ACADEMIC EMERGENCY MEDICINE July 1999, Volume 6, Number 7

693

CLINICAL INVESTIGATIONS
Differentiating Systolic from Diastolic Heart Failure
Using Impedance Cardiography
RICHARD L. SUMMERS, MD, JAMES C. KOLB, MD,
LOUANN H. WOODWARD, MD, ROBERT L. GALLI, MD

Abstract. Objective: Differentiating systolic from

diastolic congestive heart failure (CHF) is often difficult in the ED. Impedance cardiography (IC) allows
for the noninvasive evaluation of systolic function
and measurement of diastolic time intervals. This
study was designed to assess the ability of IC to accurately measure isovolumic relaxation time (IVRT)
and determine relative cardiac contractility, thereby
differentiating systolic from diastolic mechanisms in
acute CHF. Methods: In an evaluation of the technique, the average differences in the diastolic time
intervals measured in normal subjects by both IC
tracings and phonocardiography were compared.
Likewise, the average Heather index (HI) of patients
with known systolic dysfunction (ejection fraction <
30% by echo-cardiography) was compared with the
mean HI measured in the normal subjects. In a retrospective analysis, the clinical performance of the
method was examined by extracting the values of
IVRT and HI from IC tracings of patients presenting
with CHF. The determined IVRT and HI values were
then correlated to clinical markers for diastolic and
systolic dysfunction. Results: Analysis of 280 IC tracings in eight healthy volunteers revealed an average

ARDIAC output and circulatory flow are a

balance of the pumping ability of the heart
as determined by the Frank-Starling curve with
the venous-return relationship as defined by Guyton and colleagues.1,2 Congestive heart failure
(CHF) is the condition in which the cardiac output
is unable to meet the metabolic demands of the
body. This condition can vary in severity from a
simple elevation in cardiac filling pressures (comFrom the Department of Emergency Medicine, University of
Mississippi Medical Center, Jackson, MS (RLS, JCK, LHW,
RLG).
Received May 7, 1998; revision received December 15, 1998;
accepted December 29, 1998. Presented at the SAEM annual
meeting, Chicago, IL, May 1998.
Supported by the Department of Emergency Medicine, University of Mississippi.
Address for correspondence and reprints: Richard L. Summers,
MD, 2500 North State Street, Department of Emergency Medicine, University of Mississippi Medical Center, Jackson, MS
39216. Fax: 601-984-5583; e-mail: rsummers@pol.net

difference of 0.0075 seconds (95% CI = 0.0067 to

0.0217) when IVRT intervals measured by phonocardiography and IC are compared. The HI in this normal group averaged 14.2 (95% CI = 9.4 to 19.0), contrasting to the much lower value of 2.8 (95% CI = 1.98
to 3.62) seen in eight subjects with documented systolic dysfunction. In 26 patients with decompensated
CHF, there was a close correlation (r = 0.81) of the
measured IVRT to left ventricular hypertrophy by
voltage criteria and while a fall in the HI was correlated with intravascular volume expansion. Though
there was considerable overlap (46%) in mechanisms
of CHF, 35% of the patients were found to have only
systolic dysfunction (HI < 5 and IVRT < 0.125), while
19% had a predominantly diastolic etiology (IVRT >
0.125 and HI > 5) for their failure. Conclusion: IC
measures of contractility and diastolic time intervals
are a potentially effective method for differentiating
the dominant mechanisms of CHF in the emergent
setting and categorizing CHF patients into different
subsets. Key words: impedance cardiography; cardiac
output; congestive heart failure; diastolic dysfunction. ACADEMIC EMERGENCY MEDICINE 1999; 6:
693 699

pensated failure) to severe hypoxia and edema (decompensated failure). In the past, CHF was
thought to result from a failure in the contractile
elements of the heart during the systolic phase of
the cardiac cycle. More recently it has been recognized that limitations in cardiac filling during
diastole can also result in an abnormal circulatory
flow. Diastolic CHF, or diastolic dysfunction, is
defined as the condition in which there is evidence
of the clinical signs of CHF in the presence of normal systolic functioning.35 It is usually associated
with abnormalities in diastolic time intervals such
as the prolongation of the isovolumic relaxation
time (IVRT).3,4 A prolonged IVRT (active energydependent interval between aortic valve closure
and mitral valve opening) is common in patients
with long-standing hypertension and left ventricular hypertrophy (LVH).3,4 Longer ventricular relaxation time during diastole infringes upon the
cardiac filling time. Conditions that are responsi-

