Base Excess

1
Base Excess Strong Ion Theories

• (the real truth about ABGs)
• Steve Anisman MD
• Renal Wolf Pack Jan 31, 2003

2
But first

• Whats up with asparagus pee?

40 of the British population (based on a 1989
paper in British Journal of Clinical Pharmacology
in which 115 people were studied) or 100 of the
French population (103 subjects) make metabolites
of asparagusic acid, a substance found only in
asparagus. These metabolites are variants on
methyl mercaptan, aka methanethiol, which is a
sulfur-containing derivative of the amino acid
methionine. Methyl mercaptan can also be
metabolized via other pathways, and is
responsible for the characteristic odors of
garlic, onions, rotten eggs, and skunk secretions.
3
And another thing

• 10 of people (300 Israelis were tested) cant
  smell the odor in their urine or in other
  peoples urine even if the odor is present.

So before you get all high mighty and
convinced that your pee doesnt smell, get a few
people to accompany you to the bathroom.
And be aware that there is a widely held belief
that people with asparapee tend to have higher
IQs then those bland folks who cant mount an
appropriate response to an asparagus challenge.
4
..
5
The case

• A 50 yo M psychiatrist is brought to the ED with
  recent vomiting, diarrhea, SOB/COPD exacerbation.
  He was believed to have been unconscious on the
  floor for two days after a lithium overdose. He
  has a long history of abuse of loop and thiazide
  diuretics. He has been self-medicating with
  bicarbonate tablets and Renagel. He has been
  taking 30 Oscal-D pills/day, in addition to 200mg
  of lisinopril in the belief that they would be
  renally protective protection he needs, given
  his chronic use of Gentamicin and 5g Motrin/day.

He has a 120-pack/year smoking Hx, is S/P
pulmonary lobectomy, is on 5L home O2, uses CPAP
at night for his OSA, and has recently been
experiencing hemoptysis. V/Q scan is high prob.
6
The case

• In order to prevent his frequent episodes of DKA,
  he has begun a regimen of glyburide and lantus,
  the dosages of which he calculates daily after
  consulting a formula which he has devised,
  incorporating both the phase of the moon and the
  color of his aura.

He is scheduled for MWF hemodialysis in
Belchertown, but has not been for 2 weeks because
he believes the nurses are putting too much
acid in his dialysate.
How would you quantify the acid and base
components in this mans blood?
7
Exam Labs

• Exam reveals an imaginary person. No JVD, no
  extra heart or lung sounds, no edema.

There is a way
8
Respiratory PCO2

• End of story. pCO2 is directly measured (not
  calculated), and is a reliable indicator of
  respiratory acid-base disturbances. The
  correlation between pCO2 and respiratory pH is
  direct, consistent, and linear.

And theres an equivalent measurement for
metabolic
9
and its NOT bicarb

• In pure metabolic disorders, bicarb is a useful
  measurement, but if youll remember the
  equilibrium formula

H20 CO2 ? H2CO3 ? H HCO3-
youll notice that HCO3 can be affected by
respiratory (CO2) or metabolic (H) components,
and therefore isnt a specific marker for either.
In fact, the relationship between metabolic
acidosis and bicarbonate is neither consistent
nor linear.
10
Two approaches

• Strong Ion Theory

Base Excess
Lets begin, shall we?
11
Strong Ions
Na Cl-
K
HCO3-
H
OH-

• You need electroneutrality, or you would glow.

If your blood was saline, Na would have to equal
Cl-.
If you added potassium bicarbonate
And then added a bunch of other ions
Which ones of these matter, and which are clutter?
12
Strong Ions
Na Cl-
K
Mg
Ca
Others (lactate, etc)

• These are the Strong Ions, so-called because
  they do not readily combine with other ions or
  lose their charge. Conversely, H and HCO3-
  readily combine, and are called weak ions.

