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J Thorac Cardiovasc Surg 1998;116:468-472
© 1998 Mosby, Inc.
Surgery for Adult Cardiovascular Disease |
Supported in part by the Garfield Weston Trust (C.I.O.B.) and by theScott Rhodes Research Fund, the Clinical Research Committee of the RoyalBrompton, and the Garfield Weston Trust.
Received for publication Jan 7, 1998. Revisions requested March 16, 1998; revisions received April 17, 1998. Accepted for publication May 13, 1998. Address for reprints: Andrew N. Redington, MD, Department of PediatricCardiology, Royal Brompton National Heart/Lung Institute, Sydney St, Chelsea,London SW3 6NP, United Kingdom.
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Abstract |
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsDiscussionConclusionReferences |
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1,2Maintaining optimal function in the perioperative period requires carefulmyocardial protection during cardiopulmonary bypass (CPB), but there is evidencethat standard cardioplegic techniques do not adequately protect the RV function,particularly in the context of RV hypertrophy and coronary artery disease. 3-6 Assessment of RV performance at this time is difficult because there isno generally accepted method of measuring RV volume and because routinelymeasured indices of function (eg, ejection fraction and maximum rate of rise ofventricular pressure) are all critically load dependent. The conductancetechnique has been used to overcome the same problems when left ventricular (LV)performance is being assessed; but to date, there are no data concerning its usein the RV of patients undergoing cardiac operation.
Although experimental and human RV data have been obtained under othercircumstances, the intraoperative use of conductance catheters in the RV remainssubject to a number of theoretic limitations. First, measurement of 
,defined as the ratio of conductance-derived volumes to true ventricular volumes,requires comparison against a gold standard, which is not readily available forthe RV. Consequently, most studies have compared conductance stroke volumes withthose derived from thermodilution or pulmonary artery flow probes andextrapolated absolute volumes from these values. 7-9Furthermore, is dependent on the internal geometry of the RV cavity andon the position of the catheter in the ventricle, both of which can changeduring the course of an operation. Second, the parallel conductance is alsomarkedly dependent on the experimental setting in which it is measured and ithas been suggested that the thin RV myocardium may allow greater current leakagefrom the cavity. This would result in a larger parallel conductance (Vc) andpotentially introduces greater errors into absolute volume estimations. 10 Finally, conductance theorydictates that accurate volume measurements can only be obtained if the catheterlies along the central axis of an interrogated chamber. The RV cavity, however,has 2 separate axes (one from the tricuspid valve to RV apex and one from RVapex to outflow tract), and it may therefore not be possible for a singleconductance catheter to interrogate both axes simultaneously.
We conducted 3 validating studies to examine the clinical utility of thisnovel approach to the intraoperative assessment of RV performance: study 1, todetermine the influence of catheter position within the RV cavity, on alpha (),Vc, and the calculated RV volume; study 2, to assess the reproducibility ofthese data in the clinical setting; and study 3, to apply the findings to theexamination of RV contractile function immediately after CPB in patientsundergoing coronary artery operation.
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsDiscussionConclusionReferences |
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Study 1: Influence of catheter position
Ten patients were studied. After sternotomy and before CPB, a 6F pigtailconductance catheter (Cordis Webster, Inc, Baldwin Park, Calif) and a 2.5Fmicromanometer (Millar Instruments, Inc, Houston, Tex) were inserted into the RVapex via 2 different routes—either through the right atrium (RA) via theright atrial appendage and tricuspid valve or through a small incision in the RVoutflow tract (RVOT) as close to the pulmonary valve as possible. The RA routewas studied first in all cases. We used conductance catheters with a totalinterelectrode distance of 6 to 8 cm, depending on RV size. Correct positioningof the pigtail catheter in the ventricular apex was determined by palpation andconfirmed by demonstration of pressure and segmental volume signals withappropriate phase relationships.
