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* From the Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Belgium.
Correspondence to: Jean-Louis Vincent, MD, PhD, FCCP, Department of Intensive Care, Erasme University Hospital, Route de Lennik 808, B-1070 Brussels, Belgium; e-mail: jlvincen{at}ulb.ac.be
| Abstract |
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O2) by identical increases in cardiac
index (CI) and oxygen extraction ratio (O2ER). In
critically ill patients, the relationship between CI and
O2ER may be different. Patients with an altered cardiac
function may have a decreased CI/O2ER ratio, whereas
patients with sepsis may have an increased CI/O2ER ratio.
We hypothesized that the analysis of the CI-O2ER
relationship could help us to assess the adequacy of cardiac function
in critically ill patients with anemia. Design: Prospective, observational study.
Setting: Thirty-one-bed medicosurgical ICU of a university hospital.
Patients: Sixty patients equipped with arterial and
Swan-Ganz catheters presenting with anemia, which was defined as a
hemoglobin level
10 g/dL in the absence of active bleeding.
Patients were classified into those with compromised cardiac function
(group 1; n = 40), and those with normal cardiac function
(group 2; n = 20).
Measurements and results: In addition to the pertinent clinical data, initial hemodynamic measurements, including pulmonary artery occlusion pressure (PAOP), CI, and O2ER, were collected in all patients at the onset of anemia. As anticipated, group 1 patients (n = 40) had lower CIs, higher O2ER levels, and lower CI/O2ER ratios than group 2 patients. However, there was no significant difference in PAOP values between the groups. The CI/O2ER ratio was < 10 in 27 of 40 group 1 patients but only in 4 of 20 group 2 patients. Of these latter four patients, three were found to be hypovolemic, and one patient with sepsis had severe myocardial depression. There was no statistically significant difference in PAOP in group 2 patients with or without hypovolemia ([mean ± SD] 12.3 ± 2.1 mm Hg) vs 13.7 ± 4.3 mm Hg; p = 0.21). In group 1, survivors had a higher CI and CI/O2ER ratio than nonsurvivors. In group 2, however, such a relationship did not reach statistical significance.
Conclusions: The relationship between CI and O2ER level can help interpret the CI in anemic patients. In anemic patients with no cardiac history, a low CI/O2ER ratio (< 10) suggests hypovolemia even when CI is not depressed.
Key Words: cardiac index hemodynamics hypovolemia invasive monitoring isovolemic hemodilution oxygen extraction sepsis
| Introduction |
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O2). Although a high CI in an
anemic patient may appear to be adequate, if analyzed in isolation, the
cardiac response may still be inadequate for the degree of anemia.
Indicators of peripheral vascular mechanisms involved in maintaining
O2, mixed venous oxygen
saturation (SVO2) and
O2ER, may be useful in interpreting the CI under
these conditions. Various studies have shown that during isovolemic
hemodilution, healthy individuals increase their CIs and
O2ER levels to a similar extent to maintain
O2.4
5
6
7
8
9
Hence,
the relationship between CI and O2ER could be
used to interpret the adequacy of CI in anemic patients and can be
visualized easily on a computer or even on a sheet of paper at the
bedside.10
The CI/O2ER ratio, which
is around 12 (3:0.25) in healthy humans, is relatively stable in
healthy individuals with isovolemic
hemodilution.4
5
6
7
8
In critically ill patients, the
relationship between CI and O2ER may be
different. In particular, patients with an altered cardiac function or
with hypovolemia may have a decreased
CI/O2ER ratio, whereas patients with sepsis
may have an increased CI/O2ER
ratio.11
12
We hypothesized that the analysis of the
CI-O2ER relationship would help to assess
the adequacy of the CI during anemia in critically ill patients. | Materials and Methods |
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The initial measurements of complete hemodynamic data at the onset of
anemia with hemoglobin
10 g/dL were obtained by a physician using a
standard procedure. After intravascular pressure measurements, the CI
was determined by the thermodilution technique, using 10-mL injections
of iced 5% dextrose in water via a closed system (CO-set; Baxter) and
a cardiac output computer (SC 9000; Siemens; Danvers, MA). In
patients receiving mechanical ventilation, the bolus injection was
started at the end of the inspiratory phase. The CI was averaged from
three to five injections, the values of which were within 5 to 10% of
each other.13
14
Immediately after CI determination,
arterial and mixed venous blood samples were simultaneously collected
anaerobically for the immediate measurement of arterial and mixed
venous blood gas levels in an automatic analyzer providing rapid
results (model ABL3; Radiometer; Copenhagen, Denmark). The
arterial oxygen saturation (SaO2) and
SVO2 were measured by a co-oximeter
(Hemoximeter OSM3; Radiometer). O2ER was
calculated as
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All data are represented as the mean ± SD. Differences between the two groups were analyzed by a Students t test for unpaired data. A p value of < 0.05 was considered to be statistically significant.
