Acidosis vs Alkalosis: Perspectives from Cardiology and from Pulmonology
Authors: Justin D Pearlman, MD, PhD, FACC and Larry H Bernstein, MD, FCAP
Acidosis vs Alkalosis: Perspectives from Cardiology
Justin D Pearlman, MD, PhD, FACC
Your concern about alkylosis is justified. The concentration of free protons H+ is indeed not generally given the strict and prompt attention it deserves, to prevent harm from too little H+ (alkylosis) as well as to much (acidosis).
Your concern about deleterious impact on vasomotor control of microcirculation is valid. In addition, precise control of acidity is vital not only for proper auto regulation, but also protein conformation and enzyme activities throughout the body.
The use of the term pH by physicians can be considered pedantic. It shows doctors can share discussions with chemists, who deal with H+ values that shift many orders of magntude, but it belies the fact that the body does not tolerate such ranges. Rather, life requires H+ to stay well within the range 10 – 90 and it strongly prefers the range of 35-45, both for bio control such as metarterioles and precapillary sphincters, and for protein conformations and enzyme functions. Clinically, H+ should be maintained near 40 mEq/L, and I attribute my high success rate with code blue situations to paying close attention to that fact.
SOURCE
From: Justin MDMEPhD <jdpmdphd@gmail.com>
Date: Saturday, September 19, 2015 at 4:43 PM
To: “Dr. Larry Bernstein” <larry.bernstein@gmail.com>
Cc: Aviva Lev-Ari <AvivaLev-Ari@alum.berkeley.edu>
Acidosis vs Alkalosis: Perspectives from Pulmonology
Larry H Bernstein, MD, FCAP
As the state of alkalosis develops, there is a disequilibrium across the cell membrane with excess OH- uncompensated by a positive ion. This leaves a disequilibrium across the cell membrane that can only be balanced by the movement of Na+ from within the cell. If the OH- was taken up by the RBC, it would have to produce water through carbonic anhydrase, which would disrupt the mechanism for release of CO2. In the case of the kidney, I don’t see a mechanism for compensation across the cell membrane. There is a reciprocal loss of H+ and K+. The H+ has to be retained to balance the OH-, and the end result would be a net loss of K+. A continued loss of K+ would lead to cardiac arrest.
All cells in the body are seriously hurt by alkalosis. In medical intensive care there is a preoccupation with metabolic acidosis, the result being that the retained H+ has to be captured in H2CO3 in the RBC and in the kidney, and CO2 is exhaled in the alveoli. There is also the reciprocal loss of K+, which is interchangeable with H+ in the kidney. The kidney does not handle acidosis well, and the most efficient mechanism is respiratory via conversion of H2CO3 to H2O and CO2.
The sphincters opening in response to acidotic blood. This supplies oxygen, etc to the capillary bed*
I am not familiar with the precapillary sphincters, but can see merit to this statement. The sphincter would control the volume of blood entering the capillary, and it would determine the volume of blood entering the venuous circulation. The gas exchange is at the capillary level.
Acidosis is itself problematic, and it is associated with a low flow state and with acute renal failure.
ALL mechanical respirators are preset to retain alkalosis* I am not aware of this.
Complete renal shutdown with complete recovery is only possible if he is not on life support systems, which are currently used everywhere.*
I think that the goal of respiratory support should be to maintain efficient gas exchange, to eliminate H+ ion formed from peripheral vasoconstriction, and a corellary should be to maintain a neutral pH. While there is a mechanism for eliminating H+ ion, I think that it is the case that excess OH- is more difficult. The kidney has no mechanism I can think of for balancing a metabolic acidosis.
The large volume of fluid used in resuscitation is only to maintain volume of plasma.
In not so recent history, the ICU was not serviced by the main laboratory, but pulmonary had its own blood gas measurements. This became unfeasible, and especially when the demands of open heart surgery needed support that pulmonary could not provide. I still remember the situation in 1982, when the laboratory, and not pulmonary were entrusted with servicing the cardiovascular program. Measurement of blood gases includes the measurement of pH.
SOURCE
From: “Dr. Larry Bernstein” <larry.bernstein@gmail.com>
Date: Saturday, September 19, 2015 at 3:18 PM
To: Aviva Lev-Ari <aviva.lev-ari@comcast.net>
Cc: Justin MDMEPhD <jdpmdphd@gmail.com>
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