Cardiac output and stroke volume were estimated by thermodilution. A 7Fflotation thermodilution catheter (Arrow International, Inc, Reading, Pa) wasused, and cardiac output was assessed conventionally with an injection of 10 mLof cold saline solution into the right atrial port. Measurements were repeateduntil 3 readings were within 10% of one another. The stroke volumeobtained by this method was used to determine (= conductance strokevolume/thermodilution stroke volume). Vc was estimated by a modification of thehypertonic saline solution injection method developed by Baan and colleagues. 11 A slow bolus of 7 mL of 10%saline solution was injected into the superior vena cava (SVC) causing atransient change in conductivity of the blood within the RV cavity without anydetectable change in RV pressure.
Study 2: Reproducibility of RVOT measurements
The effect of small changes of catheter position within the RV on thepressure-volume data was assessed by removal and replacement of the catheterthrough the RVOT in 7 additional patients. The RA route was not studied. Theprotocol was identical to that described in study 1. Baseline values of ,Vc, end-diastolic volume (EDV), and contractile function were compared withthose obtained after the catheter had been removed and replaced through the sameincision. Repeat measurements were obtained immediately and were not associatedwith any significant change in the hemodynamic variables. Load-independentindices of ventricular performance, such as the slope of the end-systolicpressure-volume relations (ESPVR) and preload recruitable stroke work (PRSW)were determined by gradual preload reduction with a snare placed around the SVC.All measurements were obtained in duplicate, and the mean of the two values wereused for comparison.
Study 3: The effect of CPB on RV performance
In an additional 8 patients, RV function was compared before and afterCPB, with the pericardium opened. The protocol before CPB was identical to thatdescribed in study 2, except that an integrated custom-made conductance catheterand micromanometer (Millar Instruments) was used. After baseline data had beencollected in duplicate, the conductance catheter was removed and the patient wasput onto CPB. Myocardial protection was achieved with ventricular fibrillationwith intermittent aortic crossclamping. After revascularization, the conductancecatheter was reinserted through the same incision in the RVOT, and the patientwas weaned from CPB. Pressure-volume data were recorded in duplicateimmediately, then again approximately 15 minutes later, after protamine had beengiven. Thermodilution cardiac outputs and Vc estimations were also repeatedafter protamine.
The conductance catheter was removed before CPB in studies 1 and 2 andafter the last set of data collection in study 3. Hemostasis was secured with apurse-string suture, and routine postoperative care was provided.
Data acquisition and analysis
The amplified pressure signal (Fylde Isotransducer Amplifier, Preston,United Kingdom) was fed directly to a committed personal computer (Viglen Ltd,Alperton, United Kingdom) where it was combined with volume andelectrocardiographic data in custom software.
The total conductance signal was generated and processed in a Sigma-5 DFunit (Cardiodynamics, Zoetermeer, The Netherlands). The principles ofconductance catheter technology are described in detail elsewhere. 11 In brief, the conductance catheteris a modified angiography catheter with a series of equally spaced electrodes atthe distal end, designed so that the proximal and distal electrodes span as muchof the ventricular cavity as possible. A 30-µA 20-kHz current is generatedbetween the proximal and distal electrodes, and the intervening electrodesmeasure conductances between electrode pairs located in the RV. The conductancesare summed and converted to a time-varying volume signal.
The volume (V) of the ventricle at a given time (t) is:
{eq}V(t) =(1/)L2µ[G(t) – Gc],
where L is theinterelectrode distance, µ is the blood resistivity that is measured, andG(t) is the sum of conductances at any time.
Care was taken to ensure that segmental conductance changes were in phaseto exclude the possibility of atrial sampling when the transtricuspid route wasused.
The pressure and volume data were sampled at 250 Hz and transferredthrough a 12-bit, 16-channel, A to D converter into custom software andcalculations of , Vc, corrected EDV, and contractile function were madeoff-line.
All measurements were made in duplicate with ventilation held atend-expiration and then averaged. In addition, in study 1 the absolutedifference between duplicate measurements from each route was compared. Thus,conductance stroke volumes were determined from 2 recordings at steady state. Ineach recording, the maximum and minimum volume for 5 consecutive cardiac cycleswas identified, and the stroke volume for that run was defined as the meandifference between maximum and minimum volumes. This was then repeated for thesecond recording, and the mean of the 2 stroke volumes was divided by thethermodilution stroke volume to yield .
