The document provides information on interpreting arterial blood gases (ABGs), including: - A 6-step process for interpretation involving assessing pH, identifying the primary disorder as respiratory or metabolic, evaluating compensation, calculating anion gap, and considering differential diagnoses. - Tables listing normal ranges for ABG components like pH, PaCO2, HCO3, and bases for common acid-base disorders. - Explanations of key components like pH, partial pressure, base excess, bicarbonate, and their relationships in respiratory and metabolic acidosis/alkalosis. - Causes and mechanisms of respiratory and metabolic acidosis and alkalosis are outlined.

1. Dr. Mohamed Elbahnasawy
Ass. lecturer of emergency medicine
Tanta university

2.  The following six-step process helps ensure a
complete interpretation of every ABG. In addition,
you will find tables that list commonly
encountered acid-base disorders.
 Many methods exist to guide the interpretation
of the ABG. This discussion does not include
some methods, such as analysis of base excess
or Stewart’s strong ion difference. A summary of
these techniques can be found in some of the
suggested articles. It is unclear whether these
alternate methods offer clinically important
advantages over the presented approach, which
is based on the “anion gap.”

3. 7.35-7.45pH
80-100 mmHgPaO2
35-45 mmHgPaCO2
95-100%O2 saturation
22-26 mEq/LHCO3
Or - 2+BASE excess

4. pH
 pH is a - ve logarithmic scale of the concentration of hydrogen ions in a solution.
It is inversely proportional to the concentration of hydrogen ions.
 When a solution becomes more acidic the concentration of hydrogen ions
increases and the pH falls.
 Normally the body’s pH is closely controlled at between 7.35 – 7.45. This is
achieved through buffering and excretion of acids.
 Buffers include plasma proteins and bicarbonate (extracellular) and proteins,
phosphate and haemoglobin (intracellularly).
 Hydrogen ions are excreted via the kidney and carbon dioxide is excreted via the
lungs.
 Changes in ventilation are the primary way in which the concentration of H+ ions
is regulated. Ventilation is controlled of the concentration of CO2 in the blood.
 If the buffers and excretion mechanisms are overwhelmed and acid is continually
produced, the he pH falls. This creates a metabolic acidosis.
 If the ability to excrete CO2 is compromised this creates a respiratory acidosis.
 Note that a normal pH doesn’t rule out respiratory or metabolic pathology. This
why you must always look at all the values other than pH as there may be a
compensated or mixed disorder

5. Partial pressure (PP)
 Partial pressure is a way of assessing the number of
molecules of a particular gas in a mixture of gases. It is
the amount of pressure a particular gas contributes to the
total pressure. For example, we normally breathe air
which at sea level has a pressure of 100kPa, oxygen
contributes 21% of 100kPa, which corresponds to a partial
pressure of 21kPa.
 When used in blood gases, Henry’s law is used to ascertain
the partial pressures of gases in the blood. This law states
that when a gas is dissolved in a liquid the partial pressure
(i.e. concentration of gas) within the liquid is the same as
in the gas in contact with the liquid. Therefore you can
measure the partial pressure of gases in the blood.
 PaO2 is the partial pressure of oxygen in arterial blood
 PaCO2 is the partial pressure of carbon dioxide in arterial
blood.
NB Kpa = 7.6 x mmHG.

6. Base excess (BE)
• This is the amount of strong base which
would need to be added or subtracted from a
substance in order to return the pH to normal
(7.40).
• A value outside of the normal range (-2 to
+2 mEq/L) suggests a metabolic cause for the
acidosis or alkalosis.
• In terms of basic interpretation
• A base excess more than +2 mEq/L
indicates a metabolic alkalosis.
• A base excess less than -2 mEq/L
indicates a metabolic acidosis.

7. Bicarbonate (HCO3)
• Bicarbonate is produced by the kidneys
and acts as a buffer to maintain a normal pH.
The normal range for bicarbonate is 22 –
26mmol/l.
• If there are additional acids in the blood
the level of bicarbonate will fall as ions are used
to buffer these acids. If there is a chronic
acidosis additional bicarbonate is produced by
the kidneys to keep the pH in range.
• It is for this reason that a raised
bicarbonate may be seen in chronic type 2
respiratory failure where the pH remains normal
despite a raised CO2.

