aOdos (produced, for example, by an increase in the rate or depth of ventilation or by breathing supplemental oxygen) is accompanied by a rise in the arterial oxygen saturation. However, because of the shape of the dissociation curve ( figure 1 ), the proportional increases are very different. Since the dissociation curve is relatively flat when the oxygen saturation is >90%, increases in PaO2 have relatively little impact on saturation or content in this range. Clearly, as SaO2 approaches 100% (equivalent to a PaO2 greater than about 17 kPa or 128 mmHg), there can be no further increase in saturation however high the PaO2 rises. However, breathing increasingly higher oxygen concentrations continues to increase the PaO2 and there will also be a small, progressive rise in oxygen content of the blood, due to the small, though increasing, amount dissolved (as, indeed, would also happen with water exposed to a high PO2). Paradoxically, however, a very high PaO2 may reduce oxygen delivery to the tissues due to other physiological effects such as vasoconstriction or reduction in cardiac output .
By contrast, when PO2 falls below 8 kPa (60 mmHg) there is a steep decline in oxygen saturation ( fig. 1 ). This situation has been described as a “slippery slope” as small reductions in PaO2 are accompanied by disproportionately large reductions in oxygen saturation and content and therefore in oxygen delivery. To some extent the reduced oxygen delivery is countered by the greater ease with which oxygen can be “offloaded” to the metabolising tissues.
Generally, a rise in P
aO2 in a severely hypoxaemic individual is likely to result in a marked improvement in oxygen saturation, content and supply. This phenomenon underlies the use of only small increments of inspired oxygen (e.g. using a Venturi mask to deliver 24% or 28% oxygen compared with 21% in room air) in the treatment of patients with hypercapnic respiratory failure, in whom higher oxygen concentrations are likely to result in worsening hypercapnia [2, 3].
For most adult patients the optimal target oxygen saturation is 94–98%; an important exception is those at risk of CO2 retention, in whom a lower target saturation is appropriate, because a greater increase in arterial oxygenation in these patients is likely to cause a concomitant and potentially harmful rise in the arterial CO2 pressure (PaCO2) .
Just as, although not, so it portion of the dissociation curve would be considered a “life-rescuing escalator” once the a little upsurge in P
The relation between blood oxygen saturation (or content) and partial pressure is not constant, even within an individual. Classically the factors recognised to influence the oxygen dissociation curve (ODC) include the local prevailing CO2 partial pressure (PCO2), pH and temperature. The curve is shifted to the right (i.e. lower saturation for a given PO2) by higher PCO2, greater acidity (lower pH) and higher temperature. The effect of PCO2 (known as the “Bohr effect”) is mediated largely by the accompanying change in acidity; in vitro studies have shown that PCO2 itself also has an independent effect, which becomes most evident under more acidic and severely hypoxic conditions https://datingranking.net/pl/love-ru-recenzja.
The factors which shift the ODC to the right (lower pH, higher temperature and PCO2) are directly relevant to the conditions which prevail in metabolising tissues and consequently, as blood flows through the tissues, the ODC shifts to the right. This implies a reduction in the affinity of the blood for oxygen (for a given PO2, venous blood contains less oxygen than arterial blood), which is advantageous as it facilitates the unloading of oxygen from haemoglobin in the tissues. The converse occurs during passage through the pulmonary capillaries, with the greater affinity accompanying a shift of the ODC to the left aiding the uptake of oxygen.