NDT Advance Access originally published online on April 12, 2006
Nephrology Dialysis Transplantation 2006 21(6):1474-1481; doi:10.1093/ndt/gfl167
© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Editorial Comment
Evaluation of cardiac function in the dialysis patient—a primer for the non-expert
Eric H. Y. Ie and
Robert Zietse
Department of Medicine, Erasmus MC, Rotterdam, The Netherlands
Correspondence and offprint requests to: E. H. Y. Ie. Department of Medicine, Erasmus MC, P.O. Box 2040, 300 CA Rotterdam, The Netherlands. Email: e.ie{at}erasmusmc.nl; yuhanyang{at}hotmail.com
Keywords: echocardiography; haemodialysis; hypervolaemia; left ventricular function; load dependence
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Introduction
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Cardiovascular disease is a major cause of renal insufficiency,
but conversely, renal insufficiency itself contributes to cardiac
pathology in several ways. At least half of all the patients
starting dialysis therapy have overt cardiovascular disease
[
1]. Chronic pressure and volume overload lead to left ventricular
(LV) remodelling, with the development of a concentric or eccentric
LV geometry and LV hypertrophy. The prevalence of LV hypertrophy
increases with progressive renal insufficiency [
2] to about
75% in dialysis patients [
3,
4]. Amplifying factors include hyperparathyroidism,
hyperphosphataemia, angiotensin II, aldosterone, endothelin
and plasma catecholamines [
5–7]. In uraemia, LV hypertrophy
is characterized by cardiomyocyte dropout, with diffuse interstitial
fibrosis and hypertrophy of the remaining myocytes and microvascular
disease [
8]. These structural changes are associated with impaired
LV perfusion and function. Decrease in myocardial capillary
density and increase in myocyte size adversely affect myocardial
oxygen supply and flow reserve [
9]. Epicardial coronary artery
disease is common in uraemic patients, and may lead to an acute
coronary syndrome. LV dysfunction, however, seems to be related
to microvascular disease [
10]. LV function is also impaired
by cardiomyocytes being replaced by fibrosis, leading to decreased
contractile capacity and compliance. LV pressure–volume
measurements have shown the steep relationship between end-diastolic
pressure and volume in dialysis patients [
11]. As LV remodelling
is common in dialysis patients, a high prevalence of LV dysfunction
is expected. However, cardiac function assessment in dialysis
patients is fraught with pitfalls. The changing circulatory
pressure–volume relations not only affect LV structure
and function, contributing to cardiac morbidity, but also hamper
LV function assessment. In this review, we will briefly discuss
LV physiology in relation to the changing volume status in dialysis
patients, explain the principles of conventional and newer LV
function tests, and provide recommendations to optimize the
evaluation of cardiac function in the dialysis patient.
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Changing loading conditions and left ventricular function in dialysis patients
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The essential function of the heart as a pump is to provide
an appropriate cardiac output (CO), which is the product of
stroke volume (SV) and heart rate (HR). Within normal physiological
range, SV depends on end-diastolic volume (EDV). This is known
as the Frank–Starling mechanism, which states that: ‘the
output of the heart is determined by the amount of blood flowing
into the heart’ [
12]. Therefore, the heart must be able
to obtain an adequate level of filling, and requires adequate
pumping force, usually referred to as LV diastolic and systolic
function, respectively. The circulation is a closed-loop system,
and the interaction between the heart and the vascular system
is reflected in terms of loading conditions.
Preload is the distending force of the ventricular wall, which is directly related to myocardial sarcomere length at the beginning of the contraction, and therefore refers to the resting tension of the muscle. It can be measured as the end-diastolic LV pressure (or volume). The actual level of the preload depends not only on the diastolic myocardial properties, but also on the effective blood volume and the venoatrial system properties [13].
Afterload is the force opposing contraction, and can be defined as arterial input impedance. It is related to the myocardial muscle tension during the shortening phase of contraction. The actual level of the afterload depends not only on the systolic myocardial properties (contractile state), but also on the effective blood volume and the arterial system properties, which consist of systemic vascular resistance (SVR), arterial compliance and the inertia of blood [13].
