Archive for the ‘ L1-ABG ’ Category

L1- Arterial Blood Gas Interpretation

Arterial Blood Gas Interpretation

Normal Arterial Blood Gas Values*


The Key to Blood Gas Interpretation:

4 Equations, 3 Physiologic Processes


1) PaCO2 equation:

PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation




Hypercapnia (elevated PaCO2) is a serious respiratory problem.  The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the amount of the body’s CO2 production (VCO2).  Since alveolar ventilation (VA) equals total or minute ventilation (VE) minus dead space ventilation (VD), hypercapnia can arise from insufficient VE, increased VD, or a combination.


Examples of inadequate VE leading to decreased VA and increased PaCO2:  sedative drug overdose; respiratory muscle paralysis; central hypoventilation

Examples of increased VD leading to decreased VA and increased PaCO2:  chronic obstructive pulmonary disease; severe restrictive lung disease (with shallow, rapid breathing)

Clinical assessment of hypercapnia is unreliable

-The PaCO2 equation shows why PaCO2 cannot reliably be assessed clinically.  Since you never know the patient’s VCO2 or VA, you cannot determine the VCO2/VA, which is what PaCO2 provides.  (Even if tidal volume is measured, you can’t determine the amount of air going to dead space.)

-There is no predictable correlation between PaCO2 and the clinical picture.  In a patient with possible respiratory disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional change in PaCO2.  A patient in respiratory distress can have a high, normal, or low PaCO2.  A patient without respiratory distress can have a high, normal, or low PaCO2.

Dangers of hypercapnia

-Besides indicating a serious derangement in the respiratory system, elevated PaCO2 poses a threat for three reasons:

1)  An elevated PaCO2 will lower the PAO2 (see Alveolar gas equation), and as a result lower the PaO2.

2)  An elevated PaCO2 will lower the pH (see Henderson-Hasselbalch equation).

3)  The higher the baseline PaCO2, the greater it will rise for a given fall in alveolar ventilation, e.g., a 1 L/min decrease in VA will raise PaCO2 a greater amount when the baseline PaCO2 is 50 mm Hg than when it is 40 mm Hg.  (See next slide)

PCO2 vs. Alveolar Ventilation

-The relationship is shown for metabolic carbon dioxide production rates of 200 ml/min and 300 ml/min (curved lines).  A fixed decrease in alveolar ventilation (x-axis) in the hypercapnic patient will result in a greater rise in PaCO2 (y-axis) than the same VA change when PaCO2 is low or normal.  (This situation is analogous to the progressively steeper rise in BUN as glomerular filtration rate declines.)

-This graph also shows that, if alveolar ventilation is fixed, an increase in carbon dioxide production will result in an increase in PaCO2.



1.  What is the PaCO2 of a patient with respiratory rate 24/min, tidal volume 300 ml, dead space volume 150 ml, CO2 production 300 ml/min?  The patient shows some evidence of respiratory distress.

2.  What is the PaCO2 of a patient with respiratory rate 10/min, tidal volume 600 ml, dead space volume 150 ml, CO2 production 200 ml/min?  The patient shows some evidence of respiratory distress.

3.  A man with severe chronic obstructive pulmonary disease  exercises on a treadmill at 3 miles/hr.  His rate of CO2 production increases by 50% but he is unable to augment alveolar ventilation.  If his resting PaCO2 is 40 mm Hg and resting VCO2 is 200 ml/min, what will be his exercise PaCO2?


1.  First, you must calculate the alveolar ventilation.  Since minute ventilation is 24 x 300 or 7.2 L/min, and dead space ventilation is 24 x 150 or 3.6 L/min, alveolar ventilation is 3.6 L/min.  Then


2.   VA  = VE – VD

= 10(600) – 10(150)

= 6 – 1.5 = 4.5 L/min



Exercise increases metabolic CO2 production.  People with a normal respiratory

system are always able to augment alveolar ventilation to meet or exceed the

amount of  VA necessary to excrete any increase in CO2 production.  As in this

example, patients with severe COPD or other forms of chronic lung disease

may not be able to increase their alveolar ventilation, resulting in an increase in

PaCO2.  This patient’s resting alveolar ventilation is


Since CO2 production increased by 50% and alveolar ventilation not at all, his exercise PaCO2 is


2) Alveolar Gas Equation

PAO2 = PIO2 – 1.2 (PaCO2)*

-where PAO2 is the average alveolar PO2, and PIO2 is the partial pressure of inspired oxygen in the trachea.

