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INSPIRED GAS
Monitoring the fraction of inspired oxygen (FiO2) is necessary to prevent the
adverse effects of both hypoxaemia and excess oxygen. The inspired oxygen
tension (PiO2) of humidified gas is determined by the FiO2, the barometric
pressure (BP) and the saturated vapour pressure of water (47 mmHg (6.11 kPa)
):
Pio2 = Fi02 x (BP 47)
ALVEOLAR GAS
In a patient receiving 100% oxygen, alveolar PO2 in individual lung units
can range from <40 mmHg to >600 mmHg (<5.2 >78 kPa). Consequently,
end-tidal PO2 monitoring is of little value.
Raised Aa gradient
1. Diffusion defect (rare)
2. V/Q mismatch
3. Right-to-left shunt (intrapulmonary or cardiac)
4. Increased oxygen extraction (CaO2CvO2). Although the Aa gradient is
a component of the
APACHE II, III and IV scoring systems,17,18 several drawbacks limit its
clinical usefulness. They include:
1. Normal values that vary with FiO2 and age. The normal Aa gradient breathing
air is 7mmHg (0.91kPa) in young adults and 14mmHg (1.82kPa) in
the elderly. On 100% oxygen, these values become 31mmHg (4kPa) and
56mmHg (7.3kPa) respectively.
2. An exaggerated FiO2 dependence in intrapulmonary shunt (Fig. 18.1) and even
more so in V/Q mismatch.
CONTENT-BASED INDICES
Venous admixture (Qs/Qt)
Venous admixture is another construct based on the three-compartment
lung model (see above). It represents the proportion of mixed venous blood
flowing through the shunt (V/Q=0) compartment. It is determined according
to the formula:
where CcO2, CaO2 and CvO2 are the oxygen contents of pulmonary end-
capillary, arterial and mixed venous blood respectively. CaO2 and CvO2 are
calculated using data from arterial and mixed venous blood gas analysis and CO-
oximetry. CcO2 must be derived differently, since pulmonary end-capillary blood
cannot be sampled. PcO2 is assumed to equal PAO2 as derived from the alveolar
gas equation. ScO2 (normally close to 1) can then be computed from an algorithm
for the HbO2 dissociation curve.
Arteriol blood
Indices of arterial oxygenation are PaO2 and SaO2. They are linked by the
HbO2 dissociation curve. Hypoxaemia is defined as PaO2<60mmHg
(7.8kPa) or SaO2<0.9. These values lie near the descending por
tion of the HbO2 dissociation curve, so that a further drop in PaO2 leads to a
marked fall in SaO2 and thus CaO2.
TEMPERATURE CORRECTION
All measurements are at 37C. Temperature-corrected values can be
calculated if the core temperature of thepatient is entered into the device software.
Most clinicians interpret blood gas data at 37C, except when evaluating the Aa
gradient (Acidbase balance and disorders).
PULSE OXIMETRY
Pulse oximetry determines SpO2 from the absorbance of light at
wavelengths 660nm (red) and 940nm (infrared) by tissue capillary beds
such as fingers, forehead, earlobes and the nasal septum. Two light-emitting
diodes cycle on and off at multiples of the mains frequency. A single photodiode
detects the transmitted light, and applies a correction for background ambient
light. The emergent signal is pulsatile due to arterial volume fluctuations.
Subtraction of the background signal (tissue, capillary blood and venous blood)
isolates the arterial component.
For both wavelengths, absorbance (A) is determined as follows:
A = log 10 (I0 /I)
where I0=incident light intensity and I=emergent light
intensity. For a given chromophore, A is proportional to its concentration (Beers
law) and to the path length( Lamberts law). From the pulsatile (AC) and
background (DC) absorbance signals at both wavelengths, a ratio (R) is derived:
R = (AC660 /DC660 )/(AC940 /DC940 )
SpO2 is then computed from R, using software look-up tables of
empirically derived relationships between R values and either SaO2 or FHbO2
measured in the arterial blood of volunteers breathing hypoxic gas mixtures.
SpO2 is usually displayed as a percentage. Since the signal is derived from
two wavelengths there is an inherent incorrect assumption that HbO2 and Hb are
the only haemoglobin species in the light path. However, with normal
dyshaemoglobin concentrations the error is trivial. Some manufacturers calibrate
R against FHbO2 (fractional saturation) rather than SaO2 (functional saturation).
Provided volunteers generating the data have normal dyshaemoglobin
concentrations, differences between the two calibrations are small.
SPEED OF RESPONSE
SpO2 is averaged over 36 seconds, and updated every 0.51 second. With
forehead probes a sudden reduction in FiO2 produces a response within 1015
seconds, whereas with finger probes and peripheral vasoconstriction the delay can
exceed 1 minute.
ACCURACY
In the 9097% saturation range, SpO2 has a mean absolute bias of <1%,
and a precision (SD of bias) of <3%. At SaO2<0.8 there is significant
imprecision and a tendency towards negative bias. This is because very low SaO2
values are unsafe in volunteers, necessitating extrapolation from SpO2/R
relationships at higher saturations.
ERROR
Causes of error are set out in. A falsely high SpO2 is of greatest concern.
Unlike CO-oximetry, pulse oximetry is not subject to interference from bilirubin,
lipid emulsions and HbF.
Dyshaemoglobins and pulse oximetry
Pulse oximeters cannot distinguish COHb from HbO2. When [COHb] is
elevated, SpO2 tends to overestimate SaO2. SpO2 can thus provide false
reassurance when hypoxaemia is combined with a high [COHb], for example after
an inhalational burn injury. MetHb has more complex effects, since it absorbs
both wavelengths. At normal saturations, increased [MetHb] causes
underestimation of SaO2, but at very low oxygen tensions overestimation is
possible. At [MetHb]35%, the R value becomes unity, which translates
to SpO2=85%.
PULSE CO-OXIMETRY
Additional continuous real-time non-invasive monitoring of absolute total
haemoglobin concentrations and trends becomes possible with these
multiwavelength devices. Accuracy remains acceptable in low perfusion states
and in patients requiring vasopressor support.
DO2/VO2 RELATIONSHIPS
Nearly 40 years ago an association was reported between hyperdynamic
oxygen flow patterns and survival after high-risk non-cardiac surgery. This led to
the concept that maintaining an induced perioperative hyperdynamic state to
prevent an acquired oxygen debt might be protective. Although supported at a
singlecentre level, this hypothesis was not validated by large multicentre studies.
In fact, aggressive pursuit of hyperdynamic goals seemed counterproductive for
the broad ICU population.
Common therapeutic goals were CI>4.5L/min/m2, DO2
I>600mL/min/m2, VO2 I>170mL/min/m2. How ever the VO2 I
target was especially difficult to achieve. The focus subsequently narrowed to the
DO2 I target alone, which removed the need for PA catheterisation. On this basis
there is better emerging evidence of benefit in high-risk surgery,4143 although
definitive multicentre confirmation is awaited.
MEASURING DO2I
Although DO2 I determinations require accurate measurements of CI and
CaO2 , a PA catheter is not essential. Normal ranges can be quoted, but oxygen
demand in critical illness is so variable that isolated DO2 I measurements are
difficult to interpret.
MEASURING VO2I
The two methods of measuring VO2 I are the reverse Fick method and
indirect calorimetry.
Indirect calorimetry
Indirect calorimetry has better accuracy. VO2 I is determined from the
volumes and oxygen concentrations of inspired and expired gas. However, high
FiO2 settings introduce error. Newer devices retain accuracy up to
FiO2=0.8, with relative errors of <5%.