The goal of LV systolic function is to eject a physiologically adequate volume of blood into the aorta. This results from the complex interaction between adequate cardiac filling, contractility, HR and afterload [14]. Sympathetic stimulation increases SV not only by increasing contractility and reducing end-systolic volume (ESV), but also by increasing diastolic filling time and EDV, and thereby increasing the preload of the muscle fibers. Therefore, sympathetic stimulation improves cardiac pump function by stimulating the two key functions of the LV: contractility and preload recruitment.
LV diastolic function is the ability to provide a physiologically adequate preload, resulting in sufficient sarcomere length necessary for the next contraction. Diastole is usually divided into an isovolumic relaxation phase followed by a filling phase, which can be subdivided into an early filling phase and late filling due to atrial contraction. LV diastolic function results from both an active relaxation process and the passive elastic properties that determine LV compliance. From the above, it can be concluded that LV diastolic and systolic function are intrinsically load-dependent. This renders the measurement of cardiac function in dialysis patients difficult. The loading conditions of the circulation reflect the combined effect of intrinsic myocardial properties, vascular properties and the effective blood volume. During the dialysis procedure, volume withdrawal acutely alters these loading conditions, independently of LV function. Furthermore, elevated cardiac filling pressures, a hallmark of congestive heart failure, may reflect extracellular volume overload in renal failure, and may require adjustment of dry weight. The diagnosis of heart failure in dialysis patients can only be made when elevated cardiac filling pressures are found in the presence of LV dysfunction. Therefore, especially in dialysis patients, there is a need for the so-called ‘load-independent’ LV function measurements. Since LV function is intrinsically load-dependent, as outlined above, this is actually a misnomer, and could more correctly be named ‘volume status-independent’ LV function assessment.
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Left ventricular function assessment
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Cardiac function is routinely measured in daily clinical practice
with the use of imaging techniques. These yield parameters that
can only provide indirect information on the actual physiological
processes. Of these techniques, echocardiography is the most
important and most commonly used diagnostic tool.
Systolic function assessment
Several parameters are used to assess LV systolic function. SV is the difference between LV end-systolic and end-diastolic volume:
LV volumes can be
calculated from one-dimensional (1D) M-mode or from 2D images,
but conversion to the 3D parameter volume leads to amplification
of measurement inaccuracies. Furthermore, assumptions about
the shape of the LV affect these SV measurements. A common way
to measure SV from two-dimensional images is the method of discs,
in which multiple equally spaced diameters along the LV cavity
are converted to a disc area measurement (Simpson's rule). Addition
of the disc segments yields LV volume. Delineating the LV cavity
by the tracing of the endocardium can be done manually or by
means of automated border detection.
SV can also be assessed from Doppler blood flow measurements in the LV outflow tract. In the absence of significant valvular regurgitation, SV equals aortic ejection volume. SV is the product of the LV outflow tract area (A) and the Doppler mean flow velocity (V) – ejection time (T) integral. A is calculated as 
r2, in which r is the radius of the aortic annulus.
SV can be expressed in absolute volume units (ml),
but also as volume fraction of the EDV. This is the LV ejection
fraction (EF), which is the most commonly used echocardiographic
parameter of LV systolic function.
LV
systolic dysfunction is usually defined as an (EF) <50% [
15].
In reporting the echocardiographic assessment of the LV contraction pattern, an alternative approach is to report the myocardial fractional shortening (FS), which is the difference between end-diastolic diameter (EDD) and end-systolic diameter (ESD) relative to EDD:
Normal
FS is >28% [
16]. This parameter describes the contraction
pattern in one dimension in a certain LV segment. However, to
be useful, FS at endocardial level can only provide information
on overall LV systolic function if the LV has a normal shape
and uniform function. Midwall FS has been proposed as a less
geometry-dependent measurement of contraction [
17].
Diastolic function assessment
Pulsed Doppler transmitral flow velocity measurements are generally used to assess LV diastolic function. A decreased peak early transmitral flow velocity (E) due to impaired diastolic filling with an increased contribution of atrial contraction (A) results in a decreased E/A ratio (<1), the so-called ‘impaired relaxation’, which is considered diagnostic of diastolic dysfunction. It is one of the four distinct E/A ratio patterns, which forms a grading system representing a continuum from normal to severe diastolic dysfunction (Figure 1). While the E/A ratio is >1 with normal diastolic function, decreased early filling in diastolic dysfunction results in a pattern of delayed relaxation with E/A <1. Progression of diastolic dysfunction leads to pseudonormalization, in which the increase in left atrial pressure leads to a ‘normal’ E/A ratio >1. The impairment in LV relaxation can also become manifest as an increase in E deceleration time and isovolumic relaxation time. Finally, severe diastolic dysfunction results in a restrictive pattern with E/A >2, in which the stiff ventricle with an initially low intraventricular pressure allows abnormally increased early filling velocity, but very little subsequent filling due to a rapid increase in intraventricular pressure.