The difference between the strong cations and
strong anions is called the Strong Ion Difference
(SID), and indicates the net ionic charge of the
weak anions so it indicates the relative
strength of H and HCO3-.
13
Strong Ion Theory

• Alright, already so far its basically anion
  gap with a new name. But, the Strong Ion Theory
  goes a step further and adds a few other factors
  pCO2, SID, and non-volatile weak acids (buffers).
  Additionally, the Gibbs-Donnan equilibrium needs
  to be considered

Just for the record weve already considered
pCO2 and were done with it. More on SID coming
up 2 slides from now...
14
The Non-Volatile Buffers

• In blood, were dealing mainly with hemoglobin,
  albumin, and phosphate. Stick with me here

A- Ionized weak acid buffer HA Non-ionized
weak acid buffer ATOT Total weak acid buffer
?
ATOT A- HA
Dissociation for these HAs is HA ? A- H
so HA K ? A- H
so You can calculate A- if you know pH ATOT
15
Strong Ion Difference

• Remember, SID strong cations strong anions.
  It indirectly measures weak ions (HCO3 and A-).

SID HCO3- A-
Just for the record, HCO3 A- was called
Buffer Base as far back as the 1950s SID was
invented by Stewart in 1980.
You can get HCO3 by Henderson-Hasselbach if you
know pCO2 and pH (this is the calculated ABG
value).
You can get A- if you know ATOT and pH.
16
Base Excess

• Definition The amount of a strong acid (like
  HCl) needed to bring blood to 7.40.
• Assumes 100 oxygenation, 37oC, and pCO2 of 40.

Normal 0
Used to calculate the metabolic component of an
acid-base disturbance.
17
Base Excess calculations

• Calculated the same way, in practice, as SID

Buffer Base HCO3- A-
HCO3 calculated by pH pCO2 (blood gas machine)
A- calculated using pH hemoglobin (whole
blood) OR A- calculated using albumin phos
(plasma)
BE Buffer Base expected buffer base
(expected if pH 7.4 and pCO2 40)
18
Membranes Ions you guys should feel right at
home!

• There are flavors of Base Excess Base
  ExcessErythrocyte Base ExcessPlasma Base
  ExcessECF (entire extracellular fluid) Base
  ExcessWhole Blood how do we decide what to use?

The Gibbs-Donnan equilibrium describes the
behavior whenever a membrane separates
impermeable ATOT buffer (Hgb) while allowing
passage of other ions (Cl-, HCO3-).
19
Gibbs-Donnan

• It means, for our purposes, that you can predict
  what will happen to plasma pH if you add acid to
  whole blood.

Trust me on this part Base Excess of
Extracellular Fluid is the one that we like.
Extensively studied, reliable, good stuff.
Siggaard-Andersen validated it extensively in
actual people lots of them during the polio
epidemics of the 1950s. Really, trust me. In
fact, it even has its own name
20
Standard Base Excess

• aka Base Excess of ECF. ECF includes plasma,
  red cells, and the surrounding interstitial
  fluid. Its where the action takes place in the
  body regarding acid-base movement.

