Hyperbaric oxygen (HBO) exerts its effects by elevation of the inspired gas together with an increased proportion of inspired oxygen. The consequences of the latter will be discussed in the present chapter. In this context oxygen has to be considered a drug with its pharmacological properties, indications, contraindications and side effects.
The term "oxygen transport" encompasses the global balance between supply and demand of oxygen. Overall oxygen supply can be determined in the clinical setting whereas the assessment of oxygen demand is much more difficult.
Oxygen moves down a pressure gradient from inspired to alveolar gas, arterial blood, the capillary bed, across the interstitial and intercellular fluid to the sites of utilization within the cell (perioxome, mitochondria, endoplasmic reticulum). Under normobaric conditions, the gradient of oxygen partial pressure (pO2) known as the "oxygen cascade"1 starts at 21.2kPa (159mm Hg) and ends up at 0.5-3kPa (3.8-22.5mm Hg) depending on the target tissue.
The pO2 of the alveolar gas may be calculated by the alveolar gas equation (see chapter 1.3, section 2.3.1).
This equation is applicable for hyperbaric conditions. PaCO2, water vapour pressure and respiratory quotient (RQ) do not vary significantly between 100kPa and 300kPa (1 - 3bar). Thus, for example2, the inhalation of 100% oxygen at 202.6kPa (2ata) provides an alveolar PO2 of 1423mm Hg. The alveolar gas equation calculates the "ideal" alveolar gas without consideration of influencing factors like ventilation-perfusion inequalities or pre-existing atelectasis.
In a next step, the alveolar oxygen passes the alveolar-capillary space and diffuses into the venous pulmonary capillary bed according to Fick's Laws of Diffusion. The majority of the oxygen is then transported bound to haemoglobin, whilst a very small amount remains dissolved in plasma which may be quantified and formulated in the "oxygen content equation" (see next page).
There is still controversy about the oxygen-combining capacity of haemoglobin with values ranging between 1.306mL/g to 1.39mL/g in an adult depending on the mode of analysis.
The fraction of oxygen bound to haemoglobin is quantitatively most important whereas the fraction of dissolved oxygen is very small. However, the amount of oxygen dissolved in plasma is mainly responsible for the availability of oxygen diffusing through the interstitial fluid and the cell membrane. The amount of oxygen dissolved in the blood is determined by Henry's Law, which states that the concentration of a gas in a fluid (mL of gas dissolved/unit volume of water) is proportional to its pressure and to its solubility coefficient:
O2 content = Hb-bound O2 + O2 dissolved in plasma CaO2 = SaO2 x Hb x 1.34 + 0.003 x PaO2
CaO2 = mL O2/100mL arterial blood;
SaO2 = percentage of haemoglobin saturated with O2, expressed as decimal fraction Hb = haemoglobin content (g/100mL blood) 1.34 = Oxygen-binding capacity of haemoglobin (Hufner's number)
indicating that 1g Hb may bind 1.34mL O2 when fully saturated with oxygen 0.003 = solubility constant for dissolved O2 in plasma corresponding to
0.003mL O2/100mL plasma/mm Hg PaO2 PaO2 = arterial blood pO2
With air breathing 0.32mL of O2 are dissolved in 100mL plasma (% by volume) increasing up to 6.8mL O2/100mL plasma with breathing 100% O2 at 303.9kPa. This amount equates to the global arterial/mixed venous oxygen content difference (C[a-v] O2) which is able to cover the basic metabolic needs of an individual at rest with normal cardiac output. Boerema3 verified this hypothesis in his fundamental animal experiment "Life without blood" which became a hallmark in hyperbaric medicine research.
Arterial blood pO2 is influenced by the pulmonary ventilation/perfusion pattern (V/Q ratio) and by the amount of pulmonary venous admixture or right-to-left intrapulmonary or intracardiac shunting. To some extent, exposure to HBO may affect pathologic conditions due to the large increase of PaO2. Nevertheless, acute or chronic alterations of gas exchange may provide an insufficient level of PaO2. Therefore, monitoring of blood gases is important to evaluate whether the desired level of oxygen as a therapeutic goal is reached in the hyperbaric environment.
Transport of oxygen from the lung to the cell1 is achieved by the circulatory system. The quantity of oxygen globally transported to cells is known as "oxygen delivery" which is proportional to cardiac output and arterial oxygen content. Oxygen delivery may be determined according to the following equation:
DO2 = delivery of oxygen (mL/min). CO = cardiac output (mL/min).
According to the Fick principle, the amount of oxygen consumed by the whole body per unit of time (VO2) is equal to blood flow (i.e., cardiac output), multiplied by the amount of oxygen extracted by the body. This can be calculated as the difference between the content in the arterial blood and that in the mixed venous blood within the pulmonary artery (C[a-v]O2). Thus, hypothetically, the increased supply of oxygen under hyperbaric conditions could favour an augmentation of oxygen consumption and a better coverage of metabolic demands in conditions where VO2 depends on DO2.
Equally, oxygen consumption of any organ can be calculated as the difference between the amount of oxygen delivered by its arterial supply and the amount of oxygen in its venous drainage multiplied by the blood flow:
Q = organ perfusion (L/min)
[O2]a = CaO2 arterial blood entering the organ (measured) [O2]v = CvO2 venous blood leaving the organ (measured).
Oxygen extraction ratio (EO2) is defined as the ratio between consumed and delivered oxygen:
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