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Fig. 1. Grading system of diastolic dysfunction based on Doppler patterns of peak early (E) and atrial (A) transmitral flow velocity.
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Newer Doppler applications include Doppler tissue imaging (DTI)
and colour M-mode Doppler (
Figure 2). With the use of DTI, mitral
annulus peak tissue velocities can be assessed during early
diastole (
e) and atrial contraction (
a), which depend on LV
relaxation. With increasing age, normal values for
e decrease
and for
a increase. Normal values have been reported as
e>10
cm/s in younger subjects and
e>8 cm/s in older subjects,
and diastolic dysfunction has been defined as
e<8 cm/s [
18,
19].
With the use of colour M-mode Doppler, the diastolic flow propagation
velocity (
Vp) from the mitral orifice to the apex cordis over
time is assessed, also a parameter of LV diastolic function.
Diastolic dysfunction has been defined as
Vp<45 cm/s [
18].
Recently,
e was found to be a more sensitive parameter than
Vp in the detection of mild to moderate diastolic dysfunction
[
20].
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Fig. 2. Peak early (E) and atrial (A) transmitral Doppler flow velocities and deceleration time (DT) of E. Using Doppler tissue imaging, one distinct signal is obtained during systole (s), and two during early (e) and late (a) diastole. Flow propagation velocity (Vp) is measured from colour M-mode recordings as the slope of the first aliasing velocity during early filling from the mitral valve plane into the LV cavity.
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Load dependence of left ventricular function parameters
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The success of EF as a measure of LV systolic function in clinical
conditions is probably derived from the observation that, when
LV contractility is reduced, SV is maintained at an increased
EDV, leading to a reduced EF. However, the preloaded ventricular
pump needs to eject against a given afterload, so determination
of SV or EF does not characterize pump function alone. Interpretation
of LV performance indices as measures of LV systolic function
is only meaningful with concomitant information on LV volumes
and afterload [
15,
21]. This information is often not provided
or taken into account. Performance indices such as EF and SV,
which describe the entire cardiovascular system rather than
the intrinsic properties of the myocardium, are affected by
the changes in loading conditions, and are therefore called
‘load-dependent’ [
22–24].
The influence of load is particularly important when evaluating cardiac function in dialysis patients [25]. It is well-known that the changes in volume status in these patients, resulting in substantial changes in preload and afterload, affect LV function measurements. However, to what extent the changing loading conditions contribute to a change in LV function parameters is difficult to determine. A lower EF after dialysis may result from a decrease in contractility, but also from a decreased preload, an increased afterload or a combination thereof. The issue of load dependence is particularly important in the assessment of LV diastolic function, as the effect of cardiac filling pressure is part of the grading system of LV diastolic dysfunction mentioned before. The pre-load dependence of pulsed Doppler transmitral flow measurement is an important confounding factor [26]. During infusion of nitroglycerine, decreased cardiac filling pressures induced changes in Doppler transmitral flow profile that resembled those commonly taken as proof of LV diastolic dysfunction [27].
The pre-load dependence of these measurements hampers the assessment of LV diastolic function in dialysis patients. Pre-dialysis volume overload increases peak early filling velocities and preload, and could mask impairment of early diastolic filling [28]. Conversely, intravascular hypovolaemia resulting from ultrafiltration during haemodialysis may reduce preload, which could mimic a pattern of LV diastolic dysfunction [11,27]. Sequential Doppler measurements during dialysis showed that early filling progressively declined in hypotension-prone dialysis patients, to the point that just prior to the onset of hypotension diastolic filling was almost entirely the result of atrial contraction [28,29]. Left atrial pressure also affects Doppler pulmonary vein flow. Diastolic forward flow velocity has been shown to reflect both LV diastolic function and preload [30]. Therefore, it is crucial to correct for the effect of preload when evaluating LV diastolic function by means of these conventional Doppler flow velocity measurements.
