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Right Ventricular End-Diastolic Volume
J. Boldt
“Since during critical illness maintenance of the cardiac output may depend upon
right ventricular function, the clinician needs to be able to discern the presence of
right ventricular dysfunction ...” (William Hurford, Intensive Care Medicine, 1988)
Introduction
Improvements in surgical techniques and perioperative anesthetic management
have led to surgery and intensive care therapy for patients who would have never
been acceptable candidates before. Accurate assessment of hemodynamic status is
a ‘conditio sine qua non’ when managing the critically ill. There has been a
tremendous increase in the availability of monitoring devices over the last years.
Ongoing developments in monitoring techniques have shed new light on our
knowledge of pathophysiologic processes associated with critical illness and have
influenced our therapeutic approaches.
The interest in hemodynamic monitoring is focused mostly on the ‘dominant’
left side of the heart. The tendency to ‘overlook’ the right ventricle as an important
part of the circulatory system is due to the fact that it has traditionally been regarded
as a passive conduit, responsible for accepting venous blood and pumping it
through the pulmonary circulation to the left ventricle [1]. Maintenance of normal
circulatory homeostasis, however, depends on an adequate function of both ventricles. Changes in dimension and performance of one ventricle influence the
geometry of the other (Fig. 1). There is growing interest in the importance of the
neglected right side of the heart, particularly in patients suffering from sepsis,
trauma, acute respiratory distress syndrome (ARDS), and in heart transplanted
patients [2].
Why May A Closer Look at Right Ventricular Volumes be of Interest?
Ventricular interdependence is a complex interplay of interactions mediated by
the common myocardial fiber bundles, the interventricular septum, the constraining influence of the pericardium, and the pulmonary circulation (Fig. 2). Thus
alterations in right ventricular (RV) function may have detrimental consequences
on the function of the left side of the heart (Fig. 3). The consequences on altered
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Fig. 1. Geometry of the right ventricle (RV) in combination with changes of the shape of the left
ventricle (LV)
Fig. 2. Coupling of the right ventricle (RV) with the left ventricle (LV)
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Fig. 3. Influence of changes in right ventricluar (RV) hemodynamics on the left ventricle. CO:
cardiac output; RVEF: right ventricular ejection fraction; RVEDV: right ventricular end–diastolic
volume; IVS: interventricular septum; RCA: right coronary artery; CBF: coronary blood flow
loading (e.g., increased preload) and unloading (e.g., increased afterload) conditions differs widely between the two ventricles (Fig. 4). Another important aspect
for understanding the (patho-) physiology of RV performance is represented by
the compliance, that describes the relationship between end-diastolic volume and
end-diastolic pressure of the ventricle.
How to Assess Preload Conditions?
RV preload is often assessed by measuring filling pressures such as central venous
pressure (CVP) or right atrial pressure. Both, however, do not correlate with RV
end-diastolic volume (RVEDV) [3, 4]. For several years, pulmonary capillary
wedge pressure – better named pulmonary artery occlusion pressure (PAOP) –
has been used as the primary surrogate for left ventricular (LV) preload. It has
been demonstrated that monitoring of RVEDV is easier and more accurate than
PAOP, especially in patients with high levels of positive end-expiratory pressure
(PEEP) or other ventilatory support that may raise intrathoracic pressure [5].
Monitoring of Right Ventricular Volumes by Thermodilution
With conventional pressure monitoring, assessment of RV preload is not accurately possible. Hoffman et al. [4] demonstrated no significant correlation between CVP and RVEDV and emphasized that the preload factor in the original
Frank-Starling hypothesis had nothing to do with pressure but volume.
RV loading and performance are difficult to measure by conventional monitoring techniques because of the functional anatomy and complex geometry of the
right ventricle [6]. Bing et al. [7] were the first to propose the principle of indicator
dilution measurement to quantify RV volumes. Although the response time of
conventional thermistors was sufficient to measure thermodilution cardiac output,
they were, however, not rapid enough to accurately measure beat-to-beat step
changes in temperature required to calculate ventricular volumes. Mounting fastresponse thermistors on conventional thermodilution pulmonary artery catheters
(PACs) allows rapid detection of changes in pulmonary artery temperature.
