Arterial Blood Gas

Interpretation
Joseph Brian L. Costiniano, MD, DPCP
American Thoracic Society
ABG Reading Guidelines
• https://www.thoracic.org/professionals/clinical-
resources/critical-care/clinical-education/abgs.php
 Components of ABG

Blood Gas

Oxygenation Ventilation Acid-Base

PaO2, SaO2 PCO2 pH, HCO3, BE

Critical Care Medicine
ABG Interpretation
6-stepwise approach
Step 1: Assess the internal consistency of the values using
the Henderson-Hasselbach equation:

[H+] = 24(PaCO2)
[HCO3-]

Kaufman, D., American Thoracic Society

• If the pH and the [H+] are inconsistent, the ABG is
probably not valid.
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
Kaufman, D., American Thoracic Society
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

Kaufman, D., American Thoracic Society

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

Kaufman, D., American Thoracic Society

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 factor
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ±2
Acute respiratory acidosis Increase in [HCO3-]= ∆ ±3
PaCO2/10
Chronic respiratory Increase in [HCO3-]= 3.5(∆
acidosis (3-5 days) PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 +
0.6(∆HCO3-)
Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆
PaCO2/10)
Chronic respiratory Decrease in [HCO3-] = 5(∆
alkalosis 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.
Kaufman, D., American Thoracic Society
Step 5: Calculate the anion gap (if a metabolic acidosis
exists): AG= [Na+]-( [Cl-] + [HCO3-] )-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
• 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

Kaufman, D., American Thoracic Society

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.

Kaufman, D., American Thoracic Society

Selected etiologies of respiratory acidosis

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

Kaufman, D., American Thoracic Society

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

Kaufman, D., American Thoracic Society

Selected causes of metabolic alkalosis

o Hypovolemia with Cl- depletion

o GI loss of H+
o Vomiting, gastric suction, villous adenoma, diarrhea with
chloride-rich fluid
o Renal loss H+
o 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

Kaufman, D., American Thoracic Society

 Selected etiologies of metabolic acidosis

oElevated anion gap: oNormal anion gap: will have increase in [Cl-]GI
o Methanol intoxication loss of HCO3-
o Uremia o proximal RTA
o Diabetic ketoacidosisa, alcoholic o Diarrhea, ileostomy, proximal colostomy,
ketoacidosis, starvation ketoacidosis ureteral diversion
o Paraldehyde toxicity oRenal loss of HCO3-
o Isoniazid o carbonic anhydrase inhibitor
o Lactic acidosisa (acetazolamide)
o Type A: tissue ischemia oRenal tubular disease
o Type B: Altered cellular metabolism o ATN
o Ethanolb or ethylene glycolb intoxication o Chronic renal disease
o Salicylate intoxication o Distal RTA
o Aldosterone inhibitors or absence
o NaCl infusion, TPN, NH4+ administration

Kaufman, D., American Thoracic Society

 Selected mixed and complex acid-base disturbances
Disorder Characteristics Selected situations Disorder
Respiratory acidosis with ↓in pH •Cardiac arrest Respiratory acidosis with
metabolic acidosis ↓ in HCO3 •Intoxications metabolic acidosis
↑ in PaCO2 •Multi-organ failure

Respiratory alkalosis with↑in pH •Cirrhosis with diuretics Respiratory alkalosis with

metabolic alkalosis ↑ in HCO3- •Pregnancy with metabolic alkalosis
↓ in PaCO2 vomiting
•Over ventilation of
COPD
Respiratory acidosis with pH in normal range •COPD with diuretics, Respiratory acidosis with
metabolic alkalosis ↑ in PaCO2, vomiting, NG suction metabolic alkalosis
↑ in HCO3- •Severe hypokalemia

Respiratory alkalosis withpH in normal range •Sepsis Respiratory alkalosis with

metabolic acidosis ↓ in PaCO2 •Salicylate toxicity metabolic acidosis
↓ in HCO3 •Renal failure with CHF
or pneumonia
•Advanced liver disease
Metabolic acidosis with pH in normal range •Uremia or ketoacidosis Metabolic acidosis with
metabolic alkalosis HCO3- normal with vomiting, NG metabolic alkalosis
suction, diuretics, etc.
Kaufman, D., American Thoracic Society
SAMPLE PROBLEMS
CASE: The patient is a 35 year -old female with AIDS brought to the emergency room
with a fever of 39oC and a three month history of copious diarrhea.