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In search of ‘volume status-independent’ left ventricular function assessment in dialysis practice
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There are two possible strategies to assess cardiac function
independently of volume status. One way is to accurately measure
extracellular volume, and with the use of that information,
perform LV function assessment in a normovolaemic state. The
main problem is the accurate volume measurement. The determination
of a patient's correct dry weight state is one of the most elusive
problems in dialysis practice, despite advances in technology
that have been used as adjuncts to clinical criteria for dry
weight, such as the absence of overt oedema or orthopnea before
dialysis. Studies with radioactively labelled albumin showed
that plasma refilling continues after the completion of the
haemodialysis procedure, until volume equilibrium has been reached
between 1 and 2 h after dialysis [
31]. However, the cessation
of inter-compartimental fluid shifts does not necessarily mean
that normovolaemia has been reached. Equilibrium can also be
reached with the patient in a state of mild hypervolaemia after
dialysis, due to incorrect determination of dry weight and insufficient
volume withdrawal.
The other possible strategy is ‘volume status-independent’ LV function assessment. This has been an important issue in cardiology research for many years, and at first glance, appears to be a more successful approach in dialysis patients than focusing on assessment of their volume status. The newer Doppler parameters, DTI and colour M-mode, have been reported as relatively ‘load-independent’ [32–36]. These techniques could, therefore, have a potential benefit in the assessment of LV function in dialysis patients. However, these parameters were found to exhibit a pattern of preload dependence similar to that displayed by the conventional Doppler flow velocity measurements (Figure 3) [37]. This was confirmed for mitral annulus velocity by DTI in a larger cohort [38]. Similarly, systolic mitral annulus velocity by DTI was shown to depend on changes in load [39].
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Fig. 3. Change in transmitral flow velocities, mitral annulus velocities and flow propagation velocities following haemodialysis with ultrafiltration.
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With several new techniques, it is possible to obtain more global
myocardial imaging. Colour tissue velocity imaging (TVI) measures
mean velocities in multiple myocardial segments and has been
claimed as less load-dependent [
24,
40]. 3D echocardiography
and cardiac magnetic resonance imaging (MRI) may hold a promise
for the future [
41,
42]. These more complicated and expensive
techniques may trade better imaging for practical value. They
offer, however, a more general assessment of myocardial contraction
and relaxation patterns than two-dimensional echocardiography
and Doppler studies. MRI studies have demonstrated the systolic
twisting motion of LV contraction, resembling the wringing out
of a wet towel, and the diastolic untwisting motion of LV relaxation
[
14]. It is feasible that in the future, LV dysfunction could
be defined not only by
quantifying these motion velocities,
but also
qualitatively, i.e. as a pathological contraction–relaxation
pattern. Conceivably, this could be useful in dialysis patients.
However, we have to keep in mind that LV function is intrinsically
load-dependent, and that the changing volume status in dialysis
patients remains a confounding factor. All imaging techniques
still provide indirect information only, lacking LV pressure
measurement.
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Left ventricular pressure–volume relations in clinical practice
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LV volume measurements can be combined with simultaneous information
on LV pressure to establish the LV pressure–volume relationship,
or elastance E (the incremental pressure–volume ratio,
P/
V), throughout the cardiac cycle to measure the changes in
myocardial contractility [
13]. The end-systolic pressure–volume
relationship represents the mechanical properties of a fully
contracted ventricle. End-systolic elastance (
Ees) is an inherent
characteristic of a given LV, and is a parameter of LV systolic
function that is almost insensitive to changes in preload and
afterload [
14]. During acute changes in load, the pressure–volume
loops representing consecutive cardiac cycles show the end-systolic
pressure–volume relationship to be linear (
Figure 4) [
13].
The slope of this line represents
Ees. A decreasing
Ees value
within the same patient over time, therefore, indicates deterioration
of LV systolic function.
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Fig. 4. (Left) Pressure–volume (PV) loop with the four phases of the cardiac cycle: (a) isovolumic relaxation; (b) filling; (c) isovolumic contraction and (d) ejection. An acute change in load generates different PV loops (dotted line loops). The upper left corners of these loops form a linear end-systolic PV relationship (ESPVR). The end-diastolic PV relationship (EDPVR) is curvilinear. (Right) The slope of the ESPVR line is end-systolic elastance (Ees). When systolic dysfunction develops, Ees is reduced (dotted line).