8. pH is closely controlled in the human body and
there are various mechanisms to maintain it at a
constant value. It is important to note that the
body will never overcompensate as the drivers
for compensation cease as the pH returns to
normal. In essence compensation for an
acidosis will not cause an alkalosis or visa
versa.

9.  • If a metabolic acidosis develops the change is
sensed by chemoreceptors centrally in the medulla
oblongata and peripherally in the carotid bodies.
 • The body responds by increasing depth and rate
of respiration therefore increasing the excretion of
CO2 to try to keep the pH constant.
 o The classic example of this is ‘Kussmaul
breathing’ the deep sighing pattern of respiration
seen in severe acidosis including diabetic
ketoacidosis. Here you will see a low pH and a low
pCO2 which would be described as a metabolic
acidosis with partial respiratory compensation (partial
as a normal pH has not been reached).

10. •In response to a respiratory acidosis, for
example in CO2 retention secondary to COPD,
the kidneys will start to retain more HCO3 in
order to correct the pH.
•Here you would see a low normal pH with
a high CO2 and high bicarbonate.
•This process takes place over days.
•It is important to ensure that the
compensation that you see is appropriate, i.e.
as you would expect. If not then you should
start to think about mixed acid base disorders.

12.  Step 1: Assess the internal consistency of the
values using the Henderseon-Hasselbach
equation:
 [H+] = 24 x (PaCO2/HCO3)
 PH = 6.1 X (HCO3/.003XPaCO2)
 If the pH and the [H+] are inconsistent, the
ABG is probably not valid.

13. Ph Approximate [H+]
(mmol/L)
7.00 100
7.05 89
7.10 79
7.15 71
7.20 63
7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
7.55 28
7.60 25
7.65 22

14. Is there alkalemia or acidemia present?
pH < 7.35 acidemia
pH > 7.45 alkalemia
This is usually the primary disorder
 Remember: an acidosis or alkalosis may be
present even if the pH is in the normal range
(7.35 – 7.45)
 You will need to check the PaCO2, HCO3-
and anion gap

15. Is the disturbance respiratory or metabolic?
What is the relationship between the direction
of change in the pH and the direction of
change in the PaCO2?
In primary respiratory disorders, the pH and
PaCO2 change in opposite directions;
in metabolic disorders the pH and
PaCO2 change in the same direction

16. Acidosis Respiratory pH ↓ PaCO2 ↑
Acidosis Metabolic& pH ↓ PaCO2 ↓
Alkalosis Respiratory pH ↑ PaCO2 ↓
Alkalosis Metabolic pH ↑ PaCO2 ↑

17.  Is there appropriate compensation for
the primary disturbance?
 Usually, compensation does not
return the pH to normal (7.35 – 7.45).

18. Disorder Expected compensation Correction
factor
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ± 2
Acute respiratory
acidosis
Increase in [HCO3-]= ∆
PaCO2/10
± 3
Chronic respiratory
acidosis (3-5 days)
Increase in [HCO3-]= 3.5(∆
PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 +
0.6(∆HCO3-)
Acute respiratory
alkalosis
Decrease in [HCO3-]= 2(∆
PaCO2/10)
Chronic respiratory
alkalosis
Decrease in [HCO3-] = 5(∆
PaCO2/10) to 7(∆ PaCO2/10)

19. Calculate the anion gap (if a metabolic acidosis
exists):
AG= [Na+]-( [Cl-] + [HCO3-] )=12 ± 2

20.  A normal anion gap is approximately 12 meq/L.
 In patients with hypoalbuminemia, the normal
anion gap is lower than 12 meq/L; the “normal”
anion gap in patients with hypoalbuminemia is
about 2.5 meq/L lower for each 1 gm/dL
decrease in the plasma albumin concentration
(for example, a patient with a plasma albumin of
2.0 gm/dL would be approximately 7 meq/L.)
 Corrected anion gap = AG + 2.5(4-albumin)
 If the anion gap is elevated, consider calculating
the osmolal gap in compatible clinical situations.
◦ Elevation in AG is not explained by an obvious case
(DKA, lactic acidosis, renal failure
◦ Toxic ingestion is suspected
 OSM gap = measured OSM – (2[Na+] -
glucose/18 – BUN/2.8
◦ The OSM gap should be < 10

