UHS PBL: Interpretation of Blood Gas Analysis

Learning Objectives
 What are the parameters analyzed in a blood gas report?
 pH  SO2 (Sa; Sv; Sc)
 PCO2  ABE (actual base excess)
 HCO3  SBE (standard base excess)
 PO2 (Pa; Pv; Pc)  Others (lactate; electrolytes; Hb)

 What are the normal values for all the parameters?

 pH:
o 7.25 – 7.45 in neonates
o 7.35 – 7.45 in children
 PaCO2: 35 – 45 mmHg
 HCO3:
o 18-25 mEq/L in neonates
o 20-27 mEq/L in children
 PO2:
o 70-100 mmHg in neonates
o 90-100 mmHg in children)
 SaO2: ≥ 95%
o Low SaO2 is preferred in premature babies to avoid retinopathy of prematurity
(therefore it is maintained at 90 – 94%) as PO2 >100 will damage the retina.
 ABE: -2 to +2

 What are the differences between arterial, venous, and capillary blood gas values?
 Capillary blood gas values depend on how arterialized the blood is.
 The most commonly used one is CBG. You can rely on all values of CBG except PO 2 (you
use pulse oximetry with it).
 In critical cases (ex: shock), you need an ABG.

Arterial Venous Capillary

pH 7.35 – 7.45 7.31 – 7.41 7.35 – 7.45
PaCO2 35 – 45 mmHg 40 – 50 mmHg 35- 45 mmHg
(mean: 40 mmHg) (mean: 46 mmHg)
HCO3 21 – 27 mEq/L 21 – 27 mEq/L 21 – 27 mEq / L
PO2 ≥ 80 mmHg 36 – 42 mmHg < arterial
(mean: 40 mmHg)
SaO2 ≥ 95% 60-80% (mean: 75%) < arterial
 Pulse Oximetry
 It measures peripheral arterial oxygen saturation (SpO 2) to reflect the level of tissue
oxygenation.
 Uses spectrophotometry  determines proportion of Hb saturation with O2
 Advantages: rapid; non-invasive; continuous data
 Limitations: unable to detect hyperoxemia; unable to measure arterial oxygen tension;
unable to measure ventilation

 Oxygen Dissociation Curve

 PO2 of 80 gives above 95% saturation

 Shift to right: decreased oxygen affinity

o Increased PCO2 or decreased pH
o Increased temperature
o Increased 2,3-DPG concentration
(occurs in high altitudes)

 Shift to left: increased oxygen affinity

o Decreased PCO2 or increased pH
o Decreased temperature
o Decreased 2,3-DPG concentration
o HbF
o CO poisoning

 Metabolic acidosis, metabolic alkalosis, respiratory acidosis and alkalosis; and how
compensation occurs in these conditions
 Metabolic acidosis  compensated by respiratory alkalosis
o It is due to either the loss of HCO3 ions or the addition of H+ ions
o Compensation: hyperventilation (Kussmaul breathing) – respiratory alkalosis
 Metabolic alkalosis  compensated by respiratory acidosis
o It is due to either increased HCO3 or decreased H+
o Compensation: hypoventilation – respiratory acidosis
 Respiratory acidosis  compensated by metabolic alkalosis
o It is caused by a decrease in the RR and thus CO2 retention
o Compensation in chronic cases: increased renal excretion of H + ions + increased
reabsorption of HCO3- - metabolic alkalosis
 Respiratory alkalosis  compensated by metabolic acidosis
o It is caused by an increase in the RR and thus loss of CO2
o Compensation in chronic cases: decreased renal excretion of H + ions + decreased
reabsorption of HCO3- - metabolic acidosis
 What is anion gap and causes of acidosis with increased anion gap and normal anion gap
 Anion gap: [Na+] – ([HCO3-] + [Cl-])
 Normal value:
o If K+ is included: 14 +/- 2
o If K+ is not included: 10 +/- 2
 Causes of increased anion gap metabolic acidosis (due to the production of exogenous
acid)
o General classification:
 DKA
 Uremia
 Drugs (alcohol; aspirin; ethylene glycol; propylene glycol; iron tablets)
 Lactic acidosis (congenital or acquired like shock)
 Organic: inborn error of metabolism (like propionic academia)
o A MUDPILE
 Alcohol / aspirin  Ingestion / inborn error of
 Methanol metabolism
 Uremia  Lactic acidosis
 DKA  Ethylene glycol
 Paraldehyde
 Causes of normal anion gap metabolic acidosis (due to the loss of bicarbonate from
gut/kidney or impaired acid secretion by the kidney):
o Diarrhea
o Renal tubular acidosis
o Vomiting (initially alkalosis; but by the time he is admitted to the hospital he will
be acidotic b/c by the time he comes, he would have stopped eating and thus
exhausted his glycogen storages and instead is metabolizing fats - unless he has
pyloric stenosis) – acidosis may lead to the persistence of vomiting; so ketosis
needs to be corrected (IV line: glucose + fluids  the vomiting stops)