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a
b
Fig. 4. Effects of changes in afterload (a) and preload (b) on right and left ventricular performance
Measurement of RV volumes (RVEDV, RV end-systolic volume [RVESV]) and
RV ejection fraction (RVEF) by thermodilution is an easy to perform technique
with no accumulation of toxic indicators based on the use of a fast-response
thermistor. This enables accurate detection of rapid step changes in the staircase
curve of the downstream temperature change (Fig. 5). The catheter is equipped
with a fast-response thermistor and electrodes for intracardiac electrocardiographic (EKG) recording. The typical downslope thermodilution washout curve
follows an exponential decay, interrupted by the diastolic plateaus (Fig. 5). The
ratio between the temperature change of two successive diastolic plateaus represents the fraction of blood remaining in the right ventricle (=residual fraction
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Fig. 5. Principle of measuring right ventricular volumes and ejection fraction
[RF]). RVEF is calculated from EF=1-RF. The thermistor of the thermodilation
volumetric catheter is able to measure beat-to-beat temperature variations of the
downstream temperature changes after injection of an (ice-cold) indicator (e.g.,
dextrose) or – nowadays – (almost) continuously by using heating filaments
mounted on the catheter by which energy is transmitted to the circulating blood.
As cardiac output and stroke volume are calculated by the microprocessor, RVEDV
can be derived from stroke volume/RVEF and RVESV=RVEDV-stroke volume.
The accuracy and validity of this technique have been shown by using radionuclear methods in humans as well as in the animal model and it has been proved to
be valid and accurate for measuring RV volumes (and RVEF) in comparison to
radiographic, radionuclide, and echocardiographic methods [8–12]. Measurement
of RV volume by thermodilution shows reproducible results (coefficient of variation of near 7%) [13]. Moreover, measuring RVEDV by thermodilution is unaffected by arbitrary and often poorly reproducible zero points for pressure
transducers that are necessary to measure filling pressures (e.g. CVP, PAOP).
Problems With Measuring Right Ventricular Volumes
All monitoring devices have their pros and cons. While close monitoring of RV
volumes (and RVEF) using thermodilution technique was assessed as a useful
monitor [14], others stated good reproducibility, but less certain accuracy [15].
The major problems associated with RV volumetric catheters are:
• injection technique
• irregular heart rate (arrhythmias, atrial fibrillation)
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intracardiac shunt
tricuspid regurgitation
place of injection of cold indicator
mathematical coupling
higher costs
Injection Technique
The accuracy of the intermittent thermodilution technique is reported to range
from ±3% to ±30% [16]. Its accuracy depends on several factors including constant injection, technique (=homogeneity) of injection, temperature of the injectate bolus, timing of the indicator injection within the respiratory cycle, and
others [17–19]. The question concerning the optimal technique for measuring
cardiac output by intermittent bolus thermodilution is still controversial. One of
the major problems appears to be the timing of the thermal injection. Both endexpiratory and end-inspiratory points on the ventilatory cycle are used for measurement of cardiac output. Others have suggested averaging three thermal injections distributed equally over the ventilatory cycle or to calculate four to five
thermal injections carried out at random relative to the ventilatory cycle [19].
Recently it has been demonstrated, in a study in critically ill patients on mechanical ventilation, that for correct measurement of RVEDV using the thermodilution
technique, multiple determinations at equally spaced intervals, or at least eight at
random injections in the ventilator cycle are necessary due to ventilatory modulation of RV volumes and interindividual differences therein [20].
Arrhythmias
When using the thermodilution technique to assess RV volumes, accurate sensing
of R-waves is a prerequisite to calculate residual temperature. When the R-R-interval is irregular (e.g., secondary to atrial fibrillation) volumes (and ejection
fraction) cannot correctly be determined. Aside from irregular heart rate, RV
monitoring using RV volumetric catheters may become less reliable at higher
heart rates (e.g., tachycardia >150 beats/min), because the R-R-interval is too
short to identify ejection fraction [21, 22].
Place of Injection
Conventional thermodilution measurements involve positioning of the catheter
injectate port in the right atrium – in immediate proximity to the tricuspid valve.
In an animal study in pigs, the effects of catheter position on thermodilution
RVEF measurements were studied. A RV thermodilution catheter was placed in
the pulmonary artery, an injectate catheter in the right atrium, an atrial pacing
electrode, and a systemic arterial catheter [23]. RVEF measurements were determined using thermodilution with incremental increases in pulmonary valve to
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thermistor distance and with incremental increases in injectate port to tricuspid
valve distance. Measurements were obtained at a paced rate of 102 beats/min and
repeated with pacing-induced tachycardia (140 beats/min). There were no significant differences in thermodilution RVEF measurements with the thermistor positioned 0 to 10 cm from the pulmonary valve at either heart rate. A significant
reduction in RVEF occurred with the injection port located 5 to 7 cm proximal to
the tricuspid valve, with this decrease becoming more pronounced during tachycardia. The authors concluded that thermodilution RVEF measurements (and
RVEDV) appear to be independent of thermistor position within the pulmonary
artery. However, large distances from the injectate port to the tricuspid valve
reduced RVEF measurements.