21. If an increased anion gap is present, assess the
relationship between the increase in the anion gap and
the decrease in [HCO3-].
Assess the ratio of the change in the anion gap
(∆AG ) to the change in [HCO3-] (∆[HCO3-]):
∆AG/∆[HCO3-]
This ratio should be between 1.0 and 2.0 if an
uncomplicated anion gap metabolic acidosis is present.
If this ratio falls outside of this range, then another
metabolic disorder is present:
If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-
anion gap metabolic acidosis is likely to be present.
If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic
alkalosis is likely to be present

22. Disorder pH Primary problem Compensation
Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2
Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2
Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-]
Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]

23.  Airway obstruction
- Upper airway obstruction like FB , acute epiglottitis
- Lower
◦ COPD
◦ asthma
◦ other obstructive lung disease
 CNS depression
 Sleep disordered breathing (OSA )
 Neuromuscular impairment
 Ventilatory restriction
 Increased CO2 production: shivering, rigors,
seizures, malignant hyperthermia, hypermetabolism,
increased intake of carbohydrates
Incorrect mechanical ventilation settings

24. o CNS stimulation: fever, pain, fear, anxiety,
CVA, cerebral edema, brain trauma, brain tumor,
CNS infection
o Hypoxemia or hypoxia: lung disease,
profound anemia, low FiO2
o Stimulation of chest receptors: pulmonary
edema, pleural effusion, pneumonia,
pneumothorax, pulmonary embolus
o Drugs, hormones: salicylates, catecholamines,
medroxyprogesterone, progestins
o Pregnancy, liver disease, sepsis,
hyperthyroidism

25. o Hypovolemia with Cl- depletion
o GI loss of H+
 Vomiting, gastric suction, villous adenoma, diarrhea with
chloride-rich fluid
o Renal loss H+
 Loop and thiazide diuretics, post-hypercapnia (especially
after institution of mechanical ventilation)
o Hypervolemia, Cl- expansion
o Renal loss of H+: edematous states (heart failure, cirrhosis,
nephrotic syndrome), hyperaldosteronism, hypercortisolism,
excess ACTH, exogenous steroids, hyperreninemia, severe
hypokalemia, renal artery stenosis, bicarbonate administration

26.  Elevated anion gap:
◦ Methanol intoxication
◦ Uremia
◦ Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation
ketoacidosis
◦ Paraldehyde toxicity
◦ Isoniazid
◦ Lactic acidosisa
 Type A: tissue ischemia
 Type B: Altered cellular metabolism
◦ Ethanolb or ethylene glycolb intoxication
◦ Salicylate intoxication
Rhabdomyolsis

27. o Normal anion gap:
will have increase in [Cl-]
o GI loss of HCO3-
 Diarrhea, ileostomy, proximal colostomy, ureteral diversion
o Renal loss of HCO3-
 proximal RTA
 carbonic anhydrase inhibitor (acetazolamide)
o Renal tubular disease
 ATN
 Chronic renal disease
 Distal RTA
 Aldosterone inhibitors or absence
 NaCl infusion, TPN, NH4+ administration

29. Disorder Characteristics Selected situations
Respiratory
acidosis with
metabolic acidosis
↓in pH
↓ in HCO3
↑ in PaCO2
 Cardiac arrest
 Intoxications
 Multi-organ failure
Respiratory
alkalosis with
metabolic alkalosis
↑in pH
↑ in HCO3-
↓ in PaCO2
 Cirrhosis with diuretics
 Pregnancy with vomiting
 Over ventilation of COPD
Respiratory
acidosis with
metabolic alkalosis
pH in normal
range
↑ in PaCO2,
↑ in HCO3-
 COPD with diuretics,
vomiting, NG suction
 Severe hypokalemia
Respiratory
alkalosis with
metabolic acidosis
pH in normal
range
↓ in PaCO2
↓ in HCO3
 Sepsis
 Salicylate toxicity
 Renal failure with CHF or
pneumonia
 Advanced liver disease
Metabolic acidosis
with metabolic
alkalosis
pH in normal
range
HCO3- normal
 Uremia or ketoacidosis with
vomiting, NG suction,
diuretics, etc.