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Acid-Base Balance and the
Anion Gap_tut
Wesam Farid Mousa
Assist prof Anesthesia &
ICU
Dammam University
1. The body strives for electrical neutrality
Cations = Anions
One of the cations is very special, H+, and its concentration is
monitored and regulated very closely
2. Blood pH is described by the Henderson-Hasselbalch
equation
3- Basically, the regulation of arterial pH includes
a.Respiratory system regulation of PaCO2.
b. Kidneys regulation of HCO3 and chemical buffering in
the form of NH4 + and H2PO4 secretion by the distal
convoluted tubule cells.
4. So how does it all work under normal circumstances to
keep our pH about 7.4?
a.Normally, CO2 production and loss are matched
PaCO2 is maintained at about 40 mmHg
PaCO2 is regulated by respiration rate, either slowing
down or speeding up respirations, to either blow off or
retain CO2.
! Control comes from the CNS by regulating respiration
rate.
!! Production rate of CO2 is not subject to regulation,
d. The kidney regulates plasma [HCO3 – ] (by extension [H+]
and pH) by three mechanisms:
a. Reabsorption of filtered HCO3 – , this is a recovery
operation
b. Formation of titratable acid, H2PO4- distal tubule
c. Excretion of NH4+ distal tubule
Get this:
The kidney glomerulus passively filters on the order of 4000
mmol of HCO3 –each day. This has to be reabsorbed and the
tubular cells must therefore secret 4000 mmol of hydrogen ions.
Prediction of the degree of respiratory compensation with a
metabolic acidosis.
PaCO2 = (1.5 X [HCO3 –]) + 8
Thus a patient with a metabolic acidosis and 12 mmol/L of HCO3 –
would be expected to have a PaCO2 between 24 and 28. If it’s higher
or lower, there is something else going on, in other words a mixed
acid/base disorder.
Basic rules to keep in mind for simple, one cause, problems.
Is a pH disturbance metabolic or respiratory in origin?
- Respiratory acidosis, PaCO2 is > 44
-Metabolic acidosis, HCO3 is < 22
-Respiratory alkalosis, PaCO2 is < 36
-Metabolic alkalosis, HCO3 is > 26
If the primary change is
- HCO3 then the underlying cause is most likely metabolic
- CO2, the underlying cause is most likely respiratory
Metabolic acidosis with calculated ion gap
Increase in the AG
Is most often due to increased
endogenous acid production
o lactate
o ketoacidosis
o accumulation of endogenous acids
with renal failure
o loss of HCO3
ii. Rarely, an increased AG may be
due to a decrease in cations such as
Ca+2,
magnesium and/or K+
Decrease in the AG
i. Increase in unmeasured cations
ii. Reduction in a major plasma
protein such as albumin (renal loss).
If only life could be this
simple all the time. But, a
person may have more
than one
disease at a time that
can cause an acid-base
disturbance. So, how do
you know?
With the coexistence of two
metabolic acid-base disorders may be
made apparent by calculating the
difference between the change in the
anion gap (delta AG), and the change
in the serum CO2 (delta CO2).
This value goes by several names,
either the delta or bicarbonate gap.
bicarbonate gap = delta AG - delta HCO3
-
Where
Delta AG = patient’s AG - 12 mEq/L
Delta HCO3 = 27 mEq/L - patient’s HCO3
-
If there is just one acid-base abnormality, there should be a 1:1 negative correlation between
the rise in the anion gap and a corresponding drop in the bicarbonate.
Example: if the AG goes up by 10, then the HCO3 should drop by 10.
Delta AG - delta HCO3 = 10-10=0
Just one acid-base problem here.
Variation of the bicarbonate gap from zero, either + or –
means there is a mixed acid-base problem. However, it
certainly doesn’t tell you the type.
Let’s see how this operates with two different mixed acid-base conditions.
Case : This 22 year-old man presents with several days of vomiting, nausea and
abdominal pain. His blood pressure is low and he has tenting of the skin. His
electrolytes are Na+ = 144, Cl- = 95, K+ = 4.2, HCO3 = 14
AG = 35
Delta AG = 23 (35 – 12)
Delta HCO3
27-14=13
HCO3- gap = +10
The high HCO3- gap indicates there are two conditions at work.
- Metabolic acidosis from dehydration and poor tissue perfusion
- Metabolic alkalosis from vomiting and loss of stomach acid.
A case of renal related acidosis: A 24 year-old female developed acute renal failure after a
perforated ulcer with peritonitis and shock.
Her labs are Na+ 140 mEq/L, K+ 4 mEq/L, Cl- 115 mEq/L, pH = 7.12, PaCO2 13 mmHg, and
HCO3- 4 mEq/L.
Delta AG = 9 = (21-12)
Delta HCO3 27-4=23
HCO3- gap = -14 = delta AG – delta HCO3
-
Her anion gap is up, her Delta (HCO3- ) is significantly off at
-14 mEq/L; that is 14 mEq/L lower than would be expected
given her excess anion gap of 9 (above normal). Were this a
simple ‘one cause’ acidosis, the acid causing her drop in pH
should have lowered her HCO3 to only about 18 mEq/L. The
fact that her HCO3 is actually 4 mEq/L means there must an
additional reason forheracidosis.
In this case a hyperchloremic metabolic acidosis, which is
commonly seen with renal failure. Below are her two renal
related problems.
o Uremia fromkidney failure causing the elevated AG.
o The tubular related problem of HCO3- recovery and acid
secretion, which leads to a non-ion gap acidosis with
hyperchloremia.