PIO2  =  FIO2 (PB – 47 mm Hg)

-FIO2 is fraction of inspired oxygen and PB is the barometric pressure.  47 mm Hg is the water vapor pressure at normal body temperature.

*Note:  This is the ‘abbreviated version’ of the AG equation, suitable for most clinical purposes.  In the longer version, the multiplication factor “1.2” declines with increasing FIO2, reaching zero when 100% oxygen is inhaled.  In these exercises “1.2” is dropped when FIO2 is above 60%.
PAO2 = PIO2 – 1.2 (PaCO2)
where PIO2  =  FIO2 (PB – 47 mm Hg)

-Except in a temporary unsteady state, alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2).  As a result, whenever PAO2 decreases, PaO2 does as well.  Thus, from the AG equation:

-nIf FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia). nIf FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease (suffocation causes hypoxemia). nIf PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease (mountain climbing causes hypoxemia).


1.  What is the PAO2 at sea level in the following

circumstances?  (Barometric pressure = 760 mm Hg)

a)  FIO2 = 1.00, PaCO2 = 30 mm Hg

b)  FIO2 = .21, PaCO2 = 50 mm Hg

c)  FIO2 = .40, PaCO2 = 30 mm Hg

2.  What is the PAO2 on the summit of Mt. Everest in the following

circumstances?  (Barometric Pressure = 253 mm Hg)

a)  FIO2 = .21, PaCO2 = 40 mm Hg

b)  FIO2 = 1.00, PaCO2 = 40 mm Hg

c)  FIO2 = .21, PaCO2 = 10 mm Hg


1.  To calculate PAO2 the PaCO2 must be subtracted from the PIO2.  Again, the barometric pressure is 760 mm Hg since the values are obtained at sea level.  In part

a),   the PaCO2 of 30 mm Hg is not multiplied by 1.2 since the FIO2 is 1.00.

In parts b) and c)   the factor 1.2 is multiplied times the PaCO2.

a)  PAO2 = 1.00(713) – 30 = 683 mm Hg

b)  PAO2 =  .21(713) – 1.2(50) = 90 mm Hg

c)  PAO2 =  .40(713) – 1.2(30) = 249 mm Hg

2.  The PAO2 on the summit of Mt. Everest is calculated just as at sea level, using the barometric pressure of 253 mm Hg.

a)  PAO2 = .21(253 – 47) – 1.2(40) = – 5 mm Hg

b)  PAO2 = 1.00(253 – 47) – 40 = 166 mm Hg

c)  PAO2 = .21(253 – 47) – 1.2(10) = 31 mm Hg

3) Oxygen Content Equation = P(A-a)O2

-P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen.  It is commonly called the “A-a gradient,” though it does not actually result from an O2 pressure gradient in the lungs.  Instead, it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance).

-PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure.

-PaO2 is always measured, on an arterial blood sample in a ‘blood gas machine’.

-Normal P(A-a)O2  ranges from @ 5 to 25 mm Hg breathing room air (it increases with age).  A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries.  Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of  problem within the lungs.

Physiologic causes of low PaO2


Ventilation-Perfusion imbalance

-A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O2.

-By far the most common cause of low PaO2 is an abnormal degree of ventilation-perfusion  imbalance within the hundreds of millions of  alveolar-capillary units.  Virtually all lung disease lowers PaO2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary edema, COPD.

-Diffusion barrier is seldom a major cause of low PaO2 (it can lead to a low PaO2 during exercise).