On physical exam the patient is a well-developed, thin female in moderate distress.

Vital signs-(supine) blood pressure 100/60, pulse 100 and (standing) blood pressure
80/40, pulse 125, respirations 18 and she was afebrile. HEENT exam was normal.
Cardiac exam demonstrated an S1 and S2 without S3, S4 or murmur. Lungs were
clear to auscultation and percussion. The abdomen was supple and minimally tender
to palpation. Bowel sounds were hyperactive.

pH 7.35
PCO2 32 mmHg
PO2 90 mmHg
HCO3 14 mmol/L
With O2 via NC @4LPM
• Primary Disorder?
• Compensated? Mixed or Pure?
• FiO2?
• Expected PO2 for Age?
• Oxygenation? Corrected or Uncorrected?
• Primary Disorder? METABOLIC ACIDOSIS
HCO3 14
MEAN HCO3 24
DIFFERENCE OF 10

PCO2 32
MEAN 40
DIFFERENCE OF 8
• Primary Disorder? METABOLIC ACIDOSIS
• Compensated? Mixed or Pure?
PaCO2 = (1.5 X HCO3) + 8
= (1.5 X 14) + 8
= 29 +-2
PaCO2 OF PATIENT: 32 → RESPIRATORY ACIDOSIS
• FiO2?
FiO2 = 20 +(4 x LPM)
FiO2 = 36
• DESIRED PO2 for Age?
104 – (0.43 X AGE)
104 – (0.43 X 35)
= 88.95
• Expected PO2 = FiO2 x 5
= 36 x 5
= 180
• Oxygenation? Corrected or Uncorrected?
PO2 = 90 < Expected PO2 180
UNCORRECTED HYPOXEMIA AT AN FIO2 OF 36

MIXED METABOLIC ACIDOSIS WITH RESPIRATORY ACIDOSIS with

UNCORRECTED HYPOXEMIA AT AN FIO2 OF 36%
IV DRIPS COMPUTATION
• Norepinephrine
• potent vasoconstrictor and inotropic stimulant
• Usually started at 2 to 4 mcg/min
• Ceiling: 15 mcg/min
• Usual prep: 8mg in 100cc D5W or 16mg in 250 D5W
IV DRIPS COMPUTATION
• Dopamine
• Augments BP and cardiac output in cardiogenic shock
• May be used to increase HR in patients with blocks
• Usual prep: 200mg in 250 cc D5W → single strength
• 400 mg in 250 cc D5W → double strength
• Dose: <2 mcg/kg/min – RENAL
• 2-10 – inotrope. Norepinephrine release. Increased CO
• >10 – Increased vascular resistance
IV DRIPS COMPUTATION
• Dobutamine
• DOC for myocardial dysfunction
• Positive inotropic action
• As dose increased → may cause HYPOTENSION by VASODILATION
• Usual prep: 500mg in 250cc D5W
IV DRIPS COMPUTATION

• Concentration Factor = (Prep) mg/mL x 1000

60

• Actual dose = CF x rate

wt (kg)
SAMPLE
• Calculate the actual dose of the following Norepinephrine drip:

Levophed 16 mg in 100cc D5W @ 30cc/hr in a 60kg female patient.

• Actual dose = CF x rate CF = 16/100 x 1000 CF = 2.67

wt (kg) 60

AD = 2.67 x 30 AD = 1.33
60