|Year : 2017 | Volume
| Issue : 4 | Page : 280-283
The partial pressure of oxygen in arterial blood: A relation with different fraction of inspired oxygen and atmospheric pressures
NK Agarwal, Sumit Trivedi
Department of Anasthesiology, JNMC, DMIMS (Deemed to be University), Wardha, Maharashtra, India
|Date of Web Publication||17-May-2018|
Dr. N K Agarwal
Department of Anasthesiology, JNMC, DMIMS (Deemed to be University), Sawangi (M), Wardha, Maharashtra
Source of Support: None, Conflict of Interest: None
As an anesthesiologist and critical care intensivist, it is mandatory to have thorough knowledge of variable partial pressure of oxygen, at different fraction of inspired oxygen (FiO2), and effect of various atmospheric pressures in alveoli, diffusion, and transport of oxygen to tissue. The partial pressure of oxygen in arterial blood gas shall always be expressed with respect to the atmospheric pressure and FiO2; unless these conditions are mentioned, one may not be able to assess the exact respiratory status of patient.
Keywords: Alveolar ventilation, Arterial blood (partial pressure of oxygen), fraction of inspired oxygen
|How to cite this article:|
Agarwal N K, Trivedi S. The partial pressure of oxygen in arterial blood: A relation with different fraction of inspired oxygen and atmospheric pressures. J Datta Meghe Inst Med Sci Univ 2017;12:280-3
|How to cite this URL:|
Agarwal N K, Trivedi S. The partial pressure of oxygen in arterial blood: A relation with different fraction of inspired oxygen and atmospheric pressures. J Datta Meghe Inst Med Sci Univ [serial online] 2017 [cited 2019 Jul 16];12:280-3. Available from: http://www.journaldmims.com/text.asp?2017/12/4/280/232580
| Introduction|| |
As an anesthesiologist and critical care intensivist, it is mandatory to have thorough knowledge of variable partial pressure of oxygen, at different fraction of inspired oxygen (FiO2), and effect of various atmospheric pressures in alveoli, diffusion, and transport of oxygen to tissue. The partial pressure of oxygen in arterial blood gas (ABG) shall always be expressed with respect to the atmospheric pressure and FiO2; unless these conditions are mentioned, one may not be able to assess the exact respiratory status of patient.
We are presenting few respiratory equations which may be useful to assess and evaluate the alveolar ventilation and diffusion of gases; we are also suggesting a new equation to assess the percentage of lung damage at alveoli level.
The atmosphere is composed of various gases such as O2, N2, CO2, inert gases, and water vapors. The normal pressure is 760 mmHg, at absolute zero, which is comprised of the following when described in terms of percentage:
- O2– 20.8%
- N2 – 78%
- CO2– 0.45%
- Inert gases – 0.2%
- Water – 0.65%.
These all to be multiplied by 7.6 to have partial pressure of each gases in atmosphere; this may be expressed like
The alveoli are main respiratory surface in human being, they are small sacs of branching of bronchioles, and they are one cell thick and provide large area for gas exchange.
If all other factors are kept constant, the main factors are surface area and thickness of alveoli. The gas exchange is hence inversely proportional to thickness; the more is the thickness, less will be diffusion. Patients with chronic bronchitis, chronic obstructive pulmonary disease, fibrosis pneumonia, and acute respiratory distress syndrome have changes in thickness and surface area.
Partial pressure of H2O is 47 mmHg.
If the patient is given 100% oxygen, all the gases are replaced by oxygen except H2O and CO2; this is denitrogenation.
Hence, to calculate the partial pressure of oxygen in alveoli at different FiO2,
The formula is as given,
As per the change in ambient pressure, there is change in partial pressure of oxygen; however, the FiO2 remains same, i.e. 0.21, but as we go up to higher altitudes, there is a decrease in atmospheric pressure simultaneously with partial pressure of gases (Eq. 1).
At different altitude, the partial pressure of oxygen PiO2, PAO2, and PaO2 is given in [Table 1].
|Table 1: The partial pressure of oxygen PiO2, PAO2, and PaO2 at different altitude|
Click here to view
Similarly, as we go under sea, there is addition of ambient pressure to atmosphere; for every 33 ft drop in sea level, there is an addition of one atmospheric pressure, hence increase in partial pressure of gases [Table 2].
