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Arterial blood gas analysis applies blood gas analysis to a sample taken from an artery, providing a time-specific observation of systemic arterial gas tensions and acid-base state. Arterial oxygen partial pressure concerns oxygen tension, while arterial carbon-dioxide partial pressure and pH provide different information. The arterial qualifier is a sampling condition, not merely a label attached to any blood result.^[ref]

The measurement chain includes obtaining an identified sample, preserving its gas composition and analyzing it with a checked instrument. Air contamination, fluid contamination and analysis delay can change the specimen after it leaves the circulation. A reproducible analyzer reading cannot repair a specimen that no longer represents the intended physiological state.^[ref]

Equal oxygen tension need not mean equal arterial oxygen content. An original illustrative carrier model writeswhere $H$ is hemoglobin concentration, $s$ its oxygen-bound fraction and $h$ the carrier capacity per gram. Choose $h=1.34$ mL/g, $\alpha =0.003$ mL/(dL·mmHg), $s=0.98$ and $P_{\mathrm{a}{O}_2}=100$ mmHg. Samples with $H=15$ and $H=7.5$ g/dL then contain about 20.00 and 10.15 mL O${}_2$/dL, respectively. They have identical stipulated tension and saturation but very different oxygen content. The constants define the illustration; these are not patient results or diagnostic thresholds.

Interpretation also depends on the conditions when the sample was obtained. Inspired oxygen fraction, ventilator settings when applicable and sampling time help distinguish a changed respiratory state from a changed measurement condition. A later pulse oximetry reading is neither a simultaneous sample nor a measurement of carbon-dioxide tension.

Arterial blood gas analysis supplies evidence about gas transport and acid-base balance, but no individual number alone identifies the entire cause of an abnormal result. Measured co-oximetry and calculated oxygen saturation should also be distinguished when unusual hemoglobin species matter.^[ref]

Hypoxemia, also spelled hypoxaemia, is reduced oxygenation of arterial blood. Its characterization must identify what was measured: arterial oxygen partial pressure, oxygen saturation and arterial oxygen content are related quantities with different meanings. Hypoxia concerns inadequate oxygen availability to tissue, rather than simply naming an arterial measurement.

An arterial blood gas analysis measures the pressure of dissolved oxygen. Pulse oximetry instead estimates oxygen saturation optically; its output is not a direct partial-pressure measurement.^[ref] This distinction explains why the observation and instrument should accompany a report of reduced oxygenation.

A counting example separates saturation from oxygen amount. Suppose 100 available hemoglobin binding sites have 90 oxygen molecules bound: the occupied fraction is $90/100=0.90$. Doubling the number of sites to 200 while keeping that fraction gives 180 bound molecules. The saturation is unchanged although the amount bound has doubled. This is a constructed binding-site count, not a conversion between oxygen saturation and partial pressure.

Likewise, oxygen carried per unit blood and blood delivered per unit time enter different factors. If $C_a$ is arterial oxygen content and $Q$ is blood flow, then the transported amount per unit time is $Q{C}_a$. Stipulated values $C_a=0.20\mathrm{L}{\mathrm{L}}^{-1}$ and $Q=5\mathrm{L}\mathrm{mi}{\mathrm{n}}^{-1}$ give $1\mathrm{L}\mathrm{mi}{\mathrm{n}}^{-1}$; halving $Q$ halves that transport without changing $C_a$. The example shows why one arterial oxygen measurement cannot by itself describe oxygen delivery to every tissue. It is not a diagnostic reference range or a treatment rule.

Pulse oximetry estimates arterial oxygen saturation noninvasively from wavelength-dependent optical signals that vary with the arterial pulse. A typical sensor combines red and infrared light-emitting diodes with a photodetector. The pulsatile component helps distinguish changing arterial blood contribution from relatively steady tissue and blood contributions; it is not a direct measurement of arterial oxygen partial pressure.

A primary instrument-design note implements 660 nm and 940 nm illumination, a shared photodetector and alternating channel acquisition. It separates pulsatile and steady components before estimating saturation.^[ref] These wavelengths and electronics describe that implementation rather than every possible sensor.

Writing pulsatile and steady signal magnitudes as AC and DC, a common normalized optical quantity isFor original channel values AC${}_{\mathrm{red}}=0.01$, DC${}_{\mathrm{red}}=1.0$, AC${}_{\mathrm{IR}}=0.02$ and DC${}_{\mathrm{IR}}=1.0$, this ratio is 0.5. Halving both red-channel magnitudes leaves the ratio unchanged. This illustrates intensity normalization; it does not determine a saturation without a validated relation between $R$ and saturation.

That relation is experimentally checked against an independent reference. The FDA's technical guidance describes comparing oximeter readings with simultaneous co-oximetry of arterial samples during controlled inspired-oxygen changes in volunteers, and reporting an accuracy statistic.^[ref] Such comparisons test the whole sensor–algorithm measurement chain, rather than only the arithmetic of a two-channel ratio.

One summary is the root mean square differenceFor invented paired errors $-2,0,+2$ percentage points, $A_{\mathrm{rms}}=\sqrt{8/3}\approx 1.63$ percentage points even though mean error is zero. A small mean bias does not guarantee small individual errors.

Motion, weak pulsatile signals and additional absorbing hemoglobin species can invalidate assumptions behind a simple estimate. Pulse oximetry does not measure pH, carbon-dioxide tension or hemoglobin concentration. A stable displayed percentage therefore cannot establish every aspect of ventilation, oxygen content or gas exchange.