(Circulation. 1995;92:1994-2000.)
© 1995 American Heart Association, Inc.
Articles |
From the Cardiovascular Division, Washington University School of Medicine, St Louis, Mo.
Correspondence to Michael Courtois, MA, Washington University School of Medicine, Cardiovascular Division, 660 S Euclid, Box 8086, St Louis, MO 63110.
| Abstract |
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Methods and Results Using two-dimensional echocardiography, we determined H in the LVs of seven normal patients (five male, two female; age, 49±9 years) undergoing routine cardiac catheterization. H was determined from a left parasternal short-axis view and calculated as the average distance between end diastole and end systole of the endocardium of the uppermost segment of the LV anterior wall below the fourth or fifth intercostal space of the left sternal border on the anterior surface of the chest wall, with the patient in the supine position. A micromanometer/fluid-filled lumen catheter was then positioned in the LV, and we compared the micromanometer LV minimum pressure (LVPmin) obtained when the reference fluid-filled transducer was aligned at midchest with the LVPmin obtained when the reference fluid-filled transducer was aligned at H. LVPmin referenced to a midchest fluid-filled external transducer was measured as 5.1±1.6 mm Hg (range, 2.4 to 7.2 mm Hg) versus -0.6±0.6 mm Hg (range, -1.6 to 0.4 mm Hg) when referenced to H (P<.001). A significant linear relation was found to exist between patient anterior-posterior chest diameter and the magnitude of hydrostatic pressure influences related to pressure referenced at midchest (r=.88; P<.01).
Conclusions External fluid-filled transducers should be used with the goal of removing hydrostatic pressure and other influences so that the presence of subatmospheric pressure during diastole in any of the cardiac chambers is accurately measured. To achieve this goal, intracardiac pressure should be referenced to an external fluid-filled transducer aligned with the uppermost blood level in the chamber in which pressure is to be measured. The current practice of referencing the zero level of LV diastolic pressure to an external fluid-filled transducer positioned at the midchest level results in systematic overestimation due to hydrostatic effects and produces physiologically significant error in the measurement of diastolic intracardiac pressure.
Key Words: diastole pressure ventricles
| Introduction |
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In cardiovascular research, the standard for measurement of intracardiac pressure waveforms is the micromanometer catheter. Despite the ability of micromanometers to produce reasonably stable and accurate high-fidelity pressure waveform recordings free of the problems and artifacts associated with fluid-filled pressure measurement systems, micromanometer catheters are generally referenced to fluid-filled systems to correct for any drift in the micromanometer signal and to establish a common zero pressure reference level, ostensibly to remove errors due to hydrostatic pressure influences. The proper removal of hydrostatic pressure that allows for the meaningful and useful comparison of LV pressures, especially diastolic pressures, between patients is the subject of this report.
A great variety of reference levels for measurement of cardiac pressure have been proposed,13 14 none of which have met with universal acceptance. We believe that the persistent problem related to the choice of proper zero pressure reference level arises from two sources. First, there is a misunderstanding among many clinicians and researchers as to how hydrostatic pressure influences pressures measured with fluid-filled catheter systems. Second, to the best of our knowledge, no explicit logical position has been enunciated detailing the goal that the ideal zero pressure reference level should meet. Thus, in the first part of our study, we sought to assess the extent to which physicians trained in cardiology understand how hydrostatic pressure influences measurements made with fluid-filled catheter systems. In the second part of the study, we proposed an anatomically and physiologically appropriate reference level for the measurement of cardiac pressures, the objective being the accurate detection of subatmospheric pressure when it is present within any cardiac chamber. We then presented LV diastolic pressure measurements obtained by reference to our proposed new zero level and compared them with measurements obtained by reference to another commonly used level (midchest).
| Methods |
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Determination of the Uppermost LV Blood Level
Using
two-dimensional echocardiography, we
determined the uppermost LV blood-endocardial interface (H) in the LVs
of seven normal patients (five male, two female; age, 49±9 years)
undergoing routine cardiac catheterization for the
evaluation of chest pain. All patients had normal
ventricular function and volume, without any sign of
significant cardiac disease. H was calculated from a left parasternal
short-axis view of the LV chamber during quiet respiration (Fig
3
). Because H varies slightly (
1 cm) throughout the
cardiac cycle, this measure was calculated as the average distance
between end diastole and end systole of the endocardium of
the uppermost segment of the LV anterior wall below the fourth or fifth
intercostal space of the left sternal border on the anterior surface of
the chest, with the patient in the supine position. With a yardstick
equipped with a bubble-in-fluid level, each individual patient's
anterior-posterior chest diameter was measured as the distance
equivalent to the perpendicular distance from the point on the anterior
surface of the chest at which the echocardiographic
view was obtained to the table.