Blood-gas machines calculate SBE as SBE 0.9287
(HCO3- - 24.4 (14.83 (pH 7.4)))
And guess what it turns out that ATOT, while
fascinating, doesnt really matter clinically. A
nice advantage for SBE.
21
And SBE makes a pretty nomogram.
Compare Contrast
22
And the math is easier.
How do you figure out if compensation is normal?
In metabolic acidosis, If ?pCO2 SBE, then its
normal.
In metabolic alkalosis, If ?pCO2 SBE 0.6,
then its normal.
23
And the math is easier.
In acute respiratory disorders, if SBE 0 (/-
5), then its normal.
In chronic respiratory disorders, if ?pCO2 0.4
SBE, then its normal.
24
How about an improved Anion Gap?
If you apply the same logic that weve already
used, you can guess that there might be fancier
ways to calculate anion gap than what we now do.
This method should give you a gap of 12 (not
12-19)
AG pH ((1.16 alb) (0.42 phos)) (5.83
alb) (1.28 phos)
Turns out this doesnt work so well, but its a
version of a new trend called Strong Ion Gap. A
nice version of this involves the
25
Fencl-Stewart corrections!!
Theres an interesting paper in Critical Care
Medicine by Balasubramanyan 199927(8)1577-81
showing that this version of the Strong Ion Gap
works. Fencl Stewart basically said that BE had
some virtues, but that it missed the beautiful
things of the strong ion theory and that you
could apply the strong ion concepts to Base
Excess and pick disorders you might have missed
otherwise.
26
Fencl-Stewart corrections!!
BE caused by free water (BEfw) 0.3 (Na
140) BE caused by changes in Cl- (BEcl) 102
(Cl 140/Na) BE caused by changes in albumin
(BEalb) 3.4 (4.5 - albumin) BEnet BEfw
BEcl BEalb BEUA ua unmeasured anions BEUA
BEnet (BEfw bEcl BEalb)
If there were no abnormalities in sodium,
choride, albumin, or unmeasured anions, then BE
would be equivalent to BEUA.
27
Fencl-Stewart corrections!!
In a PICU, checking for BEUA picked up about 25
more abnormalities than BE alone, and about 15
more abnormalities than BE with normal gap
(!!!!). And BEUA was the strongest predictor of
mortality stronger than gap, stronger than BE,
stronger than lactate.
Even stronger than BEUA was the act of checking
a lactate, but thats a different conversation
28
Controversies
The use of SBE was accepted decades ago by Europe
(who published in Lancet), but shunned by the US
(particularly Boston, NEJM), leading to the
Great Trans-Atlantic Debate. This disagreement
has since been replaced by derision for Strong
Ions
Says Siggaard-Andersen this reveals that the
Stewart approach is absurd and anachronistic
this interpretationis contrary to all previous
rational thinking...
29
And a few words about Hasselbach
Henderson was the real McCoy. Hasselbach was an
miscreant, a rabble-rouser, and neer-do-well.
Henderson H HCO3- K CO2 H2O
(1908)
No muss, no fuss, no bother, no inverse
relationships, nothing that a high-school student
couldnt understand. In fact, if you remove H2O,
which doesnt vary, and change CO2 to pCO2, you
get
Modified Henderson H HCO3- K pCO2
Hasselbach
pH pK log (HCO3- / CO2) (1916)
30
And a few words about tight control
Youll read everywhere that pH is tightly
controlled by the body in a narrow range. What
a load of malarkey.
Logarithms introduce a false sense of tight
clustering. When the pH changes by 0.3 units,
(say from 7.5 to 7.2), this represents a doubling
of the hydrogen ion concentration (from 40 nMol/L
to 80). Even normal variation between 7.35 and
7.45 represents 25 variation in H.That is not
tight.
Sorry, I just had to get that off my chest.
31
..
32
Example 1
21 yo M with cardiomyopathy, admitted with acute
abdomen. Normal lytes, normal gap. Next day,
cyanotic hypotensive.
7.13 / 19 / 109 / -20 (SBE)
Acidosis.
Base Deficit 20 (Base Excess - 20), so
metabolic.
BE 20, ?pCO2 21. No respiratory component.
33
Example 2
67 yo F with COPD admitted for dyspnea,
intubated, soon extubated. Eats lunch, becomes
lethargic, reintubated.
First Intubation 7.19 / 70 / 249 / 0 Second
Intubation 7.10 / 85 / 50 / 0
Acidosis.
Base Deficit 0, so purely respiratory.
34
Example 3
51 yo M nephrologist. Thats all we know.
7.49 / 44 / 90 / 6 (SBE) Na148 Cl98 Alb2.1
Free water effect 0.3 (Na 140) -2.4
Cl effect 102 (Cl 140/Na)
9.3
Albumin effect 3.4 (4.5 alb)
8.16
Explained ion effect -2.4 9.3 8.16 15.06
BEua (Unexplained ions) 6 15.06 -9
35
Example 3
51 yo M nephrologist. Thats all we know.
7.49 / 44 / 90 / 6 (SBE) Na148 Cl98 Alb2.1
BEua -9
Alkalosis.
SBE ?pCO2 0.6, so pure metabolic.

• Unexplained ions are anions
• metabolic acidosis is also present
• need to check lactate, ß-OHb

36
Thank you!
At this time, Im happy to refer any questions to
Dr. OShea