Similarly, two injections of hypertonic saline solution were used tocalculate Vc. End-systolic and end-diastolic volumes (ESV and EDV) fromindividual cardiac cycles during the saline solution injection were plotted, andthe lines were regressed to the point where ESV = EDV; this volume wastaken as Vc. The correlation coefficient for the regression line was recorded asan index of precision; coefficients of less than 0.9 were not accepted.
Calculation of contractile function during SVC snaring was performed withat least 5 consecutive cardiac cycles. The ESPVR slope was determined by linearregression from the points of maximum pressure/volume in each cycle during thesnare. The PRSW slope was calculated from the plot of stroke work against EDV(defined by the electrocardiogram R wave). The end-diastolic pressure-volumerelation (EDPVR) slope was determined by both linear and exponential regressionof the same pressure-volume data at end-diastole according to the equationsp = aV+c and p = Ae, where p = pressure(mm Hg), V = volume (mL), a = slope of linearp/v relation (mm Hg/mL), and B = myocardial stiffness constant. The datapresented are therefore for the constants a andB.
Statistics
Paired values of and Vc were compared with Wilcoxon's sign ranktest. Absolute differences between duplicate measurements and comparisons beforeand after CPB were made with the paired Student's ttest.
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Results |
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TopAbstractIntroductionPatients and methodsResultsDiscussionConclusionReferences |
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The regression coefficient for Vc estimations was more than 0.91 in 92%of measurements, and there was no significant difference between routes.
Duplicate data were available from the RVOT in all patients; but, becauseof poor data quality (r < 0.85), singlevalues only had to be accepted from the RA route in 2 patients.
Gain constant,
(Table I). Duplicate data were available from both routes in allpatients. The mean (± SD) for the RVOT was 0.52 ± 0.2and for the RA was 0.39 ± 0.17, P =.01.
The mean absolute difference between duplicate measurements for the RVOTwas 0.02 ± 0.02 and for the RA was 0.03 ± 0.02,P = .73
Absolute RVEDVs
The corrected EDV with the mean values of duplicate and Vc weresimilar for both routes: RA = 118.2 ± 50.1 mL; RVOT =112.5 ± 44.1 mL; P = .34.Meaningful volumes were not obtainable from 2 patients via the RA route becauseof difficulties with Vc estimation.
The SVC snare
The SVC was chosen as the site of the venous snare because it is moreaccessible than the IVC and more easily repairable in the event of a tear duringmobilization. There were no such complications during these studies, and theapplication of the snare produced a significant, but variable, preloadreduction. The mean stroke work reduction was 44% (range, 5.6% to91.1%), but the change in EDV was much smaller, approximately 5%.
Technical considerations
Correct positioning of the conductance catheter is technically mucheasier through the RVOT than through the RA, mainly because the RV free wall iseasily accessible. We also found that the data obtained via the RVOT were bothof superior quality and more reproducible than those from the RA route (TableI). There were no complications associated with this study. Blood loss wasreduced by the use of purse-string sutures at both sites of insertion and wasnegligible, particularly during insertion through the RVOT.
The shape of the pressure-volume relations from both routes was similarwithin individual patients. Most patients had poorly defined periods of eitherisovolumic contraction or relaxation resulting in the characteristic "triangular"or "trapezoid" pressure-volume loops (Fig. 1). Only 1 patient had "square"loops, and this finding could not be explained by the presence of eitherpulmonary hypertension or acute ischemia.
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Study 3: The effect of CPB on RV performance
After CPB there was a significant change in both systolic and diastolicindices of RV performance with an increase in both EDV and ESV, a fall in thestroke volume, a fall in the slope of the PRSW, and an increase in the slope ofthe linear EDPVR. There was a tendency for the ESPVR slope to fall and theexponential EDPVR slope to increase, but these changes did not reachsignificance.
The mean (± SD) RVEDV increased from 118.4 ± 33.2 mLto 153.9 ± 36.4 mL, P = .03;and the ESV increased from 61.6 ± 28.7 mL to 102.9 ±38.1 mL, P = .025. The slope of the PRSWfell from 15.6 ± 3.8 mm Hg to 11.0 ± 5.1 mm Hg,P = .01; the linear EDPVR slope increasedfrom 0.05 ± 0.02 mm Hg/mL to 0.14 ± 0.06 mm Hg/mL,P = .001; and the exponential EDPVR slopeincreased from 0.019 ± 0.027 to 0.065 ± 0.099,P = .16. The slope of the ESPVR fell from0.5 ± 0.09 mm Hg/mL to 0.38 ± 0.16 mm Hg/mL,P = .29 (Table III; Figs. 1
and 2).