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IMPEDANCE CARDIOGRAPHY

ble for diastolic dysfunction have been shown to be

present in as many as 10% to 30% of the patients
presenting to the ED with CHF.5,6
Although the clinical manifestations of systolic
and diastolic CHF are frequently similar, their underlying pathophysiologic processes are decidedly
different, and each requires special treatment considerations.5,6 Refractory CHF may indicate a predominant diastolic mechanism that typically responds poorly to aggressive diuresis or reductions
in preload. Such therapies may even worsen circulatory flow in these conditions. Differentiating
systolic from diastolic CHF in the ED is often difficult. Limited availability of angiography or echocardiography in the acute setting has made it necessary for most emergency physicians to rely upon
inconsistent clinical clues to distinguish between
the two clinical entities. The development of thoracic electrical bioimpedance (TEB) and impedance
cardiography (IC) technology for cardiac output determination provides a readily accessible tool for
the rapid and noninvasive evaluation of hemodynamic status and may also be used for measuring
cardiac time intervals.79 This unique combination
of functions has the potential for the differentiation of systolic from diastolic mechanisms in the
patient with acute CHF. The purpose of this study
was not to reconfirm the well-documented ability
of the TEB technology to accurately determine cardiac output and contractility.1014 This study was
designed to assess the ability of IC to determine
diastolic time intervals (specifically IVRT) and the
relative myocardial contractile state in the clinical
setting and to demonstrate its usefulness in differentiating the dominant mechanisms of CHF in the
emergent patient.
Thoracic Electrical Bioimpedance. Thoracic
electrical bioimpedance and IC technology was
first developed by NASA in the 1960s.15 Since that
time it has been used primarily for continuous
noninvasive monitoring of cardiac output.7 Numerous studies have demonstrated reliable and reasonable accuracy of IC in measuring cardiac output
and contractility when compared with thermodilution and echocardiography, and it has received
Food and Drug Administration (FDA) approval for
this use in the intensive care unit.12 However, more
than just a monitoring device, this technology may
be used in the acute setting as a diagnostic adjunct. Along with cardiac output determination,
the bioimpedance waveform can be used to calculate systolic time intervals and, therefore, allows
an estimation of the cardiac contractility. The
waveform is the time-dependent change (dZ/dt) of
the transthoracic impedance (Z, in ohms) during
the cardiac cycle.15 This dZ/dt is measured by a series of electrodes that detect the impedance to a
generated high-frequency, low-magnitude current

Summers et al. SYSTOLIC VS DIASTOLIC HEART FAILURE

that traverses the patients thorax. While several

methodologies are available to estimate contractility from systolic time intervals determined by the
waveform, we have chosen the Heather index (HI)
because of its reported accuracy (HI = dZ/dtmax /
QZ1; where dZ/dtmax is the maximum deflection of
the initial waveform and QZ1 is the time from the
beginning of the Q wave to peak dZ/dt).16 Systolic
and diastolic time intervals are also available from
the IC tracings by the methodology of Lababidi et
al.8,9 In this method the primary deflection of the
bioimpedance waveform is correlated with the systolic time intervals and stroke volume, while diastolic time intervals such as IVRT as determined
by phonocardiography are found to coincide with
the second deflection of the IC waveform (Fig. 1).
The X to O period represents the IVRT that begins
with the aortic valve closure as documented by
phonocardiographic tracing and ends at the point
of the maximum second deflection when the
sounds of mitral flow begin. The beginning of the
QRS complex on the electrocardiogram (Q) and the
start of the primary IC waveform signifies the end
of diastole. Baseline impedance of the thoracic cavity (Z0) has also been strongly correlated with intravascular fluid volumes by the thoracic fluid volume index (TFVI).17,18

