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 ven- tricles. 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 constrain-
ing 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
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)
loading (e.g., increased preload) and unloading (e.g., increased afterload) condi- tions 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 accu- rately possible. Hoffman et al. [4] demonstrated no significant correlation be- tween 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 monitor- ing 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 fast- response thermistors on conventional thermodilution pulmonary artery catheters (PACs) allows rapid detection of changes in pulmonary artery temperature.
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
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 electrocardiog- raphic (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 repre- sents the fraction of blood remaining in the right ventricle (=residual fraction
Fig. 4. Effects of changes in afterload (a) and preload (b) on right and left ventricular performance ba
[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 radionu- clear 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 vari- ation of near 7%) [13]. Moreover, measuring RVEDV by thermodilution is unaf- fected 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)
Fig. 5. Principle of measuring right ventricular volumes and ejection fraction
• 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 con- stant injection, technique (=homogeneity) of injection, temperature of the injec- tate 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 end- expiratory and end-inspiratory points on the ventilatory cycle are used for meas- urement of cardiac output. Others have suggested averaging three thermal injec- tions 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 mechani- cal 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 modula- tion 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-in- terval 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 deter-
mined using thermodilution with incremental increases in pulmonary valve to
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 signifi- cant differences in thermodilution RVEF measurements with the thermistor posi- tioned 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 tachy- cardia. 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 mathe- matical 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 cor- related well with both the thermodilution-derived cardiac output and the inde- pendently 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 monitor- ing, 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. More- over, 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 nega-
tive sequelae (Fig. 6). Introduction of RV volumetric measurement into a PAC has
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 venti- lation 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 predic- tor of preload than PAOP:
Fig. 6. Reasons for right ventricular (RV) decompensation and its consequences
• 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 interven- tions [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. Mainte- nance of intravascular preload and use of open abdomen techniques are essen- tial. 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 ven- tricular function [10, 32, 33]. In this situation, RVEDV and RVESV vary inde- pendently 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 propor- tional 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 end-
diastolic 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 tech-
niques. 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 pa-
tients, 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 inot-
ropes).
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: cardio- pulmonary 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
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 pre- load. These patients clearly benefited from the additional information derived from ventricular volume measurements. Additionally, clinicians who are reluc- tant to take off-PEEP PAOP may also find this catheter useful [38]. Others demon- strated 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 hemody- namics 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) pro- tection 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 parame- ters 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 hemody- namics.
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-
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 inade- quately-trained, misinterpreting physician may be a great risk for the patient – “A fool with a tool is still a fool”.
References
1. Sibbald WS, Drieger AA (1983) Right ventricular function in acute disease states: Pathophysi- ologic consideration. Crit Care Med 11:339–345
2. Zwissler B, Briegel J (1998) Right ventricular catheter. Curr Opin Crit Care 4:177–183 3. Reuse C, Vincent JL, Pinsky MR (1990) Measurements of right ventricular volumes during
fluid challenge. Chest 98:1450–1454
4. Hoffman MJ, Greenfield LL, Sugerman HJ (1983) Unsuspected rightventricular ventricular dysfunction in shock and sepsis. Nucl Med 198:307–312
5. Durham R, Neunaber K, Vogler G, Shapiro M, Mazuski J (1995) Right ventricular end-dia- stolic volume as a measure of preload. J Trauma 39:218–23
6. Hurford WE, Zapol WM (1988) The right ventricle and critical illness: a review of anatomy, physiology, and clinical evaluation of its function. Intensive Care Med 14 (Suppl 2):448–457 7. Bing R, Heimbecker R, Falholt W (1951) An estimation of residual volume blood in the right
ventricle of normal and diseased human hearts in vivo. Am Heart J 42:483–502
8. Urban P, Scheidegger D, Gabathuler J, Rutishauser W (1987) Thermodilution determination of right ventricular volume and ejection fraction: a comparison with biplane angiography.