3.  For each of the following scenarios, calculate the P(A-a)O2 using the abbreviated alveolar gas equation; assume PB = 760 mm Hg.  Which of these patients is most likely to have lung disease?  Do any of the values represent a measurement or recording error?

a)   A 35-year-old man with PaCO2 50 mm Hg, PaO2 150 mm Hg, FIO2 .40.

b)   A 44-year-old woman with PaCO2 75 mm Hg, PaO2 95 mm Hg, FIO2 0.28.

c)   A young, anxious man with PaO2 120 mm Hg, PaCO2 15 mm Hg, FIO2 0.21.

d)   A woman in the intensive care unit with PaO2 350 mm Hg, PaCO2 40 mm Hg, FIO2 0.80.

e)    A man with PaO2 80 mm Hg, PaCO2 72 mm Hg, FIO2 0.21.



a)  PAO2 = .40 (760 – 47) – 1.2(50) = 225 mm Hg; P(A-a)O2 = 225 – 150 = 75 mm Hg

The P(A-a)O22 is elevated but actually within the expected range for supplemental oxygen at 40%, so the patient may or may not have a defect in gas exchange.

b)  PAO2 = .28(713) – 1.2(75) = 200 – 90 = 110 mm Hg; P(A-a)O2 = 110 – 95 = 15 mm Hg

Despite severe hypoventilation, there is no evidence here for lung disease.  Hypercapnia is most likely a result of disease elsewhere in the respiratory system, either the central nervous system or chest bellows.

c)  PAO2 = .21(713) – 1.2(15) = 150 – 18 = 132 mm Hg; P(A-a)O2 = 132 – 120 = 12 mm Hg

Hyperventilation can easily raise PaO2 above 100 mm Hg when the lungs are normal, as in this case.

d)  PAO2 = .80 (713) – 40 = 530 mm Hg (Note that the factor 1.2 is dropped since FIO2 is above 60%)

P(A-a)O2 = 530 – 350 = 180 mm Hg

P(A-a)O2 is increased.  Despite a very high PaO2, the lungs are not transferring oxygen normally.

e)  PAO2 = .21 (713) – 1.2(72) = 150 – 86 = 64 mm Hg; P(A-a)O2 = 64 – 80 = -16 mm Hg

A negative P(A-a)O2 is incompatible with life (unless it is a transient unsteady state, such as sudden fall in FIO2 — not the case here).  In this example, negative P(A-a)O2 can be explained by any of the following:  incorrect FIO2, incorrect blood gas measurement, or a reporting or transcription error.

SaO2 and oxygen content CAO2

-Tissues need a requisite amount of oxygen molecules for metabolism.  Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood.  How much is provided by the oxygen content, CaO2 (units = ml O2/dl).  CaO2 is calculated as:

CaO2 =  quantity O2 bound to hemoglobin   +     quantity O2 dissolved in plasma

CaO2 =  (Hb x 1.34 x SaO2)   +      (.003 x PaO2)

-Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma:  .003 ml dissolved O2/mm Hg PO2.

Oxygen dissociation curve:  SaO2 vs. PaO2

-Also shown are CaO2 vs. PaO2 for two different hemoglobin contents:

15 gm% and 10 gm%.  CaO2 units are ml O2/dl.

P50 is the PaO2 at which SaO2 is 50%.

Point ‘X’ is discussed on later slide.


SaO2 – is it calculated or measured?

-You always need to know this when confronted with blood gas data.

-SaO2 is measured in a ‘co-oximeter’.  The traditional ‘blood gas machine’ measures only pH, PaCO2 and PaO2,, whereas the co-oximeter measures SaO2, carboxyhemoglobin, methemoglobin and hemoglobin content.  Newer ‘blood gas’ consoles incorporate a co-oximeter, and so offer the latter group of measurements as well as pH, PaCO2 and PaO2.

-You should always make sure the SaO2 is measured, not calculated.  If it is  calculated from the PaO2 and the O2-dissociation curve, it provides no new information, and could be inaccurate — especially in states of CO intoxication or excess methemoglobin.  CO and metHb do not affect PaO2, but do lower the SaO2.

Carbon monoxide – an important cause of hypoxemia

-Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO (higher in traffic-congested areas)

-CO is colorless, odorless gas, a product of combustion; all smokers have excess CO in their blood, typically 5-10%.

-CO binds @ 200x more avidly to hemoglobin than O2, effectively displacing O2 from the heme binding sites.  CO is a major cause of poisoning deaths world-wide.

-CO has a ‘double-whammy’ effect on oxygenation:

1) decreases SaO2 by the amount of %COHb present, and

2) shifts the O2-dissociation curve to the left, retarding unloading of oxygen to the tissues.

