3. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG
6. Assess delta ratio
7. Urine anion gab
8. Formulate acid-base diagnosis
4. • Step 1.
History taking and physical examination
Comprehensive history taking and physical
examination can often give clues as to the
underlying acid-base disorder
5. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG
6. Assess delta ratio
7. Urine anion gab
8. Formulate acid-base diagnosis
10. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG
6. Assess delta ratio
7. Urine anion gab
8. Formulate acid-base diagnosis
11. Metabolic acidosis
Expected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2)
Metabolic alkalosis
Expected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5)
“If the actual pCO2 or [HCO3
-]
is different from the predicted values,
You must suspect a 2nd acid-base disorder”
12.
13. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG
6. Assess delta ratio
7. Urine anion gab
8. Formulate acid-base diagnosis
14. Basis of Metabolic Acidosis
H+ + HCO3- H2O + CO2
Added
acids
Loss of
NaHCO3
New A- No New A-
(rise in plasma AG) (no rise in plasma AG)
(Exhaled)
15. Electrochemical Balance in Blood
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
CATIONS ANIONS
Sulfate
Phosphate
Mg- OA
K - Proteins
Ca-HCO3
Na- Cl
UAUC
Na
Cl
HCO3
16. • (Na + K) + UC = (Cl + HCO3) + UA
• The anion gap is defined as the quantity of
anions not balanced by cations.
• Anion Gap= measured cation- measured
anion.
• AG = [Na + K] – (Cl + HCO3) = 12 ± 4 meq/L
• Corrected AG (in Hypoalbuminemia):
4-alb*2.5
18. Basis of Metabolic Acidosis
H+ + HCO3- H2O + CO2
Added
acids
Loss of
NaHCO3
New A- No New A-
(rise in plasma AG) (no rise in plasma AG)
(Exhaled)
19. Electrochemical Balance in Blood
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
CATIONS ANIONS
Sulfate
Phosphate
Mg- OA
K - Proteins
Ca-HCO3
Na- Cl
UAUC
Na
Cl
HCO3
20. 1. History taking and physical examination
2. Assess accuracy of data (validity).
3. Identify the primary disturbance
1. Check arterial pH-------- acidosis or alkalosis
2. HCO3
- & pCO2 analysis---primary disorder.
4. Compensatory responses
5. Calculate AG
6. Assess delta ratio
7. Urine anion gab
8. Formulate acid-base diagnosis
22. Delta ratio Assessment Guidelines
< 0.4 Hyperchloremic normal anion gap acidosis
< 1 High AG & normal AG acidosis
= 1 Pure Anion Gap Acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1
due to urine ketone loss
> 1 High AG acidosis and a concurrent metabolic
alkalosis
25. Ketoacidosis
• In patients with IDDM, alcoholics and pts undergoing fasting or
starvation
• due to the overproduction of ketone bodies (Ketosis) leading to
accumulation of ketones in plasma (Ketonemia) and urine
(Ketonuria).
• In starvation states where plasma glucose levels are low or in states of
low plasma insulin where uptake of glucose by cells is diminished,
fatty acids will be mobilized and transported to tissues (brain, skeletal
muscle, heart) for fatty acid oxidation and energy production.
• acetyl CoA from fatty acid oxidation can not be oxidized and is instead
converted to the generation of ketone bodies. (acetoacetate and β-
hydroxybutyrate) Which serve as a source of fuel
26. Treatment of KA
• Fluids: IVF
• Insulin infusion
• Potassium replacement
• Bicarb replacement: If pH < 7.1 and/or cardiac instability
present
27. Lactic Acidosis
• Dead-end product of glycolysis
• Occurs when the body must regenerate ATP without oxygen
• Normal lactic level is maintained at 0.7-1.3 mEq/L
• Eliminated in liver (50%), kidneys (25%), heart and skeletal
muscles
• Normal Lactate/Pyruvate ratio suggest that the cause is not related
to anaerobic metabolism or anoxia
28. Treatment for Lactic Acidosis
1. Identification of the primary illness and correction of that
disturbance.
2. Restoration of tissue oxygen delivery through hemodynamic
and/or respiratory support is the key therapeutic goal in type A
lactic acidosis.
3. the use of sodium bicarbonate in lactic acidosis is controversial,
particularly in patients with circulatory and respiratory failure.
Despite the controversy most physicians support administration
of NaHCO3 for very severe acidemia and will give small
amounts of NaHCO3 to maintain the arterial pH above 7.10,
since a pH beyond this value will promote the development of
arrhythmias and cardiac depression.
29. Actual Bicarbonate Loss
Normal Plasma Anion Gap
• Direct loss of NaHCO3
• Gastrointestinal tract (diarrhea, ileus, fistula or T-tube
drainage, villous adenoma)
• Urinary tract (RTA, use of carbonic anhydrase inhibitors)
30. Renal Tubular Acidosis
• Inability of the kidney to reabsorb
the filtered HCO3
-
• Inability of the kidney to excrete
NH4
+
31. Proximal RTA Distal RTA RTA IV
cause impairment of
HCO3-
reabsorption in
the proximal
tubules
Acidification
defect
Hypoaldosteronis
m or
Pseudohypoaldost
eronism
Type of
Acidosis
Hyperchloremic
metabolic
acidosis
Hyperchloremic
metabolic
acidosis
Hyperchloremic
metabolic acidosis
S.Potassiu
m
low low high
Urine pH < 5.5 >5.5 < 5.5
Urine
HCO3 loss
+++ ++ ++
32. Metabolic Acidosis in
Renal Failure
• Normal AG acidosis results from failure of the kidney to
generate new HCO3
- from a reduced rate of synthesis and
excretion of NH4
+
• Increased AG acidosis results from the reduced GFR,
with accumulation of anions: HPO4
35. • Bicarbonate is probably not useful in most cases
of high anion gap acidosis
• Bicarbonate therapy may be useful for
correction of normal anion gap acidosis
