Contents:

Approach
History and Physical
M7 studies
Other venous studies
ABGs
Anion Gap
Non Anion Gap
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
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An approach
Obtain history and physical
Obtain venous blood values
Obtain arterial blood gas

Then:
Determine acidemia or alkalemia

Determine if a primary respiratory and/or metabolic process is present

Determine if an anion gap is present

If MAcidosis, determine if respiratory compensation is adequate

If AG MAcidosis, determine other underlying disturbances

The only compensatory change rule useful is Winter's formula. Nomograms cannot
make a diagnosis.
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History and physical exam
Identify potential processes in the history:

-Renal failure = metabolic acidosis

-Vomiting = metabolic alkalosis
-CHF = respiratory alkalosis
-Pneumonia = respiratory alkalosis
-Heroin overdose = respiratory acidosis
-Acetazolamide use = metabolic acidosis
-COPD = chronic respiratory acidosis and metabolic alkalosis (diuretics)
-Pul Edema = respiratory alkalosis followed by respiratory acidoisis and metabolic
acidosis (lactic acid)
-Septic shock = respiratory alkalosis and metabolic acidosis (lactic)
-Hepatorenal = respiratory alkalosis plus metabolic acidosis (renal failure)
Look for clues in the physical:

-Tetany=alkalosis
-Jaundice = respiratory alkalosis
-Cyanosis = respiratory acidosis
-Kussmaul breathing = metabolic acidosis
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M7 studies

Total CO2: if normal, mixed or no disturbance

AG: present (>12), metabolic acidosis

AG = Na - (Cl + HCO3)

With AG metabolic acidosis, look for multiple distubances:

change Anion gap/ change plasma HCO3

Normal is between 1.1 and 1.6

<1 = RAlk + AG MAcid or non-AG MAcid + AG MAcid
>2 = MAlk + AG MAcid or Pre existing RAcid + AG MAcid

or

1) Calculate the change in AG above 12

2) change + measured HCO3 = "corrected" HCO3
3) If "corrected" HCO3 > 24, there's an underlying metabolic alkalosis, otherwise,
there's an underlying non AG metabolic acidosis.

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Other Venous blood studies

Potassium: can point to the direction of pH change (Usually, alkalosis decreases K

while acidosis increases K)

Renal Function: BUN/Cr

Liver Function: LFT's, Bili's, Alk Phos

Sepsis: WBC, Blood Cultures

Look for osmolar gap:

Calculated osmolality = 2(Na) + BUN/2.8 +Glu/18

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Arterial blood gases
Acidosis (pH < 7.38) or Alkalosis (pH >7.42)

-In a primary respiratory acidois, pCO2 > 40

-In a primary metabolic acidosis, HCO3 < 24
-In a pure respiratory alkalosis, HCO3 is never below 10
-In a pure metabolic alkalosis, PCO2 is rarely above 60
-In a pure metabolic acidosis, Winter's formula applies for respiratory compensation:

PCO2= 1.5 * HCO3 + 8 (+/-2)

A-a gradient
PAO2 = FIO2 * (PB - PH20) - (PCO2/0.8)

PAO2 = FIO2 * 713 - (PCO2/0.8)

(at sea level)
PAO2 = 150 - (PCO2/0.8)
(at sea level on room air)

Age correction = 2.5 + 0.25 * age

Normal A-a is <10, abnormalities indicate respiratory failure, Pulmonary emboli, etc.
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Anion Gap Metabolic Acidosis
(Normochloremic)

AG = Na - (Cl + HCO3)

MUDPILES

Methanol
Uremic
DKA (or alcoholic, starvation ketosis)
Paraldehyde
Ischemia
Lactic
Ethanol
Salicylates
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Non Anion Gap Metabolic Acidosis
(Hyperchloremic)
F-USED CARS
Fistulas (pancreatic)
Ureteral enteric fistulas
Saline (IVF)
Endocrine (hyperparathyroidism)
Diarrhea
Carbonic anhydrase inhibitors
Arginine/lysine/chloride (TPN)

RTAs
Spirolactones/Sulfur

RTAs (Urine Anion Gap positive):

Urine Anion Gap = Urine Na + K - Cl

-Type I (Distal, classic): Hypo K, hypercalcemia, renal stones, drug toxicity, urine pH >
5.3
-Type II (Proximal): Hypo K, Fanconi syndrome, heavy metal exposure, urine pH varies
(can be less than 5.3)
-Type IV (Hypoaldo, hyporenin): Hyper K, diabetics, urine pH usually < 5.3
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Metabolic Alkalosis
Primary defect is an increase in serum bicarbonate

Look at urine chloride:

UCl < 10 implies saline responsive
NG suction
Vomiting
Diuretics
Post-hypercapnia

UCl >10 implies saline resistant

Elevated BP:
Primary aldosteronism
Cushing's
Renal artery stenosis

Normal BP:
Hypomagnesium
Hypokalemia
Bartter's syndrome
NaHCO3 administration
Licorice (inhibits cortisol degradation)
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Respiratory Acidosis
Increase in pCO2

Acute:
For every 10 that pCO2 increases, pH decreases by 0.8, serum HCO3 increases by 1

Chronic:
For every 10 that pCO2 increases, pH decreases by 0.03, serum HCO3 increases by 3-
4

Chest cavity: Neurologic, Muscular, Kyphoscoliosis, Effusions, Pneumothorax

Central: Sedation, respiratory center hypofunction

Lung/Airways: Pneumonia, Pulmonary edema, Broncospasm/laryngospasm, COPD,

Obstruction
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Respiratory Alkalosis
Decrease in pCO2

Acute
For every decrease in pCO2, HCO3 decreases by 2.5

Chronic
For every 10 decrease in pCO2, HCO3 decreases by 5

Systemic: Sepsis, Salicylates, Liver Failure, Hyperthyroid, Pregnancy

Central: Ischemia/CVA, Tumor, Infection, Progesterone, Anxiety

Pulmonary: Pulmonary embolus, Restrictive lung disease, Hypoxemia

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8/10/97 by K Hsu

Note: Every effort has been given to ensure accuracy. However, no liability or warranty
for errors or ommissions exists, expressed or implied.