Zacharia Grami

5/1/2017
PBL
Learning Issue:
Use and Interpretation of ABGs

The ABG consists of several values, including pH, SaO2, PaO2, [HCO3-], PaCO2; important non-gas values used in
ABG interpretation include Na+ and Cl-. From the aforementioned value, the A-a gradient, anion gap and delta gap will be
calculated; some sources suggest calculating base excess as well. Interpreting the ABG is utilized in assessing the acid-base
status of the patient, via establishing the simple acidemic or alkalemic state, as well as via establishing the acidosis and alkalosis
mechanisms present. Interpreting the ABG requires a step-wise approach; below I will be describing my approach from my
review of the literature.
First and foremost, a working knowledge of normal values is needed. See Table 1.
Table 1: Normal ABG Values (Theodore & Manaker, 2017) (Altalag, Road, & Wilcox, 2009)
pH 7.40; 7.35-7.45
PaCO2 ~40; 35-45 mmHg
PaO2 >80mmHg; empirical; value where tissue hypoxia occurs has not been defined
SaO2 >95%; empirical; value where tissue hypoxia has not been defined
-
[HCO3 ] ~24; 21-27 mEq/L
P(A-a)O2 10-15 mmHg; predict nl with (Age/4) + 4
PAO2 = PIO2 – PaCO2/R; use to calculate the P(A-a)O2

The steps of my approach to the simplistic interpretation of an ABG are as follows:

1. Evaluate SaO2 and PaO2 to determine whether a hypoxemia is present; if so, begin evaluation to determine the cause of
this condition. See Figure 1, (West & Luks, 2012). If needed, calculate PAO2 for the A-a gradient.

Figure 1: Features of Different Types of Hypoxemia or Tissue Hypoxia (West & Luks, 2012)
 2. Check pH to determine whether pH is normal, acidemic or alkalemic. pH lower than normal is acidemic, pH higher
than normal is alkalemic.
a. Note: At this point, it is a good time to establish the difference between acidemic and acidosis, and vice versa
for the alkaline; emic states refer to the blood pH, while the osis refers to the physiologic process and how it
contributes to the overall pH.
3. Determine whether the predominant process is metabolic or respiratory.
a. This process is fairly intuitive in clinical cases for our purposes; respiratory processes modulate PaCO2 levels
while metabolic processes modulate HCO3- levels. See Table 2.
b. An example of this is as follows: If the patient is acidemic and PaCO2 is high, the expected HCO3= is higher
and the process is respiratory. Note that the fluctuation in PaCO2 matches the expected change in pH while
the HCO3= moves in an opposite direction.
Table 2: Assessing Metabolic or Respiratory Basis of Acidemia or Alkalemia

Respiratory Acidosis Predominated High PaCO2; Expected High HCO3=

Respiratory Alkalosis Predominated Low PaCO2; Expected Low HCO3=
Metabolic Acidosis Predominated Low HCO3=; Expected Low PaCO2
Metabolic Alkalosis Predominated High HCO3=; Variable Presence - High PaCO2
4. Determine the compensation (Berend, de Vries, & Gans, 2014).
a. This varies depending on whether the predominant process is metabolic or respiratory; in metabolic
processes, reliable prediction of compensation can be gauged by the winter’s formula only for metabolic
acidosis.
b. Metabolic Causes
i. Metabolic Acidosis:
1. Winters Formula for Expected PaCO2 = 1.5[HCO3-]+8 ± 2; (Berend, de Vries, & Gans,
2014)
2. If PaCO2 is less than expected, there is a concomitant respiratory alkalosis.
3. If PaCO2 is more than expected, there is a concomitant respiratory acidosis.
ii. Metabolic Alkalosis
1. Complex formulae do exist, but are not reliable at predicting the secondary respiratory
response in metabolic alkalosis (Berend, de Vries, & Gans, 2014). One such formula is
a. Predicted PaCO2 = 0.7 * [HCO3-] + 20 mmHg
c. Respiratory Causes – underlined are the most important as the others are intuitive.
i. Respiratory Acidosis
1. Concomitant Metabolic Acidosis: < 1 mmol/L increase in [HCO3-] per 10 PaCO2 > 40.
2. Acute: 1 mmol/L increase in [HCO3-] per 10 PaCO2 > 40.
3. Chronic: 5 mmol/L increase in [HCO3-] per 10 PaCO2 > 40
4. Concomitant Metabolic Alkalosis: > 5 mmol/L increase in [HCO3-] per 10 PaCO2 > 40
ii. Respiratory Alkalosis
1. Concomitant Metabolic Alkalosis: <2 mmol/L decrease in [HCO3-] per PaCO2 < 40.
2. Acute: 2 mmol/L decrease in [HCO3-] per 10 PaCO2 < 40.
3. Chronic: 5 mmol/L decrease in [HCO3-] per 10 PaCO2 < 40.
4. Concomitant Metabolic Acidosis: > 5 mmol/L decrease in [HCO3-] per 10 PaCO2 > 40.
 d. To Summarize the Compensation in another format, see Table 3.
Table 3: Summary of Determination of Duration and Compensation in Acid-Base Disturbances
State Compensation
Respiratory Alkalosis, Acute HCO3- drop of 2 per 10 drop in PaCO2
Respiratory Alkalosis, Chronic HCO3- drop of 5 per 10 drop in PaCO2
Respiratory Acidosis, Acute HCO3- rise of 1 per 10 drop in PaCO2
Respiratory Acidosis, Chronic HCO3- rise of 5 per 10 drop in PaCO2
Metabolic Acidosis Pred PaCO2 = 1.5[HCO3-]+8 ± 2
Metabolic Alkalosis Not reliable to predict.