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Determination of LV Minimum Pressure Referenced at Midchest
and H
A micromanometer-angiographic catheter (model SPC-474A, Millar
Instruments) was then positioned in the LV of each patient by standard
catheterization techniques. We then compared the LV
minimum pressure (LVPmin) obtained when the reference
fluid-filled transducer was aligned at midchest with the
LVPmin obtained when the fluid-filled transducer was
aligned at H. To do this, an LV pressure signal was obtained via the
fluid-filled lumen of the micromanometric catheter with the external
transducer positioned at midchest. The
micromanometer pressure signal was then aligned
during diastasis with this fluid-filled catheter signal (Fig
4
), and LVPmin was determined from the
micromanometer signal during brief end-expiratory
apnea. The external transducer was then repositioned at H, the
micromanometer and fluid pressure signals were
realigned, and LVPmin was determined again from the
micromanometer signal.
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Statistical Analysis
A value of P<.05 was
considered significant.
Student's t test was used for paired data.
| Results |
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Midchest and H pressure reference levels. The average
anterior-posterior chest diameter, as measured from the table to the
point on the anterior surface of the patient's chest at which the echo
transducer was positioned (fourth or fifth intercostal space at the
left sternal border), was 24.9±4.0 cm (Table
). As shown
in Fig 5
, this resulted in an average midchest value of
12.4±2.0 cm below the anterior surface of the chest. Measurement of H
by echocardiography indicated that the uppermost LV
blood-endocardial interface in the LVs of the seven patients was
5.3±0.9 cm below the anterior surface of the chest.
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Determination of LVPmin by a
micromanometer signal aligned to a fluid-filled
transducer signal referenced at midchest or at H (Table
).
LVPmin (diastolic) measured using midchest
versus H as the zero reference level produced significantly different
results. At the midchest reference level, LVPmin for the
group was 5.1±1.6 mm Hg (range, 2.4 to 7.2 mm Hg). At the H
transducer reference level, LVPmin for the group was
-0.6±0.6 mm Hg (range, -1.6 to 0.4 mm Hg). This difference
was
significant (P<.001). With H as the reference level, five
of seven patients (71%) displayed subatmospheric pressures during the
early diastolic filling phase (Table
).
Hydrostatic pressure influences as a function of
anterior-posterior chest diameter. Assuming LVPmin as
measured at reference level H to be free of LV hydrostatic pressure
influences, Fig 6
represents the relation
between pressure measurement error due to hydrostatic pressure
influences and anterior-posterior chest diameter when LV pressure is
referenced to an external fluid-filled transducer positioned at the
midchest level (r=.88; P<.01).
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| Discussion |
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Although such a result appears counterintuitive, examination of Fig
8
clarifies the effect. Removal of the water cylinder
from the configuration presented in Fig 2
results in the
catheter tip being positioned 30 cm below the transducer, producing a
pressure reading of -30 cm H2O. Replacement of the
cylinder would add a hydrostatic component of 40 cm H2O.
Thus, the resulting pressure reading would be 10 cm H2O. In
Fig 7
, by the same reasoning, a catheter positioned 9 cm above
the
transducer, contributing a pressure component of 9 cm H2O,
plus 1 cm of hydrostatic pressure would also produce a fluid-filled
transducer pressure reading of 10 cm H2O.
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It follows that the proper level to position a fluid-filled transducer
to remove all hydrostatic pressure influences would be even with the
top of the fluid column in the chamber or vessel in which the pressure
is being measured. In this way, pressure measured with a fluid-filled
catheter at any level within the vessel would indicate a zero
hydrostatic pressure component, as shown in Fig 9
. Thus,
any additional pressure added by compression or removed by a mechanism
generating suction would be measured accurately, essentially free of
any hydrostatic pressure effects caused by the LV blood level. Removal
of hydrostatic pressure influences, for example, would be a crucial
first step for the accurate determination of certain properties of the
LV such as equilibrium volume, which, by definition, is based on the
precise measurement of the generation of subatmospheric pressure by the
LV.15 This level would also provide a superior method for
patient-to-patient comparison of LV filling pressures in the everyday
measurement of LV pressures in the catheterization
laboratory.