-CO does not affect PaO2, only SaO2.  To detect CO poisoning, SaO2 and/or COHb must be measured (requires co-oximeter).  In the presence of excess CO, SaO2 (when measured) will be lower than expected from the PaO2.

CO does not affect PaO2 – be aware!

-Review the O2 dissociation curve shown on a previous slide.  ‘X’ represents the 2nd set of blood gases for a patient who presented to the ER with headache and dyspnea.

-His first blood gases showed PaO2 80 mm Hg, PaCO2 38 mm Hg, pH 7.43.  SaO2 on this first set was calculated from the O2-dissociation curve at 97%, and oxygenation was judged normal.

-He was sent out from the ER and returned a few hours later with mental confusion; this time both SaO2 and COHb were measured (SaO2 shown by ‘X’):  PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2 53%, carboxyhemoglobin 46%.

-CO poisoning was missed on the first set of blood gases because SaO2 was not measured!

Causes of Hypoxia
A General Classification

1.  Hypoxemia (=low PaO2 and/or low CaO2)

  • a.  reduced PaO2 – usually from lung disease (most common physiologic mechanism:  V-Q imbalance)
  • b.  reduced SaO2 — most commonly from reduced PaO2; other  causes include carbon monoxide poisoning, methemoglobinemia, or rightward shift of the O2-dissociation curve
  • c.  reduced hemoglobin content — anemia

2.  Reduced oxygen delivery to the tissues

  • a.  reduced cardiac output — shock, congestive heart failure
  • b.  left to right systemic shunt (as may be seen in septic shock)

3.  Decreased tissue oxygen uptake

  • a.  mitochondrial poisoning (e.g., cyanide poisoning)
  • b.  left-shifted hemoglobin dissociation curve (e.g., from acute alkalosis, excess CO, or abnormal hemoglobin structure)

How much oxygen is in the blood, and is it adequate for the patient?
PaO2 vs. SaO2 vs. CaO2

-The answer must be based on some oxygen value, but which one? Blood gases give us three different oxygen values:  PaO2, SaO2, and CaO2 (oxygen content).

-Of these three values, PaO2, or oxygen pressure, is the least helpful to answer the question about oxygen adequacy in the blood.  The other two values — SaO2 and CaO2 — are more useful for this purpose.


-Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin, PaO2 cannot tell us “how much” oxygen is in the blood; for that you need to know how much oxygen is also bound to hemoglobin, information given by the SaO2 and hemoglobin content.


-The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO2).  Note that SaO2 alone doesn’t reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content.


-Tissues need a requisite amount of O2 molecules for metabolism.  Neither the PaO2 nor the SaO2 provide information on the number of oxygen molecules, i.e., how much oxygen is in the blood.  (Neither PaO2 nor SaO2 have units that denote any quantity.)  Only CaO2 (units ml O2/dl) tells us how much oxygen is in the blood; this is because CaO2 is the only value that incorporates the hemoglobin content.  Oxygen content can be measured directly or calculated by the oxygen content equation:

CaO2 =  (Hb x 1.34 x SaO2)   +   (.003 x PaO2)


Below are blood gas results from four pairs of patients.  For each letter pair, state which patient, (1) or (2), is more hypoxemic.  Units for hemoglobin content (Hb) are gm% and for PaO2 mm Hg.

a)  (1)  Hb 15, PaO2 100, pH 7.40, COHb 20%

(2)  Hb 12, PaO2 100, pH 7.40, COHb 0

b)  (1)  Hb 15, PaO2 90, pH 7.20, COHb 5%

(2)  Hb 15, PaO2 50, pH 7.40, COHb 0

c)  (1)  Hb 5, PaO2 60, pH 7.40, COHb 0

(2)  Hb 15, PaO2 100, pH 7.40, COHb 20%

d)  (1)  Hb 10, PaO2 60, pH 7.30, COHb 10%

(2)  Hb 15, PaO2 100, pH 7.40, COHb 15%



(1)  CaO2 = .78 x 15 x 1.34 = 15.7 ml O2/dl

(2)  CaO2 = .98 x 12 x 1.34 = 15.8 ml O2/dl

The oxygen contents are almost identical, and therefore neither patient is more hypoxemic.  However, patient (1), with 20% CO, is more hypoxic than patient (2) because of the left-shift of the O2-dissociation curve caused by the excess CO.


