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Acid-Base Physiology

Normal values: pH 7.38-7.42, PCO2 35-45, HCO2 22-26

pH < 7.35 acidemic, pH > 7.45 alkalemic
pH / paCO2 mmHG / PaO2 mm Hg / HCO3
at sea level, avg PO2=
PaO2 = 104.2 - (0.27 x age)
In the alveolus a reciprocal relationship exists between oxygen and carbon dioxide. Carbon dioxide accumulation as a result of inadequate ventilation
displaces oxygen. Also, a normal gradient of about 10 mmHg exists between alveolar oxygen pressure (P AO2) and the arterial oxygen pressure (PaO2)
(A-a gradient). Generally, there is no gradient between the alveolar carbon dioxide pressure (P ACO2) and the arterial PaCO2.
O2 = FiO2(700) - (PACO2 x 1.25)

ABG: pH and PCO2 are directly measured, HCO3 is calculated using henderson hasselbach (get lytes/chem panel if you want direct HCO3)
... To analyse a gas
1) determine acidemia vs alkalemia
2) determine primary disturbance(s)...look at PCO2 and HCO3
3) for metabolic acidosis, det anion gap ... if hi gap, det corrected serum bicarb, to find out if there are other acid-base disturbances
4) for respiratory disturbance, determine acute vs chronic
5) In all disorders, determine if degree of compensation is appropriate. If not, look for mixed d/o.
If pH > 7.45: alkalemic, if <7.35 acidemic.
The underlying physiologic disorders determine if an alkalosis or acidosis is present.
Anion Gap: cations - anions. Na - (Cl- + HCO3-). The overall ion balance is neutral but there is usually an 'anion gap' of 8-12, because there are
unmeasured anions (proteins,ie albumin, phosphates, sulfates, organic acids). For calculation purposes, use normal anion gap= 12 +/- 2. Anion gap
may be due to acidosis or !alkalemia!.
Important considerations: if albumin is low (cirrhosis, nephrotic syndrome), the anion gap is smaller. It decreases by 2 for every 1 g/dl decrease in
serum albumin. Therefore in severe hypoalbuminemia if the anion gap increases and approaches 12, one must suspect an additional metabolic cause
for the increased anion gap. Also in alkalosis, (fewer H+ ions), more negative charges on albumin molecules are exposed... therefore more negative
charges means a greater anion gap.
Fine detail: there are also unmeasured cations Ca, K, Mg, which number about 11 meq/L, however the unmeasured anions number about 23
meq/L). Also, if the anion gap is >/= 20mmol/L, there is a primary metabolic
acidosis regardless of the pH or serum bicarbonate concentration
Corrected Serum bicarb:
- a simple anion gap acidosis is the result of adding acid to the system. the extra acid reacts with bicarb, which is neutralized. we therefore lose a
bicarb ion, and the anion gap increases (excess anion gap). To see if there is more going on (ie an underlying metabolic akalosis or an additional nongap met acidosis, calculate the corrected serum bicarb:
1) Excess anion gap = measured gap - normal gap (usually 12)
2) corrected bicarb = excess gap + measured HCO3
Analysis of corrected serum bicarb
1) In a simple gap acidosis, the HCO3 falls by an amount equal to the excess gap (the excess acid consumes the bicarb) and the corrected bicarb will
be normal 22-26
2) if corrected bicarb is high (>30), there is an underlying metabolic alkalosis also
3) if corrected bicarb is low (<23), there is an additional non-gap acidosis
- renal compensations begin after several hours and is maximal at 4 days: suppression of acid secretion/production of bicarb, or excretion of
bicarb...the pH may fully correct.
- respiratory compensations occur immediately... the pH usually does not fully correct
- if compensation does not correlate with predictions, expect a mixed disorder
- Remember that the body does not fully compensate even for chronic acid-base disorders. Over time, the pH approaches, but does not completely
return to normal. This concept will help in determining the primary disorder (respiratory or metabolic) responsible for the acid - base abnormality.

Primary respiratory process: use the 0.08 and 0.03 rules to look PCO2 and calculate expected pH
In resp acidosis, for every increase in PCO2 by 10, expect pH to be decreased by 0.03 if chronic, full compensation has occurred, or 0.08 if acute,
limited compensation has occurred.
In resp alkalosis, for every decrease in PCO2 by 10, expect pH to elevated by 0.03 if chronic compensation, 0.08 if acute.
Primary metabolic process: look to see if PCO2 is in the range for simple compensation.
Met Acidosis: compare PCO2 to expected PCO2=1.5 x bicarb + 8 (+/- 2). IF PCO2 < expected, resp alk is present. If PCO2 > expected, resp
acidosis is present.
Met alkalosis: hypoventilation to compensate, ie will bring PCO2 above 40 but the PCO2 will never go above 50-55. If PCO2 > 50, there is a
primary respiratory acidosis to (pathologic hypoventilation), and the pH could be normal or acidemic. If PCO2 < 40, there is a primary resp
... To analyse a gas
1) determine acidemia vs alkalemia
2) determine primary disturbance(s)...look at PCO2 and HCO3
3) Then determine acute vs chronic (in resp disturbances) or in metabolic disturbances check if compensation (pCO2) is as expected for a simple
process, if not then a mixed d/o is present. For a gap metabolic acidosis also measure bicarb against its expected value.