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Thus, external transducer reference position is crucial to the assessment of LV filling pressures. To the best of our knowledge, no proper goal for referencing intracardiac pressure measurement to the atmosphere has ever been suggested. We therefore propose that external fluid-filled transducers should, optimally, be positioned with the goal of removing hydostatic pressure from the measurement so that subatmospheric pressure generation during diastole by any cardiac chamber is free of this confounding influence. The average error of up to 5.7 mm Hg for the measurement of LVPmin produced in our study by transducer alignment at midchest level is clearly unacceptable for meaningful comparison of diastolic pressures and diastolic pressurederived indexes between patients.
In both clinical and animal research involving measurement of intracardiac hemodynamic pressure with micromanometers, two methods appear to be most widely used for referencing these pressure measurements to the atmosphere. A typical example of the first method can be found in an experiment conducted by Sabbah et al16 in which minimum LV diastolic pressure was measured in 15 patients with mitral stenosis. In that study, micromanometer pressure measurement was referenced to the atmosphere by holding the transducer in the air and adjusting its zero baseline to atmospheric pressure before placing the micromanometer in the LV. Using this approach, the investigators found an average minimum pressure in the LVs of these patients of -2±4 mm Hg. Subatmospheric pressures were demonstrated in 10 (67%) of 15 patients studied. From these results, the authors concluded that ventricular suction plays an important role in the dynamics of LV filling. Similarly, Paulus et al17 measured LV minimum pressure in 23 patients with mitral stenosis. However, that group referenced their micromanometer pressure measurements against lumen pressure referenced to an external fluid-filled transducer zeroed to atmosphere at the level of the midchest. The results of their study indicated that of 23 patients with mitral stenosis, only 3 (13%) were found to have LV subatmospheric pressures. The average LVPmin for their group of patients was found to be 2±3 mm Hg.
It is clear that in each of these studies, significant differences in
hydrostatic pressure influences resulted from the techniques used for
setting the zero reference pressure. This methodological difference
probably contributed importantly to the differences in results reported
by the two groups of investigators. Assuming that the results reported
by Paulus et al17 included a systematic error of
5
mm Hg due to hydrostatic pressure influences, their corrected data
would result in an average LVPmin of -3 mm Hg for the
group, and correcting the individual data points by this same factor
would imply generation of subatmospheric pressure in 19 of 23 patients
(83%). Assuming a conservative component of 1 mm Hg due to submersion
of the micromanometer under the blood in the LV
cavity in the study by Sabbah et al,16 correction by this
amount would result in a group average LVPmin of -3
mm Hg, with generation of subatmospheric pressure in 13 of 15 patients
(87%).
Summary and Implications for Clinical Pressure Measurement and
Research Studies of Diastolic Function
Appropriate external transducer
reference position is pivotal in
the assessment of LV filling pressures. In addition, our study
indicates that a misunderstanding exists among some researchers and
clinicians as to how hydrostatic pressure influences the measurement of
pressure by use of fluid-filled catheter systems. We conclude that the
practice of referencing diastolic pressure to external
fluid-filled transducers positioned at midchest
level14 18
merits reconsideration. The midchest level has no consistent
relation to the position of the heart within the chest, and, as can be
seen in Fig 6
, the magnitude of hydrostatic pressure influences
is
related directly to anterior-posterior chest thickness. For example,
from the equation expressed in Fig 6
, the error incurred by
measurement
of pressure at midchest level due to hydrostatic pressure in a patient
with an anterior-posterior chest diameter of 30 cm would be 7.5
mm Hg.