Crit Care Med 15:652–655
9. Matuschak GF, Potter AM, Schauble JF, Rogers MC (1982) Overestimation of pediatric cardiac output by thermal indicator loss. Circulation 65:380–383
10. Dhainaut JF, Pinsky MR, Nouria S, Slomka F, Brunet F (1997) Right ventricular function in human sepsis: a thermodilution study. Chest 112:1043–1949
11. Jardin F, Gueret P, Dubourg O, Farcot JC, Margairaz A, Bourdarias JP (1985) Right ventricular volumes by thermodilution in the addult respiratory distress syndrome. Chest 88:34–39 12. Kay HK, Afshari M, Barash P (1983) Measurement of ejection fraction by thermodilution
techniques. J Surg Res 34:337–346
13. Le Tulzo Y, Seguin P, Gacouin A, et al (1997) Effects of epinephrine on right ventricular function in patients with severe septic shock and right ventricular failure: a preliminary descriptive study. Intensive Care Med 23:664–670
14. Hines R, Rafferty T (1993) Right ventricular ejection fraction catheter: toy or tool? Pro: a useful monitor. J Cardiothorac Vasc Anesth 7:236–240
15. Schauble JF(1993) Right ventricular ejection fraction catheter: toy or tool? Con: a premature step. J Cardiothorac Vasc Anesth 7:241–242
16. Segal J, Pearl RG, Ford AJ, Stern RA, Gehlbach SM (1989) Instantaneous and continuous cardiac output obtained with a doppler pulmonary artery catheter. J Am Coll Cardiol 13:1382–1392
17. Daper A, Parquier JN, Preiser JC (1986) Timing of cardiac output measurements during mechanical ventilation. Acute Care 12:113–116
18. Snyder JV, Powner DJ (1982) Effects of mechanical ventilation on the measurement of cardiac output by thermodilution. Crit Care Med 10:677–682
19. Jansen JR, Schreuder JJ, Settels JJ, Kloek J, Vesprille A (1990) An adequate strategy for the thermodilution technique in patients during mechanical ventilation. Intensive Care Med 16:422–425
20. Groeneveld AB, Berendsen RR, Schneider AJ, Pneumatikos IA, Stokkel LA, Thijs LG (2000) Effect of the mechanical ventilatory cycle on thermodilution right ventricular volumes and cardiac output. J Appl Physiol 89:89–96
21. Maruschak GF, Schauble JF (1986) Limitation of thermodilution ejection fraction: Degration of frequency response by catheter mounting of fast response thermistor. Crit Care Med 13:679–682
22. Nelson LD (1997) The new pulmonary artery catheters: continuous oximetry, right ventricu- lar ejection fraction, and continuous cardiac output. New Horiz 5:251–258
23. Spinale FG, Zellner JL, Mukherjee R, Crawford FA (1991) Placement considerations for measuring thermodilution right ventricular ejection fractions. Crit Care Med 19:417–421 24. Chang MC, Black CS, Meredith JW (1996) Volumetric assessment of preload in trauma
patients: addressing the problem of mathematical coupling. Shock 6:326–329
25. Diebel LN, Myers T, Dulchavsky S (1997) Effects of increasing airway pressure and PEEP on the assessment of cardiac preload. J Trauma 42:585–90
26. Nelson LD, Safcsak K, Cheatham ML, Block EF (2001) Mathematical coupling does not explain the relationship between right ventricular end-diastolic volume and cardiac output. Crit Care Med 29:940–943
27. Conrad SA (2001) Right ventricular volumetric measurements: New tricks for an old dog. Crit Care Med 29:1081–1082
28. Diebel L, Wilson RF, Heins J, Larky H, Warsow K, Wilson S (1994) End-diastolic volume versus pulmonary artery wedge pressure in evaluating cardiac preload in trauma patients. J Trauma 37:950–955
29. Diebel LN, Wilson RF, Tagett MG, Kline RA (1992) End-diastolic volume. A better indicator of preload in the critically ill. Arch Surg 127:817–821
30. Dennis JW, Menawat SS, Sobowale OO, Adams C, Crump JM (1992) Superiority of end-dia- stolic volume and ejection fraction measurements over wedge pressures in evaluating cardiac function during aortic reconstruction. J Vasc Surg 16:372–377
31. Cheatham ML, Safcsak K, Block EF, Nelson LD (1999) Preload assessment in patients with an open abdomen. J Trauma 46:16–22
32. Mitsuo T, Shimazaki S, Matsuda H (1992) Right ventricular dysfunction in septic patients.
Crit Care Med 20:630–634
33. Parker MM, McCarthy KE, Ognibene FP, Parrillo JE (1990) Right ventricular dysfunction and dilatation, similar to left ventricular changes, characterize the cardiac depression of septic shock in humans. Chest 97:126–31
34. Boldt J, Kling D, Hempelmann G (1988) Right ventricular function and cardiac surgery.
Intensive Care Med 14 (Suppl 2):496–498
35. Boldt J, Kling D, Dapper F, Hempelmann G (1990) Myocardial temperature during cardiac operations: influence on right ventricular function. J Thorac Cardiovasc Surg 100:562–568 36. Boldt J, Zickmann B, Thiel A, Dapper F, Hempelmann G (1992) Age and right ventricular
function during cardiac surgery. J Cardiothorac Vasc Anesth 6:29–32
37. Boldt J, Zickmann B, Herold C, Dapper F, Hempelmann G (1992) Right ventricular function in patients with reduced left ventricular function undergoing myocardial revascularization.
J Cardiothorac Vasc Anesth 6:24–28
38. Yu M, Takiguchi S, Takanishi D, Myers S, McNamara JJ (1995) Evaluation of the clinical usefulness of thermodilution volumetric catheters. Crit Care Med 23:681–686
39. Eddy AC, Rice CL, Anardi DM (1988) Right ventricular dysfunction in multiple trauma victims. Am J Surg 155:712–715
40. Polak JF, Holman BL, Wynne J, Colucci WS (1983) Right ventricular ejection fraction: an indicator of increased mortality in patients with congestive heart failure associated with coronary artery disease. J Am Coll Cardiol 2:217–24