 Renal Tubular Acidosis

It is a state of systemic hyperchloremia due to impaired urinary acidification.
 Type I (Distal):
o Inability to excrete H+  high urine pH (>6.5)
o Causes: medications / inherited
o Associated with: hypokalemia; hypercalcuria
 Type II (Proximal):
o Impaired reabsorption of HCO3 from the proximal tubule
o Associated with: other proximal tubular dysfunction (phosphaturia & glycosuria –
Fanconi syndrome)
o This is more common in pediatrics.
 Type IV (Hyperkalemic):
o Inadequate aldosterone production or inability to respond to it
o Seen in: acute pyelonephritis; obstructive uropathy
 How does acidosis occur in a case of shock?
 Shock  inadequate tissue perfusion  hypoxia  anaerobic metabolism  pyruvate
& lactic acidosis  increased anion gap metabolic acidosis

 Acidosis in a Case of DKA

 Acute insulin insufficiency  increased free fatty acid metabolism into ketones 
increased anion gap metabolic acidosis  acute abdominal pain & vomiting + Kussmaul
breathing
 Ketones: acetoacetate, acetone, beta-hydroxybutyrate

Blood Gas Interpretation - 1

1. Ali, a 2-year-old child from the UAE was admitted to the hospital with fever, impalpable
pulses, and unrecordable BP. Blood gas analysis was as follows:

pH: 7.05 (↓) pCO2: 26.0 mmHg (↓) HCO3: 10.0 mEq/L (↓)
PO2: 80 mmHg O2 saturation: 92% (↓) ABE: -14.5 (↓)

 Metabolic acidosis with partial respiratory compensation

 Cause: shock

2. He received IV fluids, antibiotics, and NaHCO 3. His blood pressure returned to normal. He
then vomited and suddenly became distressed and was cyanosed. ABG was and the
results were:

pH: 7.18 (↓) pCO2: 60.0 mmHg (↑) HCO3: 25.0 mEq/L
PO2: 70 mmHg (↓) O2 saturation: 90% (↓) ABE: -2.0

 Uncompensated respiratory acidosis (b/c metabolic compensation needs time) +

hypoxia
 Cause: aspiration  sudden bronchospasm  distress

3. Ali then became more distressed and he was intubated and started on mechanical
ventilation. One hour later, his ABG results were as follows:

4.
pH: 7.5 (↑) pCO2: 25.0 mmHg (↓) HCO3: 25.0 mEq/L
PO2: 90 mmHg O2 saturation: 99% ABE: 0

 Uncompensated respiratory alkalosis

 Cause: high mechanical ventilation settings
5. Ventilatory changes were made. Ten hours later, his ABG results were:

6.
pH: 7.3 (↓) pCO2: 65.0 mmHg (↑) HCO3: 30.0 mEq/L (↑)
PO2: 80 mmHg O2 saturation: 93% (↓) ABE: +4.0 (↑)

 Respiratory acidosis with partial metabolic compensation

 Cause: hypoventilation (the settings were decreased too much)

7. After another 10 hours, these were his ABG results:

8.
pH: 7.4 pCO2: 65.0 mmHg (↑) HCO3: 37.0 mEq/L (↑)
PO2: 80 mmHg O2 saturation: 95% ABE: +9.0 (↑)

 Respiratory acidosis with complete metabolic compensation

 Cause: chronic hypoventilation so there was time for metabolic compensation
Note: If you do not have a scenario, you can’t know what the compensated abnormality is
(ex: either compensated metabolic acidosis or compensated respiratory alkalosis).