Mathematical Coupling
Another concern regarding RV volumetric catheters is based on possible mathematical coupling [15]: measurement of cardiac output and RVEDV both use the
thermodilution principle. Since the RVEDV is calculated by dividing the stroke
volume by the ejection fraction, it appears that the relationship between cardiac
index (CI) and stroke volume causes the statistical correlation. Chang et al. [24]
measured cardiac output by the Fick principle and RVEDV by thermodilution and
thus removed the possible effect of mathematical coupling. Others have also
argued that the better correlation of RVEDV with CI versus PAOP and CI is not
due to coupling per se [25]: Durham et al [5] showed that RVEDV correlated more
closely with CI than PAOP in 38 critically ill patients, even after correction for
mathematical coupling. Nelson et al. [26] measured RVEF and cardiac output by
the intermittent bolus thermodilution method and continuous cardiac output by
a pulsed thermal energy technique. RVEDV calculated from thermodilution correlated well with both the thermodilution-derived cardiac output and the independently measured continuous cardiac output. Because random measurement
errors of the two techniques differ, mathematical coupling alone does not explain
the correlation between RVEDV estimates of preload and cardiac output.
Cost Considerations
RV volumetric monitoring adds considerable costs to conventional PAC monitoring, especially when using (near) continuous measurement techniques. Nelson
[22] reported an addition of +20% to the costs of the traditional PAC. These are
only estimated data, because costs vary widely between different countries. Moreover, hardware costs (another bed-sided computer system) have to be added.
Is Monitoring of RVEDV useful from a Clinical Point of View?
RV decompensation may result from several insults and may have various negative sequelae (Fig. 6). Introduction of RV volumetric measurement into a PAC has
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Fig. 6. Reasons for right ventricular (RV) decompensation and its consequences
broadened the overall assessment of cardiac function in the critically ill (27).
Enlarging our monitoring armamentarium by measuring RV volumes has several
advantages:
• bedside monitoring system
• no risk of indicator accumulation (repeated measurements)
• no more invasive than a standard PAC
• additional information besides pulmonary artery pressure, PAOP, and cardiac
output
• less expensive than other techniques for assessing RV function
• (near) continuous RV hemodynamic monitoring possible
RVEDV correlates well with CI. This correlation between RV preload and LV
function appears to be of particular value when considering volume challenge in
patients with inadequate cardiac output [22]. Cardiac preload is often assessed by
monitoring PAOP. However, there is increasing evidence that PAOP appears to be
poor predictor of the preload status. In the critically ill, the assumption that PAOP
reflects left atrial pressure and thus LV end-diastolic pressure (LVEDP) is often
incorrect most likely due to changes in ventricular compliance. Mechanical ventilation and use of PEEP are reasons for the dissociation of PAOP and preload
status. In mechanically ventilated trauma patients, PAOP was not able to reflect
preload, whereas RVEDV was a reliable indicator of preload [28, 29]. Several other
studies in the critically ill have demonstrated that RVEDV is a much better predictor of preload than PAOP:
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• RVEDV was reported to be a better predictor of preload-recruitable stroke
volume by a fluid challenge than filling pressure, so that a high volume may
preclude a further rise in cardiac output with fluids, independent of filling
pressures [3, 20].
• In patients undergoing aortic reconstruction, monitoring of RVEDV using a
thermodilution technique provided a better means of evaluating the cause of
decreased cardiac output during surgery and led to direct appropriate interventions [30]. Additionally, changes in CI with aortic cross-clamping correlated
with the degree of coronary artery disease and were not reflected by PAOP.
• Intra-abdominal hypertension and abdominal compartment syndrome cause
significant morbidity and mortality in surgical and trauma patients. Maintenance of intravascular preload and use of open abdomen techniques are essential. Multiple regression analysis demonstrated that RVEDV is superior to PAOP
and CVP as an estimate of preload status in patients with an open abdomen [31].
• Sepsis may be associated with complex changes in RV function related to
multiple factors both directly and indirectly altering diastolic and systolic ventricular function [10, 32, 33]. In this situation, RVEDV and RVESV vary independently of changes in right atrial pressure and ejection pressure most likely
due to the fact that the RV is a highly compliant chamber during filling and thus
changes in RVEDV do not alter RV wall stress (preload) or ejection efficiency
(RVEF). The slope of the RVESV/RVEDV relation should be inversely proportional to ejection efficiency [10].
