Arterial Blood Gas: metabolic acidosis & alkalosis,

respiratory acidosis & alkalosis

Youtube video:https://youtu.be/EML9vE1nOgk

Interpretation of ABGs

Interpretation of Arterial Blood Gases (ABGs)

David A. Kaufman, MD
Chief, Section of Pulmonary, Critical Care & Sleep Medicine
                Bridgeport Hospital-Yale New Haven Health
Assistant Clinical Professor, Yale University School of Medicine
(Section of Pulmonary & Critical Care Medicine)

Introduction:

Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other
health care personnel. ABG interpretation is especially important in critically ill patients.

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.”

6-step approach:

Step 1:  Assess the internal consistency of the values using the Henderseon-Hasselbach equation:

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

[H+] = 24(PaCO2)
           [HCO3-]

If the pH and the [H+] are inconsistent, the ABG is probably not valid.

Step 2:  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

Step 3:  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 PaCO 2? In primary respiratory disorders, the pH and PaCO2 change
in opposite directions; in metabolic disorders the pH and PaCO 2 change in the same direction.
 Acidosis Respiratory pH ↓ PaCO2  ↑

Acidosis Metabolic& pH ↓ PaCO2  ↓

Alkalosis Respiratory pH ↑ PaCO2  ↓

Alkalosis Metabolic pH ↑ PaCO2   ↑

Step 4:  Is there appropriate compensation for the primary disturbance?  Usually, compensation does not return
the pH to normal (7.35 – 7.45).

Disorder Expected compensation Correction f

Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ±2

Acute respiratory acidosis Increase  in  [HCO3-]= ∆ PaCO2/10 ±3

Chronic respiratory acidosis Increase  in  [HCO3-]= 3.5(∆ PaCO2/10)

(3-5 days)

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)

If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder
is

present.

Step 5:  Calculate the anion gap (if a metabolic acidosis exists): AG= [Na+]-( [Cl-] + [HCO 3-] )-12 ± 2

 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.)
 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

Step 6:  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.

It is important to remember what the expected “normal” anion gap for your patient should be, by adjusting for
hypoalbuminemia (see Step 5, above.)

Table 1:  Characteristics of acid-base disturbances

Table 2:  Selected etiologies of respiratory acidosis

Disorder pH Primary problem Compensatio

Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2

Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2

Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-]

Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]

o Airway obstruction
-Upper
-Lower

o COPD
o asthma
o other obstructive lung disease

o CNS depression

o Sleep disordered breathing  (OSA or OHS)

o Neuromuscular impairment
o Ventilatory restriction

o Increased CO2  production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased
intake of carbohydrates

o Incorrect mechanical ventilation settings

Table 3:  Selected etiologies of respiratory alkalosis

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

o Incorrect mechanical ventilation settings

Table 4:  Selected causes of metabolic alkalosis

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

Table 5:  Selected etiologies of metabolic acidosis

o Elevated anion gap:

o Methanol intoxication
o Uremia
o Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation ketoacidosis
o Paraldehyde toxicity
o Isoniazid
 o Lactic acidosisa

 Type A:  tissue ischemia

 Type B:  Altered cellular metabolism

o Ethanolb or ethylene glycolb intoxication

o Salicylate intoxication

a Most common causes of metabolic acidosis with an elevated anion gap

b Frequently associated with an osmolal gap

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

Disorder Characteristics Selected situations

Cardiac arrest
Respiratory acidosis with ↓in pH
Intoxications
 Multi-organ failure
metabolic acidosis ↓ in HCO3
↑ in PaCO2

Cirrhosis with diuretics

Respiratory alkalosis with ↑in pH Pregnancy with vomiting
metabolic alkalosis ↑ in  HCO3-   Over ventilation of COPD
↓ in PaCO2

COPD with diuretics, vomiting, NG suction

Respiratory acidosis pH in normal range
Severe hypokalemia
with metabolic alkalosis ↑ in PaCO2,
↑ in  HCO3-

Sepsis
Respiratory alkalosis pH in normal range Salicylate toxicity
with metabolic acidosis ↓ in PaCO2 Renal failure with CHF or pneumonia
↓ in HCO3 Advanced liver disease

Uremia or ketoacidosis with vomiting,

Metabolic acidosis pH in normal range
NG suction, diuretics, etc.
with metabolic alkalosis HCO3- normal

Table 6:  Selected mixed and complex acid-base disturbances

Suggested additional reading:

 Rose, B.D. and T.W. Post. Clinical physiology of acid-base and electrolyte disorders , 5th ed. New York:
McGraw Hill Medical Publishing Division, c2001.
 Fidkowski, C And J. Helstrom. Diagnosing metabolic acidosis in the critically ill: bridging the
anion gap, Stewart and base excess methods. Can J Anesth 2009;56:247-256.
 Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—first of
two parts. N Engl J Med 1998;338:26-34.
 Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—second of two parts. N
Engl J Med 1998;338:107-111.  