Thank You

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Acid base tut

  • 1. Acid-Base Balance and the Anion Gap_tut Wesam Farid Mousa Assist prof Anesthesia & ICU Dammam University
  • 2. 1. The body strives for electrical neutrality Cations = Anions One of the cations is very special, H+, and its concentration is monitored and regulated very closely
  • 3. 2. Blood pH is described by the Henderson-Hasselbalch equation
  • 4. 3- Basically, the regulation of arterial pH includes a.Respiratory system regulation of PaCO2. b. Kidneys regulation of HCO3 and chemical buffering in the form of NH4 + and H2PO4 secretion by the distal convoluted tubule cells.
  • 5. 4. So how does it all work under normal circumstances to keep our pH about 7.4? a.Normally, CO2 production and loss are matched PaCO2 is maintained at about 40 mmHg PaCO2 is regulated by respiration rate, either slowing down or speeding up respirations, to either blow off or retain CO2. ! Control comes from the CNS by regulating respiration rate. !! Production rate of CO2 is not subject to regulation,
  • 6. d. The kidney regulates plasma [HCO3 – ] (by extension [H+] and pH) by three mechanisms: a. Reabsorption of filtered HCO3 – , this is a recovery operation b. Formation of titratable acid, H2PO4- distal tubule c. Excretion of NH4+ distal tubule
  • 7. Get this: The kidney glomerulus passively filters on the order of 4000 mmol of HCO3 –each day. This has to be reabsorbed and the tubular cells must therefore secret 4000 mmol of hydrogen ions.
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  • 11. Prediction of the degree of respiratory compensation with a metabolic acidosis. PaCO2 = (1.5 X [HCO3 –]) + 8 Thus a patient with a metabolic acidosis and 12 mmol/L of HCO3 – would be expected to have a PaCO2 between 24 and 28. If it’s higher or lower, there is something else going on, in other words a mixed acid/base disorder.
  • 12. Basic rules to keep in mind for simple, one cause, problems. Is a pH disturbance metabolic or respiratory in origin? - Respiratory acidosis, PaCO2 is > 44 -Metabolic acidosis, HCO3 is < 22 -Respiratory alkalosis, PaCO2 is < 36 -Metabolic alkalosis, HCO3 is > 26 If the primary change is - HCO3 then the underlying cause is most likely metabolic - CO2, the underlying cause is most likely respiratory
  • 13. Metabolic acidosis with calculated ion gap Increase in the AG Is most often due to increased endogenous acid production o lactate o ketoacidosis o accumulation of endogenous acids with renal failure o loss of HCO3 ii. Rarely, an increased AG may be due to a decrease in cations such as Ca+2, magnesium and/or K+ Decrease in the AG i. Increase in unmeasured cations ii. Reduction in a major plasma protein such as albumin (renal loss).
  • 14. If only life could be this simple all the time. But, a person may have more than one disease at a time that can cause an acid-base disturbance. So, how do you know?
  • 15. With the coexistence of two metabolic acid-base disorders may be made apparent by calculating the difference between the change in the anion gap (delta AG), and the change in the serum CO2 (delta CO2). This value goes by several names, either the delta or bicarbonate gap.
  • 16. bicarbonate gap = delta AG - delta HCO3 - Where Delta AG = patient’s AG - 12 mEq/L Delta HCO3 = 27 mEq/L - patient’s HCO3 - If there is just one acid-base abnormality, there should be a 1:1 negative correlation between the rise in the anion gap and a corresponding drop in the bicarbonate. Example: if the AG goes up by 10, then the HCO3 should drop by 10. Delta AG - delta HCO3 = 10-10=0 Just one acid-base problem here. Variation of the bicarbonate gap from zero, either + or – means there is a mixed acid-base problem. However, it certainly doesn’t tell you the type.
  • 17. Let’s see how this operates with two different mixed acid-base conditions. Case : This 22 year-old man presents with several days of vomiting, nausea and abdominal pain. His blood pressure is low and he has tenting of the skin. His electrolytes are Na+ = 144, Cl- = 95, K+ = 4.2, HCO3 = 14 AG = 35 Delta AG = 23 (35 – 12) Delta HCO3 27-14=13 HCO3- gap = +10 The high HCO3- gap indicates there are two conditions at work. - Metabolic acidosis from dehydration and poor tissue perfusion - Metabolic alkalosis from vomiting and loss of stomach acid.
  • 18. A case of renal related acidosis: A 24 year-old female developed acute renal failure after a perforated ulcer with peritonitis and shock. Her labs are Na+ 140 mEq/L, K+ 4 mEq/L, Cl- 115 mEq/L, pH = 7.12, PaCO2 13 mmHg, and HCO3- 4 mEq/L. Delta AG = 9 = (21-12) Delta HCO3 27-4=23 HCO3- gap = -14 = delta AG – delta HCO3 -
  • 19. Her anion gap is up, her Delta (HCO3- ) is significantly off at -14 mEq/L; that is 14 mEq/L lower than would be expected given her excess anion gap of 9 (above normal). Were this a simple ‘one cause’ acidosis, the acid causing her drop in pH should have lowered her HCO3 to only about 18 mEq/L. The fact that her HCO3 is actually 4 mEq/L means there must an additional reason forheracidosis. In this case a hyperchloremic metabolic acidosis, which is commonly seen with renal failure. Below are her two renal related problems. o Uremia fromkidney failure causing the elevated AG. o The tubular related problem of HCO3- recovery and acid secretion, which leads to a non-ion gap acidosis with hyperchloremia.