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Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California 90509
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Stringer, William W., James E. Hansen, and K. Wasserman.
Cardiac output estimated noninvasively from oxygen uptake during
exercise. J. Appl. Physiol. 82(3):
908-912, 1997.
Because gas-exchange measurements during
cardiopulmonary exercise testing allow noninvasive measurement of
oxygen uptake (
O2), which
is equal to cardiac output (CO) × arteriovenous oxygen
content difference [C(a-vDO2)],
CO and stroke volume could theoretically be estimated if the
C(a-vDO2)
increased in a predictable fashion as a function of %maximum
O2
(O2 max) during
exercise. To investigate the behavior of
C(a-vDO2)
during progressively increasing ramp pattern cycle ergometry exercise,
5 healthy subjects performed 10 studies to exhaustion while arterial
and mixed venous blood were sampled. Samples were analyzed for
blood gases (pH, PCO2,
PO2) and oxyhemoglobin and hemoglobin
concentration with a CO-oximeter. The
C(a-vDO2)
(ml/100 ml) could be estimated with a linear regression [C(a-vDO2) = 5.72 + 0.105 × %O2 max;
r = 0.94]. The CO estimated from
the C(a-vDO2)
by using the above linear regression was well correlated with
the CO determined by the direct Fick method
(r = 0.96). The coefficient of
variation of the estimated CO was small (7-9%) between the lactic
acidosis threshold and peak
O2. The behavior
of C(a-vDO2),
as related to peak
O2, was similar regardless of cardiac function compared with similar measurements from
studies in the literature performed in normal and congestive heart
failure patients. In summary, CO and stroke volume can be estimated
during progressive work rate exercise testing from measured O2 (in normal subjects and
patients with congestive heart failure), and the resultant linear
regression equation provides a good estimate of
C(a-vDO2).
ramp pattern cycle ergometer exercise; arterial oxygen content; mixed venous oxygen content; direct Fick cardiac output
INTRODUCTION TO AVOID ARTERIAL and mixed venous blood sampling, a
noninvasive method for estimating cardiac output (CO) during exercise has been sought for over 100 years. Prior noninvasive methods of
estimating CO have relied on the rate of solution of inert gases or the
estimation of CO2 contents of
mixed venous and arterial blood by analyzing expired gases (indirect
Fick method) (1, 3, 4). These methods require sophisticated equipment,
considerable technical expertise, and subject cooperation during the
required breath-holding maneuvers. These measurements are likely to be invalid during exercise in patients with heart and lung disease with
varying degrees of ventilation-perfusion mismatching and lactic
acidemia. The end-tidal concentration will not reflect the arterial
concentration, and in the case of the indirect Fick method, the
assumption of mixed venous pH cannot be used during heavy exercise.
Cardiac output or stroke volume (SV) can be expressed as CO = SV × heart rate (HR) and as CO = O2 uptake
( In two previously published studies (11, 14) involving both normal and
heart failure subjects,
C(a-vDO2) and
CO were measured as a function of
We therefore hypothesized that if
C(a-vDO2) as a
function of exercise intensity
(% METHODS
O2)/arteriovenous content
difference
[C(a-vDO2)].
Because both HR and O2 can be easily measured during standard incremental cardiopulmonary exercise testing (12, 13), both CO and SV could be accurately quantitated if the
simultaneous
C(a-vDO2) could
be estimated.
O2. In both studies, the
C(a-vDO2)
increased linearly as a function of %peak
O2
(O2 peak). Furthermore, in normal subjects as well as in patients with heart failure
{ranging from patients with little or no impairment in aerobic
capacity [maximum O2
(O2 max) > 20 ml · kg
1 · min1]
to severe impairment
(O2 max < 10 ml · kg1 · min1)},
the maximum
C(a-vDO2) was
~13-14 ml/dl or an extraction ratio [C(a-vDO2)/arterial
O2 content] of 75% at peak
exercise.
O2 max) increased in
a predictable fashion, it would be possible to estimate CO
noninvasively throughout exercise. To test this hypothesis, we measured
C(a-vDO2)
during progressive ramp pattern cycle ergometer exercise while
continuously measuring O2
and generated a regression of
C(a-vDO2) as a
function of %O2 max.
