Minh Kosfeld, PhD, MLT(ASCP)CM

As a working medical laboratory scientist and educator, I have found blood gas testing a challenging concept for many, coworkers and students alike. In this brief case I will provide a basic example of blood gas analysis to illustrate its use in the diagnosis of a blood gas disorder.

A child was found unconscious in a smoke-filled apartment and brought to the ED. Results of the initial blood tests (venous blood gases, CO-oximetry, whole blood electrolytes, and lactic acid) are shown in the table below. The blood gas analyzer used was a Radiometer ABL800 Flex, which uses selective electrodes to measure pH, pCO2, pO2, electrolytes, and glucose, and CO-oximetry to determine the relative concentrations of carboxyhemoglobin (CO-Hb), methemoglobin (Met-Hb), oxyhemoglobin (O2-Hb), and hemoglobin (H-Hb).

RADIOMETER ABL800 FLEX

Sample type   Venous  
Temperature   37oC  

1. pH and blood gases

      

pH

 6.705   7.32-7.42
pCO2 112 mmHg 41-51
pO2 49.8 mmHg 30-55
2. CO-oximetry values      
tHB 9.6 g/dL 11.5-13.5
FO2Hb 45.4 % 94-98
FCOHb 38.7 % 0.5-1.5
FMetHb 3.2 % 0.0-1.5
       
Calculated:      
SO2 78.2 % >70
ctO2 6.2 Vol% ~15
BE -20.5 mmol/L -2 to +2
p50 28.37 mmHg 25.3 – 26.8
3. Electrolytes and metabolites      
iCa2+ 1.00 mmol/L 1.15-1.29
Na+ 149 mmol/L 136-146
K+ 4.0 mmol/L 3.4-4.5
Cl+ 113 mmol/L 98-106
Anion Gap, K ↑↑ mmol/L 10-16
tCO2 16.6 mmol/L 18-27
Glucose 285 mg/dL 70-106
Lactic acid 20.4 mmol/L 0.5-2.2

 

Blood gas testing helps to assess the function of the respiratory, cardiovascular, and renal systems by determining the acid-base balance and oxygen status of the blood. Usually, arterial blood is preferred for blood gas measurement. However, correlation between COHb levels and pH in venous and arterial blood is good,1 and the easy and rapid availability of a venous draw made it the sample of choice in the ER, given the criticality of the presentation.

The pH reflects the acid-base status of a patient’s blood, and the Henderson-Hasselbalch equation makes clear its dependence on the concentration of bicarbonate (HCO3–) and the partial pressure
of CO2 (pCO2): pH = 6.1 + log ([HCO3–]/0.03 x pCO2).

Blood pCO2 levels are dependent on the balance between the rate of production of CO2 by metabolic processes and the rate at which it is removed by the lungs. Blood HCO3– levels are maintained by the kidneys as a means of buffering acids added to the blood by metabolism or ingestion and as a means of transporting carbon dioxide from the tissues to the lungs where it can be discharged.

As is apparent from the equation above, pH will fall as HCO3– falls and/or as pCO2 rises, and pH rises if these changes are reversed. pCO2 can be directly assessed, but HCO3– is more of a challenge, as it acutely changes in the same direction as any change in pCO2 since they are in equilibrium with one another through carbonic acid (unrelated to compensation by the kidney, which takes longer). So, to easily assess HCO3–, a parameter called the base excess (BE) is calculated, and it tells whether there is an excess of HCO3– (metabolic alkalosis when BE is +), or a deficit (metabolic acidosis when BE is –).

The present case reflects a mixed acidosis with both a respiratory component (elevated pCO2) and a metabolic component (diminished HCO3– as reflected by the extremely negative BE). The elevated pCO2 is consistent with hypoventilation resulting from smoke inhalation causing loss of consciousness and diminished respiratory drive. The diminished HCO3– is likely related to hypoxia. Several factors can cause a reduction in the partial pressure of oxygen (pO2) in the blood following smoke inhalation, including the reduced rate of ventilation (as suggested by the elevated pCO2), a decrease in pO2 in the environment, and a reduction in the efficiency of gas exchange in the lungs (due to the toxic effects of smoke)2. Our patient’s pO2 was not low upon arrival, likely due to prior administration of O2, but there is evidence of hypoxia, nonetheless.

What is important for the delivery of oxygen to the tissues is the blood’s oxygen content (ctO2), which is the product of the fraction of total hemoglobin that is oxygenated (FO2Hb), the hemoglobin (Hb) level and the O2 carrying capacity of Hb. In this case it is very low (6.2 Vol%), because of a low Hb (unknown whether there was a preexisting anemia or whether it was the result of fluid resuscitation), but more importantly, because of a low FO2Hb. The latter is because CO binds Hb at least 200x as avidly as O2 and so displaces O2 from Hb. In addition, CO reduces the release to the tissues of whatever O2 that is bound, so that tissue hypoxia is compounded. The resulting tissue hypoxia leads to anaerobic metabolism and the production of high levels of lactic acid, causing the high anion gap metabolic acidosis present in this case.

It should be noted that sO2 and FO2Hb both represent the percentage of total Hb saturated by O2 but define total Hb differently. FO2Hb calculation includes all types of Hb in total Hb, while sO2 estimation (from the measured pO2 and a standard oxyhemoglobin dissociation curve) excludes dyshemoglobins like COHb. So, if COHb is present, as in this case, FO2Hb will be smaller than sO2.

References

  1. Gerald F. O’Malley, DO, Rika O’Malley, MD, Carbon Monoxide Poisoning, October 2017 https://www.merckmanuals.com/professional/injuries-poisoning/poisoning/carbon-monoxide-poisoning
  2. Karen L. Wood , MD, Measurement of Gas Exchange, October 2017 https://www.merckmanuals.com/professional/pulmonary-disorders/tests-of-pulmonary-function-pft/measurement-of-gas-exchange
  3. Bishop M, Fody E, Schoeff L, eds. Clinical Chemistry: Principles, Procedures, and Correlations. 8th ed. Philadelphia, Pennsylvania: Wolters Kluwer; 2018.
  4. Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS. Smoke Inhalation Injury Workup; Nov 06, 2018 https://emedicine.medscape.com/article/771194-workup
  5. NSW Agency for Clinical Innovation. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0004/220675/ABG_poster_large.pdf

Minh Kosfeld is program director of IMS and assistant professor of Clinical Health Sciences at Saint Louis University in St. Louis, Missouri.