 (total of 15mg).


    One hour later...

    • Repeat ABG: 7.31/33/90/18

    • Repeat Lactate: 6.8 mEq/L


    • Wheeze significantly improved
    • Dyspnea worsened
    • More tachycardic (150 BPM)
    • More tachypneic (32)

    What would YOU do?


    There is only ONE biochemical pathway in the entire body that produces L-Lactate. This is the reduction of pyruvate by NADH. The idea here is that, without oxygen as a final electron acceptor, NADH would accumulate (and not be useful in cellular respiration). In order to eliminate NADH (and regenerate NAD+), we donate electrons to pyruvate. This forms lactate.


    Type A Lactic Acidosis

    Requires the presence of hypoxia or hypoperfusion. Think of distributive, obstructive, hypovolemic or cardiogenic shock, cardiac arrest & other ischemic syndromes.

    Type B Lactic acidosis

    Requires the absence of hypoxia or hypoperfusion. Think of alcoholism, malignancy, HIV, mitochondrial dysfunction, drugs (like metformin, sympathomimetics).

    D-Lactic acidosis

    This is uncommon and not often measured by routine labs. D-Lactate is a stereoisomer of L-Lactate. D-lactic acidosis is caused by things like DKA, GI disease (like short gut syndrome, small intestinal bacterial overgrowth) and propylene glycol ingestion.


    The paradoxical albuterol-lactate-dyspnea cycle

    Type BLA.jpg


    • Beware the temptation to administer beta agonists for 'dyspnea' without re-evaluating your patient
    • Re-evaluate your patient
    • Re-evaluate your patient
    • Did we mention you need to re-evaluate your patient?
    • Asess the patient's oxygenation & ventilation
    • Look for signs of hypoperfusion, end-organ dysfunction
    • Identify discrepancies between worsening dyspnea but improved ventilation (decreased wheeze, improved peak flow)

    Unstudied strategies:

    • Stop albuterol and observe?
    • Decrease albuterol dose?
    • Switch to ipratropium?

    Further reading:

    AMAZES Trial

    AZISAST Trial

    CHEST Study on Albuterol Induced Lactic Acidosis

    Empirical evidence for Albuterol Induced Lactic Acidosis


    “Sad Marimba Planet”, "It's a Mystery", "Looking back",  and "4th Ave. Walkup" by Lee Rosevere is licensed under CC BY-NC 4.0 / Song has been cropped in length from original form

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    Jeremy AmayoComment