5. Begin to determine the etiologic agent of the disturbance (Berend, de Vries, & Gans, 2014).
a. Respiratory Acidosis
i. Determine the A-a gradient. See Table 1.
ii. Normal – Hypoventilation without intrinsic lung disease (Hypoventilation, High Altitude)
iii. High – hypoventilation with intrinsic lung disease, v/q mismatch, both.
b. Metabolic Acidosis
i. Determine the anion gap: AG = [Na+] – [HCO3- + Cl-]; correct for albumin, where each albumin
drop of 1 g/dL increases the anion gap by 2.5; normal AG is 12.
ii. Normal AG: HARDASS (FirstAid) – Hyperalimentation, Addison, Renal TA, Diarrhea,
Acetazolamide, Spironolactone, Saline Infusion
iii. High AG: MUDPILES (FirstAid) – Methanol, Uremia, DKA, Propyelene Glycol, Iron/INH, Lactic
Acidosis, Ethylene Glycol, Salicylates
c. Respiratory Alkalosis
i. Again, consider evaluating the A-a gradient.
ii. Normal – Hyperventilation without intrinsic lung disease, including fever, pregnancy.
iii. High -- Hyperventilation with intrinsic lung disease, v/q mismatch, both.
iv. Causes from FirstAid include: Hysteria, Hypoxemia, Tumor, Pulmonary Embolism
d. Metabolic Alkalosis
i. HCO3- excess or H+ loss from loop diuretics, vomiting, antacid use, hyperaldosteronism.

Anion Gap and Non-Ion Gap Disturbances

There are some sources that suggest calculation the anion gap in every patient (Sherman, 2009). In cases where the

anion gap is increased (when corrected for albumin, as above in step 5.b.i, or when compared to the patient’s baseline) there is

the presence of an anion gap metabolic acidosis (AGMA), either concomitant or predominating (there is another negative ion

present that is acid derived).

In cases of metabolic acidosis, the delta gap is to be calculated as well (Sherman, 2009) (Altalag, Road, & Wilcox,

2009); the basis of the delta gap measurements and interpretation is that in cases of AGMA, the drop in HCO3- is expected to be
related to the AG directly; when it doesn’t match, there is a concomitant non-ion gap metabolic acidosis. This enables for the

detection of additional metabolic alkalosis or acidosis. Delta gap can be calculated by (AG-ExpAG)-(24-HCO3-).

In a predominant AGMA, when the delta gap is >6, there is an AGMA and a concomitant metabolic alkalosis. When

the delta gap is <-6, there is an AGMA and a NAGMA.

In a predominant NAGMA, for every raise in Cl- by 1, there should be a drop in HCO3- by 1 (+- 5). If the drop in

HCO3- is less than expected, there is both a NAGMA and a metabolic alkalosis.

Figure 2: Summary of Anion and Delta Gap in Metabolic Acidosis (Sherman, 2009)

Further Exploring Metabolic Alkalosis

Metabolic alkalosis can be due to many causes, but these are generally broken into grouping based on etiology; the

commonality is an increased [HCO3-] in the blood. The causes broadly include the following (Kasper, Hauser, Jameson, & Fauci,

2015):

1. Exogenous HCO3-

2. Effective ECFV Contraction, normotension, hypokalemia and secondary hyperreninemic hyperaldosteronism

3. ECFV Expansion, hypertension, K+ deficiency, mineralcorticoid excess

4. Gain-of-function mutation of renal sodium channel with ECFV expansion, hypertension, K+ deficiency, and

hyporeninemic-hypoaldosteronism

Generally speaking, exogenous alkali is not common, and thus most cases of metabolic alkalosis require the loss of acid

(generative stage) and the failure of renal compensation to excrete HCO3- (maintenance stage) (Kasper, Hauser, Jameson, &

Fauci, 2015) (Rennke & Denker, 2014).

Effective ECFV Contraction, normotension, hypokalemia and secondary hyperreninemic hyperaldosteronism

GI Origin – Isotonic Saline

Loss of H+ from vomiting à HCO3- retention. Recall that H+ and HCO3- are produced by parietal cells via CA.