From these estimates, we calculated CO and compared these estimates
with CO determinations by the direct Fick method.
O2 max, defined as
the O2 averaged over the
last 30 s of exercise.
O2 and
CO2 output (CO2) (both
STPD) were calculated as whole
breath averages for each 30-s exercise period, as previously reported
(9). The LAT was determined from a plot of millimoles
CO2 vs. millimoles O2 (V-slope plot) as
described by Beaver et al. (2).
Blood samples.
Blood was sampled simultaneously from the pulmonary artery and brachial
artery during rest, unloaded cycling, and at each minute of increasing
work rate exercise.
Blood analysis.
The blood samples were agitated and immediately chilled in an ice
slurry. Blood-gas analysis was performed with an Instrumentation Laboratories 1306 blood- gas machine for pH,
PCO2,
PO2, and on a 482 CO-oximeter for
total hemoglobin (Hb) and oxyhemoglobin saturation (Lexington, MA).
Data analysis and statistics.
Data from the first and second tests from each subject were treated
separately. The following standard equations were utilized in the data
analysis
|
(1) |
|
(2) |
|
(3) |
![O<SUB>2</SUB> content = 1.34 &z.ccirf; [Hb] &z.ccirf; O<SUB>2</SUB> saturation](/content/vol82/issue3/fulltext/908/img004.gif)
|
(4) |
|
|
(5) |
![Extraction ratio = [C(a-vD<SUB>O<SUB>2</SUB></SUB> )/arterial O<SUB>2</SUB> content]](/content/vol82/issue3/fulltext/908/img007.gif)
|
(6) |
O2 max by the use
of linear regression analysis. A P < 0.05 was considered
significant. All values are expressed as means ± SE, unless
otherwise specified.
RESULTS
The subject's physical characteristics and aerobic parameters were age
25 ± 6 (SD) yr, height 179 ± 4 cm, weight 72 ± 5 kg, resting arterial Hb 15.4 ± 0.21 g/dl, maximum work rate 296 ± 50 W, O2 max 3.77 ± 0.61 l/min, and LAT 1.84 ± 0.36 l/min (49% of
O2 max; see Table
1).
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In Fig. 1, the group mean direct Fick CO,
HR, O2,
CO2, lactate, SV,
O2 content, and
O2 pulse responses are displayed
as a function of
%O2 max during
exercise for the 10 exercise studies in the 5 study subjects (means ± SE). In Fig. 1A, the group
mean CO (each minute during exercise) increases to ~80% of the
maximal value at the LAT O2
(which is 48% of
O2 max, on average) and then increases more gradually for the remainder of exercise. HR (Fig.
1B), in contrast, continues to
increase at the same rate throughout exercise. This results in a peak
in SV at approximately the LAT (Fig.
1D), with a subsequent small but
statistically significant fall as exercise progresses (final value
differs from LAT value, P < 0.05).
The absolute values of
O2 and
CO2 are plotted against %O2 max (Fig.
1C).
CO2 exceeds
O2 after the LAT (respiratory exchange ratio >1.0) as would be expected. Figure
1E presents the arterial and mixed
venous O2 content and
C(a-vDO2)
during exercise. Arterial O2
content increases slightly due to the increase in [Hb] (~1 g/dl)
and to a lesser degree to an increase in arterial PO2 above the LAT. Mixed venous
O2 content progressively decreases
during exercise, resulting in a continuous increase in
C(a-vDO2).
Importantly, the increase in
C(a-vDO2) as a
function of %O2 max
appears to be linear, increasing 51% to the LAT (49% of
O2 max) and 49%
between the LAT and
O2 max. Finally,
O2 pulse (Fig.
1F) increases throughout exercise,
with the majority of this increase occurring before the LAT (~66%).
All of the increase in O2 pulse
above ~48% of O2 max
is attributable to the increase in
C(a-vDO2).
O2),
CO2 output
(CO2), lactate, stroke volume
(SV), O2 content, and
O2 pulse
(O2-P) responses are shown
as functions of %maximum
O2
(O2 max) during
ramp pattern cycle ergometer exercise. LAT, lactic acidosis
threshold; Art, arterial; MV, mixed venous; A-V Diff, arteriovenous
difference.