METHODS
Study Design. A retrospective case series was
collected and analyzed to determine the ability of
IC technology to measure the IVRT and relative
contractile state of the myocardium and to demonstrate its usefulness in differentiating the dominant mechanisms of CHF in the emergent patient.
Institutional review board approval was waived
due to the retrospective nature of the study. The
study was divided into three parts. The first two
parts were designed to examine the accuracy of IC
in measuring IVRT and distinguishing broad differences in cardiac contractility with the equipment available. After establishing the capabilities
of the technology, IC measurements were then
used in a feasibility study to differentiate the
mechanisms of CHF in patients in the acute clinical setting. This determination was then correlated with clinical markers that are commonly
used to distinguish diastolic from systolic CHF.
Study Setting and Population. The clinical portion of the study included a review of the records
of patients presenting to a university hospital ED
(Level 1 trauma center) from November 1997 to
January 1998 in an area with a base population
known for a high prevalence of hypertension. Inclusion criteria were adults (age > 18 years) presenting in the acute phase of decompensated CHF

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695

documented by pulmonary edema on chest radiographs. Patients were excluded if there was evidence of an acute myocardial infarction or cardiogenic shock (blood pressure < 80 mm Hg). Also
excluded were patients with known valvular heart
disease or idiopathic hypertrophic subaortic stenosis (IHSS) due to limitations in the technology
for accurate readings under these conditions. Intubated patients were likewise not included in the
study. Patients with evidence of bundle branch
block on electrocardiography or those with a pacemaker were not used in order to maintain consistency in the measurements of LVH by voltage criteria. Since the extremes of heart rates may
influence cardiac time intervals and contractility,
only waveforms sampled when the rate was between 120 and 60 beats/min were used. Normal
subjects used in the validation of the diastolic time
interval measurements and for baseline normal HI
averages were healthy adult volunteers (male and
female; age < 30 years; with no known cardiovascular or metabolic disease) who had assisted in the
calibration and testing of the IC equipment. Patients with ejection fractions less than 30% as measured by two-dimensional (2D) echocardiography
were randomly selected for comparison with the
normal subjects.
Study Protocol. To determine the ability of the
IC technology to estimate diastolic time intervals,
specifically IVRT, bioimpedance tracings were obtained (during equipment calibration) in young
normal subjects while simultaneously recording
heart sounds by phonocardiography (Sorba Medical Systems, Inc., Brookfield, WI). Cardiac time intervals were then measured by the two methods
(IC tracings vs phonocardiography) and the average differences were compared.
To ascertain the ability of the IC to grossly estimate systolic function, the average HI of randomly selected patients with systolic dysfunction
(ejection fraction < 30% by 2D echocardiography)
was retrospectively compared with the mean HI
measured in the normal subjects noted above.
These low-ejection-fraction patients were chosen
as they became available during the study period
when both IC and echocardiography were used to
evaluate the cardiac contractility concurrently and
they were found to have severe systolic dysfunction.
Clinical performance of the method was examined in a retrospective analysis of IC tracings originally obtained for diagnostic assessment of patients presenting to the ED in decompensated
CHF. This group included all those patients with
acute CHF in our ED over a three-month time period in which IC was used in their clinical evaluation. The choice of patients in which IC was used

Figure 1. The primary deflection of the bioimpedance

waveform is correlated with the systolic time intervals
and stroke volume, while the isovolumic relaxation time
(IVRT) as determined by phonocardiography coincides
with the second deflection of the impedance cardiography (IC) waveform. The X to O period represents the
IVRT, which begins with the aortic valve closure as documented by phonocardiographic tracing and ends at the
point of the maximum second deflection when the
sounds of mitral flow begin. The beginning of the QRS
complex on the electrocardiogram (Q) and the start of
the primary IC waveform signifies the end of diastole.
Baseline impedance of the thoracic cavity (Z0) determines the thoracic fluid volume index (TFVI).

was in part a convenience sampling and dependent

on the availability of the equipment operator. However, IC was used only in those CHF patients for
whom it was prospectively thought that it would
benefit the clinical decision making. Measurements used in the study were those taken upon
initial presentation of the patient when evaluation
and therapy were just beginning. The values of
IVRT and the HI were extracted from the tracings
and placed in a database. The determined IVRTs
(a standard measure of diastolic function) were
correlated to the well-established clinical marker
for diastolic dysfunction, LVH, using standard Sokolow and Lyon voltage criteria of SV1 RV5 or
RV6.3,5,6,19 Likewise, the measured values for the
HI were correlated with an indicator of systolic