(1)  CaO2 = .87 x 15 x 1.34 = 17.5 ml O2/dl

(2)  CaO2 = .85 x 15 x 1.34 = 17.1 ml O2/dl

A PaO2 of 90 mm Hg with pH of 7.20 gives an SaO2 of @ 92%; subtracting 5% COHb from this value gives a true SaO2 of 87%, used in the CaO2 calculation of patient (1).  A PaO2 of 50 mm Hg with normal pH gives an SaO2 of 85%.  Thus patient (2) is slightly more hypoxemic.


(1)  CaO2 = .90 x 5 x .1.34 = 6.0 ml O2/dl

(2)  CaO2 = .78 x 15 x 1.34 = 15.7 ml O2/dl

Patient (1) is more hypoxemic, because of severe anemia.


(1)  CaO2 = .87 x 10 x .1.34 = 11.7 ml O2/dl

(2)  CaO2 = .83 x 15 x 1.34 = 16.7 ml O2/dl

Patient (1) is more hypoxemic.

4) Henderson Hasselbalch Equation (Acid-Base Balance)


-For teaching purposes, the H-H  equation can be shortened to its basic relationships:

Picture2-pH is inversely related to [H+]; a pH change of 1.00 represents a
10-fold change in [H+]


Acid base terminology

Acidemia:  blood pH < 7.35

Acidosis:  a primary physiologic process that, occurring alone, tends to cause acidemia, e.g.:  metabolic acidosis from decreased perfusion (lactic acidosis); respiratory acidosis from hypoventilation.  If the patient also has an alkalosis at the same time, the resulting blood pH may be low, normal or high.

Alkalemia:  blood pH > 7.45

Alkalosis:  a primary physiologic process that, occurring alone, tends to cause alkalemia.  Examples:  metabolic alkalosis from excessive diuretic therapy; respiratory alkalosis from acute hyperventilation.  If the patient also has an acidosis at the same time, the resulting blood pH may be high, normal or low.

Primary acid-base disorder:  One of the four acid-base disturbances that is manifested by an initial change in HCO3- or PaCO2.  They are:  metabolic acidosis (MAc), metabolic alkalosis (MAlk), respiratory acidosis (RAc), and respiratory alkalosis (RAlk).  If HCO3- changes first, the disorder is either MAc (reduced HCO3- and acidemia) or MAlk (elevated HCO3- and alkalemia).  If PaCO2 changes first, the problem is either RAlk (reduced PaCO2 and alkalemia) or RAc (elevated PaCO2 and acidemia).

Compensation:  The change in HCO3- or PaCO2 that results from the primary event.  Compensatory changes are not classified by the terms used for the four primary acid-base disturbances.  For example, a patient who hyperventilates (lowers PaCO2) solely as compensation for MAc does not have a RAlk, the latter being a primary disorder that, alone, would lead to alkalemia.  In simple, uncomplicated MAc the patient will never develop alkalemia.

Primary acid-base disorders

-Respiratory alkalosis

Respiratory alkalosis – A primary disorder where the first change is a lowering of PaCO2, resulting in an elevated pH.  Compensation (bringing the pH back down  toward normal) is a secondary lowering of  bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not metabolic acidosis, since it is not a primary process.

-Respiratory acidosis

Respiratory acidosis – A primary disorder where the first change is an elevation of PaCO2, resulting in decreased pH.  Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO3- is not metabolic alkalosis, since it is not a primary process.

-Metabolic acidosis

Metabolic Acidosis – A primary acid-base disorder where the first change is a lowering of HCO3-, resulting in decreased pH.  Compensation (bringing pH back up toward normal) is a secondary hyperventilation; this lowering of PaCO2 is not respiratory alkalosis, since it is not a primary process.

-Metabolic alkalosis

Metabolic alkalosis – A primary acid-base disorder where the first change is an elevation of HCO3-, resulting in increased pH.  Compensation is a secondary hypoventilation (increased PaCO2) which is not respiratory acidosis, since it is not a primary process.  Compensation for metabolic alkalosis (attempting to bring pH back down toward normal) is less predictable than for the other three acid-base disorders.