for metabolic acidosis, det anion gap ... if hi gap, det corrected serum bicarb, to find out if there are other metabolic
disturbances (alkalosis or non-gap acidosis). Then check if there are additional respiratory disturbances, by checking the pCO2 against the expected
pCO2. (This can often be eyeballed by simply looking at the pCO2. If very high, a resp acidosis is obvious)
for metabolic alkalosis, PCO2 should be 40-50. If outside this range a respiratory process is also occuring.
(click for answers)

1. Respiratory Acidosis:
Respiratory acidosis results from hypoventilation which is manifested by the accumulation of CO 2 in the blood and a drop in blood pH. Examples of
specific causes can be categorized as follows:

Central Nervous System Depression (Sedatives, CNS disease, Obesity Hypoventilation syndrome)
Pleural Disease (Pneumothorax)
Lung Disease (COPD, pneumonia) s
Musculoskelatal disorders (Kyphoscoliosis, Guillain-Barre, Myasthenia Gravis, Polio)
2. Respiratory Alkalosis:
Respiratory alkalosis results from hyperventilation which is manifested by excess elimination of CO 2 from the blood and a rise in the blood pH.
Examples of specific causes are listed below:

Catastrophic CNS event (CNS hemorrhage)

Drugs (salicylates, progesterone)
Pregnancy (especially the 3rd trimester)
Decreased lung compliance (interstitial lung disease)
Liver cirrhosis
* note that deliberate respiratory alkalosis is induced to PaCO2 in the management of acutely increased ICP (CO2 causes
cerebral blood vessel dilation). A related note: the higher pH that results from respiratory (or metabolic) alkalosis is used in the treatment of PPHN to
dilate the pulmonary vasculature. So in the context of alkalosis, think of blood vessel shrinkage in the brain and dilation in the lungs.

3. Anion Gap Acidosis

Anion gap acidosis results from accumulation of acidic metabolites and is manifested by a low HCO 3- and an anion gap > 12. Examples of specific

Alcohol poisons or drug intoxication (methanol, ethylene glycol, paraldehyde, salicylates)

Inborn errors of metabolism
Anion Gap Acidosis:
M - Methanol
U - Uremia
D - DKA/AKA (EtOH w/drawal)
P - Paraldehyde/phenformin
I - Iron/INH/Inborn error of metabolism
L - Lactic acidosis
E - Ethylene glycol
S - Salicylates
One may use a mnemonic device to remember these items. MULEPAK is a mnemonic commonly used (Methanol, Uremia, Lactic acidosis, Ethylene
glycol intoxication, Paraldehyde intoxication, Aspirin, Ketoacidosis).
4. Non-Anion Gap Acidosis
Non-anion gap acidosis results from loss of bicarbonate or external acid infusion and is manifested by a low HCO 3-, but the anion gap is <12 (anion
gap calculation is discussed in step 3). Examples of specific causes:


GI loss of HCO3- (diarrhea)

Renal loss of HCO3Compensation for respiratory alkalosis
Carbonic anhydrase inhibitor (Diamox), acetazolamide)
Renal tubular acidosis
Ureteral diversion (ureterosigmoidostomy, small bowel fistula)
Other causes: extra chloride (HCl or NH4Cl infusion, Cl gas inhalation), Hyperalimentation, Addison disease,
A mnemonic device may be used to remember this list of causes. The commonly used mnemonic is ACCRUED (Acid
infusion/Acetazolamide, Compensation for respiratory alkalosis, Carbonic anhydrase inhibitor, Renal tubular acidosis, Ureteral diversion, Extra
alimentation or hyperalimentation, Diarrhea).
"HARDUP" Basically, bicarb losses through GI or renal.
H - Hyperalimentation/hyperventilation -> retention of acid/excretion of bicarb
A - Acetazolamide (carbonic anydrase inhibitor), aldosterone inhibitor, acid infusion
D - Diarrhea
U - Ureteral diversion
P - Pancreatic fistula/parenteral saline
5. Metabolic Alkalosis
Metabolic alkalosis results from elevation of serum bicarbonate. Examples of specific causes:

Volume contraction (vomiting, overdiuresis, ascites)

Alkali ingestion (bicarbonate)
Excess gluco- or mineralocorticoids
Bartter's syndrome (acts like a loop diuretic)