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The invasive character of intraventricular pressure and volume
measurements and the need for load alteration have limited the
clinical application of
Ees. To measure
Ees as a clinically
applicable method,
Ees measurement from LV pressure–area
relations was developed in the 1990s [
43]. End-systolic area
derived by continuous echocardiographic area measurement was
used as a surrogate for LV end-systolic volume. Cross-sectional
images of LV cavity changes recorded from the mid-ventricular
short-axis view, with the mid-papillary muscle level as an anatomic
landmark, have been shown to closely correlate with changes
in LV volume [
44]. Peak systolic pressure by continuous peripheral
BP measurement was used as a surrogate for end-systolic pressure.
Changes in peripheral peak pressure have been shown to correlate
with changes in LV end-systolic pressure, in the absence of
aortic stenosis or any other LV outflow tract obstruction [
45].
Ees from pressure–area loops has been validated against
Ees from pressure–volume loops in animals and humans,
with the use of automated border detection to record the changes
in LV cavity area [
43,
44]. In these studies, load alteration
was achieved by inferior vena cava obstruction. A non-invasive
alternative in a dialysis patient connected to the dialysis
machine is an intravenous bolus of nitroglycerine. As a result
of the large blood flow in an arteriovenous shunt, a 0.1–0.5
mg bolus induces acute unloading with a quick onset and short
duration [
46].
Although LV pressure–volume assessment may yield the least load-dependent information on systolic function, the use of surrogate parameters in clinical practice reduces its accurateness. Non-invasive LV pressure–volume assessment is not useful for diastolic function measurement, because of the non-linearity of the end-diastolic pressure–volume relationship. Moreover, in diastole, when the aortic valves are closed, peripheral pressure cannot be used as surrogate for LV pressure. Therefore, accurate load-independent diastolic function measurement still requires cardiac catheterization [14,47].
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Conclusions
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As many of the detrimental effects of renal insufficiency on
cardiac function start well before the onset of dialysis, evaluation
of cardiac function should be started before the patient reaches
end-stage renal disease. This is advantageous for both diagnosis
and secondary prevention of LV dysfunction (
Figure 5). In patients
with stage 3 chronic kidney disease [
48], in the absence of
clinically significant volume overload characteristic of end-stage
renal disease, the presence of moderate renal insufficiency
should not affect LV function assessment. However, it is important
to keep in mind that progressive chronic renal insufficiency
is associated with an increasing incidence of concentric and
eccentric LV hypertrophy. As LV geometry does affect EF measurement,
the use of this parameter of systolic function should not be
interpreted without concurrent LV volume assessment. At least
the EDV should be reported.
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Fig. 5. Minimal requirements for LV function assessment, depending on renal function. EDV, end-diastolic volume; LV, left ventricular.
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In dialysis patients, hypervolaemia may lead to the masking
of LV diastolic and systolic dysfunction. Consequently, both
the prevalence and severity of LV dysfunction may be underestimated
in this population. In view of the demonstrated load dependence
of both conventional and newer LV systolic and diastolic function
parameters, it is important that when echocardiographic LV function
assessment is reported in dialysis patients, the time relation
to the dialysis process is specified. Assessment of LV function
should not be performed on the haemodialysis day shortly before
dialysis, but preferably 1–2 h after dialysis. At that
moment, the patient is closest to a relatively normovolaemic
state. The routine use of DTI is recommended to help differentiate
normal from pseudonormal flow patterns. Colour M-mode Doppler
is a more time-consuming assessment. Although it appears to
be less sensitive in detecting milder degrees of diastolic dysfunction,
it may be used as an adjunct to DTI in more difficult cases.
Taking not only the high prevalence of LV hypertrophy but also
the changing volume status into account, EF in dialysis patients
should not be reported without LV volume assessment. Non-invasive
pressure–volume measurement may be applied as a less load-dependent
LV function assessment. Its application, however, is limited
by the need for acute load alteration, and consequently, the
risk of acute hypotension when applied following dialysis. Finally,
MRI and newer echo techniques such as TVI and 3D echo may prove
with time to be more than research tools and find a place as
diagnostic tools in clinical practice.
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Acknowledgments
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The authors gratefully acknowledge Ewout Hoorn for graphical
assistance.
Conflict of interest statement. None declared.
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Received for publication: 17. 1.06
Accepted in revised form: 15. 3.06
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Introduction
Changing loading conditions and...