Anion Gap

Metabolic acidosis is conveniently divided into elevated and normal anion gap (AG) acidosis.  AG is calculated as

AG = Na+  –  (Cl-  +  CO2)

Note:  CO2 in this equation is the “total CO2” measured in the chemistry lab as part of routine serum electrolytes, and consists mostly of bicarbonate.  Normal AG is typically 12 ± 4 mEq/L.  If AG is calculated using K+, the normal AG is 16 ± 4 mEq/L.  Normal values for AG may vary among labs, so one should always refer to local normal values before making clinical decisions based on the AG.

Metabolic Acid-Base Disorders

— Some clinical causes —


•Increased anion gap –lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethyelene glycol, methanol) •Normal anion gap –diarrhea; some kidney problems, e.g., renal tubular acidosis, intersititial nephritis


«Chloride responsive (responds to NaCl or KCl therapy):  contraction alkalosis, diuretics; corticosteroids; gastric suctioning; vomiting Chloride resistant:  any hyperaldosterone state, e.g., Cushings’s syndrome; Bartter’s syndrome; severe K+ dep

Respiratory Acid-Base Disorders

— Some clinical causes —


Central nervous system depression (e.g., drug overdose)

Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema)


Hypoxemia (includes altitude)



Any acute pulmonary insult, e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism

Mixed Acid-base disorders are common

-In chronically ill respiratory patients, mixed disorders are probably more common than single disorders, e.g., RAc + MAlk, RAc + Mac,       Ralk + MAlk.

-In renal failure (and other patients) combined MAlk + MAc is also encountered.

-Always be on lookout for mixed acid-base disorders.  They can be missed!

Tips to diagnosing mixed acid-base disorders

TIP 1.  Don’t interpret any blood gas data for acid-base diagnosis without closely examining the serum electrolytes:  Na+, K+, Cl- and CO2.

-A serum CO2 out of the normal range always represents some type of acid-base disorder (barring lab or transcription error).

-High serum CO2 indicates metabolic alkalosis &/or bicarbonate retention as compensation for respiratory acidosis

-Low serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis

-Note that serum CO2 may be normal in the presence of two or more acid-base disorders.

TIP 2 .  Single acid-base disorders do not lead to normal blood pH.  Although pH can end up in the normal range (7.35 – 7.45) with a mild single disorder, a truly normal pH with distinctly abnormal HCO3- and PaCO2 invariably suggests two or more primary disorders.

-Example:  pH 7.40, PaCO2 20 mm Hg, HCO3- 12 mEq/L, in a patient with sepsis.  Normal pH results from two co-existing and unstable acid-base disorders:  acute respiratory alkalosis and metabolic acidosis.

TIP 3.  Simplified rules predict the pH and HCO3- for a given change in PaCO2.  If the pH or HCO3- is higher or lower than expected for the change in PaCO2, the patient probably has a metabolic acid-base disorder as well.

-The next slide shows expected changes in pH and HCO3- (in mEq/L) for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis).

-Expected changes in pH and HCO3- for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis).


Predicted changes in HCO3- for a directional change in PaCO2 can help uncover mixed acid-base disorders.

a)   A normal or slightly low HCO3- in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO2 50 mm Hg, HCO3- 22 mEq/L.  Based on the rule for increase in HCO3- with hypercapnia, it should be at least 25 mEq/L in this example; that it is only 22 mEq/L suggests a concomitant metabolic acidosis.

b)  A normal or slightly elevated HCO3- in the presence of hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30 mm Hg, HCO3- 26 mEq/L.  Based on the rule for decrease in HCO3 with hypocapnia, it should be at least 23 mEq/L in this example; that it is 26 mEq/L suggests a concomitant metabolic alkalosis.

TIP 4.  In maximally-compensated metabolic acidosis, the numerical value of PaCO2 should be the same (or close to) the last two digits of arterial pH.  This observation reflects the formula for  expected respiratory compensation in metabolic acidosis:

-Expected PaCO2 = [1.5 x serum CO2] + (8 ± 2)

-In contrast, compensation for metabolic alkalosis (by increase in PaCO2) is highly variable, and in some cases there may be no or minimal compensation.