9. At this stage, the ventilatory rate was increased and chest physiotherapy & suction were
done. 1 hour later, his ABG was:

10.
pH: 7.55 (↑) pCO2: 40.0 mmHg HCO3: 33.0 mEq/L (↑)
PO2: 95 mmHg O2 saturation: 99% ABE: +8.0 (↑)

 Uncompensated metabolic alkalosis

 Cause: increased ventilatory rate  respiratory acidosis is corrected quickly, but
metabolic alkalosis needs time (CO2 has to be lowered slowly in order to give time for
the kidney to accommodate and thus to prevent the child from going to metabolic
alkalosis)
 Note: metabolic acidosis should be corrected slowly in DKA & in chronic renal failure
(high phosphate & low calcium; bicarb 10 pH 7.2; Ca is 1.2 normal is 2.2; high phosphate
Of 5  presents to the ER  if given bicarbonate the calcium will decrease even more –
ionization of calcium is high in acidosis; low in alkalosis --- therefore the hypocalcemia
will manifest as there will be no ionized calcium 0 convulsion)

Blood Gas Interpretation – 2

1. A 2-month-old male infant presented with projectile vomiting for the past 2 days. ABG
results were:
2.
pH: 7.60 (↑) pCO2: 40.0 mmHg HCO3: 30.0 mEq/L (↑)
PO2: 90 mmHg O2 saturation: 98% ABE: +5.0 (↑)

 Uncompensated metabolic alkalosis

 Cause: vomiting (most likely due to hypertrophic pyloric stenosis)
Oxygen Dissociation Curve
- PO2 60  SaO2 90%
- PO2 80  SaO2 95%

Explain the following:

1. pH: 7.05 (↓) pO2: 70 mmHg SaO2: 89% (↓)
 Right shift (due to acidosis)
 The decreased affinity causes decreased oxygen saturation.

2. pH: 7.18 (↓) pO2: 50 mmHg (↓) SaO2: 80% (↓)

 Right shift (due to acidosis)
 Decreased partial pressure of oxygen causes decreased oxygen saturation.

3. pH: 7.50 (↑) pO2: 50 mmHg (↓) SaO2: 87% (↓)

 Left shift (due to alkalosis)
 Partial pressure of oxygen is the same as in (2), but oxygen saturation increased due to
the left shift.

4. pH: 7.30 (↓) pO2: 60 mmHg SaO2: 87% (↓)

 Right shift (due to acidosis)
 In comparison to (3), although partial pressure of oxygen increased, the saturation
stayed the same due to the decrease in pH.

5. pH: 7.40 pO2: 60 mmHg SaO2: 90%

 No shift (as pH is normal)
 In comparison to (4), shift to the left due to increase in pH thus there is an increase in
oxygen saturation.

6. pH: 7.55 (↑) pO2: 60 mmHg SaO2: 93%

 Left shift (due to alkalosis)
 In comparison to (5), the increase in pH caused an increase in oxygen saturation.

7. pH: 7.40 pO2: 60 mmHg SaO2: 86% (↓) Temp:39˚C

 Right shift (due to elevated temperature)
 The decreased oxygen affinity causes a decrease in saturation.
8. pH: 7.40 pO2: 60 mmHg SaO2: 86% (↓) Hb: 6 g/dL (↓)
 Right shift (due to chronic anemia - decreased hemoglobin  increased 2,3-DBG)
 If anemia was acute (blood loss) there will also be a right shift, but there will be high-
anion gap metabolic acidosis (lactic acidosis).

9. pH: 7.40 pO2: 60 mmHg SaO2: 93% (↑) Neonate

 Left shift (due to fetal hemoglobin which has higher affinity)