lactic acidosis in status asthma

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We had a status asthma patient the other day. She was intubated in the ICU after some time in the ED. Her pH was 7.20. Her PaCO2 wasn't super high though--52. She had an elevated lactate, which I assumed was from having been hypoxic (though she was not after being intubated).

I thought that maybe her acidosis was from having had an elevated CO2 level prior to being intubated, but the doc believed that she was in a metabolic lactic acidosis. He explained that a severe asthma attack and cause lactic acidosis, and that the elevated lactate (don't remember the number) was not due to hypoxia but was a true metabolic lactic acidosis.

I seem to also remember that albuterol can elevate lactate levels.

Have you guys heard of this--status asthmaticus causing metabolic lactic acidosis?

how high was the lactate?

Specializes in CMICU.

Metabolic acidosis can be caused by some of the drugs given for asthma. Albuterol is a one. Especially when combined with steroids. Something to do with a hyperadrenergic state and pyruvate production.

Sorry I dont remeber the lactate level.

What was the anion gap? That would be a good place to start to determine the possible origin of the acidosis. ABGs are just a small part of the story. Non Gap acidosis in asthma exacerbations is commonly associated with respiratory muscle fatigue and tissue hypoxia. There have been studies correlating intubation and lactate levels in asthmatics. High dose albuterol has also been associated with elevated lactate levels.

If the event is severe enough, left ventricular filling becomes impeded and CO falls. That combined with hypoxemia and rise in sympathetic tone is enough to bump lactate.

If the event is severe enough, left ventricular filling becomes impeded and CO falls. That combined with hypoxemia and rise in sympathetic tone is enough to bump lactate.

Likely this.

I've seen people in shock just from increased intrathoracic pressure during a particularly severe episode (lots of breath stacking, very high auto peep). In many circumstances, I would expect that a patient's oxygen demand would rise as well simply due to work of breathing. A combination of hypoxia, impaired cardiac output, and increased oxygen demand should cause lactic acidosis.

Likely this.

I've seen people in shock just from increased intrathoracic pressure during a particularly severe episode (lots of breath stacking, very high auto peep). In many circumstances, I would expect that a patient's oxygen demand would rise as well simply due to work of breathing. A combination of hypoxia, impaired cardiac output, and increased oxygen demand should cause lactic acidosis.

I was thinking more in terms of the marked increase in negative inspiratory intrathoracic pressure causing a marked rise in venous return and RV filling, thereby compressing the LV and inhibiting filling. This all, of course, in the presence of the marked rise in pulmonary venous capacitance, further reducing return to the LV and reducing LV filling.

What you describe, though, is absolutely possible during mechanical positive pressure ventilation. As you point out, breath stacking will cause dynamic hyperinflation of the lungs, cause the intrathoracic pressure/RA pressure to exceed the mean systemic filling pressure and venous return to the RV will fall and so does the CO.

Either way, a metabolic acidosis is likely.

Specializes in ICU.

Ironically I was admitted for the same thing last week. I had a lactate of 5.3 that was worrying since I was not intubated and my sao2 was down to 86%. I was coughing non stop for just under 4 hrs from additional viral bronchospasm. My pco2 was 62.

My lactate was still high after 5 hrs and actually went up to 5.6.

Salbutamol can be toxic after surprisingly small amounts of administration. (I had had a total of 16 puffs and 3 news in 17hrs which can also increase lactate. it was considered not to be salbutamol induced lactic acidosis... But from the extreme muscle use I had used during the 4hrs of continual muscle coughing.

in summary- high lactate can also be atributed to salbutamol toxicity or by very high muscle use during the extreme coughing and use of excessory muscles in trying to breathe for extended periods.

Specializes in ER.

This is a great article on lactate, describing how you can get a high lactate without necessarily having hypoxemia.

Understanding lactate in sepsis & Using it to our advantage

Yes, I have definitely seen that in a couple of asthmatic patients who have used a lot of albuterol--usually over a couple of days preceding admission to the ICU.

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