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metabolic acidosis
SaO2
95% to 100%
The arterial oxygen saturation.
50 - 70%
-------------------------Normal: -2 to +2 mmol/L
Metabolic acidosis: < -2 mmol/L
Mild
-4 to -6
Moderate
-6 to -9
Marked
-9 to -13
Severe
to < -13
Metabolic alkalosis: > +2 mmol/L
Severe
> +13
Marked
9 to 13
Moderate
6 to 9
Mild
4 to 6
[Base excess (BE) is the mmol/L of base that needs to be removed to bring the pH
back to normal when PCO2 is corrected to 5.3 kPa or 40 mmHg. During the
calculation any change in pH due to the PCO2 of the sample is eliminated,
therefore, the base excess reflects only the metabolic component of any disturbance
of acid base balance.]
Step Four - Assess for compensation
Look at the pH, PaCO2, and B.E. / HCO3- to decide whether compensatory
mechanisms are at work.
Once the acid-base disorder is identified as respiratory or metabolic, we must look
for the degree of compensation that may or may not be occurring. we know that the
system not primarily responsible for the acid-base abnormality must assume the
responsibility for returning the pH to the normal range. This compensation may be
complete (pH is brought into the normal range) or partial (pH is still out of the
normal range but is in the process of moving toward the normal range.) In pure
respiratory acidosis (high PaCO2, normal [HCO3-], and low pH) we would expect an
eventual compensatory increase in plasma [HCO3-] that would work to restore the
pH to normal. Similarly, we expect respiratory alkalosis to elicit an eventual
compensatory decrease in plasma [HCO3-]. A pure metabolic acidosis (low
[HCO3-], normal PaCO2, and a low pH) should elicit a compensatory decrease in
PaCO2, and a pure metabolic alkalosis (high [HCO3-], normal PaCO2, and high pH)
should cause a compensatory increase in PaCO2. All compensatory responses work
to restore the pH to the normal range (7.35 - 7.45)
[ See sample problems near the bottom of the page]
Step Five - Further analysis in cases of METABOLIC ACIDOSIS
Metabolic acidosis:
1] Calculate the anion gap:
Anion gap = Na+ - [CL- + HCO3-]
Difference between calculated serum anions and cations.
Based on the principle of electrical neutrality, the serum concentration of cations
(positive ions) should equal the serum concentration of anions (negative ions).
3
However, serum Na+ ion concentration is higher than the sum of serum Cl- and
HCO3- concentration.
Na+ = CL- + HCO3- + unmeasured anions (gap).
Normal anion gap: 12 mmol/L (10 - 14 mmol/L)
2] Based on the anion gap and patient history - review potential causes:
Normal anion gap (hyperchloremic) metabolic acidosis:
Normal anion gap acidosis: The most common causes of normal anion gap acidosis
are GI or renal bicarbonate loss and impaired renal acid excretion. Normal anion gap
metabolic acidosis is also called hyperchloremic acidosis, because instead of
reabsorbing HCO3- with Na, the kidney reabsorbs Cl-. Many GI secretions are rich
in bicarbonate (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tube
drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters
into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses
bicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, which
dissociates into NH3+ and H+.
Loss of HCO3 ions is accompanied by an increase in the serum Cl- concentration.
The anion gap remains normal. Disease processes that can lead to normal anion gap
(hyperchloremic) acidosis. Useful mnemonic (DURHAM):
a) Diarrhea (HCO3- and water is lost).
b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon due
to disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary
Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the
gastrointestinal loss of HCO3-.
c) Renal tubular acidosis: dysfunctional renal tubular cells causes an inappropriate
wastage of HCO3- and retention of Cl-.
d) Hyperalimentation
e) Acetazolamide
f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and
calcium chloride (CaCl) ingestion, all of which can increase the gastrointestinal
wastage of HCO3-.
