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# Acid-Base Disorders

Summary Points
Medicine-Pediatrics

1. Know the equations for calculating acid-base disorders.

pH Acute Respiratory Acidosis = 0.08 x [(Measured PaCO
2
40)/10]
pH Chronic Respiratory Acidosis = 0.03 x [(Measured PaCO
2
40)/10]
pH Acute Respiratory Alkalosis = 0.08 x [(40 Measured PaCO
2
)/10]
pH Chronic Respiratory Alkalosis = 0.03 x [(40 Measured PaCO
2
)/10]
Anion Gap = Serum Na
+
- Serum Cl
-
- Serum HCO
3
-

Expected PaCO
2
in Metabolic Acidosis = [1.5 x Serum HCO
3
-
] + (8 +/- 2)
Corrected Bicarbonate = Measured HCO
3
-
+ (Anion gap 12)

2. Recognize the Six Step sequence that leads to a diagnosis of an acid-base disorder.

Step 1: Is the patient academic or alkalemic? If the pH is less than 7.38 then the patient is
academic. If the pH is greater than 7.42 then the patient is alkalemic.
Step 2: Is the overriding disturbance respiratory or metabolic? If PaCO
2
is greater than 40
mm Hg the respiratory contribution is the overriding disorder.
Step 3: If respiratory is overriding, is it acute or chronic? Acute defines a relationship
between pH and PaCO
2
by a factor of 0.08. Chronic defines a relationship between
pH and PaCO
2
by a factor of 0.03.
If HCO
3
-
is greater than 24 mEq/L, then the metabolic component is the overriding
disorder and Step 3 is omitted.
Step 4: If metabolic is there an increased anion gap? Measuring the difference between Na
+

and (Cl
-
+ HCO
3
-
Step 5: If metabolic, is the respiratory system compensating acidosis adequately?
Compensatory respiratory response to acidosis is hyperventilation which is predictable
from the linear relationship, [1.5 x Serum HCO
3
-
] + (8 +/- 2), between PaCO
2
and HCO
3
-
.
If the measured serum PaCO
2
is less than the calculated PaCO
2
, then

a primary
respiratory alkalosis exists. If the measured serum PaCO
2
is greater than the calculated
PaCO
2
, then

a primary respiratory acidosis exists. Compensation to metabolic alkalosis
is more difficult to predict as appropriate compensation occurs with decrease in alveolar
ventilation BUT this rarely rises to > 50 mmHg. SO a subnormal PaCO
2
(<38) indicates
concomitant primary respiratory alkalosis and a PaCO
2
> 50 mm Hg suggests
superimposed primary respiratory acidosis AND if truly compensatory the patient should
Step 6: Are other metabolic disturbances present in the patient with anion gap metabolic
acidosis? Determine if there is an increase in anion gap above normal, (Anion gap 12).
Add this value to the measured serum HCO
3
-
, Measured HCO
3
-
+ (Anion gap 12),
which then equals total HCO
3
-
BEFORE the anion gap was generated. For each
milliequivalent increase in anion gap, there is a milliequivalent decrease in serum HCO
3
-
.
A calculated HCO
3
-
< 22 indicates a preexisting non-anion gap metabolic acidosis. A
calculated HCO
3
-
> 26 indicates a preexisting metabolic alkalosis.

3. Know the differential diagnosis of each category of acid-base disorders.

Respiratory Acidosis
CNS depression as seen with sedatives, CNS disease, obesity-hypoventilation syndrome
Pleural disease typically including pneumothorax, pleural effusion
Lung disease that includes chronic obstructive pulmonary disease, adult respiratory
distress syndrome, (pneumonia and pulmonary emboli IF underlying lung disease)
Chest wall disease that can function structurally as in kyphoscoliosis, primary muscle
disease such as polymyositis, MD or by nerve disease that drives respiratory function
such as in Guillain-Barre syndrome, neuromuscular junction disease-Myasthenia
gravis/botulism toxin
Respiratory Alkalosis
Catastrophic CNS event typically involving intra-cerebral hemorrhage
Drug use of primarily salicylates, progesterones
Third trimester pregnancy
Decreased lung compliance most related to interstitial fibrosis
Anxiety
Cirrhosis of liver
Sepsis
Anion Gap Metabolic Acidosis
Renal failure once the creatinine is greater than 5 mg/dL
Ketoacidosis most commonly seen in diabetes, alcohol withdrawal
Drugs/Poisons specifically related to methanol, salicylates, paraldehyde, ethylene glycol
Lactic acidosis seen in diabetes, renal failure, liver disease, tumors, sepsis
Non-anion Gap Metabolic Acidosis
Gastrointestinal bicarbonate loss
Renal tubular acidosis
Respiratory alkalosis compensation
Carbonic anhydrase inhibitors
Ureteral diversion
HCl or Ammonium chloride infusions
Hyperalimentation/rehydration
Chlorine gas exposure
Metabolic Alkalosis
Fluid volume contraction from GI tract loss, renal loss, lung, postoperative ascites
Hypokalemia
Excess gluco/mineralcorticoids
Bartters syndrome
Alkali (bicarbonate) ingestion

4. Know normal ranges of acid-base parameters and the mechanisms and time it takes organ
systems to compensate for acid-base changes that fall out of these ranges.