The individual values of
C(a-vDO2) (in
ml/100 ml) as a function of
%O2 max (10 studies in
5 subjects) are displayed in Fig. 2. The
linear regression applied to the data reveals that the slope is ~0.10
ml · 100 ml1 · %O2 max1,
and the intercept is 5.7 ml/100 ml. The even distribution (or scatter)
of C(a-vDO2)
over the entire range of
%O2 max values is
evident as well as the close approximation by a linear regression.
O2 max. Data
were determined from systemic arterial and pulmonary arterial blood
that was simultaneously sampled each minute during 10 progressively
increasing work rate exercise tests in 5 subjects.
In Fig. 3, the group mean
C(a-vDO2)
values are plotted as a function of measured CO (±SE) with
O2 isopleths generated from the equation O2 = CO × C(a-vDO2)
overlaid on the data. Graphing of CO as a function of
C (a-vDO2)
results in a rectangular hyperbole for each
O2. This display
demonstrates three points: 1) the importance of concurrent increases in both CO and
C(a-vDO2)
to obtain the highest O2
during exercise; 2) as the LAT
is exceeded, CO increase plays a lesser role and
C(a-vDO2) plays
a greater role in the increase in
O2 (as illustrated in Fig. 1,
A and E); and
3)
C(a-vDO2)
becomes less important in estimating CO as the maximal
C(a-vDO2)
is approached because the slope of the hyperbola becomes
proportionately more shallow.
O2
isopleths. Group mean is ±SE. Isopleths are those
calculated from following equation:
O2 = CO × C(a-vDO2) for
various O2 values. Vertical hatched bars are means ± SD taken from Table 1.
O2 peak, peak O2.
In Fig. 4, the COs estimated from
O2 and
C(a-vDO2) from
the equation established from the data in Fig. 2 are plotted against the directly measured COs (calculated by the Fick principle for O2). Each point is determined
from the data set of simultaneously measured arterial and mixed venous
O2 content and
O2. Estimated CO = measured
O2/[5.721 + (0.1047 × %O2 max)].
As can be seen, the directly measured and estimated COs are highly
correlated, and the slope and intercept do not differ statistically
from one and zero, respectively. In
Fig.4B, the absolute deviation of the estimated CO and the measured (Fick) COs are displayed. In Fig. 4C, the %deviation from the measured
value across the range of COs is displayed. The deviation from the
directly measured values was almost always 15% or less across the
entire range of COs (5-28 l/min). This is comparable to the
variability of estimating CO by any of the methods currently available
(6, 7).
O2 and
C(a-vDO2) by
using the equation
[C(a-vDO2) = 5.721 + (0.1047 × %O2 max); Fig.
4A]. Absolute (Fig.
4B) and relative deviations (Fig.
4C) plotted against measured COs
(calculated by Fick principle for O2).
Table 1 displays the mean O2
values measured by gas exchange at LAT and maximum exercise and the
C(a-vDO2) and
the extraction ratios at rest, LAT, and maximum exercise. There is
considerably less variation in
C(a-vDO2) and
the extraction ratio at LAT and at
O2 max
[coefficient of variation (CV) = SD/mean 
7-9%]
than at rest (CV = 20-30%).
Figure 5 shows the data of Weber and
Janicki (14), Sullivan et al. (11), and the present study for the
values of CO and C(a-vDO2)
plotted on a graph showing the
O2 isopleths. The Sullivan et
al. study contained normal study subjects as well as patients with CHF;
the Weber and Janicki (14) study contained only CHF patients with a
range of disease severity. The reduction in measured O2 (and the subsequent
decreased ability to perform external work) during exercise in the
patients with cardiac disease was primarily related to a reduced
ability to increase CO rather than a reduced ability to increase
C(a-vDO2).
Regardless of the level of maximally measured
O2 [normal subjects
(>54
ml · kg1 ·
min1) to CHF patients
(<10
ml · kg1 · min1)],
the maximal
C(a-vDO2) at
end exercise were all 12.5-16.5 ml/100 ml. [Note the Hb values
used to calculate the
C(a-vDO2)
were not detailed in either study, and anemia in the patients would
result in a reduced maximal
C(a-vDO2)].