1.   A patient’s arterial blood gas shows pH of 7.14, PaCO2 of 70 mm Hg, and HCO3- of 23 mEq/L.  How would you describe the likely acid-base disorder(s)?

2.  A 45-year-old man comes to hospital complaining of dyspnea for three days.  Arterial blood gas reveals pH 7.35, PaCO2 60 mm Hg, PaO2 57 mm Hg, HCO3- 31 mEq/L.  How would you characterize his acid-base status?

3.  State whether each of the following statements is true or false.

a)  Metabolic acidosis is always present when the measured serum CO2 changes acutely from 24 to 21 mEq/L.

b)  In acute respiratory acidosis, bicarbonate initially rises because of the reaction of CO2 with water and the resultant formation of H2CO3.

c)  If pH and PaCO2 are both above normal, the calculated bicarbonate must also be above normal.

d)  An abnormal serum CO2 value always indicates an acid-base disorder of some type.

e)  The compensation for chronic elevation of PaCO2 is renal excretion of bicarbonate.

f)  A normal pH with abnormal HCO3- or PaCO2 suggests the presence of two or more acid-base disorders.

g)  A normal serum CO2 value indicates there is no acid-base disorder.

h)  Normal arterial blood gas values rule out the presence of an acid-base disorder.


1. Acute elevation of PaCO2 leads to reduced pH, i.e., an acute respiratory acidosis.  However, is the problem only acute respiratory acidosis or is there some additional process?  For every 10 mm Hg rise in PaCO2 (before any renal compensation), pH falls about 0.07 units.  Because this patient’s pH is down 0.26, or 0.05 more than expected for a 30 mm Hg increase in PaCO2, there must be an additional, metabolic problem.  Also, note that with acute CO2 retention of this degree, the HCO3- should be elevated 3 mEq/L.  Thus a low-normal HCO3- with increased PaCO2 is another way to uncover an additional, metabolic disorder.  Decreased perfusion leading to mild lactic acidosis would explain the metabolic component.

2.  PaCO2 and HCO3- are elevated, but HCO3- is elevated more than would be expected from acute respiratory acidosis.  Since the patient has been dyspneic for several days it is fair to assume a chronic acid-base disorder.  Most likely this patient has a chronic or partially compensated respiratory acidosis.  Without electrolyte data and more history, you cannot diagnose an accompanying metabolic disorder.


a)  false

b)  true

c)  true

d)  true

e)  false

f)  true

g)  false

Summary Clinical and laboratory approach to acid-base diagnosis

-Determine existence of acid-base disorder from arterial blood gas and/or serum electrolyte measurements.  Check serum CO2; if abnormal there is an acid-base disorder.  If the anion gap is significantly increased there is a metabolic acidosis.

Examine pH, PaCO2 and HCO3- for the obvious primary acid-base disorder, and for deviations that indicate mixed acid-base disorders (TIPS 2 through 4).

-Use a full clinical assessment (history, physical exam, other lab data including previous arterial blood gases and serum electrolytes) to explain each acid-base disorder.  Remember that co-existing clinical conditions may lead to opposing acid-disorders, so that pH can be high when there is an obvious acidosis, or low when there is an obvious alkalosis.

-Treat the underlying clinical condition(s); this will usually suffice to correct most acid-base disorders.  If there is concern that acidemia or alkalemia is life-threatening, aim toward correcting pH into the range of 7.30-7.52 ([H+] = 50-30 nM/L).

-Clinical judgment should always apply

Arterial Blood Gases – test your overall understanding

Case 1.

A 55-year-old man is evaluated in the pulmonary lab for shortness of breath.  His regular medications include a diuretic for hypertension and one aspirin a day.  He smokes a pack of cigarettes a day.

FIO2      0.21

HCO3-   30 mEq/L

pH           7.53

%COHb  7.8%

PaCO2    37 mm Hg

Hb            14 gm%

PaO2        62 mm Hg

CaO2        16.5 ml O2

SaO2        87%

How would you characterize his state of oxygenation, ventilation and acid-base balance?

Case 1 – Discussion.