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Discussion |
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TopAbstractIntroductionPatients and methodsResultsDiscussionConclusionReferences |
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9,14 and animals, 10,15,16 and it is clear from our data thatplots of the relative changes in RV pressure and volume can be obtained in humanbeings in the intraoperative setting. The potential power of this technique,however, is in the estimation of absolute ventricular volume, which is essentialfor the determination of load-independent indices of ventricular function.Clearly further validation was required before its clinical application could berecommended. The aim of this paper was to provide some of these validation dataand to examine the utility of the conductance technique in the period before anoperation.
Study 1: The influence of catheter position.
Because of technical limitations, measurement of absolute RV volumes fromconductance catheters requires calibration. In the absence of an obviouscalibrating technique, most studies, including ours, have compared conductancemeasurements with those obtained by either thermodilution or ultrasonicpulmonary artery flow probes 7-9 and have either then extrapolatedEDV from these measurements or not attempted to estimate absolute volumes atall. Although this extrapolation may not be entirely valid, as has beendemonstrated to show a degree of volume dependence in both the LV and RV, ourstudy was concerned with comparisons of at steady state derived from 2different routes of catheter insertion. We believe, therefore, that thesemeasurements are valid because any absolute volume error should apply to bothroutes studied.
Our values for , 0.5 ± 0.2 from the RVOT and 0.39 ±0.17 from the RA, in study 1 are similar to those we have described previously 19 and are comparable to thosereported by Woodard, 16Stamato, 8 Maloney 9 and their colleagues in the RV ofgreyhounds, small pigs, and human beings, respectively. These values, asexpected, are somewhat lower than those seen in the LV. We have demonstratedthat is significantly higher when the catheter is inserted into the RVapex from the RVOT, suggesting that more of the ventricular cavity isinterrogated via this route. These findings are in agreement with the only otherstudy to examine the effect of catheter position on conductance-derived volumechanges in the RV. 16
Vc in the RV has been reported to be 32.3 ± 6.3 mL in 16-kgpigs 8 and 79.1 ±18.6 mL in 40-kg pigs. 10 Inpatients with congenital heart disease, we have previously found a Vc of 89.7 ±43.7 mL and have shown that Vc is not significantly different at end-systole andend-diastole. 20 The resultsreported here, in open-chest ischemic patients, are similar in magnitude tothose described earlier but, more interestingly, demonstrate that catheterposition within the ventricle significantly affects the size of the parallelconductance. Of more importance than the absolute values of Vc, however, is thefinding that the reproducibility of Vc estimation is also superior from theRVOT: a 10.1 ± 5.1 mL versus 33.5 ± 9.8 mL differencebetween duplicate Vc estimations will clearly have implications for thedetection of small changes in contractile performance. The reason for the largervariability from the RA is probably not related to the larger absolute Vcbecause there was no correlation between difference in duplicate measurementsand absolute Vc (r = -0.05,P = .449) but is more likely explained bythe poorer quality of volume data resulting in a decreased signal to noiseratio.