Activity : ARTERIAL BLOOD GAS DISCUSSION AND INTERPRETATION

Part 1:
Identify the cases/disorder/condition per ABG interpretation:

Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

- Asthma
- COPD
- Hyperventilation
- Acute Pulmonary Edema
- panic attacks - loss of stomach acids
- Severe Obesity
- anxiety - excess antacids
- Neuromuscular disorders - increased acid
- heart attack - Diuretics
- Scoliosis production
- pain - Potassium deficiency
- Emphysema - loss of bicarbonate
- drug use (hypokalemia)
- Pneumonia - reduced ability of the
- asthma - Reduced volume of
- Conditions that affect the kidneys to excrete excess
- fever blood in the arteries
rate of breathing acids
- COPD - Heart, kidney, or liver
- Muscle weakness that
- infection failure
affects breathing
- pulmonary embolism - Genetic causes
- obstructed airways
- pregnancy
- sedative overdose
- cardiac arrest

Part 2:

1. You are asked to review a 63-year-old female who was admitted with shortness of breath. On your
arrival, the patient appears drowsy and is on 10L of oxygen via a mask.

You perform an ABG, which reveals the following results:

- pH: 7.29

-PaCO2: 68mmhg

-HCo3: 26mEq/L

Interpretation: Respiratory Acidosis (uncompensated)

2. A 17-year-old patient complaining of a tight feeling in their chest, shortness of breath as well as
some tingling in their fingers and around their mouth. There is no significant past medical history and
are not on any regular medication. An ABG is performed on the patient:

- pH: 7.49

-PaCO2: 24mmhg

-HCo3: 22mEq/L

Interpretation: Respiratory Alkalosis (uncompensated)

3. A 48-year-old male has been admitted with a 24 hour history of abdominal distention and profuse
vomiting. A CT scan reveals a large mass causing bowel obstruction. As part of the patient’s
assessment, the surgical registrar requests that you check his blood gas (on air), with the results
shown below:

- pH: 7.5

-PaCO2: 41mmhg

-HCo3: 29mEq/L

Interpretation: Metabolic Alkalosis (uncompensated)

4. You’re asked to review a 59-year-old female who has been admitted the acute medical ward of your
hospital. The nurse tells you that she appears short of breath despite currently receiving 3L/min of
oxygen via nasal cannula.

You take an arterial blood gas which reveals the following results:

- pH: 7.30

-PaCO2: 63mmhg

-HCo3: 29mEq/L

Interpretation: Respiratory Acidosis (partial compensation)

5. An 89-year-old patient presents with fever, rigors, hypotension and reduced urine output. They
appear confused and are unable to provide any meaningful history. The care home that the patient
came from has provided some basic documentation. You look through the information available and
note that the district nurse changed this patient’s catheter 24 hours ago.  The medical registrar
commences antibiotics, aggressive fluid resuscitation and asks you to perform an arterial blood gas,
with the results shown below. The patient was not on oxygen at the time of the ABG.

- pH: 7.29

-PaCO2: 41.2mmhg

-HCo3: 15mEq/L

Interpretation: Metabolic Acidosis (uncompensated)

6. A 22-year-old female is brought into the emergency room by an ambulance with a 5-day history of
vomiting and lethargy. When you begin to talk with the patient you note that she appears
disorientated and looks clinically dehydrated. At present, you are unable to gain any further details,
but the patient looks very unwell from the end of the bed. You gain IV access, send off a routine panel
of bloods and commence some fluids.  You ask the nurse to check the patient’s observations and she
notes an increased respiratory rate, low blood pressure and tachycardia. You perform an ABG as
requested. The results of the ABG are shown below (the patient was not on oxygen when this was
taken).

- pH: 7.30
-PaCO2: 30.7mmhg

-HCo3: 13mEq/L

Interpretation: Respiratory Acidosis (partial compensation)

7. A 56-year-old man was found unconscious at home with a respiratory rate of 6 breaths per minute
and pinprick pupils. An ambulance was called and the paramedics administered some naloxone. On
arrival to the emergency room his ABG showed the following (not on oxygen at the time of the ABG):

- pH: 7.31

-PaCO2: 53mmhg

-HCo3: 22mEq/L

Interpretation: Respiratory Acidosis (uncompensated)

8. A 77-year-old lady was admitted to hospital 10 days ago with a fractured neck of femur. The
orthopedic team repaired the fracture and she has been an inpatient on the orthopedic ward
recovering ever since. The patient’s nurse is becoming increasingly concerned as the patient’s oxygen
requirements are increasing (she is now on 3L) and the patient is now tachypnic (respiratory rate 35).
In addition, the patient has recently started complaining of calf pain.

You review the patient and perform an ABG which reveals the following:

- pH: 7.51

-PaCO2: 23.2mmhg

-HCo3: 21mEq/L

Interpretation: Metabolic Alkalosis (partial compensation)

9. A 18-year-old nursing student has just returned from his vacation from Palawan. In the last few
days, he has developed severe diarrhea and has now presented to emergency room. On assessment,
he is very dehydrated and tachypnic.

- pH: 7.32

-PaCO2: 30mmhg

-HCo3: 13mEq/L

Interpretation: Respiratory Acidosis (partial compensation)

10. - pH: 7.43

-PaCO2: 60mmhg

-HCo3: 38mEq/L
Interpretation: Metabolic Alkalosis (full compensation)

11. - pH: 7.36

-PaCO2: 52mmhg

-HCo3: 31mEq/L

Interpretation: Respiratory Acidosis (full compensation)