OXYGENATION:  The PaO2 and SaO2 are both reduced on room air.  Since  P(A-a)O2 is elevated (approximately 43 mm Hg), the low PaO2 can be attributed to V-Q imbalance, i.e., a pulmonary problem.  SaO2 is reduced, in part from the low PaO2 but mainly from elevated carboxyhemoglobin, which in turn can be attributed to cigarettes.  The arterial oxygen content is adequate.

VENTILATION:  Adequate for the patient’s level of CO2 production; the patient is neither hyper- nor hypo- ventilating.

ACID-BASE:  Elevated pH and HCO3- suggest a state of metabolic alkalosis, most likely related to the patient’s diuretic; his serum K+ should be checked for hypokalemia.

Case 2.

A 46-year-old man has been in the hospital two days, with pneumonia.  He was recovering but has just become diaphoretic, dyspneic and hypotensive.  He is breathing oxygen through a nasal cannula at 3 l/min.

pH   7.40

PaCO2  20 mm Hg

%COHb  1.0%

PaO2  80 mm Hg

SaO2   95%

Hb  13.3 gm%

HCO3-  12 mEq/L

CaO2  17.2 ml O2

How would you characterize his state of oxygenation, ventilation and acid-base balance?

Case 2 – Discussion.

OXYGENATION:  The PaO2 is lower than expected for someone hyperventilating to this degree and receiving supplemental oxygen, and points to significant V-Q imbalance.  The oxygen content is adequate.

VENTILATION:   PaCO2 is half normal and indicates marked hyperventilation.

ACID-BASE:  Normal pH with very low bicarbonate and PaCO2 indicates combined respiratory alkalosis and metabolic acidosis.  If these changes are of sudden onset the diagnosis of sepsis should be strongly considered, especially in someone with a documented infection.

Case 3.

A 58-year-old woman is being evaluated in the emergency department for acute dyspnea.

FIO2  .21

pH   7.19

PaCO2  65 mm Hg

%COHb  1.1%

PaO2  45 mm Hg

SaO2   90%

Hb  15.1 gm%

HCO3-  24 mEq/L

CaO2  18.3 ml O2

How would you characterize her state of oxygenation, ventilation and acid-base balance?

Case 3 – Discussion.

OXYGENATION:  The patient’s PaO2 is reduced for two reasons:  hypercapnia and V-Q imbalance, the latter apparent from an elevated P(A-a)O2 (approximately 27 mm Hg).

VENTILATION:  The patient is hypoventilating.

ACID-BASE:  pH and PaCO2 are suggestive of acute respiratory acidosis plus metabolic acidosis; the calculated HCO3- is lower than expected from acute respiratory acidosis alone.

Case 4.

A 23-year-old man is being evaluated in the emergency room for severe pneumonia.  His respiratory rate is 38/min and he is using accessory breathing muscles.

FIO2  .90  Na+  154  mEq/L

pH   7.29  K+  4.1 mEq/L

PaCO2  55 mm Hg  Cl-  100 mEq/L

PaO2  47 mm Hg  CO2  24 mEq/L

SaO2   86%

HCO3-  23 mEq/L

%COHb  2.1%

Hb  13 gm%

CaO2  15.8 ml O2

How would you characterize his state of oxygenation, ventilation and acid-base balance?

Case 4 – Discussion.

OXYGENATION:  The PaO2 and SaO2 are both markedly reduced on 90% inspired oxygen, indicating severe ventilation-perfusion imbalance.

VENTILATION:  The patient is hypoventilating despite the presence of tachypnea, indicating significant dead space ventilation.  This is a dangerous situation that suggests the need for mechanical ventilation.

ACID-BASE:  The low pH, high PaCO2 and slightly low calculated HCO3- all point to combined acute respiratory acidosis and metabolic acidosis.  Anion gap is elevated to 30 mEq/L indicating a clinically significant anion gap (AG) acidosis, possibly from lactic acidosis.  With an of AG of 30 mEq/L his serum CO2  should be much lower, to reflect buffering of the increased acid.  However, his serum CO2  is near normal, indicating a primary process that is increasing it, i.e., a metabolic alkalosis in addition to a metabolic acidosis. The cause of the alkalosis is as yet undetermined.  In summary this patient has respiratory acidosis, metabolic acidosis and metabolic alkalosis.