| Results |
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O2 was usually determined by a
greater increase in O2ER than in CI (Fig 1
). Of the 13 patients with a CI/O2ER ratio
> 10, 12 had evidence of sepsis.
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| Discussion |
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The magnitude of the physiologic response, and the mechanisms involved,
depend on the species, state of awareness (awake or anesthetized), type
of anesthesia, type of exchange solution, and condition of the heart
prior to hemodilution.11
12
19
20
21
22
Various human studies
of isovolemic hemodilution have shown an identical increase in CI and
O2ER to meet
O2.4
5
6
7
8
9
Duke and
Abelmann5
showed that when patients with chronic anemia
were treated with blood transfusions, their CIs and
O2ERs fell from 4.73
L/min/m2 and 39.6%, to 3.44
L/min/m2 and 29.4%, respectively, indicating a
proportional contribution of the CI and O2ER.
Woodson et al6
studied the effects of acute and
established anemia on oxygen transport at rest, during submaximal work,
and during maximal work in young healthy volunteers. During maximal
exercise in patients with acute anemia, they observed a 233% increase
in the CI from 4.5 L/min/m2 at rest to 10.5
L/min/m2, and a 350% increase in
O2ER from 23% at rest to 80%. During maximal
exercise with established anemia, they observed a 254% increase in the
CI from 3.4 L/min/m2 at rest to 8.5
L/min/m2, and a 300% increase in
O2ER from 29% at rest to 87%, showing
similar increases in the compensatory mechanisms (CI and
O2ER) to maintain
O2 in the presence of
anemia.6
Fontana et al7
have shown that
children can tolerate intraoperative normovolemic hemodilution to an
average hemoglobin concentration of 3 g/dL without signs of global
hypoxia or impairment of global cardiac performance. In these
conditions, CI increased from 3.4 to 4.6 L/min/m2
and O2ER increased from 17 to 44% to maintain
O2. When these patients were
reinfused with previously removed autologous blood, they reduced their
CI from 4.6 to 4.0 L/min/m2 and their
O2ER from 44 to 33%, showing a proportional
decrease in the compensatory mechanisms involved in maintaining
O2 during
anemia.7
A study by Weiskopf et al9
of
human volunteers during acute severe isovolemic anemia showed an
increase in CI from 3.1 to 5.7 L/min/m2 and a
limited increase in O2ER from 23 to 32%. This
proportionately greater increase in CI than O2ER
may have been due to an excessive catecholamine secretion by the human
volunteers during the procedure.9
Comparing CI with SVO2 would be
easier than comparing CI with O2ER, but the
curvilinear relationship between SVO2
and CI prevents a straightforward interpretation. Also,
SaO2, which directly influences the
SVO2, can vary significantly in
critically ill patients. Even in the absence of profound hypoxemia,
SaO2 still may fluctuate between 90%
(corresponding to a PaO2 of around 60
mm Hg) and > 98% (if the PaO2 is
> 120 mm Hg).10
Hence, comparing CI and
O2ER will be more useful at the bedside as
the relationship is linear and involves simpler formulas than the
calculation of
O2 and oxygen
delivery (DO2). CI and
O2ER are independently measured, avoiding the
potential problem of the mathematical coupling of data that is faced
when
O2 is plotted against
DO2.10
23
The
relationship between CI and O2ER is remarkably
independent of the hemoglobin value, so that it can be used to evaluate
the effects of hemoglobin, which becomes an independent
variable.10
On a CI/O2ER ratio
diagram, a line of reference drawn from the origin and dissecting the
meeting point of normal values represents the equal contributions of
the CI and O2ER in healthy
individuals.10
Moreover, the CI-O2ER