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IMPEDANCE CARDIOGRAPHY

Summers et al. SYSTOLIC VS DIASTOLIC HEART FAILURE

group was divided according to mechanism of CHF

in a standard hemodynamic subset analysis according to the cutoff points established from the
correlations with the clinical markers, values from
the literature, and the standards adopted by the
European Heart Association: Diastolic Failure
Working Group.1618,2023 The subsets were separated into categories by quadrant:
A. predominantly diastolic dysfunction
B. predominantly systolic dysfunction
C. mixed mechanismssevere
D. mixed mechanismsmild

RESULTS
Figure 2. Left ventricular hypertrophy (LVH, mV) is
correlated with active ventricular relaxation time (IVRT,
sec) in diastole.

dysfunction, the TFVI. The patients were then divided into mechanisms of heart failure based on
these markers and previously published indexes
for differentiation.3,5,6,16,17,18,20
Data Analysis. The average differences between
the time intervals measured by IC vs phonocardiography were compared using a paired t-test at the
95% confidence level (significance at p < 0.05), with
data expressed as the mean difference between the
measured intervals. The average HIs of the patients (ejection fractions < 30%) and the normal
subjects were compared using an unpaired t-test
level (significance at p < 0.05), with data reported
as averages for each group with confidence intervals. The values of IVRT obtained by IC were correlated with measurements of LVH by voltage criteria using linear regression analysis. The patient

Figure 3. Left ventricular contractility (Heather index

= dZ/dtmax /QZ1; where dZ/dtmax is the maximum deflection of the initial waveform and QZ1 is the time from
the beginning of the Q wave to peak dZ/dt) is correlated
with thoracic fluid volume index (TFVI, %) in diastole.

Analysis of 280 IC tracings in eight young healthy

volunteers (mean age SD = 24.8 4.7) revealed
an average difference of 0.0075 seconds (95% CI =
0.0067 to 0.0217) between IVRT intervals measured by phonocardiography and values obtained
by IC. Similarly compared systolic and total diastolic time intervals averaged less than 0.0001 seconds difference, with almost no variation. The HI
in this same group of eight normal individuals averaged 14.2 (95% CI = 9.4 to 19.0), which is consistent with that previously reported in healthy
subjects.16 This normal value contrasts to the
much lower value of 2.8 (95% CI = 1.98 to 3.62)
seen in eight subjects with a known ejection fraction of <30% (average 21%) as measured by standard 2D echocardiography.
To examine the clinical performance, the methodology was applied to 26 patients (mean age 52
years, 95% CI = 46 to 58) presenting to the ED
with decompensated CHF and pulmonary edema
and meeting the study inclusion criteria. When the
extracted IVRT values were compared with the
well-established clinical marker of diastolic dysfunction (LVH) by voltage criteria measurements,
there was a close correlation (r = 0.81) by linear
regression. The Sokolow and Lyon cutoff for ventricular hypertrophy of 3.03.5 mV corresponded
to an IVRT of about 0.125 seconds in the clinical
group (Fig. 2), which is consistent with values previously reported and is approximate to that established as a standard in the diagnosis of diastolic
dysfunction in this age group.3,19,20,24
Likewise, when the HI was correlated with an
indicator of intravascular volume expansion
(TFVI), it was noted that the volume measure began to rise precipitously when the HI reached a
point < 5 (Fig. 3). This HI value corresponds to a
plateau TFVI level of about 4.4%, which is similar
to the normal values of 3.8% from the literature
and the 4.5% average seen in our control group of
eight young subjects.17,18,25 Similar values of TFVI
have been shown to clinically depict fluid volume
overload of CHF.25 The cutoff value of 5 for the HI

ACADEMIC EMERGENCY MEDICINE July 1999, Volume 6, Number 7

is also compatible with the range of values previously noted in the literature and is consistent with
the values from our group of eight with <30% ejection fraction by echocardiography.2123 Most importantly, this HI cutoff point correlates with an ejection fraction of about 45% (derived from IC by the
Capan method in our 26 patients with CHF),
which is the standard adopted by the European
Heart Association: Diastolic Failure Working
Group as a criterion for clinical diastolic heart failure.13,20
Using the above criteria in a hemodynamic subset analysis by quadrant (A, B, C, and D in Fig. 4)
to differentiate the types of heart failure, nine of
the 26 CHF patients (35%) were found to have evidence for a systolic mechanism only (HI < 5),
while five (19%) had predominantly a diastolic etiology (IVRT > 0.125) for their future. Among the
remainder of the patients studied there was considerable overlap in the factors (systolic vs diastolic) contributing to the CHF. While seven patients (27%) had waveforms indicative of both
severe systolic and diastolic dysfunction, there was
a small subgroup of five patients who had only
mild evidence of either mechanism.

