Intensive Care Med (2018) 44:91–93
DOI 10.1007/s00134-017-4824-y
UNDERSTANDING THE DISEASE
Understanding blood gas analysis
Luciano Gattinoni1*, Antonio Pesenti2 and Michael Matthay3
© 2017 Springer-Verlag Berlin Heidelberg and ESICM
Introduction
Blood gas analysis is probably the most common diag-
nostic tool used in intensive care. In fact, a proper under-
standing and use of arterial and pulmonary/central
venous blood gas and electrolytes analysis makes it pos-
sible to correctly interpret most of the respiratory, circu-
latory and metabolic derangements which may occur in
critically ill patients.
Blood gas analysis variables
Before discussing their clinical use, we would like to
underline some the characteristics of the blood gas analy-
sis variables which are usually ignored. Indeed, it is worth
noting that:
••  The reported hemoglobin oxygen carrying capacity
coefficients ­(mLO2/g) vary quite surprisingly from
1.32 to 1.36 or 1.39; this reflects the different molecu-
lar weights attributed to hemoglobin (from 64,000 to
67,000 Da).
••  These hemoglobin oxygen-carrying capacity coeffi-
cients are used to compute other variables such as:
oxygen transport ­(DO2), the arterial–venous differ-
ence (ΔavO2), oxygen consumption by reverse Fick’s
method ­( VO2  =  ΔavO2*CO, where CO is cardiac
output in L/min  ×  10) and the Riley’s shunt frac-
tion [Qs/Qt  =  (CcO2−CaO2)/(CcO2−CvO2)] [1].
The use of different coefficients may primarily affect
the ΔavO2 and the ­VO2 if measured by reverse Fick’s
method [2].
••  The total ­CO2 given by the blood gas machines refers
to the ­CO2 content of plasma and not to the whole
blood, which is lower by 5–10  mmol/L. Indeed, the
*Correspondence: gattinoniluciano@gmail.com
1
Department of Anesthesiology, Emergency and Intensive
Care Medicine, University of Göttingen, Robert‑Koch‑Straße 40,
37075 Göttingen, Germany
Full author information is available at the end of the article
­CO2 content in the red blood cells is lower than in
plasma due to the lower pH in the red cells.
••  Different blood gas machines, for the same pH and
­PCO2, provide different values of ­ HCO3− up to
2 mmol/L in cases of severe acidosis or alkalosis, due
to differences in the implemented algorithms.
••  The base excess (BE), i.e., the difference between
the actual and the ideal buffer base (i.e., the sum of
­HCO3−, dissociated proteins, and ­HPO42−, measured
at ­PCO2 40  mmHg, pH 7.40 and proteins 70  g/L)
is equal to the strong ion difference (SID). In the
venous blood, the base excess is always higher than in
the arterial blood by 1.5–2 mmol/L due to the lower
pH and higher ­PCO2 (leading to higher ­HCO3−).
Clinical use
Arterial sampling
Arterial sampling allows the precise assessment of oxy-
genation ­(PaO2 and hemoglobin saturation, either com-
puted or directly measured by oximetry), of ventilatory
status ­(PaCO2) and of acid–base equilibrium (BE and
pH). It should be noted, however, that the oxygena-
tion status may be clinically assessed by pulse oximetry,
although keeping in mind its limitations, such as the
presence of carboxy- and meta-hemoglobin, severe ane-
mia or vasoconstriction so severe as to impede signal
transmission.
Central venous sampling
The central venous sampling is inadequate to assess the
efficacy of oxygenation, which, however, may be esti-
mated by pulse oximetry. In contrast, both venous P ­ CO2
and BE are well related to the arterial ones (3–5 mmHg
and 1–2  mmol/L higher, respectively). Therefore, res-
piratory and metabolic status may be assessed by central
venous blood plus pulse oximetry. In addition, the central
venous sampling provides the central venous oxygen sat-
uration ­(SatvO2), which is an extremely sensitive monitor
92
of variations of respiratory, hemodynamic and metabolic
homeostasis. Indeed:
VO2 (mL/min) 1
Satv O2 = Sata O2 − · ARDS patients [7]. Indeed, the computed dead space
Q(L/min) Hb(g/L) · 1.39
Metabolism 1
Satv O2 = Lung − · the shunt increases [8]. Therefore, physiological dead
Hemodynamics Oxygen carrying capacity
As shown, whatever change in lung function, hemo-
dynamics, metabolism or oxygen transport affects
­SatvO2. Indeed, S
­ atvO2 does not tell us which one of the
basic vital functions is impaired (i.e., it is not specific),
but it monitors immediately their alterations (i.e., it is
extremely sensistive). Therefore, sampling the central
venous blood in patients in whom pulse oximetry is avail-
able provides more information than the arterial blood
analysis.
Dual sampling
Several important data variables may be acquired with
the dual sampling. Here, we will focus particularly on
the shunt fraction and on the pulmonary dead space
assessment.
Shunt fraction
The shunt fraction, correctly named venous admixture if
measured at an F ­ iO2 lower than 1.0, quantifies the frac-
tion of cardiac output flowing through pulmonary units
with a low or nil ventilation/perfusion ratio. It represents
the best estimate of the oxygenation status, although
rarely used in intensive care medicine, where the oxygen-
ation assessment is usually performed by computing the
­PaO2/FiO2 (P/F) ratio (mmHg). The limits of the P/F ratio
in the oxygenation assessment [3, 4] are shown in Fig. 1,
where we plot the P/F ratio as a function of shunt at dif-
ferent levels of F
­ iO2. As shown, the same patient with
30% true shunt may be classified as severely, moderately
or even mildly hypoxemic [5], depending on the delivered
­FiO2. The discrepancy between the venous admixture
and the P/F ratio is particularly relevant for shunt frac-
tions between 0.2 and 0.3.
Pulmonary dead space
The dead space measurement requires both the P ­ aCO2
and mixed expired P ­ CO2 (physiological dead space) or
the end-tidal ­P CO2 (alveolar dead space). This meas-
urement has also been almost abandoned in the ICU,
as the ­P CO2 levels are not usually considered a rel-
evant clinical problem. However, omitting the dead
space measurement means leaving out an excellent
bedside indicator of the structural changes of the lung
[6], and one of the best prognostic factor available in
increases not only when the ventilation of the pulmo-
nary units with high VA/Q increases but also when
space is a strong indicator of the overall function of
the pulmonary gas exchanger (pulmonary dead space
and shunt).
Respiratory, hemodynamic and metabolic relationships
Beyond the shunt fraction and the dead space, the simul-
taneous sampling of arterial and central venous blood
allows the diagnosis and monitoring of several other
pathophysiologic conditions:
••  Respiratory: beyond the usual assessment of oxygena-
tion ­(PaO2 and P/F ratio) and ventilation (­PaCO2),
the measurement of venous admixture makes it pos-
sible to quantify the impact of hemodynamics on
oxygenation. Indeed, it is known (but usually forgot-
ten or ignored) that cardiac output and shunt are
related. A decrease of cardiac output decreases the
shunt and increases the oxygenation [9]. As an exam-
ple, an increase in the ­PaO2 with PEEP loses its clini-
cal pertinence if associated with a decrease in ­SvO2,
indicating a probable decline in cardiac output, and
that the change in oxygenation is more hemody-
namic than recruitment-related.
••  Hemodynamic: impending hemodynamic insuf-
ficiency may be easily detected by a decline in the
­SvO2 and by widening of the veno-arterial difference
in oxygen content; this happens as the first mecha-
nism before energy crises (tissue hypoxemia and
anaerobic metabolism) may occur. It is worth noting,
however, that a lowering of ­SvO2 and widening of
ΔavO2 are warning signals not necessarily indicating
an energy crisis.
••  Metabolic: the occurrence of energy crises due to tis-
sue hypoxemia is manifested by several signals, all
related to the partial shift of metabolism from aero-
bic to anaerobic: primarily a decrease of pH, worsen-
ing base excess, a decrease of strong ion difference
(SID), an increase of veno-arterial difference in ­PCO2
and of its ratio to the ΔavO2 [10], together with an
increase in plasma lactate. In the presence of these
signs, treatment and careful monitoring of its effects
should follow immediately.
 93