An increasing number of cases of RV ischemia and RV failure after coronary
bypass grafting have been reported [34]. Because of the relatively hazardous RV
preservation during cardiopulmonary bypass (CPB), postoperative RV function
may be impaired by myocardial areas that remain ischemic [35]. Increased enddiastolic volume (and decreased RV contractility index) may occur already prior
to CPB – especially in patients with reduced LV function or in elderly cardiac
surgery patient (Figs. 7 and 8) [36, 37]. In 30 consecutive patients with reduced LV
function (LV ejection fraction [LVEF]) undergoing myocardial revascularization,
RV hemodynamics were studied from the beginning of anesthesia until the end of
the operation [36]. The data were compared with 30 consecutive patients with
almost normal LVEF. RVEF was significantly lower in the patients with a LVEF
below 30% and RVEDV was significantly higher (Fig. 7). These patients may be
unable to make the adaptations required. Acute volume loading may lead to
further deterioration of myocardial function due to RV failure, a condition that
cannot be diagnosed readily at the bedside with conventional monitoring techniques. As ischemia of the RV myocardium seems to be the limiting factor in the
response to pressure load, reduced RV function already preoperatively may have
disastrous consequences for RV performance during and after weaning from
bypass. More attention should be focused upon the right ventricle in these patients, which can be monitored by rapid response thermodilution. Knowledge of
the complex interaction between both sides of the heart may enable us to optimize
patient management during the perioperative period (e.g., volume versus inotropes).
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Fig. 7. Right ventricular end-diastolic volume index (RVEDVI) in patients undergoing cardiac
surgery showing almost normal left ventricular function (ejection fraction >30%) in contrast to
patients with markedly reduced left ventricular function (ejection fraction <30%). CPB: cardiopulmonary bypass – modified from [37] with permission
Fig. 8. Right ventricular end-diastolic volume index (RVEDVI) in patients undergoing cardiac
surgery aged either >70 years or aged 50–70 years. CPB: cardiopulmonary bypass – modified from
[36] with permission
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Impact of RV Monitoring on Outcome
One of the most urgent questions is whether RV volumetric monitoring may help
to improve ‘outcome’. It is dubious whether a specific monitoring system is
actually able to improve ‘outcome’ (i.e., to reduce lethality). However, it is certain
that monitoring of RV volumes by a PAC yields additional beneficial information.
In a small sample of surgical patients with sepsis, ARDS, and hemorrhagic shock
(n=13), the additional information derived from RVEDV index (RVEDVI) did not
change treatment in 43 of 46 instances [38]. However, patients with increased
intra-abdominal pressures may show misleadingly high PAOP despite low preload. These patients clearly benefited from the additional information derived
from ventricular volume measurements. Additionally, clinicians who are reluctant to take off-PEEP PAOP may also find this catheter useful [38]. Others demonstrated that monitoring RVEF by using RV volumetric catheters is a predictor of
survival in trauma patients [39] and in patients with congestive heart failure
associated with coronary artery disease [40]. Thus monitoring of RV data may
contribute to the evaluation of the patient’s prognosis [2]. However, no large
clinical trials are available showing a beneficial impact of RV volume monitoring
on patient outcome. By using this sophisticated monitoring device, additional
data are available that may be associated with the danger that the untrained and
uncritical physician is confused and misled by such a mass of information.
Conclusion
RV dysfunction is recognized as an important factor in modulating hemodynamics in critical illness. Various factors can contribute to an abnormal RV
performance including perioperative RV infarction, insufficient revascularization
of the right coronary artery, RV overdistension, inadequate (hypothermic) protection of the right ventricle, or pulmonary injury (=increasing RV afterload).
With the help of conventional pressure monitoring, accurate assessment of RV
performance is not possible: The assessment of ventricular function is based upon
the measurement of both volumes and pressures. Commonly monitored parameters such as CVP, right atrial pressure, or RV pressure have been demonstrated to
be invalid for judging RV loading conditions. Further development of computer
techniques allows intermittent or (near) continuous monitoring of RV hemodynamics.
Measurement of RVEDV using the fast-response thermodilution technique
provides a more accurate estimation of (true) fiber preload. The results on the value
of monitoring RVEDV are, however, far from being uniform. The discrepancy in
the benefits of RVEDV monitoring as a surrogate of cardiac preload is most likely
due to the diverse patient populations studied [25]. It is important to stress that it
is not the absolute values of RVEDV (RVESV or RVEF) that are of interest, but the
intraindividual changes (e.g., after volume therapy, inotropes, or vasodilators).
Whether enlarging our monitoring armamentarium by using thermodilution
RV volume measurements may help to improve patient outcome remains to be
elucidated. There is no doubt that the use of monitoring devices may yield addi-
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tional information, and there is no doubt that some information may be useful. But
there can also be no doubt that the malfunctioning monitor device and the inadequately-trained, misinterpreting physician may be a great risk for the patient – “A
fool with a tool is still a fool”.
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Assessment of Fluid Responsiveness