DISCUSSION
It has been previously shown that 1030% of patients presenting with CHF will have good myocardial contractility and normal systolic function.5
These patients have been thought to have diastolic dysfunction with limitations in cardiac filling and venous return resulting in their heart failure. While some of this dysfunction may be due to
a stiff myocardium limiting the passive phase of
diastolic filling, the majority is caused by delays in
isovolumic myocardial relaxation.3,5,6,2628 Myocardial relaxation is an energy-dependent, active process that is mainly unconstrained by preload and
afterload considerations.5,6 Ventricular hypertrophy is often the end result of long-standing hypertension and is commonly responsible for delays in
IVRT due to abnormalities in calcium kinetics.5,6
Patients presenting with CHF due to diastolic dysfunction may not respond to traditional therapies
that can even be detrimental. Patients with evidence of acute decompensation secondary to a diastolic mechanism may have worsening of symptoms, hypotensive response, and reduced cardiac
output with the typical off-loading treatments of
diuretics or preload reducing medications.5,6,27
Differentiating diastolic from systolic mechanisms of CHF has been difficult in the ED. Definitive angiography is not a realistic consideration in
the decompensated patient and ED echocardiographic measurements are limited by technique,
available expertise, and load-dependent character-

697

Figure 4. Represents a typical hemodynamic subset

analysis using a measure of contractility (Heather index) plotted against the measure of diastolic function
(IVRT = isovolumic relaxation time). The quadrants correspond to demarcations for systolic and diastolic dysfunction and divide the set according to mechanisms of
dominance.

istics of the patient.36 Newly accessible IC technology, with its unique combination of functions,
has the potential for the rapid, noninvasive differentiation of systolic from diastolic mechanisms in
the patient with acute CHF. There is already considerable evidence in the literature (26 articles reviewed by the authors) correlating IC readings
with cardiac output and contractility measurements made with conventional methods.1014,29 It
has also been clearly established in previous studies that IC can be used to determine diastolic time
intervals.8,9,30 As previously stated, the purpose of
this study was not to reconfirm the well-documented ability of the TEB technology to accurately
determine cardiac function. This study was designed to assess the usefulness of IC in differentiating the dominant mechanisms of CHF in the
emergent patient. This patient application was
further examined by correlating the findings with
clinical markers currently used to differentiate
systolic from diastolic dysfunction. While the results of this preliminary study do not prove the
value or accuracy of IC to differentiate mechanism
of CHF, they do demonstrate the potential feasibility of the technology to assist in the assessment
of these patients. An interventional study that
identifies the clinical usefulness and impact on
acute patient outcomes of differentiating CHF
mechanisms would be important in the further
evaluation of the methods described.
Categorization of the patients studied is based
on the criterion that best reflects those standards
determined in a consensus statement by the European Heart Association: Diastolic Failure Working Group as diagnostic of diastolic dysfunction.20

698

IMPEDANCE CARDIOGRAPHY

While information regarding outcomes in our patients is not available, the criteria used have been
established previously to correspond to clinical responses.5,6,20 Upon examining the findings of this
study, several interesting points emerge. While the
percentage of patients with predominantly diastolic failure (19%) was consistent with that previously reported, it was surprising to see how
many patients had evidence that both mechanism
were involved in the etiology of their CHF. This
may be due to the fact that the base population
from which the study was derived is known for its
high prevalence of severe and often untreated hypertension, a risk factor for developing diastolic
dysfunction. However, it may also be that CHF as
a clinical entity is not sharply divided into systolic
and diastolic mechanisms and is more of a continuum with differing degrees of contributing factors.
This is obvious upon analysis of Figure 4 (divided
into quadrants), where there are patients with
dominantly diastolic (A), dominantly systolic (B),
and some with a mixed pattern (C). The patients
in the small group that did not have very significant systolic or diastolic dysfunction (D) were
noted to have other underlying medical conditions
such as end-stage renal disease and volume overload that could be contributing to the generation
of the pulmonary edema seen. As clinician we are
taught to recognize the traditional clues that
would grossly differentiate systolic from diastolic
mechanisms of CHF (LVH, cardiomegaly, gallops,
etc.). However, determination of the dominant
mechanisms when there is overlapping etiologies
requires a quantitative approach that IC provides.