Study 2: variability of contractility indices
Although we were able to derive a figure for the EDV using both and Vc, we have no way of estimating its accuracy. Nevertheless, because thereis no other technique capable of providing beat-to-beat pressure-volume changes,the repeatability of EDV measurements becomes more important than a systematicerror in absolute EDV. Using the RVOT route we were able to demonstrate thatboth the ESPVR and PRSW were reproducible. The 12.7% ± 10.8%and 15.3% ± 13.2% difference between baseline and repeatslopes of the PRSW and ESPVR, respectively, are similar to those reportedpreviously. Karunanithi and colleagues 21found a 7.8% ± 3.3% and 10.1% ± 6.7%difference between 3 repeated measures of PRSW and ESPVR using sonomicrometry indogs, but it is of note that in this study the ultrasonic crystals were notmoved between estimations. In 2 patients, however, there was a marked reductionin the EDV when the conductance catheter was replaced, which could be due toblood loss sustained during this maneuver but is more likely explained by achange in catheter position within the cavity. Interestingly, this volume changewas not associated with a marked shift in either the ESPVR or the PRSW; but,with such a small sample, it is not possible to draw any definite conclusionsfrom this observation. Almost all studies that have examined contractilityindices in either ventricle have used an inferior vena cava balloon to reducepreload. 8,10,18,22 Although this technique iseminently suited to catheter laboratory studies, the sterile field in anoperating theater creates problems for balloon manipulation, so we decided toinvestigate the possibility of using a snare placed around the SVC. Althoughcareful mobilization of the vein is required, the procedure takes less than 2minutes and allows both a gradual and a reproducible reduction in preload.Provided the snare is kept away from the RA-SVC junction, atrial ectopy can bekept to a minimum. With this method, the stroke work done by the RV can bereduced by a mean of 44% although a much smaller change in EDV, of theorder of 5%, is observed. This relatively small change in EDV haspreviously been described and is probably due to changes in in responseto acute preload reduction. 8,17,18,23 Because we were not using apulmonary artery flow probe in this study, we were not able to confirm thesefindings. Acute preload reduction also results in changes to Vc in the LV, 17 and it is possible that similarchanges occurring in the RV are contributing to this phenomenon.
Study 3: Changes in RV function after CPB
There are many reports of apparent RV dysfunction after CPB, 5,6,24,25and it is thought that imperfect RV myocardial protection is at least partlyresponsible for these observations. These studies, however, have used acombination of thermodilution techniques and/or radionuclide angiography toderive indices of RV function that are dependent on preload, afterload, andcontractile state, all of which can change significantly after CPB. It istherefore not appropriate to assume that changes in these ejection indicesaccurately reflect changes in the contractility of the RV myocardium. To date,there have been no studies that have directly examined RV contractile functionafter cardiac operation.
Detailed pressure-volume analysis, whether from sonomicrometry orconductance catheterization, allows derivation of "load-independent"indices of function, such as the ESPVR, PRSW, and maximum rate of rise ofventricular pressure–end diastolic volume relationship. 26,27Since they were proposed, however, a number of studies have questioned both thelinearity and the afterload sensitivity of these parameters. 28,29In the LV, Little and colleagues 28concluded that if linearity, reproducibility, and load sensitivity were allconsidered then the PRSW relation was the most reliable index of LVcontractility. Karunanithi and colleagues 21found similar results in the RV of conscious dogs. We have demonstrated, for thefirst time, a significant decline in systolic RV function, characterized by afall in the slope of the PRSW in the period immediately after CPB. Thisdysfunction was present for the duration of the study and was not affected byprotamine administration. Of note is that the magnitude of the fall in PRSW andthe standard deviation of our measurements are comparable with those reportedwith esmolol administration in experimental animals. 10 There was a similar decline in theslope of the ESPVR, but this did not reach statistical significance, probablybecause of the greater variability in the measurement of this index and it isconsistent with the findings reported earlier. 21
There was a concomitant increase in the slope of the linear EDPVR, andwhen these relations were derived with the exponential model there was a similartrend, albeit statistically insignificant, for end-diastolic stiffness toincrease. The ideal method for analysis of EDPVR is a subject of debate, 30 particularly with the pericardiumopen; but we believe there is a significant myocardial contribution to theobserved changes, at least in most patients (Fig. 1).
The cellular mechanism of this global dysfunction is unknown; butphysical trauma, perioperative temperature, ischemia-reperfusion, and theindirect effects of CPB (eg, the initiation of a systemic inflammatory response)probably all contribute.
This study was not designed to assess the efficacy of the protectionmethod used but does suggest that the conductance technique, particularly withthe RVOT route of insertion, could be used to examine myocardial protectionstrategies and their effect on RV systolic and diastolic performance with thesensitivity obtainable in experimental animal preparations. 10
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Conclusion |
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TopAbstractIntroductionPatients and methodsResultsDiscussionConclusionReferences |
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TopAbstractIntroductionPatients and methodsResultsDiscussionConclusionReferences |
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