If the
C(a-vDO2) of
the studies by Weber and Janicki (14) and Sullivan et
al. (11) (both CHF patients and normal subjects) are
plotted with the present study as a function of
%O2 max (Fig.
6), a similar regression, intercept, and
slope comparable to Fig. 2 are obtained, despite a wide variation in
cardiac function.
O2
isopleths. Normals, normal subjects.
O2 max, a similar
regression with a similar intercept and slope to those in Fig. 2 is
obtained, despite a wide variation in cardiac function.
DISCUSSION
The recognition by Fick (5) that virtually all of the heart's output
passed through the lungs and, therefore, that the law of conservation
of mass could be applied to measure CO from measured
O2 and the
O2 content differences across the
lung sets the foundation for the present study. A totally noninvasive
determination of CO and SV during exercise would be very useful in
normal subjects as well as in patients with various degrees of cardiac
insufficiency. Both CO and SV could be estimated from
O2 and HR if the behavior of
C(a-vDO2)
were known. Because
C(a-vDO2)
behaves in a consistent pattern in response to upright cycle exercise
in the present study (and in other reports) (11, 14), we believe that
CO can be estimated from O2
alone at the LAT and
O2 max on the basis of
the predictability and reduced variability of
C(a-vDO2) at these points.
We found that in normal subjects, the majority of the CO increase
occurred before the LAT (Fig. 1A),
although O2 continued to
increase throughout exercise (Fig.
1C).
C(a-vDO2)
increased in a relatively linear fashion throughout exercise (Figs.
1E and 2). Additionally, the predicted
CO with the use of the linear regression equation from Fig. 2 resulted
in small, nonsystematic deviations from the actual CO measurements
(Fig. 4). If O2 max were not reached during exercise, the CO could be estimated from a
C(a-vDO2) of
11.3 ml/100 ml (see Fig. 5) at the LAT because this level of exercise
is reached in normal subjects and in most patients with cardiovascular
and lung diseases during exercise testing. Finally, we found the
highest SV is reached at the LAT (Fig.
1D) in normal subjects; SV is
unlikely to rise much farther with increasing exercise intensity either
in patients or in normal subjects. In a comparison of the results from
the present study to prior studies in which CO and
C(a-vDO2) were
determined in normal subjects and in patients with CHF
(11, 14), the
C(a-vDO2) values were quite similar when compared at
O2 peak (Fig. 6), despite a very large range of CO responses.
Therefore, in a consideration of the interrelationships among CO,
C(a-vDO2), and
O2, as plotted in Figs. 3 and
5, and the relatively narrow ranges of
C(a-vDO2) at
the LAT and O2 peak, three major points become apparent.
1) In normal subjects, both CO and
C(a-vDO2)
increase severalfold from rest to
O2 peak. 2) In patients with cardiovascular
disease resulting in a reduced O2 peak, the CO can be
validly estimated because it is much more dependent on the
O2 peak reached than
the absolute level of
C(a-vDO2)
estimated [note the shallow slope of the isopleths as maximal
C(a-vDO2) is
approached]. 3) In CHF patients and
normal subjects, CO (and peak SV) can be well estimated from the
O2 at the
subject's LAT. Although patients with primary lung disease would be
expected to manifest a similarly low
O2 peak (see
above), the present results must be evaluated and validated in this
particular subject group.
We conclude that CO can be accurately estimated from
O2 during exercise in normal
subjects and patients with heart failure by measuring the LAT or
O2 peak. From
these data and HR, SV can be calculated. This can provide a simple and
low-cost assessment of cardiac function (CO and SV) in response to
exercise that is independent of disturbed lung physiology and acid-base
changes during exercise.
ACKNOWLEDGEMENTS
The authors thank Jay Reeck for contributions to the analysis and presentation of this manuscript.
FOOTNOTES
Address for reprint requests: W. W. Stringer, Div. of Respiratory and Critical Care, Physiology and Medicine, Los Angeles County Harbor-UCLA Medical Center, Harbor Mail Box 405, 1000 West Carson St., Torrance, CA 90509-2910.
Received 22 July 1996; accepted in final form 24 October 1996.
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