LIMITATIONS AND FUTURE QUESTIONS

Several limitations to the study are noted. The limited capacity of echocardiography and radionuclide
ventriculography to accurately determine diastolic
time intervals and baseline systolic function in the
decompensated patient makes these noninvasive
technologies poor benchmarks for correlation.36
Likewise, the inability for emergent measurements by angiography for criterion standard comparisons results in the studys relying on the previously proven efficacy of the components of the IC
waveform to accurately determine diastolic and
systolic function. This limitation is tempered by reconfirming the ICs reliability in measuring IVRT
and broadly differentiating systolic function in the
current study environment.
It is also important to note that the findings in
the CHF patient study group were consistent with
known clinical markers that distinguish systolic
from diastolic failure. The close correlation of the
degree of LVH with the delays in IVRT is concordant with what we know clinically with regard to

Summers et al. SYSTOLIC VS DIASTOLIC HEART FAILURE

diastolic dysfunction. The Sokolow and Lyon criteria were chosen over other electrocardiographic
methods for diagnosing LVH due to their superior
sensitivity and specificity when collaborated by autopsy data.31 However, demonstration of LVH by
electrocardiography alone is insufficient to conclude a mechanism of diastolic heart failure. While
this clinical marker is an indicator of probable
pathologic diastolic dysfunction, factors that physiologically hypertrophy the heart (e.g., exercise) reduce its specificity as a diagnostic marker. Electrocardiographic findings also do not allow detection
of combined diastolic and systolic dysfunction. Direct measurement of IVRT is by definition one of
the best indicators of problems with the active
phase of myocardial relaxation during diastole and
thereby has been adopted as a criterion for the diagnosis of diastolic heart failure. Similarly, the
rapid rise in central cardiac and vascular volumes
with failing contractile function is typical of systolic mechanisms of heart failure that are not usually seen in diastolic dysfunction alone. Elimination of the patients with the combined mechanisms
of failure from the study would only serve to
strengthen the already conclusive correlations.
The study may also be limited by its retrospective and convenience design. Restricting the study
to those in pulmonary edema may be selective for
those with predominantly systolic mechanisms
and therefore limit potential incongruencies that
might arise if a larger population with diastolic
dysfunction were analyzed. However, a prevalence
of 19% with predominantly diastolic dysfunction in
our study group is within the range typically found
in epidemiologic studies.5,27 Furthermore, it was a
major goal of the study to test the ability of the
technique to distinguish between the two types of
failure in those patients who had conclusive evidence of CHF. However, it is not always possible
to categorize the mechanisms as solely diastolic or
systolic. As demonstrated by our findings, overlapping mechanism are common, and CHF must be
viewed as a continuum.
The study is limited in its use of correlations to
demonstrate relationships. Except for validation of
the measures of IVRT (compared with phonocardiography) and HI (compared with echocardiography-derived ejection fractions), the evidences
of diastolic and systolic dysfunction are not compared with any criterion standard. Since the information used to differentiate the CHF mechanisms
is also that used in established international standards and since the elements of IVRT and HI have
already been previously demonstrated to accurately reflect diastolic and systolic states, criterion
standards were not incorporated in the study design.5,6,2023,30 The primary purpose of the study was
to demonstrate the feasibility of the use of this

ACADEMIC EMERGENCY MEDICINE July 1999, Volume 6, Number 7

technology to differentiate CHF mechanisms in the

emergent setting. Further study to collaborate the
findings with other modalities such as echocardiography might be used to calculate the sensitivity
and specificity of the technique.
The limitations of IC in conditions of valvular
heart disease and in patients who have been intubated preclude the use of this technology in certain groups of patients. Fortunately, these select
individuals are less commonly seen in the ED and
are also not the patients for whom differentiation
of the mechanisms of heart failure is crucial in determining the outcome.

CONCLUSIONS
Emergency physicians are often asked to make
critical decisions in a short period of time using
limited amounts of information. They frequently
are not afforded the luxury of the results of definitive tests in this decision-making process. While
further testing of the methodology is needed, IC
potentially offers a rapid and noninvasive technique for differentiating the mechanisms of CHF
in the emergent setting. This technology may be
useful for categorizing ED patients with acute
CHF into important subsets, which could affect decisions regarding therapeutic interventions.
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