Acidosis Decreases Response to Vasopressors is a guest post by Jerry Altshuler, PharmD, BCPS, BCCCP

One question I commonly encounter on rounds is “does acidosis reduce the activity of catecholamines?” While I think that at this point it is relatively clear that acidosis likely reduces LV contractility due to reduced intracellular calcium entry as well as H+ competition for calcium binding sites on myocardial troponin, I think that the notion that catecholamines “don’t work as well in acidosis” is less clear. The bulk of the data that comprises this idea can be seen in these three pictures and goes as follows:

Calif Med. 1958 Jun; 88(6): 437–440.

1) A report from 1958 describing the effects of catecholamines on dogs over varying pH values suggested less response at a pH of 6.76 than 7.27 and 7.34 (they also note that they gave 6 human patients sodium lactate, increased their pH and decreased their pressor requirement – that’s 1950’s publication standards for you).

Am J Physiol. 1988 Jan;254(1 Pt 2):H20-7.

2) A 1988 paper in chickens showed reduced beta receptor expression when the acidotic chicken’s pH fell. Isoproteronol responsiveness was concordantly reduced.

J Thorac Cardiovasc Surg. 2014 May;147(5):1698-705.

3) The most recent paper from 2014, looking at contractile force in Human mammary arteries showing INCREASED catecholamine response as the pH decreased.

In real life this is concept is obviously difficult to pinpoint as usually the degree of critical illness tends to correlate with the degree of acidosis and hypotension and can easily be misidentified as non-causative correlate.

What is everyone’s thoughts on this question?

Jerry Altshuler, Pharm.D., BCPS, BCCCP
Critical Care Pharmacy Coordinator
Director, PGY-2 Critical Care Pharmacy Residency Program 
The Mount Sinai Hospital
1 Gustave L. Levy Place
New York, New York 10029

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