500.0

400.0

300.0
FiO2 0.21
P/F rao

mild FiO2 0.40

FiO2 0.60
200.0 FiO2 0.80
FiO2 1.00
moderate

100.0

severe
0.0
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7
Shunt
Fig. 1  The ­PaO2/FiO2 ratio as a function of shunt at different ­FiO2 levels. Data computed with Kelman’s subroutine [11], assuming an oxygen con-
sumption of 250 mL/min, cardiac output 5 L/min, temperature 37 °C, ­PaCO2 40 mmHg and pH 7.40. The intervals used to define mild, moderate and
severe oxygenation impairment are represented with different colors (light blue, yellow and red, respectively)

Author details 2. Gattinoni L, Carlesso E (2009) Chapter 124: arterial and venous blood
1
 Department of Anesthesiology, Emergency and Intensive Care Medicine, gases. In: Ronco C, Bellomo R, Kellum JA (eds) Critical care nephrology,
University of Göttingen, Robert‑Koch‑Straße 40, 37075 Göttingen, Germany. 2nd edn. Saunders, Philadelphia
2
 Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, University 3. Aboab J et al (2006) Relation between PaO2/FIO2 ratio and FIO2: a math-
of Milan, Milan, Italy. 3 Cardiovascular Research Institute, University of Califor- ematical description. Intensive Care Med 32(10):1494–1497
nia, San Francisco, San Francisco, USA. 4. Karbing DS et al (2007) Variation in the PaO2/FiO2 ratio with FiO2: math-
ematical and experimental description, and clinical relevance. Crit Care
Compliance with ethical standards 11(6):R118
5. ARDS Definition Task Force et al (2012) Acute respiratory distress syn-
Conflicts of interest drome: the Berlin definition. JAMA 307(23):2526–2533
On behalf of all authors, the corresponding author states that there is no 6. Gattinoni L et al (1994) Lung structure and function in different stages of
conflict of interest. severe adult respiratory distress syndrome. JAMA 271(22):1772–1779
7. Nuckton TJ et al (2002) Pulmonary dead-space fraction as a risk factor
Ethical approval for death in the acute respiratory distress syndrome. N Engl J Med
This article does not contain any studies with human participants or animals 346(17):1281–1286
performed by any of the authors. 8. Suarez-Sipmann F et al (2013) Corrections of Enghoff’s dead space for-
mula for shunt effects still overestimate Bohr’s dead space. Respir Physiol
Funding Neurobiol 189(1):99–105
None. 9. Dantzker DR, Lynch JP, Weg JG (1980) Depression of cardiac output is a
mechanism of shunt reduction in the therapy of acute respiratory failure.
Chest 77(5):636–642
Received: 10 April 2017 Accepted: 26 April 2017 10. Mekontso-Dessap A et al (2002) Combination of venoarterial PCO2
Published online: 11 May 2017 difference with arteriovenous O2 content difference to detect anaerobic
metabolism in patients. Intensive Care Med 28(3):272–277
11. Kelman GR (1967) Digital computer procedure for the conversion of
PCO2 into blood CO2 content. Respir Physiol 3(1):111–115

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