The Curious Case of the Acidemic Asthmatic

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

 

 

The Case

HPI: 

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.

PMH: 

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:

Exam:

  • Moderate distress, uncomfortable

  • Accessory Muscle use, speaking in full sentences

  • Bilateral expiratory wheeze (all lung fields)

Vitals:

  • HR 120

  • RR 26

  • BP 155/72

  • SpO2 100% on 2L NC

Other Data:

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  • 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.

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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

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SO YOUR ASTHMATIC PATIENT HAS AN ELEVATED LACTATE...

  • 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

Attributions

“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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