relationship is obtained easily on any computer and can be viewed on a
graph at the bedside, as is the case in our ICU. We selected a
CI/O2ER ratio of 10 to assess the adequacy
of CI. Hence, in the presence of normovolemic anemia with normal
cardiac function, a CI/O2ER ratio of > 10
should suggest adequate cardiac compensation. However, if the CI
response is inadequate, the
O2
will be maintained by a proportionately larger increase in
O2ER and the
CI/O2ER ratio will be < 10.
In our study, as anticipated, the majority of patients with compromised cardiac function had a CI/O2ER ratio < 10 due to a blunted cardiac response to anemia.11 12 However, the majority of patients with sepsis in this group still had a high CI/O2ER ratio, as is typically observed in these circumstances.11 12 On the contrary, the majority of patients with normal cardiac function had a CI/O2ER ratio > 10. In the presence of sepsis, most of these patients showed a greater cardiac response than did patients with compromised cardiac function. Of the four patients with a normal cardiac function but a low CI/O2ER ratio, three were hypovolemic and one had severe myocardial depression. Hence, a CI/O2ER ratio < 10 indicates an impaired cardiac response to anemia but obviously does not help to identify the cause. An inadequate CI is generally due to impaired myocardial contractility and/or to inadequate preload. Interestingly, PAOP was not a reliable guide to assess the adequacy of patient fluid status. PAOP, which is routinely used as a guideline of left ventricular end-diastolic pressure, may be altered by a number of factors related to lung function, pulmonary hemodynamics, respiratory condition, and cardiac factors. Moreover, there are other factors involved in the reliability of PAOP data even if great care is taken in its measurement.24 Differences in clinical environment due to the differences in nurse training and in the nurse/patient ratio also may account for significant differences in the frequency of technical problems.25 Therefore, a normal PAOP may not rule out hypovolemia, and reference to the CI/O2ER ratio diagram may help to identify this problem and may be of help in practicing a goal-oriented therapeutic approach in critically ill patients, especially against a background of conflicting views on the concept of routine supranormal DO2.26 27 28
This diagram was particularly useful in the 41 patients with a CI between 2.5 and 5 L/min/m2. In these patients, a CI/O2ER ratio < 10 identified patients with an inadequate cardiac response to anemia, while a CI/O2ER ratio > 12 in patients with a history of cardiac disease was suggestive of sepsis. The use of a CI/O2ER ratio in the 10 to 12 range may be more difficult to use. It may correspond to a normal response as well as to an inadequate cardiac response associated with sepsis in a patient with preexisting cardiac disease, inadequate preload, or myocardial depression. An algorithm to interpret the CI/O2ER ratio is proposed in Figure 3 .
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| Footnotes |
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O2 = oxygen
consumption Received for publication August 3, 1999. Accepted for publication January 29, 2000.
| References |
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N. Lim, M.-J. Dubois, D. De Backer, and J.-L. Vincent Do All Nonsurvivors of Cardiogenic Shock Die With a Low Cardiac Index? Chest, November 1, 2003; 124(5): 1885 - 1891. [Abstract] [Full Text] [PDF] |
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J.-L. Vincent Monitoring Cardiac Output Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2003; 7(1): 37 - 39. [PDF] |
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