The amount of normal oxygen dissolved in plasma at FiO2 of 0.2 is 0.3 ml/dl, this increases with increase in fraction of oxygen inspired; at FiO2 of 1, it amounts to be 1.8 ml/dl, it increases with absolute atmospheric pressure.
Depending on the ambient pressure, there is linear change in partial pressure of gases mainly oxygen.
When there is an increase in FiO2 from 0.21 to 1, there is increase in partial pressure of oxygen in alveoli [Eq. 2].
The partial pressure of oxygen at alveolar level at FiO2 of 0.21 is
PAO2= 0.2 × (760 − 47) − 1.25 × 32
= 104 mmHg
At FiO2 of 0.6, the partial pressure of oxygen at alveolar level will be
PAO2= 0.6 × 713 − 40
= 427 − 40
= 387 mmHg
Similarly at FiO2 of 1 or 100% inspired oxygen,
PAO2= 1 × 713 − 40
= 673 mmHg
The atmospheric or the alveolar gases are exchanged to blood through small sacs of cell, the alveoli. Exchange is affected by as many as five factors which are
- The thickness of alveoli
- The surface of alveoli
- The pressure gradient of gases
- The molecular weight of gases
- The blood–gas solubility.
The alveolar ventilation is part of gas that participates in gas exchange.
Alveolar arterial ventilation = (tidal volume − dead space) × respiratory rate.
These are the main factors that affect the exchange of gases in the alveoli.
As the partial pressure of oxygen is increased in air simultaneously, the partial pressure increases in alveoli and hence in blood.
Mainly, oxygen is carried by hemoglobin; one gram of hemoglobin carries 1.31 ml of oxygen, and there is 0.3 ml/dl of dissolved oxygen in plasma; if hemoglobin level is 15 gm/dl, then total oxygen carried by 100 ml of blood is equal to 19.7 ml/dl; this is at normal air breathing or FiO2 of 0.21; when the FiO2 is increased, there is linear increase in dissolve oxygen in plasma, which increases up to 1.8 ml/dl.
One more gradient that plays role in assessment is P(A − a) O2 difference, which is 5–20 mmHg at FiO2 of 0.21 increases up to 110 mmHg at FiO2 of 1. This is an important gradient to assess the alveoli or parenchymal damage. When the A − a gradient is >400, it refers to severe distress.
The normal PaO2/PAO2 gradient is 5–7 mmHg, for every rise of 10% FiO2,
K is loss of gases at alveoli level (at FiO2 21%–40% = 0.05, 40%–60% = 0.10, 60%–80% = 0.15, 80%–100% = 0.2)
Using the below equation, we can calculate the lung damage
ADD = Alveolar diffusion damage
The normal PaO2/FiO2 ratio is >400 mmHg
It is an important ratio to diagnose the diffusion defect; a ratio ≤200 mmHg is indicative of acute respiratory distress syndrome according to American-European Consensus Conference criteria.
A ratio ≤250 is must to label severe community-acquired pneumonia while a ratio ≤333 is necessary to label damaged alveoli.
| Application|| |
It is mandatory to supplement oxygen under the following conditions:
- Increased myocardial demand
- Increased work of breathing
- Pulmonary hypertension
- High altitude.
This may be achieved with
- Nasal cannula
- 1–6 L/min
- PAO2 not predicted.
- Simple mask
- 5–8 L/min (minimum 5 L to flush 2 from mask)
- FiO2 0.35–0.55
- PAO2-209–352 mmHg.
- Venturi mask
- As per nozzle
- FiO2 0.24–0.5
- PAO2-131–260 mmHg.
- Partial retreater
- 6–10 L/min
- FiO2 0.50–0.70
- PAO2-260–459 mmHg.
- 6–10 L/min
- FiO2 0.50–1
- PAO2-240–673 mmHg.
These are the few basics ways which help the patients with respiratory insufficiency.