Normal physiological ranges include arterial pH ranging between 7.38-7.42; ventilation by
the pulmonary system that involve either excess elimination or retention of carbon dioxide
that functions in the normal PCO
2
range of 38-42 mm Hg; and renal metabolic control
that tries to maintain blood HCO
3
-
concentrations in a normal range between 22-26 mm
Hg.
Respiratory Acidosis is characterized by PaCO
2
elevation and pH drop (academic) which
results when the rate of CO
2
elimination is lower than rate of tissue production. Disease
influencing ventilation are characterize as acute OR chronic. Pulmonary changes
respond almost instantaneously to acute disease in which a 10 mm Hg increase in
PaCO
2
will influence pH to decrease by a factor of 0.08. Chronic disease responds by a
10 mm Hg increase in PaCO
2
influences a pH decrease by a factor of 0.03.
Compensation to chronic respiratory disease generally requires hours to initiate and is
not fully maximized until about 4 days following an acute change; however, compensation
is NEVER totally achieved as serum bicarbonate will not be able to increase enough to
normalize pH.

Respiratory Alkalosis is characterized by a PaCO
2
reduction and pH elevation (alkalemic)
as a result of increased alveolar ventilation and consequential decrease in PaCO
2
. This
process is not necessarily a compensatory response to hypoxemia. Decreased lung
compliance leads to hyperventilation EVEN in absence of hypoxia and will induce
increased ventilation. Of special note: Sepsis drives ventilatory rate also in the presence
of normal oxygenation state and must be ruled out in unexplained primary respiratory
alkalosis. Pulmonary changes respond almost instantaneously to acute disease in which
a 10 mm Hg increase in PaCO
2
will influence pH to decrease by a factor of 0.08. Chronic
disease responds by a 10 mm Hg increase in PaCO
2
influences a pH decrease by a
factor of 0.03. Renal compensation involves suppression of renal acid secretion which
subsequently consumes and decreases serum bicarbonate level. Compensation begins
during first 2 weeks and is typically not complete BUT in long standing disease states
compensation may be complete as serum bicarbonate can increase enough to normalize
pH.
Metabolic Acidosis is characterized by a reduction in serum HCO
3
-
and drop in pH
(academic). Upon recognition metabolic acidosis is next characterize as either in the
presence of an anion gap (discussed in the next point highlight) OR non-anion gap.
Ancillary findings such as exam of urine sediment/drug serum measures can be helpful in
supporting this etiology. The non-anion gap is generally caused by GI HCO
3
-
losses or
altered renal function. GI losses is associated with hyperchloremic metabolic acidosis in
compensation for bicarbonate losses. Renal mechanisms also contribute as is seen in
proximal and distal renal tubular acidosis, and pharmacologically with the used of
carbonic anhydrase inhibitors specifically acetazolamide. Other drug are also association
with non-anion gap metabolic acidosis that include amphotericin B, cyclosporins,
cholestyramine.

5. Understand the components and usefulness of an anion gap in the metabolic profile that
accompanies acid-base disorders.

The Anion Gap reflects the concentration of anions typically not measured on standard
serum analysis. Potassium is also excluded by convention in the analysis due to the
small contribution relative to sodium from the routine serum analysis. A normal anion
gap generally ranges between 10-14 mEq/L, and reflects the difference between
measured cations anions = Serum Na
+
- (Serum Cl
-
+ Serum HCO
3
-
)
Unmeasured anions Concentration
Proteins 15 mEq/L
Organic acids 5 mEq/L
Phosphates 2 mEq/L
Sulfates 1 mEq/L
Total 23 mEq/L
Unmeasured cations Concentrations
Calcium 5 mEq/L
Potassium 4.5 mEq/L
Magnesium 1.5 mEq/L
Total 11 mEq/L
Therefore Normal Gap 12 mEq/L
Respiratory alkalosis will elevate the anion gap due to exposing (increasing) negative
charges on albumin at alkaline pH. A search for sepsis should begin in the presence of
this disorder that reflects lactic acidosis contribution from inadequate tissue perfusion.
Additional etiologies resulting in elevated lactic acid includes other forms of tissue
hypoxemia, low cardiac output, peripheral shunting high cellular turn over from high
metabolic states (cancerous tissue).