Rather, intracardiac pressures should be referenced, at minimum, to an external fluid-filled transducer aligned with the uppermost level of blood in the chamber in which pressure is to be measured. We emphasize "at minimum" because, in the case of the LV, additional hydrostatic and other pressure influences, such as those resulting from the presence of the right ventricle (RV) and pericardial fluid lying above the LV, may transmit additional hydrostatic pressure influences through the interventricular septum. Additional research will be needed to determine how and under what circumstances such potential sources of hydrostatic force can and should be removed from the measurement of LV diastolic pressure. Such research will have to take into account that this form of "ventricular interaction" is dependent to some extent on the passive elastic properties of the ventricular septum.19 RV hydrostatic influences can probably be estimated by the inferior vena caval occlusion technique to measure the direct ventricular interaction, as described by Slinker and Glantz.20 In addition, the influences exerted by pericardial forces and intrathoracic pressures need to be accounted for in the in vivo state if, as would be the ultimate goal for the calculation of indexes of passive myocardial chamber properties, an accurate estimation of LV transmural pressure is to be obtained.21 22
Thus, uncontrolled hydrostatic pressure influences can result in a misrepresentation of the nature of LV filling (ie, presence or absence of ventricular recoil), which would, for example, result in potentially large errors in the determination of LV equilibrium volume, since the pressure-volume relation during early LV filling is known to closely parallel the volume axis.23 Additionally, in open-chest animal preparations, external transducers should be aligned to fit the particulars of the experimental situation.
In the setting of a busy cardiac care unit (CCU) or cardiac
catheterization laboratory, it it also important that
proper external transducer position be determined readily and
implemented easily. Proper external transducer position could be
determined by one of three approaches: (1) Make this measurement a
routine part of the normal diagnostic
echocardiographic procedure. However, not all patients
undergo this procedure and, in this cost-saving era, an available
echocardiograph and technician are unlikely practical
additions to any CCU or catheterization laboratory. (2) Use lateral
fluoroscopy in conjunction with a catheter tip directed to contact the
anterior wall to estimate H. Although a potentially accurate method of
determining H, this approach would be time-consuming in the
catheterization laboratory and impractical in the CCU.
(3) Estimate LV H level based on a large database. We believe this to
be the most practical solution. For example, in a large patient
population, H could be carefully estimated by
echocardiography for the LV, and possibly for the
other three cardiac chambers, by parasternal short-axis and long-axis
views. Based on these data, either a single standardized mean value and
SD for the H levels of the LV and other chambers might be established
for the population as a whole or individual regression equations
describing the relation of H to variables such as sex and body
surface area might be constructed. At present, based on our small
sample of patients with LV H level estimated from a parasternal
short-axis view, we recommend that in the routine clinical setting
external transducers be positioned approximately 5 cm below the left
sternal border at the fourth intercostal space. Since the H level of
the left atrium (LA) tends to be
1 cm below the H level of the LV
and the H level of the RV tends to be
1 cm above the H level of the
LV, errors due to hydrostatic influences in measurement of LA and RV
chamber pressures with the transducer positioned at the LV H level
would only be on the order of +0.8 or -0.8 mm Hg, respectively.
Since
the H level of the RA is essentially equal to the LV H level,
hydrostatic error influences during pressure measurement in this
chamber with the external transducer positioned at the LV H level
should be minimal. Thus, at present, we believe that the H level of
the LV, with its narrow range of variation as estimated in our patient
sample (SD, ±0.9 cm), is probably the most practical position and
subject to the smallest overall errors due to hydrostatic influences
for the routine measurement of pressure in any of the cardiac
chambers.
In the conduct of research, we suggest that micromanometer catheters alone should not be used for direct recordings of LV diastolic pressure because of the influence of hydrostatic pressure. Unless the catheter can be manipulated within the LV so that the micromanometer is positioned at the most anterior "surface" of the blood within the LV and held there throughout diastolic filling, errors due to hydrostatic influences will result. Micromanometer catheters can be corrected for hydrostatic pressure influences only by simultaneous use of LV cineangiography in the lateral position or echocardiography to determine the precise depth of the transducer below the LV blood pool. In this way, dynamic hydrostatic pressure influences could be accounted for on a moment-to-moment basis throughout diastolic filling. Such a method, although onerous, may be the optimal way to measure LV diastolic pressure for the purposes of research. Alternatively, fluid-filled pressure measurement systems can provide an effective reference pressure to adequately remove most of the hydrostatic pressure influences due to blood within the LV chamber. In the present study, this technique resulted in substantially different measured LV diastolic pressures compared with midchest. Placement of an external fluid-filled transducer should be done with the goal of removing hydrostatic pressure so that subatmospheric pressure during diastole in any of the cardiac chambers can be measured accurately.
| Acknowledgments |
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Received January 18, 1995; revision received March 21, 1995; accepted April 1, 1995.
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