Typically the H+ load is buffered later in the GI tract in the small intestine where the pancreas secretes HCO3-, but in vomiting

this does not occur due to the loss of H+. Other causes include chloridorrhea. Note that hypokalemia due to both GI loss and the

response of the RAAS system to the dehydration further exacerbates the alkalosis (aldosterone, angiotensin II à Na+

reabsorption, K+ loss, H+ loss) (Rennke & Denker, 2014) (Kasper, Hauser, Jameson, & Fauci, 2015)
 Renal Origin – Isotonic Saline

Thiazides and loop diuretics cause the loss of Na and Cl, diminishng the ECFV acutely but not altering the HCO3-

content à contraction alkalosis (volume depletion triggers RAAS, as discussed above) (Costanzo, 2013) (Kasper, Hauser,

Jameson, & Fauci, 2015). Furthermore, chronic diuretic use increases delivery of NaCl to the distal nephron, stimulating K+ and

H+ secretion in exchange for Na+ (Kasper, Hauser, Jameson, & Fauci, 2015). Maintenance of this alkalosis is intuitive; the

protracted volume depletion, secondary hyperaldosteronism and loss of K+ aid in maintenance.

Potassium Depletion

Hypokalemia enhances NH3 synthesis and resultantly increases H+ excretion as NH4+. (Costanzo, 2013)

Bartter’s Syndrome – Loss of Function in TALH (similar to loop diuretics)

The NKCC2 transporter is affected, leading to hypokalemia, metabolic acidosis with a hypercalciuria. Recall that the

NKCC2 is important in establishing paracellular calcium reabsorption.

Gitelman Syndrome – Loss of function in NaCl of DCT (similar to thiazides)

The NaCl channel in the DCT is mutated à hypokalemia, hypomagnesemia, hypocalciuria.

ECFV Expansion, hypertension, K+ deficiency, mineralcorticoid excess

These conditions are classified by the presence of hypertension. (Kasper, Hauser, Jameson, & Fauci, 2015)

High Renin

Renal artery stenosis

Renin-secreting tumor

Estrogen therapy

Low Renin

Primary Aldosteronism

Adenoma, Carcinoma

Adrenal Enzyme Defects

(SAME) 11B-Hydroxylase deficiency, 17a-hydroxylase deficiency

Cushing’s

Licorice and some chewing tobacco

Gain-of-function mutation of renal sodium channel with ECFV expansion, hypertension, K+ deficiency, and hyporeninemic-

hypoaldosteronism

This is essentially Liddle’s Syndrome. This is a gain of function of the ENaC channel in the collecting duct which

increases Na retention, expanding volume. There is also a loss of potassium. In Liddle, aldosterone levels are reduced due to the

expansion of volume; presents like hyperaldosteronism.

Metabolic Acidosis: The Importance of the Anion Gaps, Osmolar Gap

As discussed earlier, the anion gap is a crucial measurement. Here, I wish to simply point out that osmolarity gap is

also important; it indicates that there is the presence of a low MW toxin, namely ethylene glycol, other glycols, methanol and

ethanol. In theory, ketoacids, lactic acid and salicylate metabolic acidosis could cause this, but due to their higher MW, the

patient is not likely to survive to the theoretical elevated osmolar gap (Costanzo, 2013).

Osmolarity can be estimated by: 2[Na] + Glucose/18 + BUN/2.8

The Urine Anion gap is another useful tool. Normally, the urine anion gap is near zero or positive. In the presence of a

metabolic acidosis, excretion of NH4+ with Cl- should increase if the renal acidification is working properly. Thus, one expects

that the urine anion gap would become negative.

Urine Anion Gap = [Na+] + [K+] – [Cl-]

Think about using the urine anion gap when there is a hyperchloremic (normal anion gap) metabolic acidosis; if it is

negative (UAG), then there is likely a loss of bicarbonate through the GI tract. If it is positive, suggesting that Cl- anions were not

increased in the urine and thus NH4+ secretion is impaired, think about renal tubular acidosis.
Bibliography

Altalag, A., Road, J., & Wilcox, P. (2009). Pulmonary Function Tests in Clinical Practice. London: Springer-Verlag.

Berend, K., de Vries, A. P., & Gans, R. O. (2014). Physiolofic Approach to Assessment of Acid-Base Disturbances. The New

England Journal of Medicine, 1434-1445.

Sherman, S. C. (2009). Acid-Base Made Easy. Boston Scientific Assembly. Boston: Boston Scientific Assembly.

Theodore, A. C., & Manaker, S. (2017, March 16). Arterial blood gases. Retrieved April 17, 2017, from UpToDate:

http://www.uptodate.com/contents/arterial-blood-gases

West, J. B., & Luks, A. M. (2012). Respiratory Physiology: The Essentials (10th Edition ed.). Philadelphia: Wolsters Kluwer.

(Berend, de Vries, & Gans, 2014)

(Berend, de Vries, & Gans, 2014)
(Berend, de Vries, & Gans, 2014)
(Altalag, Road, & Wilcox, 2009)

(Altalag, Road, & Wilcox, 2009)