Increased anion gap metabolic acidosis
High anion gap acidosis: The most common causes of a high anion gap metabolic
acidosis are ketoacidosis, lactic acidosis, renal failure, and toxic ingestions. Renal
failure causes anion gap acidosis by decreased acid excretion and decreased
bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate
accounts for the high anion gap. Toxins may have acidic metabolites or trigger
lactic acidosis.
In increased anion gap metabolic acidosis, the nonvolatile acids are organic or other
inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid, sulphuric acid). The
anions of these acids are not Cl- ions. The presence of these acid anions, which are
not measured, will cause an increase in the anion gap. Useful mnemonic (MUD
PILES):
Methanol poisoning: Methanol is metabolized by alcohol dehydrogenase in the liver
to formic acid.
4
Uremia: In end-stage renal failure in which glomerular filtration rate falls below 10
20 ml/min, acids from protein metabolism are not excreted and accumulate in
blood.
Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of betahydroxybutyric and acetoactic acids (ketoacids).
Paraldehyde poisoning.
Ischemia: causes lactic acidosis.
Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid,
the end
product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the
Tricarboxylic Acid Cycle. (Causes: hypoxia, ischemia, hypotension, sepsis).
Ethylene glycol poisoning: Ethylene is metabolized by alcohol dehydrogenase to
oxalic acid in the liver. Usually there is also a coexisting lactic acidosis.
Salicylate poisoning
Respiratory Acidosis:
Central nervous depression: sedatives etc.
Neuromuscular disease (Guillain-Barr,
myasthenia gravis). Trauma.
Severe restrictive disorders: scoliosis.
COPD. Acute airway obstruction: choking
etc. CVA, pneumothorax, chest wall
disorder, tumor. Acute and chronic lung
disease.
Formulas (Compensation):
- Acute: HCO3 increases 0.1 for every
mmHg change in pCO2
- Chronic: HCO3 increases 0.35 for every
mmHg change in pCO2
Compensation:
The respiratory response to metabolic Compensation: In the presence of
alkalosis is hypoventilation. PCO2 rises respiratory acidosis the kidneys
above normal. Respiratory
compensate for the fall in pH by excreting
compensation to metabolic alkalosis is H+ ions and retaining HCO3 - ions. As a
variable and unpredictable. It is
result, pH rises towards normal and HCO3
unlikely that a conscious patient
- concentration rises above normal. Renal
breathing spontaneously will
compensation (also called metabolic
hypoventilate to a PCO2 > 7.3 kPa (55 compensation) to respiratory acidosis is a
mmHg) to compensate for metabolic
slow process. Compensation is not obvious
alkalosis.
for several hours and takes 4 days to
complete.
6
pH:
PaCO2:
HCO3:
BE:
7.44
24
16
-6
Respiratory acidosis.
Chronic ventilation failure
pH:
PaCO2:
HCO3:
BE:
7.38
76
42
+14
Uncompensated metabolic
alkalosis
pH:
PaCO2:
HCO3:
BE:
7.56
44
38
+14
(Respiratory acidosis.
acute ventilation failure
pH:
PaCO2:
HCO3:
BE:
7.26
56
24
-4
uncompensated metabolic
alkalosis
pH:
PaCO2:
HCO3:
BE:
7.56
40
34
+11
pH:
PaCO2:
HCO3:
BE:
7.44
26
18
-4
pH:
PaCO2:
HCO3:
BE:
7.40
56
34
+7
Respiratory acidosis.
Chronic ventilation failure
pH:
7.44
Respiratory alkalosis.
PaCO2: 20
Chronic alveolar hyperventilation HCO3:
16
BE:
-7
Uncompensated metabolic
acidosis
pH:
PaCO2:
HCO3:
BE:
7.24
36
14
-13
pH:
PaCO2:
HCO3:
BE:
7.52
28
22
+1
Dx - heroin overdose.
Breathing - shallow, slow.
7
ABGs:
pH: 7.30
PaCO2: 55 mm/Hg
HCO3-: 27 mEq/L
Compensated Respiratory
Alkalosis
Metabolic Alkalosis
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