This is also suggested that in cases of cardiovascular insufficiency, one must not forget to start high FiO2, as it will increase the dissolved oxygen, hence supply to tissue.,,,,,
| Case Reports|| |
A 12-year-old boy posted for laparotomy for intussusceptions under general anesthesia; during intubation, the boy aspirated. After the surgery was over, the boy was shifted to pediatric Intensive Care Unit (ICU), where he was kept on continuous positive airway pressure. The ABG values were FiO2– 1, EtCO2– 32, and PaO2: 78. The intensivist said PaO2 adequate; using above formula ours interpretation was totally different, see how?
PAO2= 1 × (760 − 47) – 1.25 × 32
= 1 × 713 − 40
= 673 mmHg
EPaO2= 0.8 PAO2
= 0.8 × 673
= 538 mmHg
With above alveolar partial pressure, expected PaO2 will be 538.
Due to damage to alveoli, there is lack in diffusion of oxygen.
Now will see how much is the damage to lungs?
= 0.85 × 100
What it was appearing on ABG was not the actual condition of the patient; there was 85% lung injury; as the FiO2 and atmospheric pressure were not considered, we lost the patient.
A 40–year-old male patient was posted for diaphragmatic hernia repair on the right side. During preoperative visit, it was noticed that the patient was clinically comfortable; there were crepts on the affected side with forced expiratory volume-1 s (FEV1), FEV1/forced vital capacity ratio near normal. The X-ray chest posteroanterior view was normal, we know thau unless the lateral view is done, respiratory investigation are not considered complete, and the lateral view was showing hazy lung fields on the right side. The surgeons were constantly pressurizing for fitness, at last we advised them to do ABG; to our expectation, it showed PaO2 57 mmHg, we calculated the probable lung damage.
PAO2 =0.2× (760 − 47) – 1.25 × 32
= 147 − 40
EPaO2 = PAO2× (1 − 0.05)
= PAO2 ×0.95
= 0.95 × 107
= 101 mmHg
We interpreted that the patient is having 44% lung damage, the surgery was postponed for 2 weeks, patient advised treatment after two weeks ABG improved to 87 mmHg, the patient did well in postoperative period.
Here, we conclude with interpretation that always ABG should be read with respect to FiO2 and atmospheric pressure and the PaO2 values are significant and change with FiO2 and atmospheric pressure. The respiratory equations available should be used to interpret the alveolar diffusion damage in ICU or in preoperative phase.,,
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Harris EA, Kenyon AM, Nisbet HD, Seelye ER, Whitlock RM. The normal alveolar-arterial oxygen-tension gradient in man. Clin Sci Mol Med 1974;46:89-104.
West JB. Respiratory Physiology – The Essentials. 4th
ed. Baltimore: William and Wilkins; 1990.
Hughes JM, Bates DV. Historical review: The carbon monoxide diffusing capacity (DLCO) and its membrane (DM) and red cell (Theta. Vc) components. Respir Physiol Neurobiol 2003;138:115-42.
Thomas EJ Healy (Editor). Respiratory Physiology. 7th
ed. Lippincott Williams & Wilkins: Wyeli and Churchill; 2005. p. 168-9.
Nunn JF. Alveolar air equation. Anesthesiology 1996;85:946.
Story DA. Alveolar oxygen partial pressure, alveolar carbon dioxide partial pressure, and the alveolar gas exchange. Anesthesiology 1996;84:1011.
Severinghaus JW, Astrup P, Murray JF. Blood gas analysis and critical care medicine. Am J Respir Crit Care Med 1998;157:S114-22.
Law R, Bukwirwa H. Update in Anesthesia. 1999. p. 20-5.
Maya Martínez M, Carrión Valero F, Díaz López J, Marín Pardo J. Barometric pressure and respiratory quotient for estimating the alveolar-arterial oxygen gradient. An Med Interna 2000;17:243-6.
Mansoor R. Murray and Nadel's Text Book of Respiratory Medicine. 5th
ed. Philadelphia, PA: Elsevier; 2014.
Paul R Knight (Editor). Wylie and Churchill Davidson. 7th
ed. Taylor and Francis Group: 2003. p. 168-9.
[Table 1], [Table 2]